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Reducing the Health Consequences of Smoking ! 25 YEARS OF PROGRESS a report of the Surgeon General 1989 1; DcvARTti+rNT OF +EA''~ AND NU:"AN SERVICES tinn'~h Snrv~cr ~~........... ~ .

PROP''"TY OF Wamb iC , C.., ' " ^:co 66L9 Z85t5 Reducing the ' Health Consequences of Smoking , 25 YEARS OF PROG1ESS a report of the ' Surgeon General ' 1989 ; . • U.S DEPARTMENT OF HEAITH AND HUMAN SERVICES PubNc H.Nth Swdn = ~ ~ Ornt.rs for Disw.. Conhd R : C.nt.r for ChnonOc da.... Pr.wrdlon and H..Mh Promotion ° l OMbx, on Srzwldnp and HaM "/MI , .. MwryIN1d 20a57 ppe;_ t

CHAPTER 1 HISTORICAL PERSPECTIVE, OVERVIEW, AND CONCLUSIONS ' ' Ei89 18SI5

FOREWORD Z089 i85TS Twenty-five years have elapsed since publication of the landmat!k report of the Sur- geon General's Advisory Committee on Smoking and Health. By any measure. these 25 years have witnessed dramatic changes in attitudes toward and uie-of tobacco in the United States. The health consequences of tobacco use will be with us for many years to come, but those consequences have been greatly reduced by the social revolution that has occurred during this period with regard to smoking. ( Since 1964, substantial changes have occurred in scientific knowledge of the health hazards of smoking, in the impact of smoking on mortality, in pubiic knowledge of the dangers of smoking, in the prevalence of smoking and using other "forms of tobacco, in the availability of programs to help smokers quit, and in the number of policies that en- courage nonsmoking behavior and protect nonsmokers from expqsure to environmen- tal tobacco smoke. These changes and other significant developments. as well ac the overall impact of the Nation's antismoking activities, are reviewed in;detail in the in- dividual chapters of this Report. Based on this review, five majcx`conclusions of the entire Report were reached. The first two conclusions highlight,important gains in preventing smoking and smoking-related disease in the United States. The last three conclusions emphasize sources of continuing concern and rcmaining challenges. The conclusions are: 1. The prevalence of smoking among adults decreased from 40 percent In 1965 to 29 percent In 1987. Nearly half of all living adults who ever smoked have quit. 2. Between 1964 and 119115, approximately three-quarters of a million smok- inR-reiated deaths were avoided or postponed as a resuit of decisions to quit smoking or not to start. F.ach of these avoided or postponed deaths repre- sented an averaRe Eain in life expectancy of two decades. 3. The prevalence of smoking remains higher among blacks, blue-collar workers, and less educated persons than in the overall population. The decline in smoking has been substantially slower among women than among men. 4. Smoking begins primarily during childhood and adokscence. The age of initiation has fallen over time, particularly among females. Smoking among high school seniors kveled off from 1980 through 1997 aafter pre- vious years of decline. 5. Smoking is responsible for more than one of every six deaths in the United States. Smoking remains the single most important preventable cause of death in our society.

ZZ89 18SZ5 TABLE OF CONTENTS Foreword ............................................................i Preface ...................................................:.........iii Acknowledgments ....................................................ix 1. Historical Perspective, Overview, and Conclusions ............. : ........ 1 2. Advances in Knowledge of the Health Consequences of Smoking..'. ....... 33 3. Changes in Smoking-Attributable Mortality ........................... 117 4. Trends in Public Beliefs, Attitudes, and Opinions About Smoking ........ 171 5. Changes in Smoking Behavior and Knowledge About Detertmnants, ...... 259 6. Smoking Prevention. Cessation, and Advocacy Activities ................ ~377 7. Smoking Control Policies ............................... . . r . . . . . . . 461 8. Changes in the Smoking-and-Health Environment: Behavioral and ; Health Consequences .................................. ....... ' 637 Glossary .................................................. ........ 677

the ks+ons we have karned in the United Staea, as detailed in this Report, will help other countries take the necessary steps to avoid the devastation caused by use of tobacco. C. Everett Koop, M.D., Sc.D. Surgeon General 9089 I85tS ACKNOWLEDGMENTS 'ihis Report was prepared by the Department of Health and Human Services under the general editorship of the Office on Smoking and Health, Ronald M. Davis, M.D.. Director. The Managing Editors were Susan Hawk, Ed.M.. M.S., and Thomas E. Novotny. M.D., Office on Smoking and Health. !, The scientific editors of the Report were: I Kenneth E. Warner, Ph.D. (Senior Scientific Editor), Professor, Depattlment of Public Health Policy and Administration. School of Public Health, Universlity of Michigan, Ann Arbor. Michigan Ronald M. Davis. M.D., Director. Office on Smoking and Health. Cenjer for Chronic Disease Prevention and Health Prontotion, Centers for Disease Control, Rockville, Maryland John H. Holbrook, M.D., Professor of Internal Medicine, Department of Internal Medicine, University Hospital, Sah [ske City, Utah Tfwmas E. Novotny, M.D., Medical Epidemiobgist. Office on Smoking and Health, Center for Chronic Disease Prevention and Health Promotion. Centers for Disease Control. Rockvilk, Maryland I Judith K. Ockene. Ph.D., Associate Professor of Medicine, and Director. Division of Preventive and Behavioral Medicine, Department of Medicine. University of Mas- sachusetts Medical School, Worcester, Massachusetts Nancy A. Rigotti, M.D., Associate Director, Institute for the Study of Smoking Be- havior and Policy, John F. Kennedy School of Government. Harvard Universiry, Cambridge, Massachusetts, Instructor in Medicine, Harvard Medical School, Bos- ton, Massachusetts The jorlowing individuals prtpared dmJr ehopttrs or portions of the Rrport. Elvin E. Adams, M.D., M.P.H., Associate Dinector. Health Department, General Con- ference of Seventh-Day Adventists, Washington. D.C. Gregory N. Connolly, D.M.D., M.P.H.. Director. Office for Nonsmoking and Health. Massachusetts Depattment of Public Health, Boston. Massachusetts K. Michael Cummin&t, Ph.D., M.P.H., Ditector, Smoking Control Program, Roswell Park Memorial Institute, Buffalo, New York I viii

. ~ The Ilenorable Coerge Sesh President of the Senate Washinston, D.C. 20515 1r.. ?Q s" ( I tNt SeC.r rAa V p1 N(Al7N AIIp NUM/1N Sc e V/CC S rAY~hO~Ow.OC Mn~ ~ It is 4 pleanre to transnlt to the Conares the ~1969 .SurReon Gneral•e Repert en the health een.puenees of nakfnR, sa :andated by Section 6(a) of the Public Realtlt Cigarette S.okina AcF of 1969. iThe report was prepared by the Centers for Disease Control's Office on Smoking and Realth. Daar Mr. Treeidents r This reprt, entitled R tn *a e. 1 b Con eawencaa of emiDR; 2S 7aars sf praarau, examines the funda.eetal de.elop.ents e.er the peat quarter century in Smoking pre.alenee and in mortality cau.ed by s.okinR. It highlights important Sains in preventing ewokNnb and saakfna-related disease, reviena changes in programs and policies designed to reduee a.oking, and mph.sises aourcee of continuing concern and ressaining challenges. During the past 25 year., Smoking behavior haa changed dramatically. ltearly half of all living adults vho e.er seaked have quit. The prevalence of Smoking has declined steedily, with a particularly l.pressi.e decline among men. Smoking prevalence a.onR .en decreased from 50 percent in 196S to 32 percent in 1997. As a result, long eaaeer mortality rates among .en are now leveling off after many decades of consistent inerease. Despite this proaress, the prevalence of Smoking reusins higher awonR blacks, blue-collar vorkers, and lese-edacated persons, than in the overall population. Smoking among high school seeiora leveled off from 1961 through 1967 after previous years,of decline. In 19139 the last year for which eatimates are available, approximately 190,000 A.erieans died as the result of past and current e.okinR. This represents more than one of every six deatha in the United States. Smoking re.ains tha single .ost iportent preventable caeae of death in our socieq. To maintain our .esnta toward a wske-free soeiet>r, we .ast focus our efforts on preventing Smoking initfation and encouraging Smoking cessation a~on{ bl{h-risk populations. Inereaaed public fnfor.atfon activities, Smoking prevention and cessation proaraws, and policies that encourage nonsmoking behavior should be pursued. Unless we meet thtn challende successfully, sookins-related mortality vill remain high well into the 21st Century. Sincerely, 0-**7'-- -„~. ,,,., Q e- Otia R. seven, M.D. Secretary 1089 Z 8 5 i S snclosere

I I CONTENTS bt89 tBStS I HistoricalPerspective ................................................ 5 Highlights of Conclusions and Findings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Major Conclusions ................................................ 11 Key New Findings ................................................. 11 Overview ..............................................• • ......13 `r Coverage of the Report .................................... .......13 1990 Health Objectives for the Nation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Limitations of Coverage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 Development of the Report .......................................... 19 Chapter Conclusions ........................................ .......20 Chapter 2: Advances in Knowledge of the Health Consequences of Sr{ioking . 20 Part 1. Health Consequences . . . . . . . . . . . . . . . . . . . . . . . . . .~.I . . . . . . 20 Part 11. The Physicochemical Nature of Tobacc.~o . . . . . . . . .•'r. . . . . . . 21 Chapter 3: Changes in Smoking-Attributable Mortality . . . . . . . . . . . . . . . . . 21 Chapter 4: Trends in Public Beliefs. Attitudes. and Opinions About Sinnoking . 22 Chapter 5: Changes in Smoking Behavior and Knowledge About ! Determinants .......................................... ....23 Part 1. Changes in Smoking Behavior . . . . . . . . . . . . . . . . . . . .:. . : . . . . 23 Part H. Changes in Knowledge About the Determinants of Smoking Behavior ..........................................24 Chapter 6: Smoking Preventlott, Cessation, and Advocacy Activities ........ 25 Part 1. Smoking Prevention Activities . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 Part It. Smoking Education and Cessation Activities . . . . . . . . . . . . . . . 25 Part Ili. Anti.cmoking Advocacy and Lobbying . . . . . . . . . . . . . . . . . . . . . 26 Chapter 7: Smoking Control Policies . . . . . . . . . . . . . . . . . . . . . . . . . : . . . . . . . . 26 Part I. Policies Pertaining to Information and Education . . . . . . . . . . . . . 26 Part II.EconomicIncentives ................................... 27 Part til. Direct Restrictions on Smoking . . . . . . . . . . . . . . . . : . . . . . . . . . 28 Chapter 8: Changes in the Smoking-and-Health Environment: Behavioral and Health Consequences ............................................. 28 References ......................................................... 30 I

1 5t89 t8SZ5 Historical Perspective Each of the last five Surgeons General of the U.S. Public Health Service (aHS) has Identified cigarette smoking as one of this Nation's tnost significant sourres of death and disease. Today, more than one of every six American deaths is the result of cigarette smoking. Smoking is responsible for an estimated 30 percent of all cancer deaths, in- cluding 87 percent of lung cancer, the leading cause of cancer mortality; 21 percent of deaths from coronary heart disease;18 percent of stroke deaths; and 82 percent of deaths fnxn chronic obstructive pulmonary disease. Other forms of tobacco u3e. including pipe and cigar smoking and use of smokeless tobacco, are also associated with sig- nificantly elevated risks of disease and death (US DHEW 1979a; US DHHS 1986b). Although the health hazards of tobacco use have been suspected for almost 400 years, the first reported clinical impressions of a relationship between tobacco and disease date from the 18th century, when tobacco use was associated with lip!cancer (US DHEW 1979a)and nasal cancer (US DHHS 1986b). However, true scidntifiic under- standing of the health effects of tobacco has been achieved only in the prrsent century. Broders (1920) published an article in the lownal of the Anterican Medical Associa- tion linking tobacco use to lip cancer, and 8 years later. Lombard and Doering (1928) published an article in the New England lournal of Medicine noting thaO heavy smok- ing was more common among cancer patients than among control groups. Later. Pearl (1938) observed in the journal Science that heavy smokers had a shorter li fe ~cpectan- cy than nonsmokers. During the 19,70s, the Nation'a Increasing rate of lung cancer and other diseases prompted the initiation of epidemiologic and laboratory studies of the relationship be- tween tobacco use and disease. In the late 1940s and early 1950s, a number of retrospec- tive epidemiologic studies, published by Wynder and Graham (1950) and by other in- vestigators, provided scientific evidence strongly linking smoking to lung cancer. This association was soon thereafter supported by the emerging early findings of major prospective (cohort) mortality studies, including the work of Doll and Hill (1954,1956) in Great Britain and Hammond and Horn (1958a, 1958b) in the United States. The stnength and consistency of these results, combined with evidence from laboratory and autopsy studies, led a national scientific study group to conclude in 1957 that the relationship between smoking and lung cancer was causal (Study Group on Smoking and Health 1957). On July 12 of that year, U.S. Surgeon General Leroy Burney issued a statement declaring that "The Public Health Service feels the weight of the evidence is increas- ingly pointing in one direction; that excessive smoking is one of the causative factors in lung cancer" (US PHS 1964). Two years later, in 1959, Surgeon General Burney said that "The weight of evidence at present implicates smoking as the principal factor in the increased incidence of lung cancer" (Burney 1959). Increases in chronic diseases in other parts of the world led health authorities in other countries to examine the relationship between tobacco and diaease, particularly in Europe and Scandinavia. ln 1957, the British Medical Research Council reported that a major part of the incnease in lung cancer was attributable to smoking (British Medi- cal Research Council 1957). Later, the Royal College of Physicians (1962) issued a S a

Joanna Ebling, Word Processing Specialist, The Circle. Inc., McLean. Virginia David Fry, Editor. The Circle. Inc., Mckan, Virginia Lynn Funkhausrr. Word Processing Specialist. The Circle. ine., McLean. Virginia Amy Garson, Student Intern, Office on Smoking and Health, Rockville. Maryland Gary A. Giovino, Ph.D.. Epidemiologist, Office on Smoking and Health, Rockville, Maryland Ametta G. Glover, Secretary, Office on Smoking and Health. Rockville, Maryland Victoria M. Grier. Conference Coordinator. The Circle. Inc., McLean, Virginia Andree C. Harric, Program Analyst. Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control. Atlanta, Georgia Evridiki Hatziandreu. M.D., Dr.P.H., Epidemic Intelligence Service Officer, Office on Smoking and Health, Rockvilk, Maryland Patricia E. Healy. Technical Information Spacialist, Office on Smoking and Health, Rockville, Maryland Timothy K. Hensley, Technical Publications Writer, Office on Smoking and Health, Rockville, Maryland Robert S. Hutchings, Associate Dineetor for Infonnation and Program Developnent, Office on Smoking and Health, Rockvilk, Maryland Karen Jacob. Senior Editor. The Circle. Inc., McLean, Virginia Beth Jacobsen. Student Intern, Office on Smoking and Health. Rockville, Maryland Sheila M. Jones. Word Processing Specialist. The Circle. Inc., McLean, Virginia Kathleen M. Keever, Secretary, Department of Public Health Policy and Administra- tion. School of Public Health. University of Michigan. Ann Arbor. Michigan Rick Keir. Senior Editor, Tfie Circle. lnc., McLean, Virginia Jennifer L. Kirxht, M.P.H., Statistics Consultant, Department of Public Health Policy and Administration, School of Public Health, University of Michigan, Ann Arbor, Michigan Laura Y. Martin, Program Andyst, Office of Program Planning and Evaluation, Centets for Disea.ce Control. Atlanta, Georgia Daniel F. McLaughlin, Editor, The Circle. Ine., McLeen, Virginia Sherry L M ills, M.D., M.P.H., Epidemic Intelligence Service Of'f+cer, Office on Smok- ing and Health, Rockville, Maryland Nancy A. Miltenberger, M.A., Senior Editor, The Circle. Inc., McLean, Virginia Elizalxth Mugge. Special Assistant, Office of the Deputy Director, Division of Cancer Prrvention and Controi, National Cancer Institute, Bethesda, Maryland Millie R. Naquin, M.Ed., Research Assistant, Office on Smoking and Heahh, Rock- ville, Maryland Regina Nwankwo, Editor, The Circle. Inc., McLean, Virginia Ruth C. Palmer, Secretary, Office on Smoking and Health. Rockville. Maryland Lida Peterson. Computer Systems Manager. The Circle. lnc., McLean, Virginia Renate Phillips. Desktop Publishing/iGraphic Artist, The Circle. lnc., McLsan, Virginia Margaret E. Pickerel, Public Information and Publications Specialist, Office on Smok- ing and Health, Rockville, Maryland Tamara Shipp. Publications Assistant, The Circle. lnc., McLean, Virginia Edwin Silverberg, Supervisor, Statistical Information Service, American Cancer Society Linda R. Spiegelman. Administrative Officer, Office on Smoking and Health, Rock- ville. Maryland Traion Stallings, Word Processing Specialist, The Circle, lnc., McLean, Virginia Daniel R. Tisch, Senior Project Manager. The Circle, Inc., Mci.ean, Virginia Pamela Wilson. Editor, The Circle, Inc., McLean, Virginia Louise G. Wiseman, Technical Information Specialist, Office on Smoking an4Health, Rockville. Maryland I 1189 t85t5 xix

I nQ aeatrMw er KAtrw re Mw.w rt.v.ets .rr...w. u. .w, . . Suggested Citation U.S. Department of Health and Human Services. Reducing the Health Consequen- crs of Smoking: 25 Years of Progress. A Report of the Surgeon General. U.S. Depart- ment of Health and Human Services. Public Health Service. Centers for Disease Con- trol. Center for Chronic Disease Prevention and Health Promotion. Office on Smoking and Health. DHHS Publication No. (CDC) 89-l441 I, Prepublication versicxl, January 11, 19R9. This is a prepublicaticxl version of the Report. The final version, with index, will be available later in 1999. tlr a..erable ,li. rrtght spo.kar ee the Ne.ao of Rqr.N.t.t1Na reohtagtea, D.C. 20313 ll.ar Mr. apoal.rl It ta 4p1...are to tr....tt to the Catttmaa H. /!N t.rge.a O.aar.1'a aeprt es the Iraltb eawt.eaeea of ..e4twg; r rnr.t.d by lLettaa a(.) ei the f.blte a.alth Clpr+tte 1.okint " o!, Hbf. Tho repert wprpar./ by the CGat.ra for at.e..e Coetrol'a Orllee as a.nktett .d sa.lth. 81S report. .atttl.d W.ala~ tlw lt.alth Ce.wt..ie.. e! artlni: 23 T.aro et h~a[reoa, es..t.oo th. . a..at• develoyaaat. e.er the wt q+arter eont.rl is .askttg rro.aleeee ..d ie .oit.ltt7 ewwA by o.altag. It higbligAto taprtant gataa to t.roreattej ..ntlng .d avokiag-r.1.taN dlaea.e, r..i..a eha.pe ia rrosr.r and plietos h.tpM to rM+ea ..ettag, .at aaph.elt.a .e.reee of eenttaalag re.pra wd rerl.tag eballeagea. ' tl.rtaa the pat 23 y.arn, .rklaa bati.Her lw eha,qd 4ra.Kiea117. taarl7 half e[ .il lt.t% N.lt. .hs e..r e.n4.d ba.* t.it. The pro..ls.ee of ...klag hr Mel1w.N atoadi:y, rtth a prtte.larly l.proaotw doelir a.a.g ..a. fstf.ag pr...lesee ..e" rn deere.ad lre. 30 pareoat ta 1li3 to 32 pareowt ta 1967. An a rea.lt, l..a caae.r .ort.ltty rat.a a.att! .aa .ta ss. le..ltag off after,rq deeMos of eea.taNat laer./ae. Ooqite tbie hragroaa, the pro.alonee of .aeltag mair higher ..aag bl.el., bl.a-eellar .orbra, and leae-edue.t.d Parae.., tlw ta tho ererall pplatlew. li.ekin{ .aoet high aeheel aaaton l.wld .[[ [roe ltai through 1l117 atter pro.leeo 7.ara of bcll.a. It 1905. tAe lNt Ta.r for sMeA ..tl.at.s ar. ..atlabl.. MPr.:irt.ly 730,000 Arrte.aa dl.l r th@ r...lt of past aad e.rn.t aettag. ZMa rahreaaata sre tAan awa of o..ry aln d.aths ta the OattM ft.toa. g.ettae ra..lr the ataale .n.t t.portant pnventdle e.rN e! Mattt t.o o.r a.elety. ?o rtwqts .ar a.aatan twad a asba-hro aootetlr, .a awt [ee.m our et[orts ea l.ra.eatittg amkta{ lattiatlen ..d oecooragtag a.ekia` ee...ttea aaaag Mgh-rtak prel.tten.. Ieeroa.ed public tntor..tlon .ctt.ittea, .uetttag pr..eattew .ad e.a..tlen presra.., and pltel.e that eneo.r.q wenasking bahavler should bN penwA. Unlo.s we aeet thta ehallenp .aee..oL.i17, .aoktft-r.l.ted asrt.llt>r .til re.aln htth well tate the 21st Ceat.ry. titae.rely, 0089 18StS 4.~ Otta l. Dow., M.D. Soeretary saeloa.r.

0£89 t85tS CONTENTS Introduction ........................................................ 37 Partl: Health Consequences .......................................... 38 Smoking and Overall Mortality ...................................... 38 Lung Cancer ..................................................... 43 Introduction ................................................. 43 Dose-Response Relationships ............................... ! ~ .. 43 Women and Lung Cancer ...................................... 46 Type of Lung Cancer and Smoking ............................... 50 Pipe and Cigar Smoking ....................................... 50 Determinants of Susceptibility .................................. 50 Familial Factors ....................................... •... 52 Other Host Factors .................................... 52 Occupational Exposures ............................... ~. . . : 52 Ambient Air Pollution ...................................... 53 Indoor Air Pollution .................................... ... 53 Diet .................................................... 54 Smoking Cessation ........................................... 55 Laryngeal, Oral, and Esophageal Cancer ....i. 56 Bladder and Kidney Cancer .....................................'...'. 56 Pancreatic Cancer ................................................. 56 Stomach Cancer ...............................................'....57 Cervical Cancer ................................................... 57 Endometrial Cancer ............................................... 58 Coronary Heart Disease ............................................ 58 Epidemiology .......................................... .. 58 Coronary Heart Disease Risk Factors ............................ 59 Pathophysiological Mechanisms ................................ 60 Clinical Correlations .......................................... 61 Smoking Cessation ........................................... 61 Cerebrovaccular Disease (Stroke) ..................................... 61 Atherosclerotic Peripheral Vascular Disease ............................ 64 Atherosclerotic Aortic Aneurysm ..................................... 65 Chronic Obstructive Pulmonary Disease ............................... 66 Pathogenesis ................................................ 67 Pathophysiology ............................................. 67 Natural History of COPD and the Role of Ciganme Smoking ......... 68 Pregnancy andlnfant Health ......................................... 71 Infant Birthweight ........................................... 72 Fetal and Perinatal Mortality ................................... 73 Congenital Malformations ................................. . . . 73 Fertility .................................................... 75 Long-Tctm Effects on the Child .................. . . . . .......... 75 Peptic Ulcer ...................................................... 76 35 I

U.S. DF.PARTMENT OF HEALTH. EDUCATION. AND WELFARE. San Diego Smoking Rr.crarrhPrnjec•t. FiwYrorStatus. U.S.DepartmentofHealthEducation,andWelfarc,Cen- tcr for Disease Control. DHEW Project No. 200-7S-0S 16:1-7, 1976. U.S. DEPARTMENT OF HEALTH. EDUCATION, AND WELFARE. The Health Canss- qnrnre.c n/SmnkinR,1977-197R. U.S. Department of Health, EAucation, and Welfare. Public Health Service. Office of the Asaistant Secretary for Health. Office on Smoking and Health. DI IF.W Publication No. (PHS) 79-Stttl6S, 197R. U. S. 1)EI'ARTMENT OF HEALTH. EDUCATION. AND WELFARE. Smnking and Health. A Report of the Sur.etnn General. U.S. Department of Health. F.ducaticxt, and Welfare. Public Health Service, Office of the Assistant Secretary for Heallh. Office on Smoking and Health. fri1t;W Publication No. (PHS) 79-5(11)66, 1()7qa. U.S DEPARTMENT OF HEALTH. EDUCATION. AND WELFARE. Healthy People. The .CurRenn Grnrrars Report nn Hrolth PrnmMinn and ni.amsr Preventinn. U.S. Department of Ikalth. F.ducatinn, and Welfare, Public Health Service. Office of the Ascistant Secretary fox Health. DIIFW Publication No. 79-55(171, 1Q79h. U.S. PUBLIC HEALTH SERVICE. SmnkinR and Health. Rennrt of the Advisory Committee to the.SurRron General ejthe Public HrahhStrvirt. U.S. Department of Health. EAocatiort, and Welfare, Public Health Service, Center ftx Disewe Control. PHS Publication No. 1103, 1964. U.S. PUBLIC HEALTH SERVICE. The Health Consequtncts nJSmnking. A Public Strvict Review: 1967. U.S. Depariment of Halth. Educatan, and Welfare. Public Health Service. Health Services and Mental Health Adminictration. PHS Publication No. 1696. revised 196Ra. U.S. PUBLIC HEALTH SERVICE. Tht Health Cnnstqrthtts of Smnking. 19tfR Srqqrlenrtnt to the 1967 Public Health Service Rrview. U.S. Depatrtment of Health. Education, and Wel- fare. Public Health Service, Health Servica and Mental Adminixtration. DHEW Publication No. 1696, 196Rb. U.S. PUBLIC HEALTH SERVICE. The Health Cnn.aqrtnees ojSmokinR. 1969 Supplement to thr 1967 Public Health Service Review. U.S. Department of Health. Education, and Wel- fare. Public Health Service. DHEW Publication No. 1969-2 (Supplement), 1969. WYNf)ER, E.L., GRAHAM, E.A. Tobacco smokin6 as a Poc.cible etioloRic factor in bronchiogenic carcitwxna: A study of 694 proved craes. Journal njtht American Medical Association 14.1:i29¢i96, May 27, 19.50, 6Z89 Z8SiS CHAPTER 2 r ADVANCES IN KNOWLEDGE OF THE HEALTH CONSEQUENCES OF SMOKINq :~:~

;7! lack E. Henningfield. Ph.D.. Chief, Biology of Dependence and Abuse Potential As- sessment Labnratory, Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland Carol J. HoFue, Ph.D.. Director. Division of Reproductive Health. Center for Chronic Disease Prevention and Health Pronation, Centers for Disease Control, Atlanta, Georgia Elvin Hityer, Associate Director for Policy Coordination, Centers for Disease Control, Atlanta. Georgia Richard lessor, Ph.D.. Professor of Psychokogy. Director of the Institute of Behavioral Science. University of Colorado at Boulder. Boulder. Colorado Lloyd D.lohnston, Ph.D.. Program Director. Institute for Social Research, University of Michigan. Ann Arbor, Michigan John T. Kalherer, Jr., Ph.D.. Deputy Director. Division of Disease Prevention, Office of Disease Prevention, Office of the Director. National Institutes of Health, Bethes- da, Maryland John H. Kelso, Acting Administrator, Health Resources and Services Administration, Rockville, Maryland Larry Kessler, Sc.D., Surveillance and Operations Research Branch, National Cancer Institute. Bethesda, Maryland A. Joan Klebba, M.A., Statistician, Division of Vital Statistics, National Center for Health Statistics, Centers for Disease Control, Hyattsville. Maryland Lloyd J. Kolbe, Ph.D.. Acting Director. Division of Adolescent and School Health. Cen- ter for Chronic Disease Prevention and Health Prorration, Centers for Disease Con- trol. Atlanta. Georgia Jeffrey P. Koplan, M.D.. M.P.H., Dinector, Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Atlanta, Georgia Lynn T. Kozlowski, Ph.D.. Head. Behavioral Research on Tobacco Use. Addiction Re- search Foundation, Toronto, Ontario, Canada Marshall W. Krcuter, Ph.D., Din.ctor, Division of Chronic Disease Control and Com- munity Intervention, Center for Chronic Disease Prevention and Health Promotion, Centers for Diseaie Ctfnhiol, Atlatna, Georgia Narry A. Lando, Ph.D., Associate Profe.ssor, Division of Epidemiology. School of Public Health, University of Minne.sota, Minneapolis, Minnesota Charles A. LeMaistre, M.D., President, University of Texas M.D. Anderson Cancer Center, Houston, Texas Claude Lenfant, M.D., Director. National Heatt, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland Eugene M. Lewit, Ph.D., Associate Profes.sor, Departments of Medicine and Preven- tive Medicine and Community Health, Office of Primary Health Care Education, UMDNJ-New Jersey Medical School, Newark, New Jersey Bryan R. Luce, M.B.A.. Ph.D., Battelle Human Affairs Research Center, Washington, D.C. Dolores M. Malvih, Dr.P.H., Dental Disease Prevention Activity, Center for Preven- tion Services, Centers for Disease Control, Atlanla, Georgia AlfnedC. Marcus, Ph.D., Associate Director, Division of Cancer Control,lexrI sson Com- prtihensive Cancer Center, UniversitK of California, Los Angele's, Los Angeles, California ' James S. Marks, M.D., M.P.H.. Deputy Director for Public Health Practice, Center for Chronic Disease Prevention and Health Pronation, Centers for Disease Control. At- lanta, Georgia James O. Mason, M.D., Dr.P.H., Director. Centers for Disease Control, Atlanta, Geor- gia ' Robin 1. Mermelstein, Ph.D., Assistant Professor, Prevention Re.search Center, School of Public Health, University of Illinois at Chicago. Chicago, ltlinois Dannie C. Middleton, M.D., Medical Officer, Document Development Branch. Division of Standards Development and Technology Transfer, National Institute for Occupational Safety and Health. Centers for Disease Control, Atlanta. Georgia Gregory J. Morou:o, Ph.D., M.P.H., Coordinator, National Heart. L{ung, and Blood Institute's Smoking Education Program, National Institutes of Htalth, Bethesda, Maryland Joseph P. Mulholland, Ph.D., Bureau of Ecorwmics, Federal Trade Commission, Washington, D.C. Hillary Murt, M.P.H., Research Associate, Departrrtent of Health SerYices Management and Policy, School of Public Health, University of Michigan, Ann Arbor, Michigan Herbert W. Nickens, M.D.. M.A., Director, Office of Minority Health. Public Health Service, Washington, D.C. Richard W. Nietneier, Ph.D., Acting Ditector, Division of Standards I?eveloPmertt and Technology Transfer, Nationd Institute for Occupational Safety and Health. Centers for Disease Control, Atlanta, Georgia Stuart L. Nightingale, M.D.. Associate Commissioner for Health Affairs, Food and Drug Administration, Rockville, Maryland Ira S. Ockene, M.D., Professor of Medicine, Director. Preventive Cardiology. Division of Cardiovascular Medicine, University of Massachusetts Medical School, Wor- cester, Massachusetts Horace O.Ogdelt, Consultattt, Oaithersbur6, Maryland Patrick M.O'Malky Ph.D.,Associate Research Scientist, Institute forSocial Research. University of Michigan. Ann Arbor. Michigan Mario A. Orlandi, Ph.D.. M.P.H., Chief. Division of Health Promotion Research. American Health Foundation, New York, New York Carole Tracy Orleans. Ph.D., Senior Investigator. Behavioral Medicine and Director of Smoking Cessation Services, Fox Chase Cancer Center, Philadelphia, Pennsylvania Gerry Oster, Ph.D.. Vice President, Policy Analysis, Inc., Brookline, Massachusetts Clifford H. Patrick, Ph.D.. Senior Public Health Advisor. Office of Minority Health, Washington. D.C. Cheryl L. Perry, Ph.D.. Associate Profesaor, Division of EPidemioingy. School of Public Health, University of Minnesota. Minneapolis. Minnesota Michael Pertschuck, J.D., Co-director, Advocacy Institute, WashingRkxt, D.C. I 6089 IBSiS xv Xiv

Ronald M. Davis, M.D.. Director. Office on Smoking and Health. Center for Chronic Disease Prevention and Health Promcxion, Centers for Disease Control. Rockville, Maryland Joseph R. DiFram.a, M.D.. Director of Research, Fitchburg Family Practice Residen- cy Program, University of Massachusetts Medical Center, Fitchburg, Massachusetts Michael P. Eriksen, Sc.D.. Director. Behavioral Research Program, Department of Can- cer Prevention and Control, The University of Texas M.D. Anderson Cancer Center, Houston, Texas David P. Fan, Ph.D.. Professor of Genetics and Cell Biology. University of Minnesota, St. Paul. Minnesota Michael C. Fiote, M.D.. M.P.H.. Assistant Professor, Department of Medicine. Center for Health Sciences, University of Wisconsin. Madison, Wisconsin Edwin B. Fisher, Jr., Ph.D.. Associate Professor of Psychology, Director. Center for Health Behavior Researrh, Washington Univenity, St. Louis, Missouri Jeffrey E. Harris, M.D., Ph.D., Visiting Associate Professor, Department of Biostatis- tics, Harvard School of Public Health, Boston, Mac.sachusetts; Clinical Associate, Medical Services. Massachusetts General Hospital. Boston, Mas.sachu.setts; As- sociate Professor of Economics, Massachusetts Institute of Technology. Cambridge, Massachusetts Jan L Hitchcock, Ph.D., Associate Director. Institute for the Study of Smoking Be- havior and Policy, John F. Kennedy School of Government, Harvard University, Cambridge, Massachusetts Thomas A. Hodgson. Ph.D.. Chief Economist, Office of Analysis and EPidemiology, National Center for Health Statistics, Hyattsville, Maryland Dietrich Hoffmann, Ph.D., Associate Director. Naylor Dana Institute for Disease Prevention, Americatt Health Foundation, Valhalla, New York Ilse Hoffmann, Research Cootdinator, Naylor Dana Institute for Disease Prevention, American Health Foundation, Valhalla, New York Juliette S. Kendrick, M.D., Deputy Chief, Ptegnancy Epidemiology Branch, Division of Reproductive Health, Center for Chronic Disease Prevention and Health Ptvnw- tion, Centers for Disease Control, Atlanta, Georgia Lewis H. Kuller, M.D., Dr.P.H., Professor and C?tairperson. Departntent of Epidetniol- ogy, Graduate School of Public Health, University of Pitt.sMtrgh, Pittsburgh, Pennsyl- vania ~ Eugene M. Lewit, Ph.D.. Associate Professor, Departments of Medicine and Preven- tive Medicine and Community Health, Office of Primary Health Care Education, UMDNJ-New Jersey Medical School, Newark, New Jersey Edward Lichtenstein, Ph.D.. Research Scientist, Oregon Research Institute; Professor of Psychology. University of Oregon, Eugene, Oregon Thomas E. Novotny, M.D.. Medical Epidemioiogist, Office on Smoking and Heahh. Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Rockville, Maryland Judith K. Ockcne. Ph.D., Associate Professor of Medicine, and Director. Division of Preventive and Behavioral Medicine, Del+artment of Medicine. University of Mas- carhucetts Medical School, Worcecter, Massachusetts Chris Leo Pashos, M.P.P., Project Coordinator, Institute for the Study'of Smoking Be- havior and Policy, John F. Kennedy School of Government, Harvard University, Cambridge. Massachusetts Richard Peto, M.A., M.Sc., ICRF Cancer Studies Unit, Radcliffe Infirmary. Oxford, England John P. Pierce. M.Sc.. Ph.D., Chief, Epidemiology Branch, Office on Smoking and Health. Center for Chronic Disease Prevention and Health Promoticm, Centers for Disease Control. Rockville, Maryland John M. Pinney, Executive Director. Institnte for the Study of Smoking Behavior and Policy, John F. Kennedy School of Government, Harvard University, Cambridge, Massachusetts Edward T. Popper, M.B.A., D.B.A., Associate Professor of Marketing. Bryant College, Smithfield. Rhode lsland Patrick L. Remington, M.D., M.P.H.. Medical Epidemiologist. Buresu of.Community Health and Pteventiott, Wisconsin Division of Health, Madison, N~isconsin Nancy A. Rigotti, M.D., Associate Director. Institute for the Study' of Smoking Be- havior and Policy. John F. Kennedy School of Govemment, Harvard University, Cambridge, Massachusetts, and Instructor in Medicine, Harvard Il4edical School, Boston, Massachusetts Jonathan M. Samet, M.D.. Professor of Medicine, Department of Medicink, Chief, Pul- monary Division, University of New Mexico. Albuquerque. New lvlexico Russell C. Sciatdra, M.A., Associate Director. Smoking Control Program, Roswell Park Memorial institute, Buffalo, New York Carol Anne Soltanek, M.D.. Resident, Southwestern Michigan Anea Health Education Center. Kalamazoo. Michigan Michael A. Stoto, Ph.D., Senior Staff OPficer, Institute of Medicine. National Academy of Scienors, Washington. D.C. I Owen T,1ltornbetry, Ph.D., Director. Division of Health Interview Statistics, Nation- al Center for Health Statistics, Centers for Disease Control, Hyattsville. Maryland Kenneth E. Wamer, Ph.D., Professor, Department of Public Health Policy and Ad- ministration. School of Public Health, University of Michigan, Ann Arbor. Michigan The editors aCbrotvleQRe with gratitude the felfowinR distinRuishtd scienti.ctc, physicians, and othtrs who tent their sapport in the development nf this Report hv conr- dinatinR manuscript preparation, contributing critical rrviPNCC. or assisting in other ways. Elvin E. Adams, M.D., M.P.H.. Associate Director. Health Department. General Con- ference of Seventh-Day Adventist.s, Washington. D.C. Charles Althafer, M.P.H.. Assistant Director for Health Promotion and Risk Aplraical, office of Program Planning and Evaluation, National Institute for Occupational Safety tutd Health, Centers for Disease Control, Atlanta, Georgia ; Lynn M. Artz, M.D., M.P.H., Senior Policy Advisor, Oflice of Diseate Prevention -and Health Pnomotion. Office of the Assistant Secretary for Health, Washington. D.C.

~ ~ tobacco use is one of 21 priority areas in which objectives are being formulated. PHS s D » intends to publish the objectives in 1990 W S ~ a E 06 . Y 6 S L 0 ~ O » o ~•~ ~ V ...yyy A C ~ C ~ Limitations of CoveraRe espite the broad scope of this Report, certain limitations have had to he placed on . ~ ~ E ~ Q qY » V,,~~ u r m ,J Y.~ m C N ~ ";;aA °og ` 0 6 E coverage. Two in particular are worthy of mention here: . (1) The Report focuses primarily, but not exclusively, on cigarette smpking, reflect- ing its dominance among forms of tobacco use, in terms of both prevalence and disease impact. This focus also reflects the desire to represent the principal interest•of the 1964 Advisory Committee in this 25th anniversary Report. Pipe and cigar smoking are much less prevalent than cigarette smoking but also carry significant health risks (US DHEW 1979a). Growing use of smokeless tobacco products (snuff and chevying tobacco), primarily by adolescent males, has focused national attention on there vaknce and health consequences of using these tobacco products (Connolly et al. 19R6).' This sub- ject was recently reviewed thoroughly by an advisory committee to the Shrgeon General (US DHHS 19R6b) and in a National Cancer Institute monograph (Boyd and Darbey, in press). i ' (2) The Report concentrates on smoking in the United States. Both vdithin the United States and around the world, tht:re is growing concern about the spread of smoking, particularly in the world's poorer countries. While per capita cigarette eonsumption is stable or falling in most developed nations, it is rising in Third World countries. Rates of smoking-related chronic diseases are also increasing rapidly, to the point that tobac- co is expected to soon become the leading cause of premature, preventable mortality in the Third World, as it is at present in the developed world (Aoki, Hisamichi, Tominaga 1988). Concentration of this Repott on smoking in the United States is no reflection on the relative importance of the international situation. Rather, it results fnom the principal objective of reviewing where this Nation has come in its efforts to control smoking-re- lated disease since the 1964 report of the Surgeon General's Advisory Committee. The Public Health Service hopes that this review; like its predecessors, will prove to be of value to scientists, health professionals, and public health officials in countries throughout the world. Development of the Report This Report was developed by the Office on Smoking and Health (OSH). Center for Chronic Disease Prevention and Health Ptorrwtion. Centers for Disease Centrol, Public Health Service of the U.S. Department of Health and Human Services, as. part of the Department's responsibility, under Public Law 91-222, to report new and current in- formation on smoking and heahh to the U.S. Congress. The scientific content of this Report was produced through the effortt of more than ILV scientists in the fields of inedicine, the biological and social sciencec, public health, and policy analysis. Manuscripts for the Report, constituting drafts of chapters or sec- tions of chapters, were prepared by 33 scientists sclected for their expertise in the tn

, Donald A. Berreth, Director, Office of Public Affairs, Centers for Disease Control, At- lanta. Georgia Gayle M. Boyd, Ph.D., Program Director, Srnoking, Tobacco and Cancer Program, Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, Maryland Allan Brandt, Ph.D., Department of Social Medicine and Health Policy, Harvard Medi- cal School. Boston, Massachusetts Lester Brcslow, M.D., M.P.H.. Professor, School of Public Health, and Director. Health Services Research, Jonsson Comprehensive Cancer. Center, University of California, Los Angeles. Los Angeles, California Clarice Brown, M.S., Data Analyst, Office of Prevention. Education, and Control, Na- tional Heart, Lung, and Blood Institute, Bethesda, Maryland David P. Brown, M.D., Deputy Director. Division of Surveillance. Hazard Evaluations, and Field Studies, National Institute for Occupational Safety and Health. Centers for Disease Control, Atlanta, Georgia Martin Brown, Ph.D., Surveillance and Operations Research Branch, Division of Can- cer Prevention and Control, National Cancer Institute, Bethesda, Maryland David M. Burns, M.D., Associate Profes.sor of Medicine. Division of Pulmonary and Critical Care Medicine, University of California. San Diego Medical Center, San Diego, California Dee Burton, Ph.D.. Assistant Professor, Prevention Research Center, School of Public Health, University of Illinois at Chicago. Chicago. Illinois Frank l. Chaloupka, Ph.D., Assistant Professor, Department of Economics, Colkge of Business Administration, University of Illinois at Chicago, Chicago, Illinois Paul D. Cleary, Ph.D., Department of Health Care Policy and The Division on Aging, Harvard Medical School, Boston, Massachusetts Alexander Cohen. Ph.D.. Deputy Director, Division of Biomedical and Behavioral Science. National Institute for Occupational Safety and Health. Centers for Disease Control, Atlanta, Georgia Joel B. Cohen, Ph.D., Distinguished Service Professor and Director. Center for Con- sumer Research, University of Florida, Gainesvilk, Florida Michael J. Cowell, F.S.A., Vice President and Corporate Actuary, UNUM Life In- sdrance Company. Portland, Maine Joseph W. Cullen, Ph.D., Deputy Director. Diviaion of Cancer Prevention and Control. National Cancer Institute, Coordinator for the National Cancer Institute's Smoking. Tohacco and Cancer Program. Bethesda, Maryland Sir Richard IMll, Emeritus Professorof Medicine, University of Oxford. Acting Dinec- tor, Imperial Cancer Research Fund, Cancer Epidemiology and Clinical Trials Unit, Oxford, England J. David Erickson, D.D.S., Ph.D.. Chief, Birth Defects and Genetic Diseases Branch, Division of Birth Defects and Developmental Disabilities, Center for Environmental Ilealth and Injury Control, Centers for Disease Control, Atlanta, Georgia Michael P. Eriksen, Sc.D., Director. Behavioral Research Program, Department of Can- cer Prevention and Control. University of Texas M.D. Anderson Cancer Center, I louctnn, Tcxas , Virginia L. Emster, Ph.D., Professor of Epidemiology. Department of Epidemiology and international Health, School of Medicine. University of California. San Francis- co, California Roberta G. Ferrence, Ph.D., Ptevetttion Studies Department. Addiction Research Foun- dation, Toronto, Ontario, Canada Jonathan E. Fielding, M.D., M.P.H., Professorof Public Health and Pediatrics. Univer- sity of California at Los Angeles, Los Angeles, California. Vice President and Health Director. Johnson and Johnson Health Management, Inc.. Santa Monica, California John R. Finnegan, Jr., Ph.D., Assistant Professor, School of Public He~lth, University of Minnesota. Minneapolis. Minnesota Martin Fishbein, Ph.D., Professor of Psychology and Research Professor, Institute of Communications Research, University of Illinois, Champaign-Urbana, Illinois Brian R. Flay, D.Phil., Associate Professor and Director. Prevention Research Center. School of Public Health, University of Illinois at Chicago. Chicago,;lllinois William H. Foege. M.D., M.P.H., Executive Director, The Carter :Center, Emory University. Atlanta. Georgia Peter L. Frommer, M.D., Deputy Director, Natiotal Heart, Lung, and Blood institute, National Institutes of Health, Bethesda, Maryland Lawrence Garfinkel. M.A., Vice President for Epidemiology and St~atistics, Director, Cancer Prevention. Arnerican Cancer Society, New York, New York Donald W. Garner,l.D., Professor of Law, Southern Illinois University Sc$tool of Law, Carbondale, Illinois i I Russell E. Glasgow, Ph.D., Research Scientist, Oregon Research Institute. Eugene, Oregon Thomas J. Glynn, Ph.D.. Program Dinctor for Smoking Research, Smoking, Tobacco, and Cancer Program, National Cancer Institute, Bethesda. Maryland Frederick K. Goodwin, M.D., Administrator, Alcohol, Drug Abuse, and Mental Heahh Administntion, Rockville, Maryland , Nancy P. Gordoe, Sc.D.. Behavioral ScieMist, Division of Research. Northern Califor- nia Kaiser Permanente Medical Care Program Leonard Gnxn, Ph.D.. Professor of Psychology, Department of Psychology, Washington Univetsity, St Louis, Missouri Ellen R. Gritz, Ph.D., Director. Division of Cancer Control, Jonsson Comprehensive Cancer Center, University of Califomia. Los Angeles, Los Angeles, California Neil E. Grunbtxg, Ph.D., Associate Professor, Department of Medical Psychology, Uniformed Services University of the Health Sciences, Bethesda. Maryland Dudley H. Hafner, Executive Vice President, American Heart Association, Da11at, Texas James A. Harrell, M.A., Acting Director. Office of Disease Prevention and Health Promotion, Office of the Assistant Secretary for Health, Washington. D.C. Jeffrey E. Harris, M.D., Ph.D., Visiting Associate Professor, Department of Biostatis- tics, Harvard School of Public Heahh, Boston, Massachusetts; Clinical Associate, Medical Services, Massachusetts General Hospital, Boston, Mapsachusetts•, As- sociate Professor of Econornics, Massachusetts Institute of Technology. Cambridge. Massachusetts 8089 18515 xiii

landmark document on smoking and health that concluded that "Cigarette smoking is the most likely cause of the recent world-wide increase in deaths from lung cancer ... is an important predisposing cause of the development of chronic bronchitis... probab- ly incrcaces the risk of dying from coronary heart disease...has an adverse effect on healing of (gastric and duodenal ( uMers ...(and) may be a contributing factor in can- cer of the mcwth, pharynx, oesophagus, and bladder." On June 1. 196 1, the presidents of the American Cancer Society, the American Public Health Assnciation, the American Heart Ac.sociation, and the National Tuberculosis Association (now the American Lung Association) urged President John F. Kennedy to establish a commission to study the health consequences of smoking. Repre- sentativcs of these organi7ations met with Surgeon General Luther L. Terry in January 1962 to reiteratc their call for action. In April, the Surgeon General presented a detailed proposal for an advisory group to reevaluate the position adopted by the Public Health Service in 1959. In calling for the advisory group. Dr. Terry cited new research on the adverse health effects of tobacco, a request from the Federal Trade Commission for guidance on policy regarding the laheling and advertising of tobacco pmducts, and the findings in the new report of the Royal College of Physicians. On July 27, 1962, following consultations between the White House and the Public Health Service, the Surgeon General held a meeting to define the work of an expert advisory group and to identify candidates for the committee. Meeting with the Sur- geon General were representatives of the American Cancer Society, the American Col- lege of Chest Physicians, the American Heart Association, the American Medical As- sociation, the Tobacco Institute, the Food and Drug Administration, the National Tuberculosis As.sociation, the Federal Trade Commission, and the President's Office of Science and Technology. The group agreed on a list of nmre than 150 scientists and physicians. Each of the organisAtions had the right to veto any of the names on the list for any reason. Persons who had taken a public position on smoking and health were not considered for inclusion on the advisory committee. Dr. Terry selected 10 individuats from the list to serve on the Surgeon General's Ad- visory Committee on Smoking and Health: Stanhope Bayne-Jones, M.D., LLD., former Dean, Yale School of Medicine; Walter J. Burdette, M.D., Ph.D., Univetsity of Utah: W illiam G. Cochrane. M.A., Harvard University; Emmanuel Farber, M.D., Ph.D., University of Pittsburgh; Louis F. Fieser, Ph.D.. Harvard University; Jacob Furth, M.D., Columbia University; John B. Hickam. M.D., Indiana University: Charles LeMaistre, M.D.. University of Texas; Leonard M. Schuman, M.D., University of Minnesota; and Maurice FI. Seevers, M.D., Ph.D.. University of Michigan. The Advisory Committee held nine meetings from November 1962 through Decem- ber 1963, during which they reviewed all the available data from animal laboratory ex- periments, clinical and autopsy studies, and rttrospective and prospective epi- demiologic studies. The Committee had access to over 7.000 publications pertaining to smoking and health, including more than 3,0(10 articles reporting research findings published after 1950. In evaluating evidence linking smoking to disease, the Commit- tec restricted judgmenk of a causal relationship to those associations for which the evidence was (I) con.sistcnt, (2) strong. (3) specific, (4) supportive of appropriate tem- pnral relationchips, atKl (5) coherent (US PHS 1964). The final Report of the Advisory Committee was released on January 11, 1964 (US PHS 1964). It concluded that "Cigarette smoking is causally related to lung cancer in men; the magnitude of the effect of cigarctte smoking far outweighs all other factors. The data for women, though less extensive, point in the same direction .... The risk of developing lung cancer increases with duration of smoking and the number of cigarettes smoked per day, and is diminished by discontinuing smoking." The Report also concluded that pipe smoking is causally related to lip, cancer, that cigarette smoking is causally related to laryngeal cancer in men, and that "Cigarette smoking is the most important of thecausesofchronic btonchitis " The Advisory Com- mittee identified significant associations between smoking and cancerof the esophagus, cancer of the urinary bladder, coronary artery disease, emphysema, peptic ulcer dis- ease, and low-birth-weight babies, but it did not consider the available data to be suf- ficient to label these associations causal. The Committee found that male cigarette smokers had a 70-percent exc~ss 'nortality rate over mcn who had never smoked and that female smokers also had an~elevated mortality rate, although less than that of males. The Advisory Committee concluded that "Cigarette smoking is a health hazard of sufficient importance in the l jnited States to warrant appropriate remedial action " "Remedial action" was initiated immediately after publication of ~the Advisory Committee's Report, when the Federal Trade Commission (FTC) proposed that cigarette packs and advertisements txar warning labels and that strict limitations be placed on the content of cigarette advertising. With passage of the Federal Cigarette Labeling and Advertising Act of 1965 (Public Law 89-92; amended in April 1970 by Public Law 91-222). Congress preemqed the FTC's recommendation: beginning in 1966, a congressionally mandated health waming appeared on all cigarette packs but not on advertisements. The Act also required the Secretary of Health. Education, and Welfare to submit an- nual reports to Congress on the health consequences of smoking, together with legis- lative recommendations. beginning no later than mid-1967. New reports of the Sur- geon General on smoking and health were issued in each calendar year beginning in 1967, except for 1970,1976,1977, and 1987. (In 1976, a volume of selected chapters from the 1971-75 Reports was published. The t+eport issued in 1978 was a joint Report for the years 1977 and 1978.) Thus, the present volume, commemorating the 25th an- niversary of the 1964 Report, is the 20th Report in the series. In addition, in 1986. PHS issued a report on the health consequences of using smokelass tobacco (US DHHS 1986h). Table I identifies the previous reports and highlights their coverage. The reports published since the 1964 Report have confirmed the scientific judgment of the Advisory Committee and have extended its findings. The evidence available today has reinforced the Advisory Committee's judgtnents of causality: converted most of its "significant associations" into causal retationships, adhering to the strict criteria described in the first Report; confirmed causal associations for relationships not con- templated in the 1964 Report (e.g., the health hazatds of involuntary smoking (US DHHS 19R6a)); and identified additional disease associations. Accompanying the growth and dissemination of scienlific knowledge has been in- crcased public understanding of the hazards of smoking, reflected in decreases in smok- I i 6 F 7

n (kteoporocis ..................................................... 76 Involuntary Smoking .................................... . •. 77 Smr.kelecs Tr,haeco ............................................. . 78 Acktictionto Smoking .............................................. 78 Part 11: The Physicochemical Nature of Tobacco .......................... 79 Thc Changing Cigarette ............................................ 85 Environmental Tohacco Smoke . . . . . . . . . . . . . . ........................ 88 Smokeless Tc.Mcco ................................................ 90 ToxicityandCarcinogenicityofTohaccoSmoke ........................ 92 Nic„tine . ................................................. 93 Riological Markers ................................................ 94 Summary .......................................................... 97 Conclucicros ....................................................... - - --- 100 Refercnce~ ........................................................ 102 I£g9 T851S 1i, i iNTRODUCTION The purpose of this Chapter is to summarize and compare the state of biornedical knowledge concerning tobacco and health in 1989 with that presented in the 1964 Sur- geon General's Report (see Table 13). The Chapter addresses major tobacco-related disonders that are well documented in the medical literature; it does rat consider many areas of current research that may prove to be important but are in an early or provisional state of investigation. The 1964 Surgeon General's Report was a landmark publication that includeb a sur- vey of trnxe than 7.000 available scientific articks on smoking and health. The Ad- visory Committee that prepared the 1964 Report reviewed and assessed epidemiolbgic, clinical, pathological, and experimental data for evidence linking smoking to disease. To reach conclusions concerning the causality of associations between smoking and disease, the Committee constructed a framework for evaluating the evidencel With regard to causality, the Committee concluded: ~' The causal aignificance of an association is a matler of judltment which goes beyond aey statement of statictical probability. To judge or evaluate the causal significance of the as- sociation between attribute or agent and the disea.ve, or effect upon health, a nu4ntxr of criteria must be utilized, no one of which is an all-sufficient basis for judgme4t. The.e criteria include: a) the consistenry of the ssociation b) the strength of the associatioe c) the specificity of the association d) the temporal relationships of the tmsociation e) the coherence of the associatioe (US PHS 1964). I These criteria were applied throughout the 1964 RepuR. When the word "cause" was used in the 1964 Report, it was felt to convey "the notion of a significant, effectual relationship between an agent and an associated disotder or disease in the host." Use of the word "caua" in relation to cigarette smoking did not exclude other agents as causes; rather, the rnembt:rs of the Advisory Committee shared "a common conception of the multiple etiology of biological processes." The principal findings on the health effects of smoking were stnnrnariud in the Sur- geon General's 1964 Report as follows: 1. Cigarette smoking is associated with a 70-percent increase in the age-specific death rates of men. 2. Cigarette smoking is causally related to hmg cancer in men; the magnitude of the effect of cigarette smoking far outweighs all other factors. The data for women, though less extersive, point in the same direction. 3. Civarette smoking is the most important of the causes of chronic bro6chitis in the United States and increases the risk of dying from chronic bronehitis and i 11

emphysema. A relationship exists between cigarette smoking and emphysema. but it has not been established that the relationship is causal. 4. It is established that male cigarette smokers have a higher death rate from coronary artery disease than nonsmoking males. Although the causative role of cigarette smoking in deaths from coronary disease is not proven, the Commit- tee considers it more prudent from the public health viewpoint to assume that the established association has causative meaning than to suspend judgment until no uncertainty remains. 5. Pipe smoking appears to he causally related to lip cancer. Cigarette smoking is a.ignificantfactorinthecausationofcanceroftixlarynxinmen. Theevidence supports the belief that an association exists between tobacco use and cancer of the esophagus, and between cigarette smoking and cancer of the urinary blad- der in men, tart the data are not adequate to decide whether these reiationships are causal. 6. Women who smoke cigarettes during pregnancy tend to have babies of lower hirthweight. It is not known whether this decrease in birthweight has any in- fluence on the biological fitness of the newborn. 7. Epidemiologic studies indicate an association between cigarette smoking and peptic ulcer that is greater for gastric than for duodenat ulcer. R. The habitual use of tobacco is related primarily to psychological and social drives, reinforced and perpetuated by the pharmacologic actions of nicotine. Since 1967. the U.S. Department of Health and Human Services has transmitted to the U.S. Congress mandated reports on the health consequences of smoking. Some of the reports have been encyclopedic reviews similar to the 1964 Report, whereas others have focused on the relationship between smoking and a specific topic. The Federal unit charged with preparing these annual neports, the Office on Smoking and Health, now has more than 57.000 documents on smoking and health in its Technical Informa- tion Center database. Research performed during the subsequent 25 years has substantiated and strengthened the conclusions of the 1964 Advisory Committee. Studies published since 1964 have atso established acsociations between smoking and disease in areas for which data did not exist in 1964. shed light on pathogenetic mechanisms of tobacco-related disease, and added scientific depth to areas mentioned only briefly in the 1964 Report. ~ ~'o a r ~ E Y ~ 'a Y Y > i A V >. ~ ~ d ~ wp' ~00 ao P0 O ~p- P =0,0 y o ~ .. .•S o °~ -. O n N ~O fV -~ N O O - N d a ..,M-ra_n N1 fV - O ~ 0. ~ v~ N P ~~ vl .-? aD VI O. a O g _a r N K O: g N~~ aD -! ~ N O: n n V1 N.D oa e.i e3 A O y'O t.i a _:o 1. ~. m Y ., V ~ PART I: HEALTH CONSEQUENCES 0 .o N ~ r . ~ Smoking and Overall Mortality (Cee Chapter 3 for more detailed discuqsion) ~ The ma jor prospective studies of the disease risks associated with smoking completed in the IWA)s and I970s contributed substantially to an underaanding of the relation- ship between smoking and disease (US DHi:W 1979). These studies provided es- timatcs of both the relative and attrihutahlc risks related to cigarette and other types of smoking (Table 1) (US DHEW 1979). Male cigarette smnkers had approximately 7() percent higher overall death ratcs than rnmsmokcrr the excess mortality of female 5 :. r 4~r 5$y~ Vf [+ g > _ „Is G ., ~~ 'A r. ~. . . ' ~ 0 O O O o 0 0 0 0 0 0 2 y Q y C C .`y$ye$ u uyt uy`ut uy v~ p 3` C tS 1' u U V U uVC~lVUV VU- UV QSC7 < ~ Yp ~ ~, ^ n a, a=~==x .~ 1 Z£89 tBStS ~t ix

Lung Association, have played a significant role in educating the public about the hazards of tobacco use. 2. Individual and group smoking cessation programs evolved from an emphasis on conditioning-based approaches in the 1960s. to the cognitively based self- management procedures of the 1970s, to the relapse prevention and phatmacologi- cally based components of the 19Rfk. 3. There has recently been an increased emphasis on targeting specific groups of smokers for cessation activities (e.g., pregnant women. Hispanics. blacks). 4. Packaging and marketing of self-help smoking cessation materials have become more sophisticated and there is more of an emphasis on relapse prevention, while much of the contents have changed relatively little over the years. 5. Mass-mediated quit-smoking programs have become an increasingly popular strategy for influencing the smoking bchavior of a large number of smokers. 6. The 1980% have seen an increase in the promotion of smoking control efforts in the workplace in response to increasing demand and opportunity for worksite wellness programs and smoking control policies. 7. In the last decade there has been an increasing interest in involving physicians and other health care professionals in smoking control efforts. Medical organizations have played a more prominent role in smoking and health during the 1980% than they had in the past. Part Ill. Antismoking Advocacy and Lobbying 1. Lobbying and advocacy efforts have expanded through the increasing commit- ment of the national voluntary health agencies to political action and the forma- tion of coalitions at the local, State, and national levels. 2. Antismok ing advocacy and lobbying have evolved over the past 25 years and now focus on a growing number of local. State, and national legislative and regulatory initiatives designed to reduce smok ing, regulate the cigarette product, and prevent the uptake of smoking by children and adolescents. Chapter 7: SmokieR Control Policies 0 Part 1. Policies Pertaining to Information and Education I. The Federal Government's efforts to reduce the health consequences of cigarette smoking have consisted primarily of providing the public with information and education about the hazards of tobacco use. Two of the most well-known mcchanisms are the publication of Surgeon General's Reports and the require- ment of warning labels on cigarette packages. A system of rotating health wam- ing lahcls is now required for all cigarette and smokeless tobacco packaging and advertisements. 2. Current laws do not require health warning labels on all tobacco products and do not require monitoring of the communications cffectivencs.s of the wamings. Fur- thcmxxe, existing laws do not provide administrative mechanisms to update the contents of labels to prevent the overexposure of current messages or to reflect advances in scientific knowledge, such as new information about the,addictive nature of tobacco use. 3. There is insufficient evidence to determine the independent effect of cigarette warning labels, particularly the rotating warning labels required since 1985. on public knowledge about the health effects of smoking or on smoking behavior. 4. Information about tar and nicotine yields appears on all cigarette adyertisements but not on all cigarette packages. Levels of other hazardous constitutnts of tobac- co smoke, such as carbon tnonoxide, hydrogen cyanide, and ammonia, are not dis- closed on packages or advertisements. Little information is available to the public about the identity or health consequences of the additives in tobacco products. 5. Declines in adult percapita cigan-tte consumption have occurred in years of major dissemination of information on the health hasards of smoking. ~hese include 1964, the year of the first Surgeon General's Report on smoking and Fiealth, and 1967-70, when antisntoking public service announcements were,4videYy broad- cast on radio and television, as mandated by the Federal Communications Commission's Fairness Doctrine. 6. In 19R5, when cigarette advertising and promotion totaled 2.5 ~illion dollars, cigarettes were the most heavily advertised product category in the outdoor media (e.g., billboards), second in magazines, and third in newspapers. Over the past decade, the majority of cigarette marketing expenditures has shiftdd itorn tradi- tional print advertising to promotional activities (e.g., free samples, coupons, sponsorship of sporting events). 7. An estimated I percent of the budget allocated to disease prevention by the U.S. Department of Health and Human Services is devoted specifically to tobacco con- trol. These expenditures totaled 39.5 million dollars in 1986. Part 11. Economic Incentives I. Cigarette excise taxes are imposed by the Federal Government (16 cents per pack). all State govemments. and nearly 400 cities and counties. On average, Federal and State excise taxes add 34 cents per pack to the price of cigarettes. Cigarette excise tax rates have fallen since 1964 in real terms because the rate and mag- nitude of periodic tax increases have not kept pace with inflation. 2. Studies demonstrate that increases in the price of cigarettes decrease smoking, particularly by adolescents. It has been estimated that an additional 100.0(10 or more persons will live to age 65 as a result of the price increases induced by the 1983 doubling of the Federal excise tax on cigarettes. 3. In 1964, smoking status was not considered in the determination of insurance premiums. Currtntly, nearly all life insurers but only a few health. disability, and property and casualty insurers offer premium discounts for nonsmokers. Few health insurers reimburse for the costs of smoking cessation programs or treat- ment. ,7

The 19R9 Report examines changes,in each of these dimensions over the past quarter century. The Report includes a Forewcxd by the Assistant Secretary for Health and the Director of the Centers for Disease Control, a Preface by the Surgeon General of the U.S. Public Health Service, and the following chapters: Chapter 1. Historical Perspective, Overview, and Conclusions Chapter 2. Advances in Knowledge of the Health Consequences of Smoking Chapter 3. Changes in Smoking-Attributable Mortality Chapter 4. Trends in Public Beliefs, Attitude.s, and Opinions About Smoking Chapter 5. Changes in Smoking F3ehaviorand Knowledge About Determinants Chapter 6. Smoking Prevention, Cessation, and Advocacy Activities Chapter 7. Smoking Control Policies Chapter 8. Changes in the Smoking-and-Health Environment: Behavioral and Health Consequences A key to abbreviations used throughout the Report is found at the end of the volume. Analysis of changes in scientific-medical understanding follows the core tradition of the Surgeon General's Report series. Chapter 2 summarizes current knowledge of the health consequences of smoking and examines how it has advanced, both qualita- tively and quantitatively, beyond that reflected in the original Surgeon General's Report. The Chapter also summarizes knowledge of the physicochemical nature of tobacco smoke. Chapter 3 examines the ultimate population impact of srnoking-disease relationships in its review of changes in smoking-attributabk mortality. The patterns of mortality have changed in predictable ways, reflecting variations in the rates and sociodemographic distribution of smoking prevalence (the subject of much of Chapter 5). In particular, smoking-attributable mortality in women has increased dramatically, the predictable consequence of the rapid growth in smoking by women in the middle decades of the century. Shifts in sociodemographic patterns of smoking, with greater prevalence now found among blue-collar workers and some minorities than among the white-collar population, presage a continuing disproportionate burden of illness for the Nation's poor and minority populations. One element of the decision of whether or not to smoke is personal understanding of the dangers involved. Chapter 4 reviews changes in public knowledge since 1964. Tlte most basic findings from scientific research on the health consequences of smoking have been conveyed to and accepted by the American public, at least at a generalized level. Nevertheles.s, survey research reveals important gaps in public understanding of the ha?.ards of smoking. Smokers report less understanding of the basic consequences of smoking than do nonsmokers; furthermore, smokers often do not internalize, or per- scnalise, the hazardt they acknowledge as applying to smokers in general. In addition, knowledge of smoking-and-health facts beyond the most basic information is not pos- sessed by significant numbers of Americans. Thus, a subaantial educational task remains. Although significant gaps rcmain, it is also clear that the public has a much better ap- preciation of the hazards of smoking than it did 25 years ago. Associated with the grow- ing acceptance of smoking as a health h;tz.ard for the smoker, and more recently as a hai.rd fix non.mokers, is a growing public dcxire to restrict smoking in public places to protect the rights of nonsmokers to breathe clean air. Opinions about smoking and the appropriate role of smoking control are also considered in Chapter 4.' The relationship between knowledge and opinion change, on'the one hand, and suh- sequent behavior change, on the other, is quite complex. Neverthcless, substantial smoking behavior change has occurred since issuance of the first Surgeon General's Report and has often followed shifts in beliefs and opinions about smoking. The many dimensions of such behavior change are explored in Chapter 5. Part I,of the Chapter examines empirical evidence on behavior change across a number of smoking behaviors and across the major sociodemographic groups. Several previous reports of the Sur- geon General have included consideration of these trends (US DHEW 1979; US DHHS 1990. 1983. 1985, 1988). Part 11 of Chapter 5 reviews the evolution of understanding of smoking behaviors and their determinants. The 1979 Surgeon General's Report devoted several chapters to the psychological and social determinants ¢f smoking (US DHEW 1979). Most tecently, the phenomenon of nicotine addicti9h was reviewed thoroughly by the Surgeon General (US DHHS 1988). Changes in public anitudes toward smoking and in the prevalence of smoking are reflected in the rapid expansion in the 1980s of State and local Iaws,and workplace policies restricting smoking. The Nation's growing nonsmoking ethos is also reflected in more attention to both voluntary and regulatory measures intended to prevent the in- itiation of tobacco use or to ussist smokers to quit. The number of sm¢kirlg-ces.sation techniques and programs has expanded. Smoking policy discussions today concern such diverse activities as excise taxation, restriction of advertising ano promotion of tobacco products, limitation of children's acoess to tobacco products, and regulation of the newly emerging nicotine-based products collectively referred to as "alternative nicotine delivery systems." Chapters 6 and 7 examine developmettts over the past quarter century in voluntary programmatic efforts and public policies directed at smoking control, respectively. Chapter 6 describes separately programs directed at smoking prevention and cessation, and highlights the work of the major voluntary health associations. The Chapter reviews such diverse efforts as comprehensive school health education curricula and antismoking public service announcements on the broadcast media. Chapter 6 c<m- cludes with a brief overview of advocacy and lobbying activities related to smoking and health. Advocacy activities are purely voluntary in nature, yet most have been directed at promoting smoking control policies, particularly in recent years. As such, a discussion of advocacy serves as a logical transition between the focus of Chapter 6 on voluntary efforts to combat smoking and concentration in Chapter 7 on policy measures. Coverage of developments in smoking control policies in Chapter 7 has few precedents in prior report.s of the Surgeon General. despite the first Report's call for "appr+npriate remedial action" a quarter of a century ago (US PHS 1964). The ma.jcx exception was the substantial attention accorded workplace and Government smoking restriction policies in the 1986 Report (US DHHS 1986a). Otherwise, the relxxt series' principal references to policy have come in the form of legislative recommen- dations to the Congress. Yet, as noted above, policies intended to diminish smoking and its disease burden have become increasingly common in both the public and .i i tG

40 . V V ~ y . N n o CS r b r 0 a ca ~ ~ ro V ; Pi IN m a " fV ~O fV = P_ - N $ ba o N r, - 19 IY - 8 ~ O~ ~ n P • .~ O r ~ e~i ri - z h - V A N OD s r ~i p .: d N N oh . % ~ N n ~ ; ££89 T8STS ~ e ~ ~ I I cigarette smokers was somewhat less than that of men, but it increased over the fol I - lowup intcrvals. A strong dose-tesponse relationship was found between exlxxore to cigarette smoke and excess mortality; cessation of cigarette smoking was associaied with a decrease in this excess mortality. The relative risks were greater for smoking- related cancers and chronic obstruetive pulmonary disease (COPD) than for coronary heartdisease(CHD); however,becauseofthehighermortalityratesforCHDthesmok- ing-attritxdahle mortality associated with CHD accounted for over one-third of the cx- ccss mortality due to smoking-tetated diseases. There have been relatively few long-term longitudinal studies that have measured the overall effects of cigarette smoking since these earlier reports. Results from a new American Cancer Society prospective study (CPS-il) and a detailed discussion of iotat cmoking-rclated mortality are presented in Chapter 3. Based on this study, cigarCtte smoking is currently estimated to account for 21 percent of all CHD deaths, 30 percent of all cancer deaths, and 82 percent of all COPD deaths. (,' The Multiple Risk Factor Intervention Trial (MRFIT) is a recent prosrcct'rye study that screened 361.662 men aged 35 to 57 years between 1972 and 1974 and I;as been following them since then, both through the Social Security Administration and the Na- tional Death Index files. To gauge smoking status, only the number of cig,arcttes smoked per day at enrollment was reported. Because fomrcr smokers were ikluded in the nonsmoker category, the risk comparisons in this study between nonsmokers and smokers are conservative in estimating the effects of smoking. Findings for the,6 yiars of followup for the MRFtT enrollees screened from 1972-73 are consistent with the studies reported in the 1960s, despite changes in the type of cigarettes in terms of tar and nicotine yield and the increased use of filters (see later section of this Chapter and Chapter 5). The MRF1T study shows that smoking status and number of cigarettes smoked per day have remained powerful predictors for total mortality and the develop- ment of CHD. stroke, cancer, and COPD. In the study population, there were an es- timated 2.249 (29 percent) excess deaths due to smoking, of which 35 percent were fmm CHD and 21 percent from lung cancer. The nonsmoker-fomter smoker group had 30 percent fewer total cancers than the smoking group over the 6-year followup. A study of a random sample of 25,129 Swedish men between 1963 and 1979 evaluated the relationship between cigarette smoking (prevalence of 32 percent). pipe smoking (27 percent), cigar smoking (5 percent), and subsequent mortality (Table 2; Carstensen, Pershagen, Eklund 1987). The all-cause relative death rate was 1.7-fold higher for those smoking greater than 15 g of tobacco per day (estimated as 16 to 25 cigarettes equaling 20 g and a package of pipe tobacco lasting 1 to 4 days equaling 16 g). The relative risks associated with cigarette smoking were consistent both with those of the current MRFIT sample and the earlier cohorts from the 1950s and 1960s. The risks were also increased for pipe and cigar smokers for many of the causes of death. Epidemiologic studies have shown that cigarette smoking exerts an adverse effect on mortality in older as well m younger age groups. The 17-year followup of the Alameda County Study (Kaplan et a1.1987) demonstrates an increased risk of death even among older cigarette smokers. The adjusted relative risk of death among smokers at entry was 1.46 (age 60 to 69) and 1.43 at age 70 or,nore. Smoking remained the strongest predictor of mortality even in this older age group. Other studies have also cubstan- 4t

80 7 o 0 s 0 s 40 30 20 10 0 19 30 1940 1950 1960 197 0 '-•-•-•Esephaqus --- Pnsbh lang -..-•--• Bbdder 1980 -- •-•-Cdoo b Roctum - - • - latkotnh ••••.•••... Pancrefs -----Stomu:h -------liver 1990 FI(:I IRE 5.-Age-adjosted cancer death rates for selected sites, males, United titates.19-i0•-!i6 'AAry.prl ~~ ihr nce ~h.~nM~h.m ~d Ihe 197(I ll.t. Cemw ~rtati~w~. Sf)r1R('1'S(Nt)ATA: N.liima('tMerfMNtahhSlmiaiia:llS.n~~.uOflheCe".w. women: the evidence ai.o provided comprehensive descriptions of d(Ke-recp(m.ce rclatilmshiin with lindingr cimiiar to those reported previously for men. Recently rcl+l,rted d(xe-re%lxoncc relationships frlmm the American Cancer Slxiety Cancer i'rcvcntinn Stndy 11 for iun} canl•er :md wlxncn extrnd these ohservcrtionc (FiFnrc 6). Rat~ per 100,00p mab ptpob0ee Age-Adjusted Cancer Death Rates• for . Selected Sites, Males , United States, 1930-1986 "~.. \\ -- "~ ~ /' - - i.. . _ .._ :~ i - . -- ..._ . - --- - ~ _ -- ~ - _ FIGURE 6.-Lnng cancer mortallty ratlos ot temak c{garette smokers, compared to never smokers, by dail7 cigarette consumptbn s SOURCE: CPS-11 191t2-R6. ACS. 1 These data also dramatically illustrate that the current lung cancer epidemic in wnmen is confined to those who smoke cigantttes (Figure 7). Agsssfand.rdlzed d.ath nlatas p.r 100,000 wonf.n 160 100 ao =NOARnfOlosrS ® Zln10kNO 64.1 25.0 M iqeae4 11"t{-01411 FIGURE 7. [.unR cancer death rates anxing temales over time Sl1URl'F CPS•1.nd CP5-11. ACS. 44 te

Public Health Cigarette Smoking Act of 1969. TThese laws required a health warning on cigarette packagcs, banned cigarette advertising in the broadcast media, and called for an annual report on the health consequences of smoking. In 1964, the Public Health Service established a small unit called the National ClearinRhouse for Smoking and Health (NCSH). Through the years, the Clearinghouse and its successor organization, the Office on Smoking and Health, have been respon- sible for the 20 reports on the health consequences of smoking previously mentioned, eight of which have been issued during my tenure as Surgeon General. In close coopera- . tion with voluntary health organi.-ations, the Public Health Service has supported high- ly successful school and community programs on smoking and health, has disseminated research findings related to tobacco use, and has ensured the continued public visibility of ant ismok ing messages. Throughout this period, tremendous changes have occurred. As detailed in this Repnrt, we have witnessed expansion in scientific knowledge of the health hazards of smoking, growing public knowledge of the dangers of smoking, increased availability of programs to prevent young people from starting to smoke and to help smokers quit, and widespread adoption of policies that discourage the use of tobacco. Most important, these developments have changed the way in which our society views smoking. In the 1940s and 1950s, smoking was chic; now, increasingly, it is shunned. Movie stars, sports heroes, and other celebrities uced to appear in cigarette advertisements. Today, actors, athletes, public figures, and political candidates are rarely seen smoking. The ashtray is following the spittoon into oblivion. Within this evolving social milieu. the population has been giving up smoking in in- creasing numbers. Nearly half of all living adults who ever smoked have quit. The most impressive decline in smoking has occurred among men. Smoking prevalence among men has fallen from 50 percent in 1965 to 32 percent in 1987. These changes represent nothing less than a revolution in behavior. The antismoking campaign has been a major public health success. Those who have participated in this campaign can take tremendous pride in the progress that has been made. The analysis in this Report shows that in the absence of the campaign, there would have been 91 million American smokers (15 to 84 years of age) in 1985 instead of 56 million. As a result of decision,c to quit smoking or not to start, an estimated 789.000 smoking-related deaths were avoided or postponed between 1964 and 19R5. Further- more, these decisions will resuh in the avoidance or postponement of an estimated 2.1 million smoking-related deaths between 1996 and the year 20(l0. This achievement has few parallels in the history of public health. It was ac- complished despite the addictive nature of tobacco and the powerful ecor.-amic forces promoting its use. The Remaining Challenges Despite this achievement, smoking will contimte ns the leading cause of preventable, premature death for many years to cMne, even if all snxokerx were to quit today. Smok- ing cessation is clearly beneficial in reducing the risk of dying from smoking-related diseases. However, for some diseases, such as hmg cancer and emphysema: quitting may not reduce the risk to the level of a lifetime nonsmoker even after many years of abstinence. This residual health risk is one reason why approximately, 390,000 Americans died in 1985 as the result of smoking, even after two decades of declining smoking rates. The critical message here is that progress In curtailing smoking must continue, and ideally accelerate, to enable us to turn smoking-related mortality around. Otherwise, the disease impact of smoking will remain high well into the 21 st century, Just maintaining the current rate of progress is a challenge. Compar4d with non- smokers, smokers are disproportionately found in groups that are harder to reach, and this disparity may increase over time. Greater effort and resources will need to be devoted to achieve equivalent reductions in smoking among those whose behavior has survived strong, countervailing social pressures. Today, thanks to the temarkable progress of the past 25 years• we c Mre to en- vision a smoke-free society. Indeed it can be said that the social tide is flving toward that bold objective. To maintain momentum, we need to direct special attention to the following groups within our society: ' Children aed Adolewenb ! As a pediatric sutgeon. and now as Surgeon General. I have dedicated.my career to protecting the health of children. In the case of smoking, children and adeAesCents hold the key to progress toward curbing tobacco use in future generations. If the adult rate of smoking were to continue at the present level, the impact of snmk- ing on the future health and welfare of today's children would be enormous. Research has shown that one-fourth or tnas of all negular cigarette smokers die of smoking-re- lated diseases. If 20 million of the 70 million children now living in the United States smoke cigarettes as adults (about 29 percent). then at least 5 million of them will die of smoking-related diseases. This figure should alarm anyone who is concemed with the future health of today's children. Two additional factors tnake tmaking among young people a preeminent public health concern: (1) the age of initiation of smoking, and (2) nicotine addiction. As this Report shows, four-fifths of smokers born since 1935 started smoking before age 21. The prvpottan of smokers who begin smoking during adolescence has been increas- ing over time, particularly amung women. In the Teenage Smoking Survey conducted by the Dep>r+tttent of Health• F.dtwation• and Welfare in 1979, respondents were asked. "What would you say is the possibility that five years from now you will be a cigatette smoker?" Among smokers, half answered "definitely not" or"probably tat." This response suggests that many children and adolescents are unaware of, or undetes<tm.te, the addictive nature of smoking. The predecessor to this volume, The Health Consequences ojSmoking: Nicotine Addiction. provided a comprehensive review of the evidence that cigarettes and other fotms of tobacco are addicting and ahat nicotine is the drug in tobacco that causes addiction. These two factots refute the vgument thd smoking is a matter of free!choice. Most smokers start smoking as teenagers and then become addicted. By the time smokers v

The last 25 years have witnessed phenomenal changes in the way Americans think about tobacco use. More people now than ever before consider smoking to be outside the social ncxrn. Antismoking pmgrams and policies have contributed to this change. This shift in societal attitudes is almost certain to generate additional efforts to further limit the use of tobacco. Almost half of all living Americans who ever smoked have quit. This is especially remarkable when one takes into account the powerful media images enticing people to smoke and the powerfully addictive nature of nicotine. As the downward trends in smoking behavior continue, we can expect to see a decline in the number of premature deaths and avoidable morbidity due to smoking. For now, however, we must recognize that continued tobacco exposure in the popula- tion will cause a great deal of human suffering for many decades. Thus, we must not rest upon the laurels of the past quarter century. As long as children and adolescents continue to find reasons to use tobacco, replacements will be recruited for at least some of the smokers who quit or who die pn:maturdy. If current trends continue, these re- placements will be found disproponionately among minority groups, among the less educated, among the most economically disadvantaged, and among women. We must look back on the last 25 years of change in order to look forward to our tasks for the future. Surely those tasks include expanding educational efforts for the young and old alike, restrictions against minors' access to tobaeco, support for cessa- tion activities, and restrictions against smoking in worksites, restaurants, transportation vehicles, and other public places. The Public Health Service is dedicated to continuing the legacy of the 1964 Report. We hope this 25th Anniversary Report will stimulate new commitment to action by public health officials, civic kaders, educators, scientists, and the public at large on the problem of tobacco use, especially among chiklrrn, adolescents, and high-risk groups. Robert E. Windom, M.D. James O. Mason, M.D.. Dr.P.H. Assistant Sectetary for Health Dinector Public Health Service Centers for Disease Control £089 I8SIS PREFACE Exactly 25 years ago, on January 1 t, 1964. Luther L Terry, M.D., Surgeon General of the U.S. Public Health Service, released the report of the Surgeon General's Ad- visory Committee on Smoking and Health. That landmark document, now referred to as the first Surgeon General's Report on Smoking and Health, was Antprica's first wide- ly publicized official recognition that cigarette smoking is a cause of cancer and other serious diseases. 'I On the basis of mae than 7,000 articles relating to smoking and disease already avail- able at that time in the biomedical literature, the Advisory Committee concluded that cigarette smoking is a cause of lung cancer and laryngeal cancer yn'men. a probable cause of lung cancer in women, and the most important cause of chronic bronchitis. The Committee stated that "Cigan:tte smoking is a health hazard of suff icient impor- tance in the United States to warrant appropriate remedial action." `' What would constitute "apptopriate retnedial action" was left unspecified. But the release of the report waa the first in a seties of steps, still being taken' 25 years later, to diminish the impact of tobacco use on the health of the American people. This 1989 Report, the 20th in a series of Surgeon General's Reports on the Health Consequences of Smoking, spells out the dtamatic progress that has been achieved in the past quarter century against one of our deadliest risks. The circumstances surrounding the rekase of the first report in 1964 are worth rernembering. The date chosen was a Saturday morning, to guard against a precipitous reaction on Wall Street. An auditorium in the State Department was selected because its security could be assured-it had been the site for pre.s.s conferences of the late Presi- dent John F. Kennedy, whose assassination had occurred less than 2 months earlier. The first two copies of the 387-page, btvwn-covercd report were hand delivered to the West Wing of the White House at 7:30 on that Saturday morning. At 9:00, ac- credited press representatives were admitted to the auditorium and "locked in," without access to telephones. Surgeon General Terry and his Advisory Committee took their seats on the platfomt. The Report was distributed and reporters were allowed 90 minutes to read it. Questions were answered by Dr. Terry and his Committee mem- bers. Finally, the doora were opened and the news was spread. For several days, the Report furnished newspaper headlines across the country and lead stories on television newscasts. Later it was ranked among the top news stories of 1964. During the quarter century that has elapsed since that report. individual citiaens, private organizations, public agencies, and elected officials have tirelessly pursued the Advisory Committee's call for "appropriate remedial action: " F.arty on, the U.S. Con- gress adopted the Federal Cigarette Labeling and Advertising Act of 1965 and the ~~;

epithelial lining of the tracheobrrxtchial tree may be damaged and lung cancer may ul- timately result. Extensive epidemiologic data from studies of uranium and other un- derground miners have established a causal association between exposure to radon daughters and lung cancer (National Research Council 1988). The committee on the Biological Effects of Ionizing Radiation (BEIR ) IV concluded that the studies of miners indicated synergism between cigarette smoking and radon decay pmducts (National Re.carch Council I9RR). The evidence, however, was not considered adequate to deter- mine if the interaction was multiplicative or suhmultiplicative. To date, cpidcmiologic investigations of domestic radon daughters as a risk factor for lung cancer have been limited and preliminary (Samet et al. 198R). However, it is assumed that radon decay products are carcinogenic in the indoor environment as they are in the mining environment. Dosimetric analyse.c indicate equivalent car- cinogenicity in the domestic and mining envir+onments (National Research Council 1988). Thus, radon must he considered one of the most important factors interacting with cigarette smoking. All smokers are exposed to radon, some at unacceptable levels. Quantitative estimates of the contribution of radon to lung cancer arc variable. The es- timates vary with the underlying assumptions and the risk model employed (Samet et al. 19RR). Although cigarette smoking is by far the major cause of lung cancer, radon must also he considered a cause of the disease. The public health burden of radon-related lung cancer is substantially increased by the synergism between cigarette smoking and radon exposure. Diet Diet has recently been considered as potentially influencing the risk of lung cancer in smokers. Nutrients of particular interest include preformed vitamin A, carotene, vitamin I- and vitamin C(Coklitz, Stampfer. Wiltett 19g7). An enlarging body of experimental and epidemiologic evidence supports the hypothesis that the risk for certain cancers varies inversely with consumption of preformed vitamin A or beta-carotene, its precursor (Peto et al. 1981; National Academy of Sciences 1982. CColditz. Stampfer, Willett 1987). The biological plausibility of this hypothesis derives frnm the known effects of vitamin A deficiency on the,differentiation of epithelial surfaces, from in vitro and in vivo models, which show that rctinoidc can suppress the development of malignancy, and from possible an- ticarcinogenic activity of beta-carotene, the principal dietary ptecursor of vitamin A ( Peto ct al. 19R 1: National Academy of Sciences 19g2). The epidemiologic evidence indicates a protective effect of dietary vitamin A intake from vegetable sources, hut not of preformed vitamin A, which is derived from meat and dairy sources, and vitamin supplcments. Clinical trials nn vitamin A and lung cancer risk are in progress. Vitamins E and C are antioxidants, which might have anticancer effects. To date. the ef+idemiologic data on these vitamins arr sparse and inconclusive (Coldiv, Stampfer. Willctt 19R?), SmokinR Cessation Cessation of cigarette smoking results in a gradual decrease in lung cancer risk. Several of the prospective and retrospective epidemiologic studies have demonstrated a reduction in lung cancer risk over time following smoking cessation. One example is provided from the U.S. Veterans study (Kahn 1966) (Figure 9). Other recent studies have continued to confirm the benefit of smoking cessation for lung cancer risk (Lubin et al. 19lWb; Alderson, Lee, Wang 1985; Pathak et a/: 1996; H iggins. Mahan. W ynder 1988). For example. Lubin and col leagues (19R46) described the pattern of reduction in risk following smoking cessation in a case-control study that Mortality Ratio 25 r 20 15 to 7.73 4.71 4.e1 2.1 J_-- I 5 0 1-4 5-9 I 10-14 15-19 20+ Nonsmoker Number of Years Stopped Smoking , FIGURE 9.-Lung cancer mortaiity ratio for male former smokers S(NlRCI? U.S. Veterae.IKrM 10M). involved 7,181 lung cancer patients and 11,(l0G controls). For men and women in this study who had smoked for less than 20 years and had not smoked for 10 years. the risks of lung cancer were approximately the same as those of lifelong nonsmokers. On the basis of the study of British physicians. Peto and Doll (1984) have suggccted that the effect of cigarette smoking cessation is to fix the age-specific risk of lung cancer at the rate achieved at the time of cessation, based on the smoking history up to that time. Ac- cording to this analysis, the former smoker's relative risk of lung cancer decline. as the background ratc for lung cancer rises with age. Therefore. smoking cessation is clearly beneficial in reducing the risk of lung cancer compared with continued smoking: but cessation may not reduce the risk to the levels of a lifetime non.moker even after many years of cessation. (See Table 2, ChaPtcr 3.) 11 0fi89 T8SiS S~

i TAIi1,F I.-Continued Highlights of Conclusions and Findings Year 1094 10R(r Suhjeel/HiEhliRhn Reviewed evidence on smokinR.nd chronk nhqrucyive luna disease (COLD). Concluded that smnkinR is the majnr cwse of COtA. accamtinR for Rn to 00 percent of C(H..D deaths in the United States. Nrwed that CnLD mtxbidity has Rreater social impact than C(nA nwirtality because of exlended disahility pcriodt of C(N,D victims (US DHHS 191N). F.xamined tdatinnship hetween emnkinR tled hv.wdan sahstances in the wrwlcplace. Fand that for the majority of.nqkers. smoking is a greater cause of ckath and disahility than their workplace envimrunent. Risk of IunE cancer frMn ashesnn eupKUre characteriml as nwhiplicative with smnking exposure. (k+served special importance of snmkinR pevcrNion among Mue.collar .wmkers hecause of their greater expnwe In workplace hasards and their hirher pevaknce nf smnlun6 (I IS tN IHS t9RS), Fwu.ed on involuntary smokinR. eonehMtinR that "Involumary smoking is a cause of disea.e. including lung cancer, in heahhy nonsme>tcers." Also found that. compned with children of nonsnwtken. children of smokera have higher incidence of tespir.tory infections and sympom.s and reduced n„es of increase in IunR function. Presented detailed examination of (trowth in nstrinion.s on smohinR in public places and workplacex. Concluded that simple separation of smol¢erx ard nnn.smohers within same airspace reduces but dnes not eliminate e.posure to envimnmentat tobacco snx+ke (US tKiHS 19Rtia). I Major Conclusions As the present Report documents, knowledge of the health consequences of smok- ing has expanded dramatically since 1964, and programs and policies to combat the hazards of smoking have proliferated. The essential chapter-specific conclusions relat- ing to these and other topics of this Report are presented at the end of each chapter and are reproduced in the final section of this introductory chapter. The major cdnclusions of the entire Report. immediately following, address fundamental developments over the past quarter century in smoking prevalence and in mortality caused by 'smoking. The first two conclusions highlight important gains in preventing smoking and smok- ing-related disease in the United States. The last three conclusions emphasize sources of continuing concern and remaining challenges. ! 1. The prevalence of snaking amonR aduks decreased from 40 percent in 1965 to 29 percent in 1987. Nearly half of all living adults who ever smoked have quit. ; f 2. Between 1964 and 1985, approximately three-quarters of a million snooh- inR-related deaths were avoided or postponed as a result of decisions to quit smoking or not to start. Each of these avoided or postponed deatIhs ~epre- sented an average gain In life expectancy of two decades. 3. The prevalence of smoking remains higher amonR blacks, blue-collar workers, and less educated persons than in the overall population. The decline In smoking has been substantially slower among women than among 19Rr," Speci.l R of.dv' ' 19RR _V "t+t) eon"nM1ee appanled by 1he SurReon General to Wudy the health consequences of smnheless tobacco. Concluded that use of smokelea tobacco can cause cancer in humans and can lead to nicotine addiction (US DHHS 19Rt+b). EuaMished nfcotine as a highly addictive >atfuannoe, cdn{arabk in its physiobEical aed psychokhtical prnperties to otAer addictive sutruances of a1mse (US DHHS 19RR). 'F.seluded fnvn cauM uf.e.in veli.nty {n kat heew.e nn new evideace w.s n;viewed. "E.. IudM frae arum ef xeie+ vahrnem in teat hrcwwit wa a SPecid Rqmnn. wot in Me +eriea deperu an vunkinR anl lWahh. inr- prevalence and, in necent years, the intensification of public and private measures to discourage smoking. A quarter century after publication of the first Repfxt, smok- inR remains the leading cause of preventable premature death in our society. hut per capita cigarette consumption is declining annually, and analyses of consumption and diccasc trends augur eventual decreases in smoking's toll. Given these chang!s, the remaining toll of tobacco-related disease. and the Surgeon reneral's objective of a smoke-free society by the year 2(ltlt) (Koop 1984). Surgeon Ccncr:ll C. Everett Koop devotes this 25th anniversary edition of the Surgeon General's Rcixin to an assessment of progress against smoking in the quarter century since the fircl Report was published. 8189 18SIS men. I 4. Smoking begins primarily during childhood and adolescence. T6e age of initiation has falkn over time, particularly among femaks. Smoking among high school seniors leveled off from 1980 through 1987 after pre- vinus years of decline. 5. SnakinR is responsl6k for more than one of every six deaths in the United States. Srnoking remains the single most important preventable cause of death in our society. Key New Findings While this Report is designed to provide a retrospective view of smoking and health over the past 25 years, several findings never previously documented in a report of the Surgeon General emerged during the process of reviewing and analyzing the voluminous materials consulted for the study. Discussed in detail throughout the Report, key new findings include the following: 10 11

(Lubin et al. 1984a; Lubin et at. 19R4b). However, dose-response relationships could not he demonstrated between relative risk and the propoation of years nonfilter brands were smoked or with a cigarette tar index. Among sustained smokers, switching from nonfilter to filter cigarettes was associated with a small reduction in risk (Lubin et al. 19R4a). The results from anothcr recent case-eontrol study conducted in Cuba also did not show a convincing association between tar intake and relative risk of lung cancer (Joly, Lubin, Caraballoso 1983). In New Mexico, a case-control study found that lifelong filter cigarette smokers and smokers of hoth filter and nonfilter cigarettes were at lower risk than lifelong smokers of nonfilter cigarettes only (Pathak et al. 1986). l lowever, there was no evidence of decreasing risk as the extent of filter smoking in- creased. In addition, few data are available on the reduced risk of smoking low-tar or filter cigarettes for any other smoking-rclated disease (see Chapter 3). Wotnen and Lung Cancer In 1964, at the time of the first Surgeon General's Repcxt, lung cancer was the lead- ing cause of cancer mortality in males, but was only the fifth leading cause of cancer mortality among women. In 1964, the male-femak ratio of death rates from lung can- cer was 6.7. The 1964 Report did not determine that smoking was causally related to lung cancer in women, although the suggestive nature of the evidence was cited in the Report's conclusion on lung cancer. The consistency of the male-female differences in lung cancer mortality with temporal trends of smoking was noted. In the 25 years that have elapsed since the 1964 Report, lung cancer mortality has in- creased dramatically in women. In 1986, lung cancer and breast cancer were the lead- ing causes of cancer death in U.S. women, accounting for approximately equal num- bers of cancer deaths (Fgute 4); lung cancer deaths are now projected to have surpassed breast cancer deaths (American Cancer Society 19RR). Lung cancer mortality for women now equals that observed for men three decades earlier and the male-female ratio of death rates has now fallen to 2.0. Since the late 1970s, the rise in the age-adjusted death rates of lung cancer among men began to level off (Horm and Kessler 1986) ((Figure 5). In contrast, lung cancer death rates among women continue to climb (Figure 4). As Figures 4 and 5 demonstrate, lung cancer is the only major cancer whose death rates have increased substantially and steadily since the 1930s. The dramatic increase among women began apt+rox imatety 30 years after the increase for men, consistent with the later adoption of smoking by women; the slope of the curve for women appears to be nearly identical to that of men 30 years earlier. Figure 4 also dcmonstrates that among women, the lung cancer death rate closely approximated the breast cancer death rate in the mid-198us. Illustrative of the importance of lung cancer in overall cancer mortality is the fact that, excluding lung cancer, the Nation's age-adjusted cancer death rate fell by 13 percent from 1950 through 19R2. Including lung cancer, the rate increased by 8 percent (Bailar and Smith 19R6). The mounting evidence on smoking and lung cancer in women led to a strengthen- ing of the tentative conclusion in the 19fi4 Report. The 1971 Report concluded that "Cigarette smoking is a cause of lung cancer in women Mlt accounts for a smaller 80 ttAt, o.r 10,00 bttt.n rtlP.ru.N COcer Desth Hstes' for r- Selected SNes, Fenales, 70 Unibed Sfts, 1930-1986 60 50 40 30 20 10 1940 1950 1wo I" -•-•-•-• Ot1tRr --- -- bast -. • _ • . _ • U/arth 1970 1980 1990 - •- • -C.bn dr Iktstwn - • • - Uukanla ------- UNr ............ p~tt~ntn FIGURE 4. ARe-adjusted earacer death rates for sekcted sites, females, United States,1930416 Adjr.kd a, oe 4e diuribaMm af die U.S. Cew... tOINPIeM111„r (he Cenwa 5()('R(TS OF DATA: NMin~l Cenle~ r~ ~~h ~~~ U's ~w proportion of cases than in men" (US DHEW 1971). The conclusion of the 1979 Report was similar (US DHEW 1979). The 1990 Report (US DHHS 1980). concerned with smoking and women. and the 1982 Report (US DHHS 1982). concerned with smoking and cancer, comprehensively reviewed the epidemiologic data and reaffirmed the ear- lier conclusions concerning the causal association of smoking and lung cancer in 47 -- ----SteeMC~

beccmie adults, when they would he expected to have greater appreciation of the health effects of smoking, many have difficulty quitting. Today. R(1 percent of smokers say they would like to quit; two-thirds of smokcrs have made at least one serious attempt to quit. Characteristically, people quit smoking several times before becoming per- manent ex-smokers. The prevalence of daily smoking among high school seniort leveled off from 1981 through 19R7, at about 20 percent, after previous years of decline. Each day, more than i,(1(10 American teenagers start smoking. If we can substantially reduce this number, we will scxm achieve a major impact on smoking prevalence among adults. Although rc.earch efforts in prevention are increasing, prevention programs are not yet reaching large numhcrs of young people. The public health community should pay at least as much attention to the prevention of smoking among teenagers as it now pays to smok- ing cessation among adults. Comprehensive school health education, incorporating tobacco use prevention, should he provided in every school throughout the country. Women S ince rrlease of the first Surgeon General's Report, the prevalence of smoking among women has declined much more slowly than among men. If current trends continue, smoking rates will be about equal among men and women in the mid-1990s, after which women may smoke at a higher rate than men. The public health impact of this trend is already being seen. Lung cancer mortality rates are increasing steadily among women, and estimates by the American Cancer Society indicate that this disease has now overtaken breast cancer as the number one cause of cancer death among women. Smoking during pregnancy poses special risks to the developing fetus and is an important cause of low birthweight and infant mor- tality. Smoking and oral contraceptive use interact to increase dramatically the risk of cardiovascular disease. Women's organizations and women's magazines have paid scant attention to these issues. The key to addressing this problem is the prevention of smoking among female adolescents. The disparity in smok ing pnevaknce between men and women is primari- ly a reflection of differences in smoking initiation. Smoking initiation has declined much more slowly among females than among maks. This difference is due, in large part, to increasing initiation rates among less educated young women. Among high school seniors, the prevalence of daily smoking has been higher among females than among males each year since 1977. In summary, women, and especially female adolescents not planning higher educa- tion, arc an important target group for prevention activities. Minorities Smok ing rates are higher in certain racial and ethnic minority grrsups, many of which already suffer from a disproportionate share of risk factors and illness. In particular, smoking prevalence has been consistently higher among black men than among white men (41 and 31 percant, respectively, In 1987). In addition, the limited data available show higher rates of smoking among Hispanic men than among white men. Trends in smoking initiation, prevalence, and quitting among blacks and whites show similar rates of change from 1974 to 1995. Thus, the gap in smoking prevalence be- tween blacks and whites is not widening.,,i3owever, to reduce the gap in smoking be- tween blacks and whites, prevention efforts must focus on blacks more successfully. The public health community is only now beginning to address this problem. The ur- gency of the situation is greater because cigarette companies are incfeasingly targeting their marketing efforts at blacks and Hispanics. Blue-collar Workers The prevalence of smoking has been consistently higher among bue-collar workers than among white-collar workers. In 1985.40 percent of blue-coll workers smoked compared with 28 percent of white-collar workers. Again, blue-collar workers are a major target of cigarette company advertising and promotional campaigns. Worksite smoking cessation programs, employee incentive programs, and pblicies banning or restricting smoking at the workplace are effective strategies to reach this group. i Toward a Smoke-Frte Fbture i Because the general health risks of smoking ane well known, because amoking is banned or restricted in a growing number of public places and worksites, and because smoking is losing its social acceptability, the overall prevalence of smoking in our society is likely to continue to decline. The progress we have achieved during the past quarter century is impressive. Equally impressive, however, are the challenges we face. During the next quarter century and beyond, progress will be slow, and smoking-related mortality will remain high, unless the health community more effectively reaches children and adolescents, women, minorities, and blue-collar workers. Organizations that represent these groups can contribute substantially to the antismoking movement. In large part, the future health of these populations will depend on the degree to which schools, educators. parents' organizations, women's groups, minority otganizations, employen, and employee unions join the campaign for a smoke-free society. Hen; in the United States, such a society is an attainable long-term goal. Unfortunately, the looming epidemic of smoking and smoking-related disease in developing countries does not encourage similar optimism. According to the World Health Organization, increases in cigarette consumption between 1971 and 1991 ex- ceeded population growth in all developing regions: by 77 percent in Africa, and by ;i0 percent in Asia and Latin America. The topic of tobacco and health intemationally, although critically important, espe- cially for developing nations, is beyond the scope of this Report. 1, can only hope that 5089 L8StS vii

private sectors. Thus, as part of the history of smoking and health, and as a determinant of progress against smoking, smoking-related policy is examined in detail in this 25th anniversary Report. Coverage of policy in Chapter 7 includes documentation of trends in specific l+olicies, analogous to the coverage afforded smoking restrictions in the 1996 RReport. Policies are grouped into three categories: policies pertaining to information and education (Part 1); economic incentives (Part 11); and direct restrictions (Part III). Where lxxcihle, ditcussion includes examination of scientific understanding of specific policy effects. Such understanding derives from a growing and increasingly sophisti- cated body of empirical social science research. Collectively, the I+mgram and policy efforts discussed in Chapters 6 and 7, combined with changing public knowledge and social norms, have encouraged tens of millions of Americans not to smoke. As examined in Chapter R, this behavioral change can he credited with the avoidance of many hundreds of thousands of premature deaths and the associated saving of millions of life-years. Chapter R reviews these and other find- ings on the behavioral and health consequences of changes in the Nation's smoking- and-health environment. Conclusions pertaining to the findings of each of the Report's chapters are reviewed in the final section of this introductory chapter. By all accounts, the 1964 Report of the Surgeon General's Advisory Committee is a landmark document in the history of public health and a seminal contribution to the Nation's effcxts to understand and combat tobacco-related morbidity and mortality. The present Report chronicks progress against smoking in the intervening 25 years, demonstrating an extraordinary array of advances in knowledge, changes in norms and behavior, and effects on the health of the American people. By any reasonable mcasure, the burden of smoking remains enormous; but the legacy of the 1964 Report is a society that has made imprcssive strides toward ridding itself of this most prevent- able source of disease, disability, and death. 19" Health Objectives for the Natbe In 1979, PHS released the first Surgeon General's Report on Health Promotion and Disease Prevention (US DHEW 1979b). The Report identified 15 priority areas, in- cluding smoking, in which significant health gains could be expected in the 1980s, with appropriate actions. Subsequently, working with health experts from both the private and public sectors, the PHS established 226 specific health objectives for the Nation (US DI IHS 19ROb). Seventeen of these pertain directly to cigarette smoking (Table 2). Many others relate to smoking as weli, because they address the prevention of heart di%ea~e, cancer, hurn injuries. and other smoking•rclated disease problems. In 1996. tthe PHS published a midcourse assessment of progress toward achieving the 226 oh- jectives (US DHHS 1986c). One of the goals of the present Report is to offer addition- al insight in this assessment as it relates to the 17 smoking objectives. This is discussed in the rclevant chapters. PI IS is currcntly developing national health goals for the year 2000, again working with organizations and individuals in the private and public sectors. The reduction of r 11. ;~ m Oe T ~ g m~O .gAD~ - u O. ~ I I a 1 M t I i 17 TZ89 T85TS

LarynReal, Oral, and FwphaReal Cancer The 1964 Surgeon General's Report concluded that cigarette smoking was causally related to laryngeal cancer in men and that pipe smoking was causally related to lip cancer (US PHS 1964). Subsequent rcports reviewed the accumulating epidemiologic evidence that established that cancers of the larynx, oral cavity, and esophagus are cau.cd by smoking in both men and women. The mortality ratios for these cancers are similar for smokers whether they smoke cigars, pipes, or cigarettes. A strong dcxe_ response rcl:uiom.hip exists, and the risk decreases with cessation, compared with con- tinued .moking. Recent studies have confirmed these findings (Blot et al. 1988: EI- w(xKi et al. 1994: Schottenfeld 19R4). (See Chapter 3.) Alcohol consumption is also a risk factor for oral, pharyngeal, laryngeal, and esophageal cancer. The combination of alcohol and smoking produces a synergistic increase in ri.k. In one study (Schottenfeld 1984), for all upper airway cancers corn-. hined, the rick was 8.6 for those smoking 30 or more cigarettes per (lay in combination with 20 oz of alcohol consumed per week. Rladder and Kidney Cancer A rclationship between smoking and bladder cancer was noted in the 1964 Surgeon General's Report. The 1979 Report concluded that cigarette smoking acts inde- pendently and probably acts synergistically with other risk factors to increase the risk of bladder cancer. The 1982 Surgeon General's Report concluded that cigarette smok- ing is a contributory factor for both bladder and kidney cancer. Cigarette smoking is estimated to account for 30 to 40 percent of bladder cancer (US DHHS 1982). Recent studies have confirmed earlier findings. For bladder cancer, in both men and women, cigarette smokers have a relative risk of 2 to 3. A dose-response relationship has been demonstrated, and the risk of bladdercancerdecneaces following smoking ces- sation (McLaughlin et al. 1984; Hartge et al. 1987; Zahm, Hartge. Hoover 1987). There is a positive association between smoking and kidney cancer, with relative risks ranging from I to mone than 5. '17rc increased risk of kidney cancer due to cigarette smoking is found for both males and females, and there is a dose-response relation- ship. a% measured by the number of cigarettes smoked per day. Pancreatk Cancer The first Surgeon General's Repott did not examine the relationship between smok- ing and cancer of the pancreas. Several subsequent reports of the Surgeon General have notcd that cigarette smoking is a contributory factor for pancreatic cancer. Ap- proximately 30 percent of pancreatic cancer mortality is attributable to cigarctte smok- ing. The m2ior Imnpective epidemiologic studies have consistently shown an increased rick of pancrcatic cancer among both male and female cigarette smokers. The mortality ratio for cigarette smokers compared with non.mokers is generally in the range of 2 to Tb89 ZBStS 3. A detailed review of the epidemiology of pancreatic cancer was written by Gonfio and Gold (19R4). For those in the MRFIT Study who smoked 40 or more cigarettes a day. the mortality ratio for pancreatic cancer was 2.3 compared with nonsmokers. Other rccent studies (Mack et al. 1996. Whittemore et al. 1985) report that cigarette smoking is strongly and consistently related to pancreatic cancer. Most epidemiologic studiec show a dose- rcsponse relationship between cigarette smoking and pancreatic cancer for both men and women and a gradual decline in the risk of developing pancreatic cance'.follow- ing smoking cessation. Autopsy studies report hyperplastic changes in the pancreatic duct cellc and,atypical changes in their nuclei among cigarette smokers compared with nonsmoker:. The pancreas is probably exposed to tobacco carcinogens or carcinogenic metaholites t present in bile or blood (US DHHS 1982). Stomach Cancer The 1964 Surgeon General's Report reviewed smoking and stomach cancer and, on the basis of the limited evidence available at that time, concluded that there was no relationship between smoking and stomach cancer. Evidence from pmspkctive and rctrospective studies available more recently has shown a small hut consistent increase in mortality ratios, averaging approximately 1.5 for smokers compared Witl4 non- smokers. Dose-response relationships have been demonstrated for the number of cigarettes smoked per day. The 1982 Surgeon General's Report concluded that cancer of the stomach is associated with cigarette smoking. Cervical Caecer Cancer of the uterine cervix was not reviewed in the 1964 Surgeon Genera)`s Report. The 1982 Report of the Surgeon General reviewed the studies published up to that time and concluded that further research was necessary to define whether there, was an as- sociation between cigarette smoking and cervical cancer. There are several risk factors for cervical cancer including early and frequent coitus. multiple sexual partners. pregnancy at an early age, and the presence of sexually trans- mitted diseases. Some of these risk factors may also be associated with smoking. Winkelstein and coworkers (1984) rreviewed 12 studies dealing with smoking and cervical cancer. and in most studies there was a positive relationship that could not he explained by other risk factors. Two studies published in 1995 confirmed these find- ings (Clarke et al. 1995; GGreenberg et al. 1985). Baron and coworkers (1986) reported on a case-control study of 1,174 patients with cervical cancer. Cigarette smoking was associated with a statistically significant in- crease in risk for cervical cancer. L.aVecchia and associates (19R6) in Italy studied the relationship between cigarette smoking and the risk of cervical neoplasia in agase-con- trol study of 183 wotnen with intraepithelial neoptacia. Cigarette smokitig was as- sociated with an increased risk of intraepithelial neoplasia and inva.ive cancer. This association could not be totally explained by potential confounding factors. In a casc- s6 57

Type of Lung Cancer and Smoking At the time of the 1964 Surgeon General's Report, the Kreyberg classification of lung tumors was being investigated. Group I Kreyberg tumors included the epidermoid and small-cell histology types: Group 2 Kreyberg tumors included adenocarcinoma and bronchioalveolar cell types. It was felt at that time that the Group I tumors, hut pmbah- ly not the Group 2 tumors, were associated with smok ing. The 1992 Surgeon General'c Report noted that smoking was related to all four major types of lung cancer: epider- moid. small cell, large cell, and adenocarcinoma. A detailed study of trends in type of lung cancer has been reported from Olmsted County. MN, a region where a large percentage of medical care is provided through the Mayo Clinic. The investigators measured the incidence by type of lung cancer during two intervals (19.i.S-34, 1975-79) over a 45-year period. The incidence rates for squamous (epidermoid), adenocarcinoma, small-celi, and large-cell lung cancer all in- creased during this time (Figure 8) (Beard et al. 19g5). Adenocarcinomas are more common than other cell types among nonsmokers, in whom lung cancer is rare. Pipe and Cigar Smoking Mortality ratios for lung cancer in those who have always smoked only cigars or pipes are significantly higher than in nonsmokers (US DHHS 1982). The mortality ratios are lower, however, than among those who have always smoked cigarettes. The risk of lung cancer increases in relation to the number of cigars smoked per day, the number of pipesful smoked per day, and the degree of smoke inhalation. The lower risk of lung cancer among pipe and cigar smokers compared with cigarette smokers is due to the lecser amount of tobacco smoked and the lower degree of inhalation. Chemical analysis of the smoke from pipes, cigars, and cigarettes indicates that car- cinogens are found in similar ievels in the smoke of all these tobacco products. Addi- tiorlally, experimental studies have shown that in a variety of animal models, smoke condensates from pipes and cigars are equally, if not mom. carcinogenic than conden- sates from cigarettes (US DHEW 1979). Determinants of Susceptibility Since the 1964 Repcxt, substantial epidemiologic and experimental investigation has been directed at the determinants of susceptibility to tobacco smoke; both environmen- tal exposures and host characteristics have been investigated. The identification of dctemlinants of susceptibility would not only further understanding of the mechanisms of carcinogenesis by tobacco smoking, but would offer new approaches for prevention (if lung cancer by identification of smokers at higher rick. Synergistic interactions among risk factors may place persons with particularly combinations of exposurcs at higher ri.k for lung cancer. Interactions among risk facaxs, such as cigarette smoking and occupational ex- pricures, may he either synergistic or antaFonistic; synergism refers to an increased ef- fect of the indcpcncknt exposures when hoth arc prescnt, whereas antagonism refers to t• 0 0 O Fl(:URE 8. Mean annual incidence rates Per 100,000 popuiation for maks of broncitogenic carcinoma by cell type, Olmsted County. MN, 19i5- 79, by decade SOURCF: Be.rd. Mrrcren. W-A-l 19R3). a reduced effect. Statistical methods are used with epidemiologic data to describe in- teractions. Either an additive or a multiplicative scale may be used to measure interac- tion statistically (Saracci 19g7). For two exposures, on an additive scale, the sum of the two independent relative risks reduced by one is compared with the relative risk ob- served when both exposures are present. On a multiplicative scale, the comparison rela- tive risk value is the product of the two independent relative ricks. For public health purposes, a positive departure from additivity is considered to represent synergism (Saracci 1987). As the extent of interaction increases.theproportionofthecxcesscases attributable to the interaction also increases (Saracci 1987). This Section briefly reviews the currcnt evidence on host characteristics and environ- mental agcnts that may modify the ri%k of cigarette smoking. I %1 cn

• Cigarette smoking is a major cause of cerebrovascular disease (stroke), the third leading cause of death in the United States. • By 19R6. lung cancer caught up with breast cancer as the leading cause of can- cer death in women. Women smokers' relative risk of lung cancer has increased by a factor of nxxt than four since the early 1960s and is now comparable to the relative risk identified for men in that earlier period. Gender differences in smok- ing behavior are disappearing; consistent with this, genderdiffetences in the rela- tive risks of and mortality from smoking-related diseases are narrowing. • Cigarette smoking is associated with cancer of the uterine cervix. • To date. 43 chemicals in tobacco smoke have been determined to be car- cinogenic. • In 1985. approximately 390.0(10 deaths were attributable to cigarette smoking. This figure is greater than other recent estimates of smoking-attributable mor- tality, reflecting the use of higher relative risks of smoking-related diseases for women and, especially in the case of lung cancer, for men. These higher rela- tive risks were derived from the largest and most recent prospective study of smoking and disease, conducted by the American Cancer Society. • Disparities in smoking prevalettce, quitting, and initiation between groups with the highest and lowest levels of educational attainment are substantial and have been increasing. Educational attainment appears to be the best single sociodemographic predictor of smoking. • There is growing recognition that prevention and cessation interventions need to target specific populations with a high smoking prevalence or at high risk of smoking-related disease. These populations include minority groups, pregnant women, military personnel, high school dropouts, blue-collar workers, un- employed persons, and heavy smokers. • One-quarter of high school seniors who have ever smoked had their first ciganttte by sixth grade, one-half by eighth grade. Associated with knowledge of this fact is a growing consensus that smoking prevention education needs to begin in elementary school. • Whereas past smoking control efforts targeting children and adolescents focused exclusively on prevention of smoking, the smoking rnntrol community has iden- tified the need to develop cessation prognims for children and adolescents ad- dicted to nicotine. • As of mid-19RR, more than 3201oca1 communities had adopted laws or regula- tions restricting smoking in public places. This compares with a total of about 90 as of the end of 1985. a more than threefold increase in 3 years. The number of new State lawc restricting smoking in public places in 1997 exceeded the num- ber Irassed in any Imcedinie year. t2 I • A growing body of evidence on the role of economic incentives in influencing health behavior has contributed to increased interest in and use of such jncen- tives to discourage ttse of tobacco products. These include excise taxation of tobacco products, workplace financial incentives, and insurance premium dif- ferentials for smokers and nonsmokers. • In marked contrast to the trends in virtually all other areas of smoking control policy, the number of legal restrictions on children's access to tobacco`qxoducts has decreased over the past quarter century. Studies indicate that vendor com- pliance with minimum-age-of-purchase laws is theexception rather than the rule. • The marketing of a variety of alternative nicotine delivery systems has heightened concern within the public health community about the future of nicotine addiction. The most prominent development in this regard wa4 the 1988 test marketing by a major cigarette producer of a nicotine delivery devite having the external appearance of a cigarette and being promoted as "t~e cieaner smoke." • While over 50 million Atttericans continue to smoke, tnore than 90 million would be smoking in the absence of the changes in the smoking-and-health environ- ment that have occurred since 1964. • Quitting and noninitiation of smoking between 1964 and 1985, encouraged by changes in that environtttent, have been or will be associated with the postpone- ment or avoidance of almost 3 million smoking-related deaths. That figure refkcts the three-quartets of a million deaths noted in conclusion 2 above, and an additional 2.1 million deaths estimated to be postponed or avoided between 1986 and the year 2000. Overvlew Coverage of the Report As the major conclusions and new findings suggest, progress against smoking is necessarily measured in several dimensions. Ultimately, the tnost important measure is the burden of mortality, morbidity, and disability associated with smoking. Secon- darily, changes in the prevalence of smoking and its distribution among sociodemographic groups fonaell the future course of smoking-rdated disease. Be- havioral changes in turn reflect a myriad of social and psychological influences that have evolved over the pa.st 25 years. 'lluse include public knowledge of smoking ha7ards and attitudes toward the behavior; availability and effectiveness of smoking prevention and cessation ptograms' and adoption of smoking-related social policies, often reflections of public attitudes and opinions. At the heart of all these phenomena is the substantial and expanding body of scientific knowledge about the he;ilth conse- quences of smoking. ;; 6t89 185TS

Part 1I1. Direct Restrictions on Smoking 1. Restrictions on smoking in public places and at work are growing in number and ccxnprehensiveness, as a result of both Government actions and private initiatives. Forty-two States and more than 320 communities have passed laws restricting smoking in public, and an estimated one-half of large businesses have a smoking policy for their employees. 2. The goal of thea smoking restrictions Is to protect individuals from the conse- quences of involuntary tobacco smoke exposure, but they may also contribute to reductions in smoking prevalence by changing the attitudes and behavior of cur- rent and potential smokers. Insufficient research has been undertaken to deter- mine the extent, if any. of these effects. 3. There arc fewer legal restrictions on children's access to tobacco products now than in 1964, despite what has been learned since then about the dangers of tobac- co use, its addictive nature, and the early age of initiation of smoking. 4. As of January 1, 1988, laws in 43 States and the District of Columbia restricted the sale of cigarettes to minors. Neverthekss, tobacco products are relatively easy for children to obtain through vending machines and over-the-counter purchases because of low levels of compliance with and enforcement of current laws. 5. Tobacco products have been exempted by law oradministrative decision from the jurisdiction of Federal regulatory agencies under whose authority they might otherwise fall. Chapter 8: Changes In the Smoking-and-Heakh Environment: Behavioral and Health Consequences 1. All birth cohorts born between 1901 and 1960 experienced neductions in the prevalence of smoking relative to the rates that would have been expected in the absence of the antismoking campaign. By 1985, the gap between actual (reported) prevalence and that which would have been expected ranged from 6 percentage points for the eldest female cohort to 28 peroentage points for the youngest male cohort. 2. In 1985, an estimated 56 million Americ.ns 15 to 84 years of age were smokers. In the absence of the antismoking campaign, an estimated 91 million would have been smokers. 3. Adult per capita cigarette consumption has fallen 3 to 8 pencent in years of major smoking-and-health events, such as publication of the first Surgeon General's Report on smoking and health in 1964. Per capita consumption fell each of the years ,the Fairness Doctrine antismoking messages were presented on television and radio (1967-70). 4. By 19R7. adult per capita cigan:tte consumption would have exceeded its actual level by an estimated 79 to 89 percent had the antismoking campaign never oc- curred. 5. One of the most substantial behavioral rosponses to concerns about smoking and health has been the shift toward filtered cigarettes in the I9.S0s and low-tar and low-nicotine cigatettes in the 1970s. The net health impact of these product chan- ges is unknown. I 6. As a result of the antismoking campaign, an estimated 789,000 deaths were postponed during the period 1964 through 1983, 112,000 in 1985 alone. The average life expectancy gained per postponed death was 21 years. 7. The avoidance of smoking-telated mortality associated with the antismoking cam- paign will represent a growing percentage of smoking-related morWity over time, as the principal beneficiaries of the campaign. younger men and women, reach the ages at which smoking-related disease is most common. Campaign-induced quitting and noninitiation through 1985 will result in the postponement or avoidance of an estimated 2.1 million smoking-related deaths between 1986 and the year 2000. 7o LZ89 iBStS 2R

specific content areas. An editorial team including the Director of OSH, a medical epidemiologist from OSH. and four non-Federal experts edited and consolidated the individual manuscripts into chapters. These draft chapters were subjected to an inten- sive outside peer rcview, with each chapter reviewed by 5 to 12 individuals knowledge- able about the chapter's subject matter. Incorporating the rcviewers' comments, the editors revised the chapters and assembled a draft of the complete Report. The draft Report was then submitted to 25 distinguished scientists for their review and comment on the entirety of its contents. Simultaneously, the draft Report was submitted to 9 in- stitutes and agencies within the U.S. Public Health Service for their review. Comments from the senior scientific reviewers and the agencies were then used to prepare the final draft of the Report, which was then reviewed by the Offices of the Assistant Secretary for Health and the Secretary. Department of Health and Human Services. Chapter Conciusions Chapter 2: Advances in Knowledge of the Health Consequences of Smoking Part I. Health Consequences I. The 1964 Surgeon General's Report concluded that cigarette smoking increases overall mortality in mert, causes lung and laryngeal cancer in men, and causes chronic bronchitis. The Report also found significant associations between smok- ing and numerous other diseases. 2. Reports of the Surgeon General since 1964 have concluded that smoking increases mortality and morbidity in both men and women. Disease associations identified as causal since 1964 include coronary heart disease, atherosclerotic peripheral vascular diseate, lung and laryngeal cancer in women, oral cancer, esophageal cancer, chronic obstructive pulmonary disease, intrauterine growth retardation, and low-birth-weight babies. 3. Cigarette smoking is now considered to be a probable cause of unsuccessful preg- nancies, increased infant mortality, and peptic uker disease: to be a contributing factor for cancer of the bladder, pancreas, and kidney; and to be associated with cancer of the stomach. 4. Accumulating research has elucidated the intetaction effects of cigarette smoking with certain occupational exposures to increase the risk of cancer, with alcohol ingestion to increase the risk of pncer, and with sekcted medications to produce adverse effects. 5. A decade ago, the 1979 Report of the Surgeon General found smokeless tobacco to be associated with oral cancer. In 1986, the Surgeon General concluded that smokeless tobacco was a cause of this disease. 6. Research in the pnesent decade hac estabiished that involuntary smoking is a cause of diseaa, including lung cancer, in healthy nonsmokers, and that the children of parents who smoke have an increased frequency of respiratory infections and symptoms. ' i. 7. In 1964, tobacco use was considered habituating. A substantial body of evidence accumulated since then, and summarized in the 1988 Surgeon General's Report. has established that cigarettes and other forms of tobacco are addicting. Given the prevalence of smoking, tobacco use is the Nation's most widcspread form of drug dependency. 8. Studies dating from the 19S0a have consistently documented the benefits of smok- ing cessation for smokers in all age groups. 9. Recent evidence, including that presented in this 1989 Report of the Surgeon General, documents that cigarette smoking is a cause of cere6rova-cular disease (stroke) and is as.cociated with cancer of the uterine cervix. Part Il. The Physicochemical Nature of Tobacco 1. The estimated number of compounds in tobacco smoke exceeds 4.006, including many 'hat are pharmacologically active, toxic, mutagenic, and carcipogenic. 2. Forty-three carcinogens have been identified in tobacco smoke. 3. Carcinogenic tobacco-specific nitrosamines are found in high conceptrations in smokeless tobacco. i Chapter 3: Changes in Sntoking-Atttibnfabk Mortality , ', 1. Lung cancer death rates irtcreaaed two- to fourfold among older male smokers over the two decades between the American Cancer Society's two Cancer Preven- tion Studies (CPS-I,19S9-6S. and CPS-I1,1982-86). Lung cancer death rates for younger male smokers fell about 30 to 40 percent during this period. 2. Lung cancer death rates increased four- to sevenfold among female smokers aged 45 years or older in CPS-II compared with CPS-i, while lung cancer death rates among younger..orrten declined 35 to SS percent. 3. 71te two-decade interval witnessed a two- to threefold increase in death rates from chronic obstructive pulmonary disease (COPD) in female smokers aged 55 years or older. 4. There was no change in the age-adjusted death rates for lung cancer and COPD between CPS-1 and CPS-11 among men and women who never smoked regularly. 5. Overall death rates from coronary heart disease (CHD) declined substantially be- tween CPS-1 and CPS-11. The decline in CHD mortality among nonsmokers, however, was notably greater than among current cigarette smokers. 6. In CPS-I1, the relative risks of death from cerebrovascular lesions were 3.7 and 4.8 for men and women smokers under age 65. Increased risks of stroke were also observed among older smokers and former smokers. Along with the recently reported results of other studies, these findings strongly support a causal role for cigarette smoking in thromboembolic and hemonfiagic stroke. 7. In 1985, smoking accounted for 87 perant of lung cancer deaths. 82 percent of COPD deaths. 21 percent of CHD deaths, and 18 percent of stroke deoths. Among men and women less than 65 years of age. smoking accounted for more than 40 percent of CHD deaths. FZ89 IBStS ,t 70

R. The large increase in smoking-attributable mortality among American women be- tween 1965 and 1995 was a direct consequence of their adoption of lifelong cigarette smoking, especially from their teenage years onward. 9. In I9R5, 99 percent of smoking-attrihutable deaths occurred among people who started smoking before the 1964 Surgeon t;,eneral's Report. For this group, the annual smoking-attributable fatality rate is about 7.000 deaths per I million per- sons at risk. 10. For 10 causes of death, a total of 337,000 deaths were attributable to smoking in 19R5. These represented 22 percent of all deaths among men and 1 I percent among women. If other cardiovascular, neoplastic. and respiratory causes of death were included-as well as deaths among newborns and infants resulting from maternal smoking, deaths from cigarette-caused residential fires, and lung cancer deaths among nonsmokers due to environmental tobacco smoke-the total smoking-attributable mortality was about 390,000 in 19R5. Chapter 4: Trends In Pabik Beliefk, Attitndes, and Opinions About Smoking 1. In the I9_S(k, 40 to 50 pencent of adults believed that cigarette smoking is a cause of lung cancer. By 1986, this proportion had increased to 92 percent (including 85 percent of current smokers). 2. Between 1964 and 1986, the proportion of adults who believed that cigarette smoking increases the risk of heart disease mse from 40 to 78 percent. A similar increase ocxurred antong smokers, from 32 to 71 percent. 3. The proportion of adults who believed that cigarette smoking increases the risk of emphysema and chronic bronchitis rose from 50 percent in 1964 to 81 percent (chronic bronchitis) and 99 percent (emphysema) in 1986. These proportions in- creased among current smokers from 42 percent in 1964 to 73 percent (chronic bronchitis) and 85 percent (emphysema) in 1986. 4. Despite these impressive gains in public knowledge, substantial numbers of smokers are still unaware of or do not accept important health risks of smoking. For example, the pt+oportions of smokers in 19R6 who did not believe that smok- ing increases the risk of developing lung cancer, heart disease, chronic bronchitis. and emphysema were 15 percent. 29 percent, 27 percent, and 15 percent. respec- tively. These percentages correspond to between 8 and 15 million adult smokers in the United States. 5. In 1995. substantial percentages of women of childbearing age did not believe that smoking during pregnancy increases the risk of stillbirth (32 percent), mis- carriage (25 percent). premature birth (24 pereent), and having a low-birth-weight baby (15 percent). Of women in this age group, 28 percent did not believe that women taking birth control pills have a higher risk of stroke if they smoke. 6. Some smokers today do not recognis.e their own personal risk from smoking or they minimize it. In 1986, only I8 percent of smokers were "very concerned" about the effects of smoking on their health, and 24 percent were not at all con- cerned. pZ89 18SZS I I I . 7. In 1986, about half of current smokers and 40 pencent of never smokers incorrect- ly believed that a person would have to smoke 10 or ntorc cigarettes per day before it would affect his or her health. g. A national survey conducted in 1983 by Louis Harris and Associates found that the public underestimates the health risks of smoking cotnpared with many other health risks. 9. Many smokers underestimate the population impact of smoking. In 1987.28 per- cent of smokers (and 16 petcent of the general population) disagreed with the statement, "Most deaths from lung cancer are caused by cigarette smoking." 10. The proportion of high school seniors who believe that smoking a pack or rnore of cigarettes per day causes great risk of harm increased from 51 percent in 1975 to 66 percent in 1986. 1 I. In 1986, about thtee-quarters of adults believed that using chewing~to4acco or snuff is harmful to health. 12. The social acceptability of smoking in public is declining, as mealkured by the proportion of adults who find it annoying to be near a person smoking cigarettes. This proportion increased from 46 percent in 1964 to 69 percent in 1986. 13. A majority of the public favors policies restricting smoking in publiC, places and worksites, prohibiting the sale of cigarettes to minors, and increa.sinj the cigarette tax to fund the Medicare ptvgtam. Recent surveys indicate that about,half the public supports a ban on cigatette advertising. ~~ Chapter S: Chattges In Smoking Beha.tor and Knowledge About Determinants Part 1. Changes in Smoking Behavior 1. Prevalence of cigarette smoking has declined substantially among mt'n, slightly among wmtten, and hardly at all among those without a high school diploma. From 1965-87, the prevalence of smoking among men 20 years of age and older decreased from 50.2 to 31.7 pt:ncent. Among women, the prevalence of smoking decreased from 31.9 to 26.8 percent. Smoking prevalence among whites fell steadily. Among blacks, the prevalence of smoking changed very little between 1965 and 1974: subsequetttly, prevalence declined at a rate similar to that of whites during the same period. Smoking prevalence has consistently been higher among blue-collar workers than tartong white-collar workers. 2. Annual per capita sales of manufactured cigarettes (18 years of age and older) decreased from 4,345 cigarettes in 1963 to 3.196 in 1987, a 26- percent reduction. Total cigarette sales increased gradually to 640 billion cigarettes in 1981 and then fell to 574 billion in 1987. 3. In 1965. 29.6 percent of adults who had ever smoked cigarettes had quit. This propcxtion (quit ratio) increased to 44.8 percent in 1987. The rate of increase in the quit ratio from 1965-85 was similar for men and women. The rate of change in quitting activity in recent years is similar for whites and blacks. Orom 1965- 85, the quit ratio increased more rapidly among college graduates than among adults without a high school diploma. ,? 21

Edward L Petsonk, M.D., Senior Medical Gfl'iar, Clinical Investigations Branch. Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health. Centers for Disease Conavl, Atlanta, Georgia John P. Pierce, M.Sc., Ph.D., Chief, Epidemiology Branch, Office on Smoking and Health. Center for Chronic Disease Prevention and Health Pnxnotion, Centers for Disease Control, Rockville, Maryland John M. Pinney, Executive Ditector, Institute for the Study of Smoking Behavior and Policy, John F. Kennedy School of Governntettt, Harvard University, Cambridge, Massachusetts Edward T. Pc,Pper, M.B.A.. D.B.A., Associate Professorof Marketing. Bryant College, Smithfield. Rhode Island William F. Raub. M.D.. Deputy Director, National Institutes of Health. Bethesda. Maryland Dorothy P. R ice, B.A., Sc.D.(Hon.), Professor in Residence. Department of Social and Behavioral Sciences, School of Nursing. University of California, San Francisco, San Francisco, California Lynn Gloeckler Ries, M.S., Division of Cancer Prevention and Control, Surveillance and Operations Research Branch, National Cancer institute, Bethesda, Maryland Ruth Roemer, J.D., Adjunct Professor of Health Law, School of Public Health. Univer- sity of California, Los Angeles. Los Angeks, California, Past President, American Public Health Association Kenneth J. Rothman, Dr.P.H., Professor of Family and Community Health. University of Massachusetts Medical School, Wonxster, Massachusetts Jonathan M. Samet, M.D., Professor of Medicine. Department of Medicine, Chief, Pul- monary Division, University of New Mexico, ARxtqnerque, New Mexico Thomas C. Schelling, Ph.D., Lucius N. Littauer PFofessorof Political Economy, Direc- tor. Institute for the Study of Smoking Behavior and Policy, John F. Kennedy School of Government, Harvard University, Cambridge, Massachusetts Marvin A. Schneidertnan, Ph.D.. National Academy of Sciences, National Research Council. Board on Environmental Studies and Toxicology, Washington, D.C. David Schottenfeld, M.D., M.Sc., John G. Searle Professor and Chairman, Department of Epidem'alogy. School of Public Health. Professor of Internal Medicine, School of Medicine, University of Michigan, Ann Arbor, Michigan Lowell E. Sever, Ph.D., Assistant Director for Science. Division of Birth Defects and Developmental Disabilities, Center for Environmental Health and Injury Control. Centers for Disease Control, Atlanta, Georgia Saul Shiffman, Ph.D.. Associate Professor, Department of Psychology, Dinxtor, Psychology Clinic, University of Pittsburgh, Pittsburgh, Pennsylvania Donald R. Shopland, Public Health Advisor, Smoking. Tobacco, and Cancer Program, Office of the Director, Division of Cancer Prevention and Control, National Cancer Institute. Bethe.sda, Maryland John Slade, M.D., Department of Medicine. University of Medicine and Dentistry of New Jersey. New Brunswick, New Jersey Jesse L. Stcinfeld. M.D., former Surgeon General, Public Health Service, San Diego, California xvi 0189 tBSZS Steven D. Stellman, Ph.D., Assistant CommisaionerforBiostatistics and Epidemiologic Research. New York City Department of Health, New York, New York ' Michael A. Stoto, Ph.D., Senior StaffOffiar, Institute of Medicine; National Academy ' of Sciences, Washington, D.C. James A. Swornley, Managing Director, American Lung Aesociation, New York, New York Owen T. Thomberry, Ph.D.. Director, Division of Health lnterview Statistics, Nation- al Center for Health Statistics, Centers for Disease Control, Hyattsville; Maryland William M. Tipping, Executive Vice President and Chief Executive Officer, American Cancer Society, Atlanta, Georgia Dennis D. Tolsma, M.P.H., Assistant Dinxtor for Public Health Practice, Centers for Disease Control. Atlanta, Georgia Frederick L. Trowbridge, M.D., Director, Division of Nutrition, Center foc'Chtonic Disease Prevention and Health Promotion, Centers for Disease Corytrol, , Atlanta, Georgia Diana Chapman Walsh, Ph.D., University Profasor. Professor of Publ'ic Health and Associate Director of the Health Policy Institute, Boston University. 8 ' oston, Mas- sachusetts I Judith P. Wilkenfeld, J.D., Program Advisor, Ciganette Advertising and Testing, Federal Trade Commission, Washington, D.C. , i Ronald W. Wilson, M.A., Director, Division of Epidemiology and Health Promotion. National Center for Health Statistics, Centers for Disease Control„ Hyattsville. Maryland Ernst L. Wynder, M.D., Ptesident, American Health Foundation, New York. New York James B. Wyngaarden, M.D., Director, National Institutes of Health, Bethesda. Maryland The editors also acknowledge the coatAbrrtions of tlu foltowinR staff "t<"'b'ers and othtrs who assisted in the preparation oJthis Rtport. Marltaret Anglin. Sectetaay.OEtice on Smoking and Health. Rockville. Maryland Charles Appiah. Project Cktk,'I1rc Circle. Inc.• McLean. Virginia John Artis, Courier, The Circk, Inc., McLan. Virginia John L. Bagrosky, Associate Director for Program Operations, Office on Smoking and Health, Rockville, Maryland Sonia Balakirsky, Secretary. Office on Smoking and Health, Rockville, Maryland Carol A. Bean, Ph.D., Project Ditector,'[1te Circle, Inc., McLean, Virginia Marissa Bernstein, Editorial Assistant. The Circle, Inc., McLean, Virginia Doreen M. Bonnett. Senior Editor,'I1te Circle, Inc., McLean, Virginia Catherine E. Burckhardt, Editorial Assistant,OfPiee on Smoking and Health. Rockvilk, Maryland Gayle A. Christman, Administtative Assistant, The Circle, Inc.. McLean; Virginia Carol K. Cummings, Secretary, Office on Smoking and Health. Rockville. Maryland Karen M. Deasy. Assistant to the Director for Special Projects. Office on Smoking and liealth, Rockville, Maryland .,,;;

Dawher et al. 197g). Improved diagnostic methods have provided a better categoriza- tion of the causes of stroke. Epidemiologic studies have shown that hypertension is the most important risk factor for stroke (US DHHS 1983). The I9(A Report of the Surgeon General stated that the large epidemiologic studies of Hammond and Hom (1958) and Dcxn (1958) had found a moderate increase in the mortality rate from cerebrovascular disease in cigarette smokers compared with non- cmokera. The 1971 Report (US DHEW 1971) reviewed six major prospective epidemiologic studies. Cigarette smokers in these studies experienced increased stroke mortality com- pared with nonsmokers. The 1980 Report (US DHNS 1990) noted that women who smoke have an increased risk of subarachnoid hemorrhage. The 1983 Report (US DHHS 1993) reviewed the data associating cigarette smoking with stroke and found an increased risk for stroke among smokers that was most evident in younger age groups. It also noted that women cigarette smokers experience an increased risk for subarach- noid hemorrhage and that the concurrent use of both cigarettes and oral contraceptives greatly increased this risk. Since the release of the 1993 Surgeon General's Report the relationship between cigarette smoking and stroke has been clarified in several large studies involving men and women. The risk of stroke was evaluated in a prospective study of 8.006 Japanese-American men living in Hawaii (Abbottet a1.19g6). After 12 years of followup, cigarette smokers had two to three times the risk of thromboembolic or hemorrhagic stroke compared with nonsmokers. The increased risk was independent of other risk factors such as hy- pertension and CHD. Those smokers who stopped smoking during the course of the study experienced more than a 50-percent reduction in the risk of stroke compared with ccxttinuing smokers. The impact of cigarette smoking on stroke incidence was assessed prospectively in the Framingham Study of 4.255 men and women (Wolf et al. 1988). This cohort was followed for 26 years. and the diagnoses were confirmed by clinical examination. Cigarette smoking made a significant, independent contribution to the risk of stroke. The risk increased ac the number of ciganettes smoked increased. Smoking cessation resulted in a significant decrease in stroke risk so that S years after stopping smoking the risk was at the level of nonsmokers. The relationship between cigarette smoking and the risk of stroke was evaluated in a prospective study of 118 S39 middle-aged women who were followed for. 8 years (Colditz. F3onita, Stampfer 1988). Compared with nonsmoking women, those who smoked I to 14 cigarettes per day had a relative risk of fatal and nonfatal stroke of 2.2. Those who smoked 25 or more cigarettes per day had a relative risk of fatal and non- fatal stroke of 3.7. In this latter group of wofnen, the relative risk of suharachnoid hemorrhage was 9.8. The contribution of cigarette smoking to increased stroke risk was independent of other risk factors. Smoking cessation resulted in a prompt decrease in stroke risk; the relative risk of stroke in women who had ctopped smoking for 2 years was 1.4. compared with women who had never smoked. Thc authors of this study also rcviewed eight prospective coh<xt audies and Ceven case-contrrl studies involving TABLE 3.-Semttlar7 dat.dks dciRairtlte =ohing Rnd stroke In women pret audror No. CotwA aia Type of tottoke of cnes ReMive rbk Prowecti.ecahon aaodk. Coldks 118.539 All 274 2.2 (9596 C7.1.S-3.3) 2.7 (9316 C1.1.9-3.7) 3.7 (939i Cl. 2.7-5.1) S.lonen 4.334 Mfirctloe 21 1.4 (9016 C1.0.4-3.0) odKr 314 0.a (9096 C1.0.3-2.2) T.rka 1.681 ~+em~ e 30 2.1(NS) al I.0 (NS) S.cco 2,421 SahanchtofA 22 1.6 veaxy 17.000 w Km age Sahar.dnoit) t3 3.0 ~k 33 1.4 l 194 6 Ceubnl daom- 66 0.5 far 15-24 efp- Dol laYde . 46.(100 bosis Subuacleoltl 20 renes/d.r Mhti 16.759 hnnmrh.ee St+bti»eMrofA 11 3.7 (90% Cl, t.tl-17.S) hanonfise other 23 4.a (90% C7.2.3-9.R) Wolf 2,421 AII 239 1.6 (pc0.tr2S) C..o-t+ontid rtudfe+ Tatw Snb.raeMo{d 124 2.6 far anearyam Se11 heo will Suba.eMoid 134 3.7(9016 Cl. 2.3-5.9) CollaborNive study hemorrha6e ~ 192 7 y 140 Abu•2'eid ~ 137 1.4 (NS) p 410 2.4(pN.001) tionna Sub,Xtiq{4 70 4.7 (939G C1. 2.9-7.6) Sonita Aemorrh.de Not t>sD.rach- 53 2.6 (95% C1.1.4-4.6) lle lus noid IetttortfiuiEe Suc(e 125 1.2 (93'16 C1.0.7-2.3) N0T8: Cl.aw/fdeneeMMerod Ns.not+itMlk.nt• SotiaCr:: Catein ttottst.We.(1"e). CotnnKna 1-14 ci6.reue+/d.y 15-24 cittneuee/dsy 225 ci6arenea/day Inetndeo 730 men Re" risk *a 2.9 for he~vr smokers ~ Risk eended to decrease with arnomM smoked ' i Smokets hd hiSAtx rialc of faul suharachnoid henwxrfia6e Bas<d on 6s fenuk cases Smokin6 doubkd risk No increased risk lncluded men ~ponx telationchip not siRnificant Included 78 mee bii89 T85tS ~ ~,~ ~ Fz

4. Of all adults who smoked at any time during the year 1985-86, 70 percent had made at least one serious attempt toquit during their lifetime and one-third stopped smoking for at least I day during that year. 5. The age of initiation of smoking has declined over time, particularly among females. Among smokers bom since 1935. ntone than four-fifths started smoking before the age of 21. 6. Trends in prevalence of ciganette smoking among time aged 20 to 24 years are an indicator of trends in initiation. By this ttte.a.sure, initiation has declined be- tween 1965 and 1987 from 47.8 to 29.5 percent. Initiation has fallen four times more rapidly among males than among females. The rate of decline has been similar among whites and blacks. Initiation has decreased three times more rapid- ly among those with 13 or more years of education than among those with less education. 7. The prevalence of daily cigarette smoking among high school senion decreased from 29 percent in 1976 to 21 percent in 1980, after which prevalence leveled off at 18 to 21 percent. Prevalence among females has consistently exceeded that among males since 1977. Prevalence was lower for students with plans to pursue higher education than for those without such plans. The difference in prevalence by educational plans widened throughout this period: in 1987, smoking rates were 14 percent and 30 percent in these two groups, respectively. R. The hest sociockntographic predictor of smoking patterns appears to be level of educational attainment. Marked differences in smoking prevalence, quining. and initiation have occurred and have increased over time between more and less edu- cated people. 9. The domestic market share of filtered cigarettes increased from 1 percent in 1952 to 94 percent in 1986. The market share of low-tar cigarettes (15 mg or less) in- creased from 2 percent in 1967 to 56 percent in 1981. after which this proportion fell slightly and then stabili>!ed at 51 to 33 percent. The market share of longer cigarettes (94 to 121 ntm) increased from 9 pencent in 1967 to 40 percent in 1986. 10. Between 1964 and 1986, use of smokekss tobacco (snuff and chewing tobacco) declined among men and women 21 years of age and older. However, among males aged 17 to 19, snuff use increased fifteenfold and use of chewing tobacco increased more than fourfold from 1970-86. 11. Differences in ptevalence of cigarette smoking and smokeles.s tobacco use be- tween young males and young females suggest that the prevalence of any tobac- co use is similar in these two groups. 12. From 1964 to 1986, the prcvalence of pipe and cigar smoking declitted by 80 per- cent among men. Part 11. Changes in Knowledge About Determinants of Smoking Behavior 1. Smoking was viewed as a habit in 1964 and is now understood to be an addiction influenced by a wide range of interacting factors, including pharmacologic effects of nicotine; conditioning of those effects to nunterous activities, emotions. and settings; socioeconomic factor.s; personal factors such as coping resources; and social influcncc f.scton. SZ89 Z8SZ5 2. Since 1964. there has been a gradual evolution of understanding of the progres- sion of smoking behavior through the broad stages of development, regular use, and cessation. Each of these stages is differentially affected by multiple'and in- teracting determinants. 3. Views of determinants of smoking are affected by the predominating theoretical and methodological perspectives. In smoking, the earlier focus on broad, disposi- tional variables (e.g.. extraversion) has given way to an emphasis on situation- specific and interactional variables: a focus on a search for a single cau<t has given way to a focus on multiple and interacting causes. Chapter 6: Smoking Prevention, Cessation, and Advocacy Activities Part 1. Smoking Prevention Activities 1. Diverse program approaches to the prevention of smoking among youth grew out of antismoking education efforts in the 1960s. These approaches inalude media- based programs and resources; smoking prevention as part of multjcomponent school health education; psychosocial prevention curricula; and a variety of other resources developed and sponsored by professional and volunt4y health or- ganis.ations. Federal and State agencies. and schools and community, gnqups. 2. Psychosocial curricula addressing youths' motivations for smoking and he skills they need to resist influences to smoke have emerged as the program approach with the most positive outcomes. Evolution in program content has been accom- panied by a shift since the 1960s in prevention program focus from youths in high school and college to adolescents in grades 6 through 8. 3. Existing prevention programs vary greatly in the extent to which they have been evaluated and used. Psychosocial prevention curricula have been intensively developed over the last decade and have been the most thoroughly evaluated and best documented; hoarover, they are generally not part of a divsemination system. More widely disseminated smoking prevention materials and programs, such as those using mass media and brochures, have not always been as thoroughly evaluated; however. they have achieved wider use in the field. 4. The model of stages of smoking behavior acquisition underlies current smoking prevention programs and suggests new intervention opportunities, ranging from prevention activities aimed at young children to cessation programs for adoks- cent smokers. 5. There has been and continues to be a lack of smoking prevention programs that target youth at higher risk for smoking, such as those from lower socioeconomic backgrounds or school dropouts. Part 11. Smoking Education and Cessation Activities 1. During the past 25 yearc, national voluntary health agencies. especially the American Cancer Society, the American Heart Association, and the American 2S

TARI,F c,__.('onfinued cnrrirrrurNr cuncenfratinn/tiFuetfe TABLE 6.-Major ccMtkretMs d tAe MrNcrlNe matter ot the mailnstresn~ smoke of noeAlter Aarette.+ (Hher vnlalilt aldrhv,k. (6) Aci•r.me tllher v.d;ni1C Ac1'wN % (t) Mi•thvwrl Other vol:uik :dcalwd.l7) Acetonitrik Other volatile nilrikc 1 Iltl Furan Other vutauk furan. (4) PyrNhne Picolinec (1) 3-Vinylpyri(line Other vntatile pyriJinec (_'S) Pyrrok PytmliAine N-MethylpyrrnliAine Vnl:nik pyraiinec /19) Melhytamine lAhcr atiphatic aminc% ( s2) AA-I 4n IIF Inn-fS3n NF sfl-Iftt1 VF Rfl-I ftn yF 1n-!(11tF` I (N)-1 Sn yr S(LRn :n-4(1 VF 45-1?5 uF` 2n-2(1()11F 1 5-1t(1 VF I(>-tnpF N1-Sfl NF.. n.1-In yF to- IR NF 2.f/-3.0 PF 1.(1-R.0 VF 4-In NF t-In NF 'Nunmhrrm m ryrrtnhr.r- verre.enl iiwlividwl rryvnrymal% wknlifirvl in a Fiven FnNM'. "Per..•m 'd hwa1 rnhaM. S/ ft' R('I . Ihdfn.an anA IkdN. in Irea.w chemical nature and cnmntratifxlc in cigarette smoke of agricultural chemicals and pcaic ides, which originate from the rcciduec of such cnm/x+unds in tobacco. There are m:fnv variatinn% in the qualitative and quantitative arpect% relative tn such agents in tobacco from region Ito region and from year to ycar. Ovcnill. the usc of agricultural chetnical% hac alu. been greatly reduceJ (Wittekinch IOR5), Neverthelcex, it is fairly certain that cnmmcrcial tohaccns ctmtain tip tt>, a few parts per million of DDT. DDD, Cnmpamd NE~E~ I 00b-).000 Nicofine 30-130 Nofnicnfine 3-13 AnMabine 5-12 Anabasine Olher toh.u.~o dkdoids (17) NA 10-30 13ipyridyh (4) 100 mNentriarnnfanc (mCnHea) Total eaevolatile hydrocabons (43P .1lJV•'wl/ 2-4 NapMhakne Olher nsphdrknes (23) I-a i 0.2-0.0 Pherrnftrenes (7) 0.03-0.1~ Anlhaceees (5) Foom" (7) Py~eees(6) 0.6-Ltf 0s•os° 0.3-0.43' Fworaahenes (3) CafeinoRenrc Pulyettfdat aromMit 0.1-0.25 Aydmcarbons (I I )` s0•-169 Phenol 61<-111(t Other phenoh (45P 20a-40U Cafeet+ol 10b-2& Other cMeeMtls (4) 200-40d' OA+erdihydro.ybeezeoes(10) 15-70 $cppfrrlelin Olher pnlypheeds (itp NA 10-70" Cyclotenes (1e 0.5 I Qoinones (7) 600-1.000 Sol.ne.aul b989 1851S 1 10

1 .s 1 ui L ce.." Total ClgsneMe Smoke % w/W FICURF, 1 i.-CompositMn of ciprette mainstream smoke S(RIR(7i: 1>,dwadl(7reee1Nnt2/. carbon dioxide ac major constituents; the particulate matter of MS contains at least 3.500 individual compounds (Figure 13: Duhe and Green 1982). Like all organic combustion prafucts, tobacco smoke contains free radicals, highly reactive oxygen- and carbon-centered types in the vapor phase, and relatively stable radicals in the particulate phase. The principal of the latter appears to be a quinonc/hydr(,quin(x)e complex capable of reducing molecular oxygen to superoxide. and, eventually, to hydrogen peroxide and hydmxyl radicals (Nakayama, Kodama, Nagata 1994: (Church and Pryor 19R5), For chemical analysis, the smoke is arbitrarily seinnlted into vapor and particulate phases. Th(,ac smokc components of which morc than 50 percent appear in the vapor phase of frc.h MS are considered volatile smoke constituents; all others are particulate phasc componcnts (Figure 13). Tables 5 and 6 list the major types of compnnents idcn- tificd and their estimated ccxlcentrati(xl in the smoke of cxle cigarctte (US DNNS 1982; I lnffmann :md Hecht, in press). The quantitative data presented here were obtained by machine smoking of cigarettes under standardized laboratory rnn(litions using the method of the Fedcral Trade Commission (Pillsbury et al. 1969): thercfore, the data do not fully reflect the human setting. This applies especially to smokcrs of low-yicld cigarettes who tend to compensate for the low nicotine delivery by (Irawing smoke more intensely and inhaling more deeply (LIS DHHS 1999). Table 6 d(.c% not contain information about the nature and concentration of at least tn mctalk in the sm(Ike. These c(mqxxmds are not listed because lesc than 1 percent of the metads in t(.hacco are transferred into the smoke and constitute together only 590 NE/g (lenkin., G(,Idcy. Williams 19R5), Tahles 5 an(16 also l.wk descriptions of the xn FS89 t85t5 TABLE S,-Major constituents of the.apor phs+e of the mainstream smoke of ' nonfilter ciRarettes Concemra(iMJciEtne" Compuune 21ro--120(nE (~6 fi4x"1 NitroRen 30-70 mE l I 1-14%") (1><ygen 4y~i5 mE (9-179i") Carhnn dioxide 14-2.1 mE (2.Rr4.h%") Cancon ttuxurxide 7-12 mE (1.4-2.4% ") Water ArRon S mE 0.5-1.0 ma Hydrogen 10-130 NE Ammonia NitroEen nxidea (NO.) I(M1-b00 VE 400-300 VE HydroRen cyanide 4 20-90 Pe Hydrogen sulfide 1.0-2.0 m` Methane 1.0-1.6 m6` qher volatik alkanes (20) 0.4-11.5 mlt Volatik alkenk- (16) 0.2-0.4 mtt Icrnnene I 25-40 Ne Buudiene 20-33 Pg Aceaykne 12-5(1 Ng Flenzene Toluene Styrene " NR 10pts 15-y0NR Chher volatile aromatic hydrocarMma (291 20Q4S00 VL Formic acid 10n-1.700 µ6 Acetic acid t'r11piO/lie 8cid IOn-:((I(1 p6 2n-?0 P6 Methyl kumate 5-10 ys` ()ther volatile acids (6) Formaldehyde 2l>-I /xl Ng 4(1M1-1.4(1DNg Acetakkhyde 6t1-141 NE Acmkin RI

Q 1" teo ~---~ t?o ,eo Iso t4o t3o t2o ~ 11o a too lOC1 .--.~. ~ so f? ~--...~ ~ eo 7o eo s4 s. so .-~ 40 3o 20 to 23 DHHS 1993; Martin et al. 1984; Fitzgerald.Oates, Nowak 19RR). Cigarette smoking also contributes to the development of coronary atherosclerosis. Possible mechanisms for this chronic effect include: repetitive endothelial injury, a decreased high-density lipoprotein (HDL)/low-density lipoprotein (LDL)cholesterol ratio, abnormalities in the synthesis of thromboxane A2 and prostacyclin. and increased neutrophil elastase ac- tivity (Holbrook, in press; Nowak et al. 1987; Weitz et al. 1987). Clinical Correlations Cigarette smoking has an adverse effeM on individuals with symptomatic or asymptomatic CHD. Compared with nonsmokers, smokers having a positive exercise test (Rautaharju et al. 1986: Gordon et al. 1986) or a history of coronary bypass surgery (Viiestra et al. 1986; Kemp et al. 19g6) face a worse prognosis. Smokers who have an- gina pectoris have a higher risk of death than nonsmokers (Hubert. Holford. Kanpel, 19R2) and have a poorer long-term prognosis after a myocardial infarction (Ronnevik; Gundersen. Abrahamsen 1985; Kuller et al. 1982). Continuing to smoke increasek the ' likelihood of recurrent acute myocardial infarction and sudden death (Hallstrom. Cbhb. Ray 1986). Smoking may alsoeause silent ischemic disturbances in patients with stable angina pectoris (Deanfield et al. 1986). i Cigarette smoking interferes with the efficacy of medication used to treat CHDsuch as propranolol. atenolol. and nifedipine (Deanfield et al. 1984). i D Non. siM orrt, w2 a+r CarH SMaC Ca11 A13 a tno S.q aMaM tNStt iACTOR 1TATtlS AT ENt1W' FIGURE 10.-Major risk 6etor eombinatlotta, 10-year incidence of first major coronary events, males aRed i0 to S9 rears at entry. PoolinR Project .we (H I. diwoNc t.e..we 2ap mmHE; eiRweue +wrok' ISM). R~: ek~MCr/ Moat ~re. ~ .npc.nlMwenlciRrene.NeMry. N(ltE: All r.rea .rws'fc.+Ajrwd Sf' tQ-yrar se Ero~ b the U.S. whUe nrk pqwtatiM. 19010. SCNlR(IE: "inlt Ieeject ReareA (Seop. Pithophysiologicai Mechsni.ents Autopcy studies indicate that cigarette smoking has a significant positive association with atherrxckrosis (US DHHS 1983). Studies have noted the strongest relationship of cigarette smoking with aortic atherosclerosis, but smokers also show increased coronary atherosclerosis compared with nonsmokers (US DHHS 1983). Smokers un- dergoing coronary angiography have more comnary artery disease than nonsmokers (Pearson 1984). Cigarette smokers who continue to smoke following transluminal coronary angioplasty may be more likely to require repeat angioplasty than nonsmokers (Gaian et al. 1989) CCigarette smok ing exerts both acute and chronic adverse coronary effects (US DHHS 1983: Holbrook et al. 1984). It contrihutes to acute ischemic and occlusive events thrmtgh several possible mechanisms: an imbalance between myocardial oxygen sup- ply and dcmand, coronary artery spasm, a hypercoagulable statc, increased platelet ad- hes'venees and aggregation, and a decreased ventricular frMrillation threshold (US Smoking Cessation Prospective epidemiologic studies have documented a substantial reduction in CHD death rates following smoking cessation (US DHHS 1983). While some studies have shown a henefet within 2 years after quining, other studies have suggested that the former smoker's CHD risk gradually decreases over a period of several years (Copk et al. 1986). For heavier smokers, the tesidual CHD risk is proportional to the total lifetime exposure to cigaretteL Cerebro.a.+talar Distase (Stroke) In the United States stroke is the third kading cause of death. It is also a major cause of ntorbidity, with tnore than 4(10,000 Americans suffering nonfatal strokes each year (Harrison's Principles of Internal Medicine 1987). There are two major types of cerebnovascular disease: (t) cerebral infarction due to occlusion of a vessel by an embolus or thrombosis, and (2) cerebral hemorrhage, in- cluding suharachnoid and parenchymal. The terms cen:brovascutar aecident and .troke ate nonspecific and usually refer to clinical syndromes. A stroke may he caused by disease of the extra- or intracranial blood vessels. Em- bolization from the heart or extracranial arteries is also an important cause of stroke. The stroke can result from hemorrhage from a blood vessel or from occlusioO of an artery because of athetosclerosis, thrombosis, or embolization. In the Framingham study. atherothmmbotic brain infarcticxt accounted for the majority of strokes (Wolf, 61

of regular smoking. Frxthepurposeof illuctration,selectedexamplesofdose-rcsponse relation.hips from Iwo of the early, large prospective epidemiologic studies are reviewed hcrc. Figure I.hows lung cancer mortality ralios for males by the number of cigarrttes smoked per day. For those who smoked more than 40 cigarcttes per day, the risk of dying of lung cancer was 23 times greater than the risk experienced by non- .mokers. Figure 2 illu.tratc% the lung cancer mortality ratios for males by self-repurted degree of inhalation of cigarctte smoke. Thcse data confirm that even those who repcmed' just puft ing" on cigarette. still had a significantly increased risk of lung cancer. Those who reported inhal ing "nwme" or "slightiy" experienced a risk of developing lung cancer that was eight timc% prc:ncr than that of nommokcrs. The relative risk increased to 17 for thow who inhaled deeply. Figure 3 show% lung cancer mortality ratios fix males by the age they began smok- ing. The risk of devcloping lung cancer was greatest for those who began smoking at an early age. Mathematical modeling of dose-response relation.ships, in the biological framework of a multistage model of can:inogenesis, has provided further insight into the nature of dose-rrsponserctaticxlshipsfcxsmokingandlungcaneer. Usingdatafmmtheprospec- tive study of British doctors, Doll and Peto (1979) have perfornxd the most widely cited analysis. They compared regular smnkers and lifelong nonsmokers and showed that lung cancer incidence increased with the square of the amount smoked daily, but with the duration of smoking raised to a power of 4 to 5. This finding implies that dura- tion of smoking is the stronger determinant of lung cancer risk and that initiation of smoking during the teenage years will have serious consequences for lung cancer risk (Peto 1986). Commercial cigarettes have continuously evolved through the addition of filters and other modi( ications designed to reduce tar and nicotine yields (US DHHS 1981). Since extensive modification of the cigarette began in the 1950s. it has only recently become possible to investigate smokers with predominant use of the newer products. Evidence from prospective and case-control studies and assessment of temporal trends of lung cancer mtxtaiity indicate somewhat lower risks for cigarettes with reduced tar and nicotine yield, although the risks remain markedly higher than for nonsmokers (US DHHS 19R2). Doll and Peto (1991) examined trcnds of Iung cancer mortality in males in the United States. Britain, and other European countries. They concluded that the international diffen:nces and the temporal trends were generally consistent with the tar yields and tar intakes across time and across countries. Relevant information is also available from case-control and prospective studies. In the United States, investigations spanning the 196(k and 1970s have shown somewhat reduced lung cancer risks in smokers who switched from nonfilter to filter cigarettes (Bross and Gibson 19<CiR; Wynder. Mahuchi, Beattie 1970; Hammond et al. 1976: W ynekr and Stellman 1979). More recent studies continue to document lower risks in smokers of filter cigarettes compared with smokers of nonfilter eigarettes. In a case- control study ccmducted in Western Europe. the relative risk for IifRlong rKxlfilter cigarette snKikcrs was approximately twice that for smokera of filter cigarettes alone 30 MortadltY R.tlo 0.0 te e ~~ ~ e Nen.meker 1'e lo-n Cigarettes Smoked Per Day FIGURF1 -LunR cancer mortaiity ratio for males by ciRarettes smoked pef day SOURCE: U.S. Vderam /K.hn 19fA1. Mortality Ratio !0 r ts f 19.0 to e 0 Nenemeker Non. 4LN S11ght MeA.rete 11 Degree of Inhalation , FIGURE 2. Lung cancer "W"ality ratio for males by degree of inhaiation SOURCE: CPS-11Hor"mrad 19Md• Age Began Smoking FiGURF, 3.-i.unf( caacer teortality ratio fer males by age began smoking SOURCF : U.S. Vewam IK.hn IOA/. I 45 SE89 t8STS 44

childhood and neaches a peak level during early adulthood (Figure 12). From the peak level, ventilatory function declines with increasing age. In cigarette smokers who develop symptomatic airflow obstnretion, a similar loss of function takes place, but at a more rapid rate than in nonsmokers and in smoke:rs who do not develop disease. A physician is likely to diagnose COPD when continued excessive kos.s of ventilatory flmctinn results in sufficient impairment to cause dyspnea and limitation of activity. v.o. FIGURF 12.--Decline of REVt at normal rate (Mlid Rne) and at an accekrated rate (dashed line) NO?E' A. pnvin ,rM0 has ulaned a "ww"Mr m.ieY/ FE V, t/wimp /wq pt aM nu.:nnl FF V, h.a Iren rcAuceA ~~^~: R. pee.a~ wMne tiy cMlaM.,e ie.pi,.u,y MreNim. i()URCF.: S~ ei d.110/ti1. The factors influencing rate of lung function decline in cigarette smokers have not yet been fully characterized. The rate of decline tends to increase with the amount smoked, and former smokers generally revert to the rate of loss of nonsmokers. In fact. the excessive decline observed in some smoker< may represent a common physiobgi- cal consequence of different pathophysioiogical mechanisms. Habib and coworkers (19R7) carefully characterized 13 subjects from a longitudinal study in Tucson with a mean annual decline in FEV t greater than fd) ml, per year. Clinically, these subjects were not unique and none had alphat-antitrypsin deficiency. Physiological assessment suggcsted that some were developing emphysema, whereas others appeared to have disease of ahe large and/or small airways. The studies of longitudinal change in lung function have spanned only segments of the full natural history of COPD, and many questions remain unanswered. It is unclear, for example, whether the excessive decline takes place at a constant rate in continuous smokers. as suggested by much of the epideminlogic evidence, or whether the ezces- sive decline occurs intermittently after some triggering event. The factors determining the susceptibility of individuals to cigarette smoking are also unclear. Current-, hypotheses emphasize determinants of protease-antiprotease imbalance, level of non-' %pecific airways reactivity, and severe respiratory illness during early childhood. Since the release of the 1964 Surgeon General's Report, abundant evidence has in- dicated the overwhelming importance of cigarette smoking in causing COPD; in fact. COPf) would he an uncommon condition in the United States without cigarette smok- ing. Unfortunately, death rates due to COPD have paralleled those for lung cancer and{ have increased ProgresFively over the last 25 years (National Center for Health Statis-; tics 1986). The trends are consistent with cohort changes in smoking: in this regari, while age-specific rates for males have been increasing at older ages, a recent decline, in COPD mortality has been observed at younger ages (US DHHS 19ft4). While im ~ pnrtant scientific questions remain unanswered concerning the pathogenesis of COPP, thc available evidence provides sufficient rationale for preventing COPD through smoking prevention and cessation. i Pregnancy and Infant Health Several endpoints have been studied to evaluate the adverse effects of smoking on pregnancy, including (1) infant birthweight; (2) fetal and infant mortality; (3) congeni- tal malformations: (4) fertility: and (5) long-term effectson the child. The 1964 Report indicated an association between smoking and low-birth-weight habies (US PHS 19fi4), hut it did not consider the evidence sufficient to establish a cau.sal relationship. The 1969 RReport (US PHS 1969) confirmed the association between maternal smok- ing and low-birth-weight bahies, an increased incidence of prematurtty, spontaneous ahnninns, stillbirths, and neonatal deaths. The 1971 Report (US DHF.W 1971) con- cludkd that maternal smoking during pregnancy exerts a retarding influence on fetal growth. The 1973 Report (US DHEW 1973) noted that cigarette smoking is a prob- able cause of increased late fetal mortality and infant mortality. The 1977-78 Repxxt tUS DHf:W 1979) nnoted a dose-response relationship between smoking and ahruptio placentae, placenta previa, bleeding during pregnancy, and prolonged premature rup- ture of inemhranes. as well as the association of smoking during pregnancy with im- paired physical and intellectual development of the offspring. The 1979 Report (lIS DIIF.W 1979) linked smoking with sudden infant death syndrome. The 1990 Report tUS DHHS 1990) noted that up to 14 percent of pn:term deliveries in the United States may hc attributed to matemal smoking. It also surveyed studies of men and womcn suFFcsting that cigarette smoking may impair fertility. I I 70 8'b89 I8St5 71

CHAPTER 3 CHANGES IN SMOKING-ATTRIBUTABL'E MORTALITY I ZL89 ZBSZS

i e e- ~O P .p r N O. O~O O~ O. ~ N N N L1 y~ M r1 N ; ,p -. O~ ^ eC ' M O • P '° ,4 r~ .., nP, Pf N N f~~f f3 N N P .O N f~•1 • O. N " N -A ~ O N N N.- r N o ~ ~ ~O vf N ~o h ing more than I pack of cigarettes per day compared with women reporting no smok 2 ing during pregnancy. Similarly, Himtnelberger, Brown, and Cohen (1978) reported a 2.3-fold higher risk of congenital abnormalities for smoking mothers than for ndn- smokers. One study has also nepotted an increased frequency of congenital malformations based on the smoking habit.s of the father (Schardein 1985). The trends with paternal smoking were independent of maternal smoking level, maternal and paternal age, and social class. The relatively low incidence of congenital nalfomtations, the different types of mal- formations, and the various possible biological mechanisms have made the study of the relationship between environmental factors and congenital malformations extremely difficult. New techniques to monitor pregnancy outcomes may enhance our under- standing of the interrelationship between cigarette smoking, other environmental fac- ton, and congenital malformations. ! Fertility A recent study has substantiated previous teports that suggested that women who smoke may have reduced fertility (Baird and Wilcox 1985). Data on smokinj history and number of noncontraceptive cycles until conception were collected from 678 preg- nant women. Of nonsmokers, 38 percent conceived in their first cycle compan;d *ith 28 percent of smokers. Smokers were 3.4 times more likely than nonsmokers to have taken greater than 1 year to coneeive. After adjtatttnent for other risk factors, it was es- timated that the fertility of smokers was 72 pencent of that of nonsmokers. Heavy smokers experienced lower fertility than light smokers. Fertility was not affected by the husbands' smoking. The effects of ciganKte smoking on sperm quality in men (Ablin 1986) were also evaluated in relation to density, motility, and morphological abnormalities in 238 age- related smokers and 135 nonsmokers. Spermatozoa from smokers possessed sig- nificantly decreased density and motility compared with those from nonsmokers. Mor- phological abnormalities of the spt:rtn were also noted more frequently among smokers than among nonsmokers (Ablin 1986). LonR-Term Efkcts on the ChNd Relatively few studies have evaluated the long-term consequences of smoking during pregnancy on the child. One of the larger recent studies looked at neurological hand- icaps among children up to 14 years of age whose mothers had smoked during preg- nancy and among control children born in northern Finland in 1966 (Rantakallio and Koiranen 1987). Seventy-eight children of smokers and 62 controls had mental retar- dation (1Qs less than 85). cerebral palsy, or epilepsy. The incidence of mental retarda- tion alone was 1.5.9/1,000 among the children of the mothers who smoked and 13.9 antnttg the controls. For any combination of mental retardation, cerebral p*ky, and epilepsy, the rates were 42.8/1,()(1() for children of smoking mothers and 34/1,(1(X) for the controls, a relative risk of 1.27 with confidence limits of 0.90 to 1.79. 75 I

control study of 480 patients with cervical cancer, there was a 50-percent excess risk of cancer among cigarette smokers (Brinton et al. 1986). This excess risk persisted after adjustment for sexual practiees associated with smoking such as age at first inter- course and numher of sexual pariners. There was a twofold exeess risk of cervical can- cer for women who smoked more than 40 cigan:ttes per day. The dose-respon* relationship persisted after adjusting for several variables. There was no increased risk of cervical cancer among former smokers. The finding of nicotine and cotinine in the cervical secretions of ciganette smokers (Sa.sson et al. 1985) and of mutagenic mucus in the cervi x of smokers (Holly et al. 1996) complements the epidemiologic findings. In summary, more than 15 epidemiologic studies have consistently shown an in. creased risk for cervical carcinoma in cigarette smokers compared with nonsmokers. Supportive clinical studies provide a plausible biological basis for the relationship. The available data confirm an association between cigarette smoking and carcinoma of the uterine cervix. Endometrlal Geeer Several studies have ttported that endontetrial cancer is kss ftequent among women who smoke cigarettes than among nonsmokers (Baron et al. 19g6)- Cigarette smoking exerts an anticstrogenic effect that may explain this inverse association. The public health significance of this association is limited because of the overall adverse impact of cigarette smoking on morbidity and mortality. Coroeary Heart Dtuase The 1964 Surgeon General•s Report (US PHS 1964) noted that mak ciganette smokers have higher death rates from CHD than nonsmokers. Subsequent reports eon- cluded that cigarette smoking can cause death from CHD and that smoking is one of the major independent risk factors for heart attack, manifested as fatal and nonfatal myocardial infanction and sudden cardiac death. Smoking also increases the risk of heart attack recurrence amoeg survivors o[a myoeatdial infaretion (US DHEW 1979). The 1990 Report (US DHHS 1980) noted the btcreised risk of CHD among women who smoke. It also described the synergistic imeaction between smoking and oral con- trsceptive use that substantially increases CHD risk. The 1983 Report (US DHHS 1983) stated that cigarette smoking is a major come of CHD and noted the decreased risk of CHD among former smokers compered with cument smokers. Epidemiolop The findings from several prospective studies involving tnae than 20 million per- son-years of observation in North America, Northern Europe, and Japan have been remarkably similarr cigarette smokers ane at incnewed risk for fatal and nonfatal myocardial infarction and for sudden death. t7verall, smokers have a 70percent greater CHD death rate, a two- to fourfold greater incidence of CHD, and a two- to. fourfold greater risk for sudden death than nonsmokers (US DHHS 1983). Although women experience lower CHD rates than men, cigarette smoking is a major determinant of CHD in women. In a recent prospective study of 119,404 female nur- ses, smoking accounted for approximately one-half of the coronary events (Willett et al. 19R7). Cigarette smoking produces a greater relative CHD risk in men and women under 50 years of age than in those over 50 years of age (Glover. Kuber et.al. 1992; RRosenberg. Miller et al. 1983). ' Dose-response relationships between cigarette smoking and CHD mortality have been demonstrated for several measures of exposure to cigarettes, including,the num- ber of cigarettes smoked per day, the depth of inhalation, the age at which smoking began, and the numberof years of smoking (US DHHS 19R3). Smoking cigarettes with reduced yields of tar and nicotine has not been found to reduce CHD risk (Ki ufman et al. 1983). Coronary Heart Disease Risk Factors The risk of experiencing a heart attack is multifactorial (US DHHS 1983). The presence of one or more of the major CHD risk factors, cigarette sm4ing. hyper- cholesterolemia. and hypertension, identifies individuals at high or very,high risk. These risk factors interact synergistically togreatly increase CHD risk (Figune 16). The risk of CHD associated with cigarette smoking is comparable to that associated with the other major CHD risk factors. The risk of CHD is greatly increased among diabetic men and women who smoke cigarettes (Suarez and Barrett-Connor 1984; Stamler, Wentworth. Neaton 1986), and the sex differences in CHD are substantially reduced among diabetics. Among the MRFIT screenees free of a history of heart attack, there were 5,245 diabetics and 350.977 nondiabetic men aged 35 to 57 years at the time of enrollment (Suarez and Barrett-Connor 1984). The CHD death rate was much higher among diabetics than among nondiabetics. Smokers had higher CHD death rates than nonsmokers among both diabetics and nondiabetics. Six-year CHD mortality was 4.0/1.0(l0 for non- smokers who were nondiabetic and 2;.2/ 1,000 for diabetics who smoked >_36 cigarettes per day. Hyperlipoproteinernia is a primary cause of premature coronary atherrcclerosis and heart attacks. Cigarette smoking substantially increases the risk of CHD among in- dividuals with genetic familial hyperlipidemias. Williams and coworkers (Williams et a1.19R6; Hopkins. Williams. Hunt 1984) studied fourlarge Utah pedigrees with familial hypercholesterolemia. They noted a substantially increased risk of CHD within the high-risk pedigrees in relation to cigarette smoking. Miettinen and Gylling (19AR) have recently completed a long-term followup of 96 patients with familial hypercholesterolemia. Cigarette smoking was a significant predictor of coronary mortality after adjustment for disease hi.tory. sex, and various metabolic parameters. ZV89 T8SZS ? SR N)

'flu I'Nr7 Report notcd that cmrtkcrs' lungs displayed airways changes and emphysema: huwcvcr. the pathcphyciololeical correlates of these changes were not explored. Suh.cqucnt inve.tigatiom., correlating structural changes with function, have dcwrilmd thc relationship between smoking-causcd changes in lung structure and airllow oh%truction. tanphy.ema and small-airway injury contribute to the physiologi- caI impairment litund in COPD: in individuals with symptomatic airflow ohstructicxl, cithcr type of injury may be prcdominant, hut hoth are probably important (US DNHS I't`t•It. Whilc the I'N,J Report dcscrihcd effcct.s of cigarette smoking on the airways, thc imrv,rlancr of the .mall airways a. a sitc of airflow oh.tnlction was not recognized 1111111 ihc late I')(dh (Ih,gg, Macklem. Thurlheck 196R). More recent investigations ha.r contirnn d that mc:l.urc% of small-airway injury arc correlated with the degree of aurllow oh.tructifm (( IS t)IIF1S 1984: Ilalc ct al. 1994: NNagai. Wcst, Thurlbeck 19R5), nuaip.v .tuilic% have shnwn that ch:mgc% in the small airways develop in the lungs of ~oung am<,kcr% and antedate the devcloprnent of symptomatic airflow obstructinn (Nicwochncr, Klcinennan, Rice 1974). The imIx,rt:mcc of emphy.ema in producing chronic airflow obstruction has also heen amply dmununk-cl since the 1964 RReport. Emphysema reduces the driving pressure for expiratc.ry flow and contributes to increased airways resistance by reducing tether- ing (,f .m:dl airways. In patients with sym f+tomalic airflow ohstruction, the extent of an:ttomtic emphysema is corrclhted with the severity of airflow ohstruction, as are small airways ahnc,nnalitics (US DIIHS 1994: Hale et al. 19R4: Nagai. West. Thurlhrck 1')R5). Thu., thc srm*ing-caused lung changes in the airways and parenchyma have fnith been unequivocally linked to airflow ohstruction. Natural History of C(1PD and the Role of Cigarette Smoking Nearly all the epidemiologic evidence reviewed in the 19fi4 Repcm was cross-sec- tiord in nature. These data estahlishcd that cigarette smoking increased respiratory .ympaom% and reduced the level of ventilatory functicm, hut they did not provide in- .iLht into the temporal evolution of COP1). Subsequent crrxs-sectional studies have provided more complete quantitative tkscrirtions of the effects of cigarette smoking tm Iung function, and new longitudinal atKlics have partially described the evolution ol Iung function changes in smc.kers and the factors determining the rate of change over ti1nc• •fhc numcrrnls cnxc-secticautl studies published since the 1964 SSurgeon General's ReIv,rt have .hown that cigarette smoking is a strong determinant of the level of ven- tilaaory functiom, which is moa often assessed by the measurement of the I-sec fcxced rxpir:ra)ry volumc wcVl), The Icvcl of FT:VI declincs as thc amount of smoking in- crca.c. tlIS t)IIIIS 1')tt4). Multiple regression techniques have been applied to data 1rom .c.rr:tl dil'fcrcnt populations to describe the quantitativc rclationship between the :1nNN1111 xmlikcd and hiss of ventilatory function. Tlxsc amalyscs indicate that ven- til:ttary t•unction drelines in a lincar fashion with cumulative consumption of cigarcttes, u.nall.• crl+rr..cd :tc pat•k-ycar. (Rurmws ct al. 1977: Dnckcry et al. 19RR). For ex- :nnl•lc, ha.rd qm amdysi. of data fnxn R,1'l l mcn and women from six U.S. cities, lk+ck- crv :tnlloah.•t. (19,44) rcpexted that malc •mokcrf of average height lose 7.4 ml. of FT•.V I on average for each pack-year and that women Ioae 4.4 mL per peck-year. Although the decline in mean level of FEV t appears small, the distributions of lung function level • in smokers and in nonsmokers are different: the distribution for smokers is skevved toward lower kvels so that a much grtater proportion of smokers than n°nsmokers have levels below the usual limit of normal (Figure 11) (US DHHS 1994. Burrovvs et at. 1977: Dockery et al. 19RR). s0 K20 10 :3,0 -2.0 -1.0 MEIGMT nOJtlSTEO •1• PO-y" IOlttaM 0.0 1.0 2.0 3.0 FEYI RESIOUpL ILITERSI FMURF. 11.--Pes•ceM dbMbt.tlat °f P'edk* "0 °t torced expiratOry vohnnle in 1-eec (F'FV t) Ie snbjects wMb.aryhtR Mk-J'tirs of smnk- Nf7rE: Triwhtk iedic.re+ Vew 1QR M toeArrMk nW. sO111tCE: Ilwro.M d.1.1 t917k Dockary 01 d. ( Nld4. The longitudinal studies publist+ed sittce the 1964 Repolt have pattially described the natural history of lung function changes in COPD (Fletcher et al, 197b: US DHHS 19R4). Ventilatory function, as measured by FEV t, for example, increases during 69

Rekrences AOKI. M.. HISAMICHI. S., TOMINAGA. S. (eds.) Smoking and Health 19R7. PracKdings of the fSih World Confirenct nn Smoking and Health. Tokro. New York: Elsevier Science Publishing, 19RR. BOYD. li.. DARHEY, C.M. (eds.) Smokeless Tobacco Use in the United Statts, NCI Monograph. National Cancer Inatitute. in prcss. BRITISH MEDICAL RESEARCH COUNCIL. Tobacco smoking and cancer of the lung. Statement by the Medical Research Council. British Medicallournal 1:1523-1524, 1957. BRODERS, A.C. Syuamous.cell epithelioma of the lip. A study of five hundred and thirty- seven cases. Journal of thr American Mrdirol Association 74(10):656-fi64, March 6, 1920. BURNEY, L.E. Smoking and lung cancer. A statement of the Public Health Service. Journal of the Amtrican Medical Association 171:1 R29-1 R37, 1959. CONNOLLY. G.N., WINN. D.M.. HECHT, S.S., HENN1NGFlELD, J.E., WALKER. B. JR., HOFFMANN. D. The reemergence of smokeless tohacco. Nrw, EnRlandlnurnal of Mtdicint z I4(16):1020-1027, April 17, 19R6. DOLL, R.. HILL, A.B. The mortality of doctors in relation to their smoking habits; a prelimi- nary report. British Medical Journal 1(4R77)r 1451-1455, June 26, 1954. DOLL. R., HI LL, A.B. Lung cancer and other causes of death in relation to smoking. A second repon on the mortality of British doctors. British Medicallournal 2:1071-10R 1, November 1, 1956. HAMMOND. E.C.. HORN, D. Smoking and death rates-Report on forty-four months of fol- low-up on I R7,7R3 men. 1. Total mcxtality. Journal of the Amtrican Mrdical Association 166(10):1159-1172, Match 8, 1958a. HAMMOND, E.C., HORN, D. Smoking and death rates-Report on forty-four months of fol- Iow-up of 1 R7,7R3 men. 11. Death ntea by cause. Journal of the Anerican Mrdical Associa- rinn 166( I I):1294-13og. March 1.5, 195Rb. KOOP. C.E. A Smnke-Free Society by the Year N)00. Julia M. Jones Lecture, presented at the annual meeting of the American Lung Association, Miami Beach. Flarida, May 20, 19R4. LOMBARD. H.L., DOERING, C.R. Classics in oncolo8y. Cancer studies in Massachusetts. 2. Habits, characteristics and envirormtetM of individuals with and without cancer. New Englandlrnrrnol of Medicine 198•4R1-4R7, 192g. PEARL. R. Tobacco smokin8 and longevity. Science 87(2252):216-217, March 4, 1938. ROYAL COLLEGE OF PHYSICIANS. Swinking ottd Health. Srmmary and Report of the Royal College of Physieians of Lnedori on Smoking In Relation to Cancer of the Lung and nthtr Distasrs. New York: Pitman Publiching Company, 1962. STUDY GROUP ON SMOKING AND HEALTH. Smoking and health. Joint report of the Study Group an Smoking and Health. Science 125(325R):1129-1133. June 7, 1957. U.S. DF.PARTMENTOFHEALTH AND HUMAN SERVICES. ThrHralthConstqusncnsof SmnkinR fiw Women. A Report of the Surgeon General. U.S. Department of Health and Human Services. Public Health Service. Office of the Assistant Secretary for Health. Office nn Smoking and Health. 1980. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. PromorinR HealthlPrtrtnt- inR Discasc: Ohjcctnr.t far the Norion. U.S. Department of Health and Human Services. Public Health Service. 1980b. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVtCES. The Health Consequtttcas of S,nMFinR. The Changing Cigarette: A Rryw,rt.,f the Surgtnn General. U.S. Department of Health and Human Services, Public Health Service. Office of the Assistant Secretary for Health. Office on Smoking and Hcahh. DHI(S Publication No. (PHS) 81-50156, 19R1. 8Z89 T88TS U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. TiK Health Constquencts bf Sm.++Hng: Cancer. A Rtport af tht Surgeon General. U.S. Department of Health and Human Services. Public Health Service. Office on Smoking and Health. DHHS Publication No. (PHS) 82 :50179, 1982. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Health Consequences of .Smoking: Cardiovascular Disease. A Rtport of the Surgeon General. U.S. Department of Health and Human Services. Public Health Service. Office on Smoking and Health. DHHS Publication No. (PHS) 84-50204.1983. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Health Constq~encts of Smoking: ChronicOlsstrartivtLungDisrasa. AReportofthtSurryKonGenaral. U.S. Depart- ment of Health and Human Services. Public Health Service. Office on Smoking and Health. DHHS Publication No. (PHS) 84-50205. 1984. U.S. DEPARTMENT OF HEALTH AND HUMAN SER V ICES. The Health Consequences of Smoking: Cancer and Chronic Lung Distatt in the Workplace. A Report of the Surgeon General. U.S. Department of Health and Human Serviees, Public Health Service. (Jffice on Smoking and Health. DHHS Publication No. (PHS) 85-50207.19R5. '' U.S. DEPARTMENT OF HEALTH AND HUMAN SERViCES. The Health Conselqutnces of Involuntary Smoking. A Report of the SurRtoe General. U.S. Department of flalth and Human Services. Public Health Service. Centers for Disease Control. DHHS Publiqation No. (CDC) 87-8398. 1986a. S U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. TGe Health CoKarquencts of Using Smokales.cTohacco. A Repat of theAdrisoryCamminet to thr Surgeon General. U.S. pepanne M of Health and Htainan Services. Public Health Service. National lnstitrata of Health. NIH Publication No. 862874,1986b. I I U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The 1990 Health Objectives for the Notion: A Midcourse Reriew. U.S. Department of Health and Human Servibes. Public Health Service. Office of Disease Prevention and Health Promotio+. November 1986c. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Health Consequences of Smoking: Nicotine Addictioh. A Report of the Suraear Gentrol.19RR. U.S. Department of Health and Human Sarviea. Public Health Ser„ice• Centers for Disease Contro). Center for Health Promotion and Edvation. Ofrtce on Smoking atd Halth. DHHS Publication No. (CDC) 88-8406,1988. U.S. DEPARTMENT OF HEALTH, EDUCATION. AND WELFARE. Thr Health CaRa- quences of Smoking. A Report ajtlr Surdton Gthtrtsl: 1971. U.S. Department of Halth. Education, and Welfate, Publie Health Service. Health Setvias and Mental Health Ad- ministration. DHEW Publication No. (HSM) 71-7513.1971. U.S. DEPARTMENT OF HEALTH. EDUCATION. AND WELFARE. TJk Health Canse- quencts of Smoking. A Report of tht Surgtoe Ger.eral: 1972. U.S. Department of Halth. Education, and Welfare. Public Health Service. Health Services and Mental Health Ad- ministration. DHEW Publkalion No. (HSM) 72-7516.1972. U.S. DEPARTMENT OF HEAL7f1. EDUCATION. AND WELFARE. The Health Con.a- quences of SmokinR. U.S. Department of Heahh. Education, aed Welfare. Public Health Ser- vice, Health Services and Mental Health Administration. DHEW Publication No. (HSM) 73- 8704,1973. U.S. DEPARTMENT OF HEALTH. EDUCAl7ON• AND WELFARE. The Health Conse- qurncts of Smoking. 1974. U.S. Department of Health. Edocation, and Welfare, Public Health Service, Center for Di.+ease Control. DHEW Publication No. ((.'DC) 74-R704,1974. U.S. DEPARTMENT OF HEALTH. EDUCATION, AND WELFARE. The Health Conse- quences of Smoking. 1975. U.S. Department of Health. Education, and Welfan:, Public Hcahh Service. Center for Disease Control. HEW Publication No. (CDC) 77-R704, 1975. 1I

In 1995. the Center for Health Promotion and Education of the Centers for Disease Control. Atlanta, GA, defined the fetal tobacco syndrome as follows. (I) The mother smoked 5 or more cigarcttes a day throughout the pregnancy. (2) The mother had no evidence of hypertension during prcgnancy, specifically no preeciampsia and documentation of normal blood pressure at least once after the flrst trimester. (3) The newborn has symmetrical growth retardation at term. 37 weeks, defined as hirthweight le.s than 2,5(p g, and a ponderal index (weight in grams divided by length) greater than 2.32. (4) There is no obvious cause of intrauterine growth retardation, that is, congeni- tal malfonnation or infection (Committee to Study the Prevention of Low Birthweight 1')R5). Infant Rirthweight A clear dose-response relationship exists between the number of cigarettes smoked during pregnancy and the hirthweight deficit (US DHHS 1980; Committee to Study the Prevention of Low Birthweight 19R5). Compared with nonsmokers, light and heavy smokcrs have a 54- and 130-pencent increase, respectively, in the prevalence of new- boms weighing less than 2, 00 g. A review of five studies including 113.000 births in the United States, Canada, and Wales found that from 21 to 39 percent of the incidence of low birthweight was attributed to maternal cigarette smoking (Committee to Study the Prevention of Low Birthweight 19R5). Also, cigarette smoking seems to be a more significant determinant of birthweight than the mother's prepregnancy height, weight, parity, payment status, or history of previous pregnancy outcome, or the infant's sex. The reduction in birthweight associated with maternal tobacco use seems to be a direct effect of smoking on fetal growth. Mothers who smoke also have increased rates of premature delivery. The newborns are also smaller at every gestational age. The infants display symmetrical fetal growth retardation with deficits in meacurements of crown-heel length, chest and head circum- ferences, and birthweight. A recent study in Boston (Nieburg et al. 19R5) attempted to evaluate the reasons for differences in rates of prematurity between blacks and whites. Of the 1.365 black women, 34.7 percent were cigarette smokers compared with only 23.4 percent of the white women. Cigarette smoking and low hematocrit levels were two of the most im- portant risk factors accounting for the differences in prematurity rates between blacks and whites. Finally, a number of careful studies have found that the effect of cigarette smoking on hirthweight is not mediated through decreased maternal appetite or weight gain (US DIIHS 19R0). The most widely accepted hypothesis relating maternal smoking and the effects on the fetus and newborn is intrauterine hypoxia (Rush and Cassano 1983). 71te hypoxia could occur as a result of factors associated with smoking, such as increased levels of carbon monox idc (CO) in the blood, reduction of blood flow, or inhibition of respiratory en7ymcs. Therc is strong experimental evidence that maternal smoking causes fetal hypoxia. 72 6b89 t85TS Several studies have demonstrated that smoking cessation prior to orduring pregnan- cy can partly reverse the reduction in the child's birthweight (Rush and Cassano 1993: Hehel. Fox, Sexton 19RR). In a large study using the 1970 British Birth Cohort ( l:ieber- man et al. 19R7), an inverse relationship between measures of social class and the prevalence of smoking was demonstrated that was similar to that seen in the United States. In all social class groups, babies of the nonsmokers weighed more than those whose mothers had smoked during prcgnancy, and the women who had stoppcd smok- ing either before or during pregnancy had babies with higher birthweiFhtc th:in women who continued to smoke throughout pregnancy. Fetal and Perinatal Mortality Kleinman and colleagues (1998) ffrom the National Center for Health Statistics used Missouri birth records from 1979-83 (Table 4) to study the rclationship! between cigarette smoking in mothers and infant mortality. Among the 134,429 prin)iparas, the infant mortality rates (adjusted for age, pariry, education. and marital status) were (per I,(1(K) subjects) 15.1 for white nonsmokers, 18.8 for whites who smoked ISSs than I pack of cigarettes per day, and 23.3 for whites who smoked more than I pack of ciga- rettes per day. For black nonsmoking women, the infant mortality rate!(per 1.000 women) was 26.0; for blacks who smoked less than 1 pack per day. 32.4; and for blacks who smoked greater than 1 pack perday. 39.9. Mortality was increased during thii fetal, neonatal, and postne(natal periods. It was estimated that if all pregnant women stopped smoking. the number of fetal and infant deaths would be reduced by approximately 10 percent. In the United States this would result in about 4,flt)0 fewer infant deaths each year. A study conducted by the Office on Smoking and Health attributed approximate- ly 2,500 infant deaths to maternal smoking in 1984 (CDC 1987). Stein and associates (1980) have studied the causes of spontaneous abortion in three New York City hospitals. They compared women with spontaneous abortion to con- trols (women who carried their pregnancy to 28 weeks or more). Within the spon- tancous abortion groups, they then compared those with evidence of chromosomal ab- normalities and those with apparently normal chromosomes. The odds of a spontaneous abortion increased by 46 percent for the first 10 cigarcttes smoked per day and by 61 percent for the first 20 cigarettes smoked. Smoking was not associated with the spon- taneous abortion of chronwsomally abnormal concePtions• but only with those in which the chromosomes were normal. These results were not confounded by such factorc as maternal age or race. Cont;enital Malfortnations Evidence that exposure to tobacco and cigarette smoking could be related to congeni- tal malformations is less clear. About 3 percent of all live births have major congeni- tal malformations (Behrman 19R7). Maternal smoking has not been demonstrated to he a ma,kx risk factor for the induction of congenitai malformations, although elevated risks have been reported in some studies. Kelsey and coworkers (197R) rcpotted an in- creascd risk of 1.6 for congenital malformations among the offspring of women srnok- 7i

wrxnen, and concluded that most of these studies had shown a positive association he- twecn cigarette smoking and stroke (Table 3). In the ongoing study of approximately 1.2 million persons (CPS-l1), cigarette smokers under the age of 65 years experienced increased risks of death from stroke. For men and wcxnen (current smokers), the relative risks of death from stroke were 3.7 and 4.9, respcctivcty. The relative risks for those over age 65 years were 1.9 and 1.5 for men and women, respectively (Chapter 3). Cigarette smoking was associated with decreased cerebral blood flow in a recent clinical %tudy involving 192 normal volunteers (Rogers, Meyer et al. 19R3). In a sub• sequcnt study of 2bR normal volunteers, abctention from cigarette smoking improved cerebral pcrfusion (Rogers, Meyer et al. 19R5). As already noted in this Chapter, cigarette smoking increases the risk for CHD, and consequently for congestive heart failure, both of which increase the risk for stroke. Data from the Medical Research Council study on the treatment of mild hypertension illustrate the impact of cigarette smoking on the efficacy of drug therapy and stroke in- cidence (Medical Research Council Working Party 19115). Nonsmokers receiving propranolol to control hypertension experienced a reduction in stroke incidence, while cigarette smokers did not. Wolf. D'Agostino, Kannel, and coworkers nxently reviewed the association between cigarette smoking and stroke and concluded that it is causal. These investigators noted that the causal connection is supported by all of the traditional epidemiologic criteria; these include an increased risk for stroke among smokers compared with nonsmokers that is independent of other risk factors, a dose-nesponse relationship, and a decrease in stroke risk with smoking cessation (Abbott et al. 1996. Wolf et al. 19811; Colditz. Bonita, Stampfer 19Rg). The aforementioned recent clinical studies also confirm that cigarette smoking increases the risk for stroke. Thus, curnent evidence indicates that cigarette smoking is a cause of stroke and that smoking cessation reduces the risk for stroke. Atherosckrotk Peripheral Vaactdar Disease Lower extremity arterial va.culardisease causes subctantial mortality and morbidity; the complications may include intermittent claudication, tissue ischemia and gangrene. and ultimately, loss of the limb. The 1964 Surgeon General's Report commented that little is known about the relationship of smoking to peripheral arteriosckrosis. Subsequent reports have described the evidence establishing that cigarette smoking is a cause of and the most powerful risk factor for atherosclerotic peripheral vascular disease and that smoking cessation is the most important intervention in the management of this problem (US nHEW 1971, 1979; US DHHS 1983). Cigarette smoking is directly related to the extent of atherosclerotic disease involv- ing large and small arteries in the lower extremity (Criqui et al. I9R5). Cigarette smok- ing also causes peripheral vasoconstriction. F.pidemiologic and clinical studies have clearly demonstrated that cigarette smokers have a higher prevalence than nonsmokers both symptomatic and asymptomatic lower extremity arterial disease (US DHHS 19R3)• alence study (>'~rchn et al. 1986).49 percent of In the Lipid Research Clinic prev compared with 30 percent individuals with claudication were current cigaren ~~ d~~veloping leg pain. of the controls. Smoking was twice as frequen in, during the exercise test. In the compared with those not developing leg i~ ~ittent claudication was directly and Framingham Study. the risk of developing amngly related to cigarette smoking (Kannel and Shurtleff 1973). . Diabetes mellitus and cigarette smoking are the~y ~u~ ~y for ~~~~~~i~mity' 1 arterial disease and subsequent amputation. Perip rcne and am-, arterial disease and infection predispose individuals with diabetes to gang puiation (Herman. Teutsch, Geiss 1987). Diabetics have a sixteenfold in rcen~of the of lower extremity amputation compared with nondiabetics; about 50 Pe lower extremity amputations in the United States are performed on diabetics. Ap- o such surgery each year. The diseasei , pmximately 31,()(x) A~~can diabetics underg r a~ in diabetic smokers than in tends to be more progressive and occurs at younge 8 ncrosmokers. ttents under the age of 60 years with In a study in Sw'~n• practically all diabetic pa gangrene were cigarette smokers (Lithner 1983). 71w prcvalence of lower extrcmitji arterial disease was evaluated for diabetic subjects. One-third of the smokers hbd rcd with only 16 percent of the non- evidence of peripheral vascular disease comPa ~ had a 30 percent lowe,r smokers. Diabetics who stopped smokmg for at least 2 yea prevalence of lower extremity arterial disease than those Z~~ n~~k19R1) Epidemiologic studies in a Rochester, MN. Poim with demonstrated that for 1,073 residents over the age of 30 i o~n ~ ~~~ne of diabetes mellitus between 1945 and 1969. about disease at the time that diabetes women had clinical evidence of periPle arterial disease among the was diagnosed. The annual incidence of lower extremity ent had diabetics was 21/1.000 for men and 17.611.000 for ""ornen; about 20 P~ ~ ent had intermittent claudication. Among diabetics with lower gangrene and - 6 perc of men and 43 percent of women had been extremity arterial diseaaer,ed7with 55 percent of normal control men and 36 percent of cigarette smokers comPa tion are the two mos tst im- normal control women. portant treatment of diabetes tneQitus and smoking ~ ral vascular portant interventions to prevent the developrrKnt of atherosclerotic periPlx disease. Atherosclewotk Aotk Aneurys>n The 1964 Report of the Surgeon General commented on the increased mortality rates for aortic aneurysm in cigarette smokers compared with nonsmokers• The 1969 Repnrt ccmcluded that there is a close 3 R iation between cigarctte~ ~o¢,~ data and nci ed sm• The 198 Report summarized the epi by aortic aneury% was 2 to g times greater in cigar,'ctte that the mortality rate for abdominal aortic aneury' logical studies have shown a sig- smokers than in nonsmokers• As already noted, pat~ FS Sb89 iBSiS 64

TABLE 6.-Coetlta.ed Co-"und PtkiR.retk NtMhyhdienes (4) 200-350 umo~ene OtAer letp eno ( 201/-2.10P Ndeeirie.eid NA 104-150 Steric.cid 5o-7s oltic.eie 44-I 10 Unokic.cid 60-150 Lhrolenie acid 150-250 Lactic acd 60-a0 lndo/e 10-13 skmle 12-16 Oner indok~ (13) Oumolines (7) NA 2-4 °Uer N-6elerocyclic Aydeoe.toe. (55) Tt+cuoh.ns (4) NA 2t1D-30p Olher O-helnoertlic Aydraenepa (42) SHtma~le~ol NA 40-70 s~~l 30-0 CrnpeMero1 20-30 Chokaeiol 10-20 Aniline 0.36 'Ioh".rc, 0.23 Oder aomak amine~ (12) 0.25 7bti.eco-apeciRc N-nkro,.myin (IIF 0-M-27 Clyrerd 120 No7t?: NA,na.wil.Ak. 'i.w ,„umhm M o..e~.lr.e. ~ry.e.,. MAI.i~,y awyew~d. de~Nfle! L. dw* a~e.e `Ser TaMe ~ fer Aeq{I. S(r IR('F.: /h/rnnm,.~d /lea#1. h pl~. SS89 185ZS md maleic hydrazide; fewer than 20 pement of these contaminants are transferred into the smoke stream. The 1964 Surgeon General's Report listed five polynuclear aromatic hydrocarbons (PAHs) and three N-heterocyclic hydrocarbons as known carcinogenic smoke con- stituents (US PHS 1964). By the criteria for carcinogenicity of chemicals as set by the International Agency for Research on Cancer (1986), the carcinogens identified to date in tobacco smoke include 11 PAHs, 4 N-heterocyclic hydrocarbons, 9 N-nitrrsamines, 3 aromatic amines. 3 aldehydes, 6 volatile carcinogens, 6 inorganic compounds, and the radioelement polonium-210 (Table 7; Hoffmann and Hecht, in press). The Changing Cigarette As discussed in Part 1, epidemiologic studies have documented a dose-respoMse, relationship between the number of cigarettes smoked and the development of cancer of the lung, larynx, oral cavity, esophagus, pancreas, bladder, and kidney (US DAHS ' 1982;1ARC 1986). Bioassays for tumorigenicity with whole smoke and with tar 14;ve also demonstrated a dose-response relationship (US DHHS 1982). Other toxic and tumorigenic agent.c, such as CO, volatile N-nitrosamines, and carcinogenic PAHs, pvere also successfully reduced (Hoffmann, Tso, Gori 1980; Hoffmann et al. 1984; US DHHS 1981). However, it was soon realized that the smoker of low-yield cigarettes tended to; compensate for reduced nicotine delivery by intensified smoking (US DHHS 19$R),' and therefore exposuse may not actually have been lowered. Based on values generated by smoking machines under standardized smoking tonditions. Figure 14 shows'the teduction in sales-weighted tar and nicotine delivery of the average U.S. cigarette. Ar- rows in the graph point to the introduction of technical changes in the manufacture of cigarettes at various times. These changes have influenced the machine-measured sates-weighted average nicotine and tar deliveries (Norman 1982). Technical issuls in the machine measunetnents of delivered tar and nicotine yields also arose during 1982; modifications of the testing procedure were suggested (Federal Trade Commission 1984). The data shown in Figiae 14 are based on the consistent testing procedures. Since 1981, the tar delivery of U.S. cigarettes has ranged between 13.0 and 12.7 mg, while nicotine delivery has remained stable at 0.9 mg per cigarette. (See Chapter 5, Table 26.) In the smoke of popular U.S. low-yield cigarettes, the reduction of nicotine, the primary pharmacologic factor in tobacco addiction (US DHHS 1988). has not oc- curred to the same extent as has the reduction of tar. The same development has been observed with cigarettes in the United Kingdom (Jarvis and Russell 1985). Some modifications in the makeup of commercial cigarettes have led to a selective reduction of toxic and tumorigenic agents. Filter tips of cellukose acetate, the most com- molt cigarette filter material, can selectively remove phenols and volatile N- nitrosamines from the smoke stream. Petforated filter tips selectively reduce CO and hydrogen cyanide (HCN) levels, and charcoal filters may selectively reduce volatile al- dehydes and HCN. The incorporation into the tobacco blend of reconstituted tobpcco sheets, expanded tobaeco, and tobacco ribs has also contributed to a selective rz'duc- lion of PAHs in cigarette smoke. The incorporation of ribs and stems and the utiti7.a- AS i

Familial Factors The 1964 Report considened and dismissed the "constitutional hypothesis" that predilections to cigarette smoking and to lung cancer share a common genetic origin. The Report did consider that genetic factors might determine susceptibility for a minority of cases. Subsequent epidemiologic studies have provided empirical evidence of possibk genetic or familial deterrninants of susceptibility (Tokuhata and Lilienfeld 1963a: I963h; Samet, Humbk, Pathak 1996: Oni e1 al. 1986). For example, in a recent case-contmi study in New Mexico (Samet, Humbk, Pathak 1986). a parental history of lung cancer was associated with a fivefold increase in lung cancer risk, after adjust- ment for cigarette smoking. Clinical studies of selected families have also indicated familial aggregation (Brisman et al. 1967: Lynch et al. 1992; Goffman et al. 1992). Research has not yet identified the mechanisms underlying the familial aggregation of lung cancer. In 1973, Kelktmann, Charles, and Luyten-Hellerman (1973) reported the promising observation that patients with lung cancer had a higher degree of in- ducibility of aryl hydrocarbon hydroxylase than did control subjects. Because this en- zyme converts polycyclic aromatic hydrocarbons to more active carcinogens and be- cause enzyme concentrations are under genetic control, this observation suggested a possible genetic determinant of lung cancer risk. However, not all subsequent studies have been confirmatory, and the inheritance of inducibility in humans has not yet been fully described (Mulvihill and Bale 1984). Other Host Factors Acquired host characteristics have also been examined as determinants of lung can- cer risk including pulmonary tuberculosis, chronic bronchitis. COPD, disorders as- sociated with interstitial fibrosis of the lung, and peripheral pulmonary scars. However, the evidence related to these disorders is incomplete and frequently is derived from case series rather than from epidemiologic investigations. Recent epidemiologic evidence, however, has indicated increased lung cancer risk for smokers with COPD comparnd with unaffected smokers (Peto et al. 19R3; Samet, Humble, Pathak 1986; Skillntd, Of- ford, Miller 1986). Occupational Exposures Diverse agents inhaled in the workplace have been shown to cause lung cancer. In- teraction between occupational exposures and smoking was the focus of the 1985 Report of the Surgeon General (US DHHS 1985). That Report concluded that "For the majority of American workers who smoke, cigatette anoking represents a greatercause of death and disability than theirworkplace envimnment." The Report also highlighted the limitations of the evidence on interactions hetween smoking and occupational ex- posures. Little new information has become available since the 1985 Report. The evidence temains strongest for interactions of smoking with exposure to radon decay products and with expcxure to asbestos (Sancci I9R7). For both exposures, the preponderance 6E89 T85Z5 of the evidence indicates synergism (Doll and Peto 1985; National Resenrch Council 1988), although the results of some individual investigations are inconsistent with synergism. Ambient Air Pollution The 1964 Report noted that lung cancer mortality rates tended to be higher in urban than in rural locations: Air pollution was considered a plausible explanation 1~br these differences. The association of lung cancer with atmospheric pollution dcrive~ l.iologi- cal plausibility from the presence of carcinogens in polluted air and has somcmipport from epidemiologic data. However, epidemiologic investigation of ambient air Ix'Illu- tion as a risk factor for lung cancer has been hampered by methodological problems. including the necessity of considering cigarette smoking and the difficulty of a`.%essing pollution exposure (NIH 1986). Recent epidemiologic invextigations have not shown strong effects of air pollution (Samet et al. 1987; Buffler et al. 1998); and Doll and,Peto (198 1). in their review of the causes of cancer. estimated that only I to 2 percwt of lung cancer was related to air pollution. lndoor Air Pollution As the hazards posed by ambient air pollution from conventional fossil ftrclr have diminished in scxne countries, the relevance of indoor air quality for health has become increasingly apparent. Studies of time-activity patterns demonstrate that rctidcnts of more developed countries, including the United States, spend on average little t ime out- doots (Spengler and Sexton 1983; Samet, Marbury, Spengler 1987). Indoor.paccs may be polluted by entry of contaminants from outdoor air and by indoor sources including those related to human activity, such as tobacco smoking, building materials, combus- tion devices, personal care and other household products, and other sources: A trend of reduced building ventilation in the aftermath of the energy problems of the I970s may have worsened indoor air quality. Two pollutants in indoor air have been causally linked to lung cancer: envimnmen- tal tobacco smoke (ETS) (US DHHS 1986a) and radon (National Research Council 198R). The evidence on ETS and cancer was comprehensively reviewed in the 1986 Report (see section on involuntary smoking in this Chapter). Radon is an inert gas that is formed from radium during the natural decay of uranium. The prcdcxninant source of radon in indoor air is the soil beneath structures. Rakm dif- fu.ses through the ground into basement and crawl spaces, and then throughout the air in a home, or crosses cracks and other penetrations in homes on concrete .Lah% to enter the indoor environment. Radon daughters are invariably prewnt in ind(x)r hir and a wide range of concentrations has been observed in homes (Samet ct A. I999). Some homes have levels comparable to those measured in uranium mines. but the majority of homes probably have levels that are currently considered acceptable. , R.-Aon decays into short-lived particulate decay products. Two af the dcc:iv pmduct% emit alpha particles, which are highly effective in damaging cetl% hccau.c (it their high energy and high mass. When these alpha emissions take place within the lung. The 51 i

CONTENTS Inratluction ....................................................... 121 A Twenty-Year Perspective: 1965-19R5 ................................ 122 The Concept of Attributable Risk ...................................... 122 Mathematics of Attributable Risk .................................... 123 Illustrative Calculation: Smoking and Lung Cancer in Women ............ 1254, Uncenaintics in Attributable Risk .................................... 12V Aggregation Bias Versus Statistical Precision ..................... 127 Age-Standardization ......................................... 127 ' Potential Biases in Applying the Results of Prospective Studies to the General Population ............................ 129 Uncertainties in Exposure ....................................129! Errmrs in the Classification of Causes of Death .................... 1:74~' Previous Estimates of Attributable Risk from Cigarette Smoking .......... 130 -- ---~ Populations at Risk: 1965 and 1985 ................................... 132. Cigarette Smoking and Other Fotms of Tobacco Use .................... 1.13 ; , Older Cohorts of Cigarette Smokers .................................. 134 Overlapping Populations at Risk ..................................... 136. ~ Changes in the Cigarette Product .................................... 139, ', Other Changes in the Cigarette Smoking Population ..................... 139 TMm Smokers Most at Risk in 1985 Were Also Smokers in 1965 .......... 140 Cancer Prevention Study I and Cancer Prevention Study 11 ................. 140 Nonsmokers' Death Rates .......................................... 141 Current Cigarette Smokeri Death Rates: Lung Cancer .................. 143 Current Cigaretle Smokers' Death Rates: Coronary Heart Disease ......... 144 Current Cigarette Smokers' Death Rates: Chronic Obstructive Pulmonary Disease .............................................. 146 Estimated Relative Risks from CPS-1 and CPS-11 ....................... 146 Endocrine and Sex-Related Cancers in Women ......................... 152 Summary ........................................................ 152 Smoking-Attributable Mortality in the United States 1965 and 1985 ......... 153 Conclusions... -....~ ...... ....................... . - 161 Rcferences ........................................................ 162 ZL89 18919 119

nificant association between cigarette smoking and atherosclerocis that is most striking in the aorta (US DHIIS 19R3). Chronk Obstructive Pulmonary DFsesse In the 1950s, increasing morbidity and mortality from chronic respiratory conditicxis prompted clinical and epidemiologic investigations of the etiology of chronic tmmchitis, emphysema, and related diamters. A variety of terms have suhsequently been applied to permanent airflow ohstntction in cigarette smokers. In the 19R4 Sar- geon General's Report, chronic obstructive lung disease (COLD) referred to chronic mucous hypersecreticxt, airways abnormalities, and emphysema. In this Report, the term COPD is used for the permanent airflow obstruction that develops in cigarette smokers. Thirty years ago, the most widely advanced hypothesis on the etiology of COPD linked progressive lung damage to recurrent respiratory infection and atmos- pheric pollution (Stuart-Harris 19.54). However, epitkmiologic investigations, largely carried out in the United Kingdom, quickly indicated the predominant role of cigarette smoking in causing COPD (Stuart-Harris 196Ra.b). By Iyli4, the evidence was sufficiently compelling to support the conclusion by the Advisory Committee to the Surgeon General that "Cigarette smoking is the most im- portant of the causes of chronic bronchitis in the United States, and increases the risk of dying from chronic hratchitis and emphysema" (US pNS 19fv1). T1te repnrt stot4w short of classifying the relationship between cigarette smoking and emphysema as causal, however. The report also noted the increased prevalence of respiratory symptoms and the reduction of lung function in smokers. The epidemiologic data cited in support of these conclusion.s were drawn from seven prospective studies of mortality in relation to cigarette smoking and about a dozen wrveys of respiratory morbidity: only one prospective study on lung function had been reported at that time. In the 25 years that have elapsed since the release of the 1964 Surgeon General's Report, the findings of numetm. laboratory, clinical, and epidemiologic studies have continued to reaffirm the predominant role of cigamtte smoking in causing COPD and have extended underctanding of the pathogenesis, pathophysiology, and natural history of this disorder. As the evidence has accumulated, the conclusions of the Surgeon General's Reports on cigarctte smoking and COPD have been strengthened. The 1967 Surgeon General's Report labeled cigarette smoking as the most important of the causes of COPD (US PHS 11>rrill). In the 1971 and 1979 Reports, the conclusions of the 1964 and 1967 Reports were strengthened (US DHEW 1979). Increased morbidity and mor- tality from chronic hronchitis and emphysema were documented in cigarette smokers compared with nonsmokers. Additionally, autopsy evidence confirmed that the IunFs of smokers were widely damaged, and the evolving pn>tease-antipmtcase hypothesis pmvickd a framework for understanding mechanisms thmugh which cigarette smoke causes emphysema. The 191t4 Surgeon General's Report focused on COLD (US DFIHS 19R4). The over- all conclusion of the Report was: "Cigarette smnking is the major cause of chronic otxtructivc lung disease in the United States for both men and women. The contribu- tion of cigarette smoling to chronic ohaructivc lung di.ease morhidity and mortality troutweighs all other factors " In contrast to the spatse evidence in the 1964 Report. Arc 1984 Report reviewed numerous cross-sectional and longitudinal studies of mor-' iMdity and mortality. The longitudinal studies described the evolution of the cigarette- Rlated decline in lung function that leads to sufficient impairment to result in a clini- c3l diagnosis of COPD. This Section provides an overview of the evidence on COPD that has accumulated tince the 1964 Report in the areas of pathogenesis, pathophysiology, and natural his- uKy of COPD and the role of cigarette smoking. ' hthnRenesis The 1964 Report described the deposition of cigarette-smoke particles and gases in the lungs and the effects of cigarette smoke on lung defenses but did not address the mrehanisms by which cigarette smoking causes COPD (US PHS 1964). Much of the! %uhseqtKnt investigation of the mechanism of lung injury by cigarette smoke wms' qvrked by the observation that homozygousdeficiency of alphat-antitrypsin, the major rrotease inhibitor, is associated with familial panlobular emphysema (Laurell and Friksson 1963: Eriksson 1964). This observation led to the hypothesis, generall)i referred to as the protease-antiprotease hypothesis, that the development of emphyser~a mults from an imbalance between proteolytic enzymes and their inhibitors (Janoff 1995; Niewtrehner 1988). Cigarette smoking is postulated to produce uncheckeo pmteolytic activity by increasing proteolytic enzyme activity In the lung while decrees- roF antiprotease activity. Experimental and clinical observations have been consistent with the protease-an- tipmtease hypothesis (US DHHS 19g4). Observations that smokers. compared with nnnsmokers, have an increased ntnnberof neutrophils in peripheral blood (Yeung and dy Buncio 19R4), in bronchoalveolar lavage fluid, and in lung biopsy specimens (Ilunninghake and Crystal 19g3) provide indirect evidence for an increased elastase hurden in smokers' lungs, since neutrophils are the primary source of elastase (Janoff 1985). Furthermore, elastase levels are elevated in bronchia) lavage fluid immediate- ly after smoking cigarettes (Fera et al. 1986). Cigarette smoking has also been shown to decrease the levels and activity of antiproteases. an effect attributed to oxidants in ci famtte smoke and the pulmonary macrophages of smokers (Janoff 1985: US DHFIS I'JR4). Animal models confirm that unchecked proteolytic activity can cause em- physema (US DHHS 19R4). The lungs of patients with COPD generally display both emphysema and abnor- malities of the small airways. Mechanisms by which cigarette smoke damages small airways have not been so extensively investigated as the factors determining the development of emphywma. t'athephvsMlOVv The lungs of smokers with COPD generally have both thickening and narmwing ctf airways and emphysema. although the extent of these two processes is variable (US I)HHS 19R4). Both the airways changes and emphysema produce airflow obstruction. 67

1 sd..•.A~AId tn (ad ttMs-.APAd akMb ta1M 0 0.0 1955 1960 1965 1970 1975 1980 1985 FIrURE 14.='Tar" and nitotine content of US. cigarettes, sales-weighted average hash,1957-87 NATE: Nicorine valnea ril. IOS7-67 re eaimre.. sf x iRCF. Ivt7-n7. wakAum / Iv7m. felunh-qu.ner eatimara rer tach year. 1 WNI-a I. FTC t 19R4 Y. 19R2-R7. Aeri.ed fmm IT(' Ama ul.r..f annual ciRarHtt crrnpany .u/wni..ila% tn IAr FTC. Thia datalo.e i% the.mle aa thal uvrd fnr the nn- Mwnr FTC alhxcro rerywt .ene.. Sinre 10111. Ihe.e rerywt. have nlw li.red Ihe .uka-weirMed lar avenEe. Hiaorical e.enh aa nlwnl in R I Revnnkl. (1W1K1. lion of more hurley varieties in the tobacco blend have led to an increase in the nitrate content of the U.S. blended cigarette from 0.5 percent to between 1.2 to 1.5 percent. This development brought about a reduction of the smoke yields of tar, phenois, and PAHc, hut has caused an increase of the nitrogen oxides in the smoke and thus ha.c in- crea.ed the potential for N-nitrosamine formation (US DHHS 1981. 1992: Hoffmann ct al. 19R4). The development of the low-yield cigarette has also necessitated an en- richment of the flavor "bouquet" in the smoke either by tobacco seiection or by addi- tion of natural or synthetic flavor compounds. These facts and the practice of smoking low-yield cigarettes more intensely make it difficult toevaiuate whether these new types of cigarettc% are in fact less hazardous to the smoker (see Chapter 8). Changes in the market share of filtered cigaRttes, lower yield cigarettes, mentholated cigarettes, and longer ciFarettc% are presented in Chapter 5. Environmental Tobacco Smoke SS i% the sm(,ke. generated during smoldering of tobacco products between puffs. When it i% ohtaine(t tinder standard laboratory cotKtitions, undiluted SS contains far higher am(„Ints of toxic and tumorigenic agents than MS, which is drawn puff by puff through the unlit end of the cigarette. Table R presents data for those toxic agents in SS th:tt are known carcinogens, tumor prr+ln(+tcrs, and cocarcinngens. The rcleace of volatile N-nitrocamincs afxi aromatic aminc% into the SS is remarkably higher than that into MS (US UI111S 1(/RR: Goerin 19R7). Whereas filter tips, especially perforated 99 LS89 T8SiS TABLE 8.-SSome toxk and tuemri8enk agents In undiluted cigarette sidestream smoke M11110und oxicity Amount in sidestream smoke (perciRarette) Amrwnl in sides-trcam %mokel amraml in mainslrcam smnke vapnr phase Carhon monnxide T 26.8-61 mg 2.5-14.9 Carbonyl sulfide T 2-3 µs 0.0.1-11.13 . Bentene C 400-400 VE 5-10 50 Fmm.ldehyde C I .300 Vt 3-Vinylpyridine SC 300-430 VE 2 HydroRen cyanide T 14-t10µE 0.06+0.4 1 Hydrazine C 90n8 3 Ni1rt+jten oxidea (NU.) T 300-2.000 Na 3.7-1 7.8 N-Nitr)sodimethylamine C 200-1.040 ng 2(1~130 N-Nifrosopyrtolidine C 30-390 nt; 6-120 + fartkrohte phau Tar C 14-30 m` t 1.1-15.7 Nicotine T 2.1-46 m8 1.3-21 Phenol Tp 70-250 µ6 1.3-3.0 CNechol C.aC 58-290 N8 0.67-12.R 3 .1A.7 o-Toluidine C µs 2 Naphtylamine C 70 ng 139 4-Aminobiphenyl C 140 ns 31 Benz(aHnthncene C 40-21MIng 2-4 Be"Mallpyrene C 40-70 ng 2.5--20 20 IS lI-11 Quinoline C p6 - NNN C 0.13-1.7 µ6 O.S-3.0 NNK C 0.2-1.4 pg 1.0-22 N-Nitmsodiethannlamine C 43 ne 1.2 72 7.2 Cadmium C µ8 0. Nickel C 0.2-2.5 µs 13-30 C 0.5-1.6 PO PnMnium-210 SC. w*Ilec~d eNCino{rn: T. toRie: TP. tumrx pn lmwer: NNN. N(7rV C.. c.ecilwlRenic: CnC. rncreino~enk: N'-NitnwwMwniawine: NNK.4dmNhyMAMMWPMOK~.pyrw} I-baanale. SOURCF.: flrtnmann and /krM. in pe+a. x9

FI(:URF 15.-Forntation of tobacco-spccifk N-nitrosamines w TABI,F 10.-Tobacco.apectfk N.nttrnsatnlnes In U.S. smokekas tobacro (ppb) PrMuct t ooce te.f tof+acco NNN 67(1-S.20o (6') NNK 380(1) NAT 2.30U(I) NAB U0(1) PhIt Wb.cco 3.404-4100 (3) S'"'1--mMt SnuR * 3.120-t33.a00(26) aQO-t3.6tlo(2S) 1.3M)-339.000(20) 1(1-4.700(16) -- y 9.00D-52.0QB(3) I.80Q-13.t10B(3) IE.Of14-3R.(IQp(3) 60.60.110f)(3) NOTE NNN. N'-N*O@onnmkvt4wNNK.4 {~/ni~n.r~:~e}1{) I}I-biu.none NAT. W-nit-nonstsbine: NAR. N'-nianwwobe.ine. ~r Nmnher in /wc+whex+ i+*e e.rohe+ed..~np4x mlreed. scxwrtcF: tu,rtmnn.nd Heclv( tma). Toxkfty and Carrinogenkity ot'Tobacco Smoke Undiluted tohacco smoke is too toxic to he tolerated by laboratory animals primari- IY hecamc of the acute toxic effects of CO. CO in cigarette smoke increases with as- cending puff number from 2 to 5 volume percent (the average CO content of cigarette smoke is 3.5 to 4.5 volume percent). The acute toxicity of tobacco smoke is also due to IJCN, nicotine, and volatile aldehydcs. In vitro short-term exposure to cigarette smoke cau%es ciliastasis, an effect primarily attributable to HCN (300 to 500 Itg/cigarette) and volatile aldehycks (5U0 to 2.Of1()Ng/cigarette). The long-tetm expo- sure of lalx,ratory animals to diluted cigarette smoke causes impairment of mucociliary ekarance, mucus hypersecretion, and epithelial lesions. Cigarette smoke constituents Rcponsible for this effect are both the gas phase. primarily HCN and volatile aldehydes, and the particulate phase (US DHEW 1979; US DHHS 1984). Long-term inhalation of diluted cigarette smoke by mice has resulted in adenomas and adenocarcinomac of the lung, whereas such inhalation in rats has only led to a few isolated tumors of the lung. In Syrian golden hamuers. long-term smoke inhalation studies have regularly induced benign and malignant tumors of the larynx and only a few lung tumors. These observations strongly suggest, and studies of particulate deposition and determination of carboxyhemoglobin (COHb) and nicotine-cotinine in the blood of the smoke-exposed animals have confirnxd, that laboratory animals do not inhale the smoke deeply. Intratracheal instillation of cigarette tar and one of its fractions has resulted in lung tumors, including bronchogenic carcinomas (Mohr and Reznik 1978. Dalbey et at. 1980: US DHHS 1982). The particulate matter (rnore often called "tar) suspended in organic solvebts has in- duced carcincma in the rat after subcutaneous injection and benign andl malignant tumors in the skin of mice and rabbits after topical application. The majof tumor in- itiators reside in the PAH-enriched neutral subfractions, whereas the tumor promoters and cocarcinogens are found in the weakly acidic fraction ac well a.a in tE+e polaric neutral subfraction (Wynder and Hoffmann 1967: Mohr and Reznik 1978.4 US DHHS 1982: Hoffmann and Hecht 1988). , As discussed earlier, combined chemical-analytical studies have led to the idehtifica- lion of several organ-specific carcinogens in cigarette smoke. The diversity of these carcinogens and those identified as contact carcinogens may cause ambiguity as to which among them are most important. Table 11. which is based on extensive laboratory studies, lists the likely causative agents associated with the increased risk of cigarette smokers for cancer of the various organs (Hoffmann and Hecht 1,9RR). Nicotine I It is generally held that nicotine is the active pharmacologic agent in tobacco that determines the addictive behavior of the tobacco smoker (US DHI IS 1988). Nicotine. together with CO, is also regarded as a majorcontributor to cigarette smokers' increased risk of cardiovascular disease (US DHHS 1983, 1988). In addition to nicotine, tobac- co contains various other alkakoids, most of which are 3-pyridyl derivatives. In the blended U.S. cigarette. nicotine constitutes 85 to 95 percent of the total alkaloids. During the smoking of a nonfilter cigarette, about 15 percent of the nicotine appears in the MS. 35 to 40 percent appears in the SS. 15 to 20 percent is deposited in the butt, and the remainder is broken down into pymlysis products. The major pymlycis prnducts of nicotine are CO. C02. 3-vinylpyridine. 3-methylpyridine. pyridine. myo- smine, and 2.3'-dipyridyl (US DHHS 1982). As discussed earlier, the absorption of nicotine from tobacco smoke is pH depend- ent. When tobacco smoke reaches the small airways and alveoli of the lung. nicotine is rapidly absorbed. In chewing tobacco and snuff with their alkaline pI l; nicotine is primarily abmxbed through the mucou% membranes of the oral cavity. Nicotine enters the blood and is rapidly transported ao the brain, which has specific receptor sitec for 6589 tBSTS 4,, 91

TABLE 1 L-Likely camaati.e aBents tor tobaceo-relsted nncers thgan IniKnor a aeeinogdt F01411c{ftarnts L.dng• txynx PAH Gtethol (eoaRineRee) weakly acidic tumor promoten NNK Anokin, erolmaldehyde (7) Polonit.n-2 tn (mina fsctor), acetaldehyde.lamatdehyde EaphaRus NNN Pancreat NNK(?) Bladder 4-AminoAiphenyl 2-NapMhylamine Oral cavity (smoking) PAH 1?ahrrol NNK,NNN Oral cavity (rnRdipping) NNK. NNN Irtilutltte (7) Heryes simplex (7) Putoniam-210 NOTE: PAN. polyn.clar rpn.ee hydroerEoM: NNK, 4{imikylai`osomio)-1 {7-oyridyl} 1-harmne: NNN, M-Ninomnanicetinc• SOURCE: HoPrmrm and /tecfit, in perw the drug. The effects of nicotine on the central nervous system are associated with the development of tobacco dependence (US DHHS 19ltg). Nicotine is primarily metabolized in the liver and, to a smaller extent, in the lung. About 10 to 15 perrent of the absorbed nicotine is excreted unchanged in the urine. The primary metabolites of nicotine ane cotinine and nicotine-N'-0xide. Cotinine is further metabolized extensively, with only 17 percent of it appearing unchanged in the urine (Benowitz 1986; Neurath et al. 19f17; US DHHS 19RR). Cotinine measurcments in saliva, serum, or urine serve as an indicator for nicotine uptake by tobacco chewers, active smokers, and involuntary smoker-.. It takes I g to 20 hr to eliminate one-half of the cotinine present in an active smoker through renal excretion: an involuntary smoker shows a considerably slower rate of elimination (Sepkovic. Haley. Hoffmann 1996; US DHHS 19RR). Blnklglal Markers Techniques for the determination of current and lifetime exposures to tobacco products include the examination of medical records and data from prospective and case-control studies as well as the utilization of biological markers. The development of highly sensitive and reproducible methods has led to increased use of biological markers for uptake of tobacco smoke constituents. I Table 12 lists those biochemical markers that are currently used to determ,ine, ex- posure to tobacco smoke components after active inhalation of MS and also after in- voluntary uptake of ETS. Some of these markers are also the basis for measuring the transfer of smoke constituents from the matemal bloodstream to a developing fetus. The tobacco-specific alkaloid nicotine ittd its major metaholite, cotinine, are most fn-quently used as serum and urine indicators of the uptake of tobacco smoke by active smokers and also to indicate ETS exposure in nonsmokers. Unlike CO, nicotine is not TABLE 112.-Biache+ekal markers for the uptake of tobacco smoke Critic~l Smoke Bioehemieal i l cnnatitue.yM marke. Substrate iNediod Sensitivity v , ue r Nicotine Nicotine Setum GC I n6hnL 0 I Urine Set.nt RIA 0.2 ng/mL 0 4 Urine Cotinine Saliva OC 3 nt/YnL 0 Saom Urine S.Nva RIA I ng/FnL 0 Senne Urine CarEoe monoxide COHb Blood Oitimeler ~O.Nb 0.9l0.796 (CO) CO p.xlrleA OC 31 ppm 5.6 42.7 ppm air Hydrollen cyanide ~ ~ sdiv. Aulowlyter 15 pnwlJ[K t0° Nm°UL ~ (SCTt- ) U n~( ion) Niuoten o.ides Nitrosoppoline Urine CC/IFA 30.4 µs/L ;.~4 -~ (NO.) t?jAykne GIoMn-adduct Blood GC tSpmo(/glth 58 i23 Hb u (CH2=(:.H2) pmo R 4-Aminobiphenyl Globimadducl Blood CC ? <70p6/Rttb Tof.eeo-. itk tpee Clnbin-~ddu~t Blood GC ? Not established nMrmwnines TriNcat vdurn. v.hKS roaM ed in nonweolCe++• 9nURCE: 1nftmariand AReecy far Re.euch on Cancer (19117). 0999 Z8STS ' 94 M

TABLE 7.-TumfKiVnk aWt.ln to6at:co and toAacco smoke P d A M Evidence for IARC evahatlion o(caRittt4tenicity Compoutds toKSae to aecb (DK R~) sn (pef cittuefle) In ktb animals In htnnan. PAN Iknr(alanthncene 20-70 nl Sufficient NA Nenm(h)ftuonnthene 4-22 ne Sufficient NA Ben?o(j)1luaamhene 6-21 ng Sufficient NA Benm(k)fluo.anthene 6-12 ng Sufheienl NA Benzo(a)pytene 0. I-90 n6 20-40 ng Sufficient Pro6ahle Chrysene 40-60 eR Sufficient NA Dibenz(a.h)rNMacene 4n# Sufficient NA Dihenzn(a.i)pyrene t.7-3.2 nj Srafficienf NA Dihento(a.l)pyrene Indeno(1.2.3tA)Pytene Present 4-20 ns Sufficient Sufficient NA NA 3-Methykhryene 0.602 Sufficient NA Az.-.renet! Quinoline 1-2 p= NA NA Dihev(a.h)aridine Dihenzfaj)acridine 0.1 ttR 3-10ng Sufficient Sufriciem NA NA 71f-Dibenzo(c.gkarbatok 0.7ns Sufficient NA N-Nkrew mines N-Nitrosodinxthylamine ND-213nS 0.1-1SOtt0 Sefrtcient NA N-Nitrowelhyl 3-13 ni; Sufficient NA tnethylamine N-Nit.o.aodiethylamine N-Nihosopynolidine N-Nittowdietlunolamine ND-360 ne ND-6.900 nS ND-23 n` 1.3-I IO n6 ND-36 n= Sufficient Sufficient Sufficient NA NA NA N'-Nittovxromicofine 0.3-R9 pS 0 12-3 7 p S ffi i . . g u c ent NA 4-(MethyIninosamieo)-I- 0.2-7 µ6 o.0R-o.77 pt Sufra:ient NA ( 3-pyridyt)-1-fanannne N'-Nilmwanahnine 0.01-1.9µ` 0.14-4.6 yR Limited NA N-Nittc><nmwxrhtd'me ND-M nR Sufficient NA TABLE 7.--Continucd Mainstram Evidence for IARC evatualion of carcinn6enicity C~~a PmcesseA tobhxo l~ ~hn) smoke (per ciRatette) In lab animals In hunana Aromatic amines 2-Toluidine 30-200 n` Sufficient 1nsd69u•K 2.Napluhylamine I-22 nS Sufficient Sufficient 1 4-AminobiPhe+ty 2-s ttS Sufficient Suffjcienl ~ AlAehydes 1 Formaldehyd• 1.6-7.4 pg 70-100 µs' Sufficient NA Aeefaldehyde • 1.4-7.4 fnR 111-I.400etS' Sufficient NA ~ Crotoauldehyde 0.2-2.4 µ` 10-20 pE NA Nr M{s"Nime"s oeR.nk C-npovrl& i 1 ~ 12~E µ` Sutfeient Su}ficienf Benneee Acrylonitrik 1. I-Dimethylhydrazine 0-147 yt 3.2-13 µs Sufficient Sufficient Litf+ifed k, NA 2-Nitropopwrc 0.73-1.21 µE Sufficient NA Ethykuhamafe 310-373 t16 20-31i n6 Sufficient NA Vinyl ehbride IaurR.nkeompounds I-16 ns Sulficient Sufficknt Sufficient Instiewave Hydraime 14-31 ng 24-43 ng Atsenie 501).-900ng 40-120n` lmdts~e s~e Suffcient Nickel 2.000-6.000n6 0-600n` Sufficienf Limited CTromium 1.000-2.000ns 4-70n` Sufficient Sufficient Cadmium 1.300-t.600ns 41-62ng Sufficient Limited Lead Pobnium•210 R-10 ps 0.2-1.2pCi 0.03-1.0PCI SutTicknt NA Inadequak NA NOTF: NO. no dN.: NA. ev.l.rion Ir. nd been done by IARC. kdific Canrninee en'S~nokM! and Heahh (19Mt) pabli%hcd valuen for the Se 'M Fourth RetrM of the MdrR'"k+M . _ 14 k.dinR U.K. ciR.ene. in I91A 1M.4 petcent of the nurkN/ °f 2b 103 ytth IR•K~ 1~•n. S9 yR) kN f. r+n.ldeh7~ ad 3Stt-1.1 ifl y/lA•ipeene (nrc.n.910 p`) foa actulAeAyde• i S( NVRC F: IMlfm.nn and Neeh4 in 0f". 9S89 t8SZS 87 96

introdnctMn EL89 tBStS In 1939. Raymond Pearl reported elevated death rates among white males who smoked tohacat, especially those aged 30 to 60 years (Pearl I91R). Pearl's study of 6.800 suhjects revealed the incrtase in mortality risk to he highest among heavy smokers. In 1954, Hammond and Horn reported on the 20-month followup of their prospcctivc study of 199,000 white men, aged 50 to 69 years (Hammond and Hom 1454). Death rates were highest among men who smoked cigarettes but not othcrtohac- c•o prmlucts, and increased with the amount of cigarette use. Overall, the nurtiher of deaths among cigarette smokers was 52 percent greater than would he cxpected from nrmsnxokcrs' mort:dity rates. Most of the increased mortality could be attributed to deaths frrxn cancer and especially from coronary heart disease (CHD). In 19h4, the Advi.ccxy Committee to the Surgeon General reviewed seven prospec- tivc studies of smoking and mortality, encompassing over 1.7 million entrants. fFor the 1.1 million male cnmllees, the overall mortality ratio, defined as the observed ~iumher of deaths in current cigarette smokers divided by the number expected from nonsmokcrs' ratcs, was 1.69. "For all seven studies," the Committee stated, "c4mnary artery di.cate is the chief contributor to the excess number of deaths of cigarette smokers over nonsmokers, with lung cancer uniformly in second place. For 411 seven studies comhined, coronary artery disease (with a mortality ratio of 1.7) accounts for 45 percent of the excess deaths among cigarette smokers, whereas lung cancer (with a ratio of Ib.R) accounts for 16 percent" (US PHS 1964, p. 30). In 1979, the Surgeon General described cigarette smoking as "the single most impor- tant preventable environmental factor contributing to illness, disability and death in the United States" (US DHEW 1979, p. vii). The 1992 Surgeon General's Report, citing an analysis by Doll and Peto (1981), estimated that forthe year 1978, tobacco use caused 122,(XK) cancer dcaths in men and women (US DHHS 1982). For 1982. the estimate for smoking-caused cancers was 129,0(X) (US DHHS 1982). The 1983 Surgeon General's Report estimated that 170.000 Americans died annually from CHD caused by cigarette smoking (US DHHS 1983). "During 1965-1977." the Report noted, "there were an estimated 2.8 million premature deaths from heart disease, primarily CI ID, in American men and women attributable to the use of tobacco" (US DHHS 19Ri, p. Fi6). The 1984 Report estimated that 80 to 90 percent of the 62.000 deaths from chronic obstructive lung disease (COLD). referred to later in this discussion as chronic obstruc- tive pulmonary disease (COPD), in the United States in 1983 were attributable to cigarette smoking (US DI 11IS 1984). "Over 50,0()() of the COLD deaths can therefore he concidered preventahle and premature since these individuals would not have died of Ct7L.D if they had not smoked" (US DIIHS 1994. p. ii). In 19R7, the Fxonomic Report (if the 1'resident stated, "Smoking presents the largest single source of health ri.k in Amcrici' (U.S. Prrsitkht 1997. p. 184). Thi-, ('haptcr further delineates the mcxtality rnnsequenees of cigarctte smoking in the United Statcc. Deaths attributable to cigarette smoking are reported for two benchmark years-1965 and 19115. Tlx Chapter focuaec cm the heahh crnnet4uences of.mokine fiir currcnt and fornxr cigarcttc stnokcrs. Dcaths of nonsmnkcrt cabccd by cnvironmcntal tohacco smoke (National Pi'wanh Council 19R6; I LC 1)1a11S 1947) and 121

l ETS (US DHHS 19R6a), the duration of expocure, and the differences in the distrihu- tion of potential carcinogens between sidestream and mainstream smoke. The 1986 Surgeon General's Report on ievoluntary smoking concluded (US DHHS 19R6): 1. Involuntary smoking is a cause of disease, including lung cancer, in healthy non- smokers. 2. The children of parents who smoke compared with the children of nonsmoking parents have an incrrased frequency of n-tpiratory infections, increased respiratory symptoms, and slightly smaller rates of increase in lung function as the lung matures. 3. The simple separation of smokers and nonsmokers within the same air space may reduce, hut does not eliminate, the exposure of nonsmokers to ETS. Another major review on involuntary smoking was released in 1996 by the Nation- al Research Council (NRC). This report concluded that the risk of lung cancer is ap- proximately 30 percent higher for nonsmoking spouses of smokers than it is for non- smoking spouses of nonsmokers (NRC 1986). Since release of the 1986 Surgeon General's Repott, five additional studies examin- ing ETS exposure and lung cancer in nonsmokers have been published (Brownson et al. 1987. Dalager et al. 1986; Humble, Samet. Pathak 1997. Gao et al. 1987; Pershagen, Hrubec, Svensson 1987). All five noted a correlation between ETS exposure and lung cancer among nonsmokers. Thus, of the 16 epidemiologic studies in the scientific literature, 14 have noted a positive association. Snmkekss Tobacco In 1979 the Surgeon General's Report included, for the first time, a review of the health consequences of using smokeless tobacco (snuff and chewing tobacco) (US DHEW 1979). In 1996. a special Surgeon General's Report, The Health Consequen- ces of Using Smokeless Tobacco (US DHHS t9Rfib), reviewed smokele,cs tobacco in depth and concluded that it can cause cancer in humans. The relationship between smokeless tobacco use and cancer is strongest for the use of snuff and for cancer of the oral cavity. Smokeless tobacco can also cause oral leukoplakia, which may progrtss to neoplastic transformation with continued use of smoketess tobacco. Addiction to Smoking The 1964 Surgeon General's Report referred to tobacco uee as habituating. Fifteen years later, the 1979 Report concluded that smoking wac "the prototypical substance abuse dependency" (US DNEW 1979). The entire 1998 Report (US DHHS 1988) was dedicated to an exhaustive review of tobacco use as an addiction. The 1998 Report concluded: t. Cigarettes and other forms of tobacco are addicting. 2. Nicotine is the drug in tobacco that causes addiction. 3. The phamiacolMgic and behavioral pmces.ses that detertnine tobacco addiction are similar to thcxe that detennine addictinn to drugs such as heroin or cocaine. I I i These findings are discussed in greater detail in Patt It of Chapter 5 oq deter- minants of smoking behavior. PART Il. THE PHYSICOCHEMICAL NATURE OF TOBACCO The 1964 Surgeon General's Report on Smoking and Health (US PHS 1964) gave impetus to intensified investigations on the physicochemical nature and composition of tobacco smoke and the identification of biologically active agents in tobao,eo and tobacco smoke and their modes of action. In 19.36 BrUckner listed 120 known components in tobacco smoke. This number grew to about 450 in 1959 (Johnstone and Plimmer 1959), to about 950 in 1969 (Sted- man 196R), and to 3.875 in 1982 (Dube and Green 19g2). Today, the estimated num- ber of known compounds in tobacco smoke exceeds 4,000, including some tpat,are pharmacologically active, toxic, mutagenic, and carcinogenic (US DHEW 19119; US DHHS 1983). Such diverse biological effects of cigarette smoke constituentsl,provide a framework for understanding the multiple adverse consequences of smoking. Since about 1960. both the composition of cigarette tobacco and the components and shape of the cigarette itself have undergone significant changes that effected reductions in standardized measunements of tar, nicotine, and other toxic agents in the smtlke (Nor- man 1982). Perhaps the greatest advances have been made in understanding, the pharmacology and toxicology of nicotine (Benowitz 1986; US DHHS 1988) and iri de- lineating the nature and mode of action of the major carcinogens in tobacco smoke (US DHHS 1992; Hoffmann and Hecht, in press). Processed, unadulterated tobacco contains at least 2,550 known compounds (Dube and Green 1982). The bulk of the dried tobacco consists of carbohydrates and proteins. Other important constituents are alkaloids (0.5 to 5 percent), with nicotine as the predominant compound (90 to 95 percent of total alkaloids). and terpenes (0.1 to 3 per- cent). polyphenols (0.5 to 4.5 percent). phytosterols (0. t to 2.5 percent). carboxylic acids (0.1 to 0.7 pen:ent), alkanes (0.1 to 0.4 percent), and alkali nitrates (0.01 to 5 per- cent). In addition, tobacco contains traces of arotnatic hydrocarbons. aldehydes. ketones. amines, nitriks. N- ard O-ht:terocyclic compounds, ptKticides• and more than 30 metallic compounds (Wynder and HofF' mann 1967; US DHEW 1979). The composition of the processed tobacco in cigantttes influences the chemistry and toxicity of the smoke. Cigarettes manufactured in the United States are made with blends of bright. twrky. and oriental tobaccos that generate weakly acidic mainstream smoke (pH 5.5 to 6.2) in which nicotine occurs in protonated form in the particulate matter. The sidestneam smoke (SS) of these cigarettes is neutral to alkaline (pH 6.5 to 8.0). and part of the nicotine in SS is present in unprotonated form in the vapor phase (Brunnemann and Hoffmann 1974). These observations are important because un- prolonated nicotine is readily absorbed through the buccal mucosa (US DHHS 1988). The 400 to 5(10 mg of mainstream smoke (MS) freshly emerging from the mouth- piece of a cigarette is an aerosol containing about 1010 particles per mL: these,range in diameter from 0.1 to 1.0 pm (mean diameter 0.2 Nm) and are dispersed in a valior phase (Ingebrethsen 19g6). About 95 percent of the MS effluents of a nonfilter cigarette ate composed of 400 to 5(10 individual gareous compounds with nitrogen. oxygen, and Z989 T8STS 79

Naeye and Peters (I9R4) investigated the mental development of smokers' children by comparing siblings whose mothers smoked in one but not in subsequent pregnan- cies and found that hyperactivity. short attention span, and lower scores on spelling and reading te.t% were more frequent for the children whose tnother had smoked during pregnancy, hut the differences were relatively small, the test scores being only 2 to 4 percent lower. Dunn at.o studied neurological and elcctmencephalographic abnor- malitics among 6-year-old children of smokers and found these cemditions to he slight- ly more common in the children of mothers who had smoked during pregnancy. but again the diffcrcnces were not statistically significant. Small sample sizes in many of these qudie% and the relative infrequency of the events of interest limit interpretation of the studies. Peptic Ulcer '1?The 1964 Surgeon General's Report noted an association between peptic ulcer and cigarette smoking. The 1979 Report stated that the relationship between cigarette smoking and peptic ulcer is .ignificant enough to suggest a eausal relationship. Peptic ulcer disease is more likely to occur, less likely to heal, and more likely to cause death in smokers than in nonsmokers. Cigarette smoking retards the healing of peptic ulcer (Sontag et al. 1984; Lane and Lee I9RR; Korman et al. I98i). A large trial of cimetidine, a drug used in the treatment of peptic ulcer, was reported in 1994 hby Sontag and associates. Uker recurrence was much meme frequent among smokers compared with nonsmokers for both the placeho• and the cimetidine-treated groups. Nicotine decreases pyloric sphincter pressure and therefore permits increased reflux of duodenal contents into the ctomach. Nicotine also decreases pancreatic bicarbonate secretion. Thie may impair neutraiization of gastric acid in the duodenum, contributing to the formation and persistence of ducxlenal ulcers. Smoking cessation probably reduces the incidence of peptic ulcer and is an important component of peptic ulcer treatment even with the available effective drug therapy. (Meoporesis The 1964 Report did not discuss ostenlxmsis. The interest in osteoporosis is fairly recent hecauce of the increasing number of older individuals, especially women, at risk of fracture; the better methods of ineasuring hone mineral mass. • and the understanding of ostcofxmnis pathophycio(ogy and risk factors. (ktcolxmxi. leading 14) fractures, especially of the hip, wrist, and spine, is an impor- tant cause of disability and ckath, predominantly among postmcnopausal women. About 15 to 20 million persons in the United States have osteoporosis. Fach year about 1.3 million fracturrs are attributed to this disease (Journal of the American Medical As- cociati<m 19R4), Smokingmayhcarickfactorfornstech+omsis(Willettetal. 198i). Woxncnsmokers have an earlier age of mcnopaurc, an important risk factor for ostccxxxosis (Willett et al. 1993). Smc,kcrn may havc a lower intake of cadc ium during aik,lcsccnce and young 76 adult life when maximum bone mineral mass ie reached (Saitdler et a1.1985). Smokers also weigh less than nonsmokers (US DHHS 1988). Obesity substantially reduces the ' risk of hip fracture (Kiel et al. 1987). Overweight women have higher endogenous estrogen levels and greater bone mass (Cauley et al. 1986). Exogenous estrogen'intake among postmenopausal women results in a decreased risk of fracture (Ernster et al: 1988). Women who smoke and ate on estrogen therapy may have reduced levels of estrogens in their blood compared with tevels for nonsmoking women. Among women who smoked and were given high doses of estradiol, blood levels of estrone and'; estradiol were only one-half of those tanong nonsmokers (lensen, Christiansen, Rodbro:1 , 19R5). Increased hepatic metabolism of exogenous oral estrogen may result in lower. estrogen levels among postrnenopausal cigarette smokers. Several case-control studies have evaluated the relationship between osteoporosis and cigarette smoking. Most find an increased risk of fractures among smokerg. However, problems with study design, especially the potential effects of confounders{ such as obesity and age, have limited the interpretation of these studies, as have con-' tradictory findings. For example, a large study of hip fractures among posmxnopaus4l women in four Connecticut hospitals did not find any differences in risk between smokers and nonsmokers (Kreiger et al. 1982). A sttdy in Iowa by Sowers (Sowers,~ Wallace, Lemke 1985) of 86 women aged 20 to 35 years did not find any relationshQ between forearm bone mineral masa and smoking during maximal bone mineralization. A study in Denmark (Jensen 1986) compared bone mineral content among 771ong i term smokers and 103 nonsmokers. Bone mineral content correlated with fat mass. For the came degrees of obesity, smokers did not have any lower level of bone mineral con; tent than nonsmokers. The results of these studies suggest that the effect of smoking as a risk factor for osteoporosis and fractute among postrrenopausal women may be primarily determined by the inverse relationship between smoking and obesity. It ;is possible that the early age of menopause among smokers may also contribute to the risk of osteoporosis. ' ItwolatMary Smoking The issue of involuntary smoking was not raised in the 1964 Surgeon General's Report. 11te first report of the Surgeon General to address the possible health effects of involuntary smoking was published in 1972 (US DHEW 1972). Over the ensuing 15 years, evidcnce on the adverse consequences of invohmttuy smoking began to amas.s, with several hundned papers being published. In 1986, the Surgeon C',eneral's Report (US DHHS 1986a) focused exclusively on this subject. I such Nonsmoking adults exposed to ETS have a higher frequency of symptano ogy as eye irritation and upper respiratory symptoms (US DHHS 19ft6a). The relationship between lung cancer among nonsmokers and ETS has been documented in both case- rnntrol and Mngitudinal studies. Most of thece studies have measured the increased risk of lung cancer among nonsmoking women, usually wives exposed to their husbands' tobacco smoke. A 1.3-fold increased risk of lung cancer has been estimated from these studies and is consistent with the amount of exposure to carcinogens from 1989 T8ST5 77

only taken up by inhalation hut also is ahsorhed through the mucous membranes in the (iral cavily. Thcrefure, it is possible to determine user uptake of hydrophilic agenta from c/n•winlg tobacco and snuff by means of nicotine-totinine measurements. The an:dytical ar-se.cmrnt of nicotine and cotinine in physiological fluids is primarily done hy gas chromatngraphy and radioimmunoassay (IARC 19R6). f3oth methods are high- ly .en.itivc ( hetween 0.2 and S ng/mL). and there is little or no interference by other smnkc crrmpment.. After cnvironmcntal exrnsure, the average nicotine and cotinine Irvclc in .aliva, plaxma, and urine of nonsmokers vary from 0.5 to 4.0 Ng/mL, whereas the average amount of nicotine in ahe serum of cigarette smokers ranges from 15 to 40 Ng/ml. and )ic% between 5(x) anct 2,(xx1 Ng/mL in saliva and urine. Cotinine concen,ra- ticm varics from 150 la 350 pg/mL in pL•rcma, from ISO to 4f)fl Ng/mL in saliva, and can go op to 2010 Itg/mL in urine (larvis et al. 1994. US DHHS 19RR). In snuff dip- pcrs and tobacco chcwers, placma nicotine levels were found between 3 to 22 ug/mL and pla.ma cotininc was 2(lfl to 4(X) ug/mL (US DHHS 19R6). One of the oldest methods fnr estimating the inhalation of tobacco smoke is the deter- minaticxr of COHh in blood. Since some CO is endogenously fornxd, the background values for COllh in the blood of nonsmokers without occupational exposure to CO range from 0.5 to 1.5 percent (National Research Council 1977). Smoking only a few ciFarenes per day elevates COHb levels to 2.0 percent. In a study of men aged 34 to 64 year., cigarette smokers. had average COHh concentrations of 4.7 percent: cigar cmoker., 2.9 percent: and pipe smokers, 2.2 percent (Wald et al.19R 1; Wald and Ritchie I9R4). The COFIh values of nonsmokers after ETS exposure do not markedly exceed 1.5 percent: thus. ('OHh cannot serve as an indicator of exposure to ETS (NRC 198b). Since CO is only slowly released from the blood in the process of exhaling, the smok- ing intensity of a cigarette smoker can also he assessed by the analysis of CO in the ex- haled hrcath. The critical value for CO. the value above that of a mmsmoker, is 5.6±2.7 f+prn in exhaled breath: again this method is not applicable to the dosimetry of non- %moker ETS expnsures. HCN, a major tobacco smoke constituent (>)OD pg/cigarette), is absorbed upon in- halation and ic dctnxificd in the liver, yielding SCN-. Since SCN- can also originate from dietary intake, only values above I()() Nmol of SCN' per L of serum as measured for cigarcttc .mnkerc are meaningful for dosimetry of uptake. In general, the average cigarette smoker has SCN- levels between 100 and 250 pmol/L of serum (US DHHS 19R7). A number of studies have clearly demonstrated that the mutagenic activity of the urine of cigarette smokers is higher than that of nonsmokers (IARC 19Rb). The most widely applied method for determining mutagenic activity-of urine samples was dcvelohcd by Yamasaki and Ames (1977), using a resin to concentrate the body fluid and, upon metalxdic activation, measuring the mutagenic activity on bacterial tester strains TA9R and TA I 5iR. In genera), the urine of cigarette smokers exhibits at least twice the mutaleenic activity as that measured in nrntsmokers' urine, )n summary, there are several biochemical indicators that enable investigators to as.ay the uptake of tobacco smoke by individuals or by groups of individuals. Whereas analyse. rif cxhaled CO, rrf C(3Fih, and r,f SCN' and nicotine-4otinine in sa)iva, scrum, and urinc are well xuited for determining the smoking intensity of an active smnker, only nicotine and cotinine determinations in serum and urine can also serve as indicatnrs, for the exposure of nonsmoken to ETS. Summary The ) 964 Surgeon General's Report was a landmark study that reviewed and asse-ed the available epidemioloRic, clinical, pathological, and experimental literature for; evidence linking cigarette smoking to disease. The principal findings of that Report!' are summari7ed in Table 13. In nxn, cigarette smoking was found to increase overall mortality and to cause lung and laryngeal cancer. Several other important conclu.ions were also drawn (Table 13). Since 1964. 20 reports of the Surgeon General (including this Report) have been released on tobacco and health that substantiate and strengthen the original cnnclusionsj ' of the 1964 Report. These reports have also established associations between smoking and disease in areas for which data did notexist, shed light on pathogenetic mechanism.s of tobacco-related disease, and added scientific depth to areas mentioned only briefly in the 1964 Report. A review of Table 13 allows the reader to quickly survey the state of knowledge onl. cigarette smoking and health in 1989 and to compare it with what was known in 1964. Of the 27 principal effects presented in Table 13, 13 were first noted in 1964: among i those 13 effects, many have been strengthened since 1964. Recent reports of the Suri gmn General have also covered important topics not even mentioned in the 1964 Report. For example, these relxxts have concluded that involuntary smoking can causf disease, including lung cancer, in healthy nonsmokers and that smokeless tobacco can cause oral cancer. The most recent Surgeon General's Report also concluded that the use of cigarettes and other forms of tobacco is addicting (US DHHS 1988). Much progress has been made in understanding the physicochemical nature of tobac- rn smoke. Today, the estimated number of compounds in tobacco smoke exceedc 4,0()(l, including some that are pharmacologically active• toxic, mutagenic, and car- cinogenic. The diverse biological effects of tobacco smoke constituents provide a framework for understanding the multiple adverse consequences of smoking. For ex- ample, the identification of 43 different carcinogenic substances in tobacco smoke helps explain why cigarette smoking can cause cancer at different sites including the lung, larynx. oral cavity, and esophagus; why cigarette smoking is a contributory factor for the development of cancer at different sites including the bladder, kidney, and pancreas: and why cigarette smoking is associated with cancer of the stomach and uterine ce The central role of cigarette smoking as a massive, preventable persona) and puh) c health problem can now be better appreciated. In the United States, it is a ma jor cause of CHD, this country'c most common cause of death: cigarette smoking is estimated to account for 21 percent of all CHD deaths. Cigarette smoking is the major cause of lung cancer, the most common cause of cancer death in the United States: smoking is es- timated to account for 87 percent of lung cancer deaths and 3() percent of all cancer deaths. While lung cancer death rates for women who are nonsmokers have not in- creased since the early 19h(k, comparable death rates for women who smoke cigarettes have inercased mc.re than fourfold. In 1986. lung cancer and breast cancer were the ow, 1999 T8515 1 07

ones, can significantly reduce the concentration of toxic and tumorigenic agents in MS, they have no reducing effect on the agents emitted into the SS (Adams. O' Mara-Adams, lloffmann 19R7). SS ia the major source of EtS. The smoke diffusing through the cigarette paper, the smoke emerging from the burning cone during active smoking, and that portion of MS that is exhaled also contribute to ETS. Table 9 prcsents some data for toxic agents resulting from tohaccocombustion in indoorenvimntnents(US DHHS 1997; Hoffmann and Ik-chtI in pre.-). The concentrations of toxic agents in ETS appear low in com- pari.on with their levels in undiluted cigarette MS. With regard to exposure factors, one needs to take into account the fact that the active inhalation of MS is limited to the time it takes to smoke each cigarette, whereas the inhalation of ETS is constant over sevenl hours spent in the polluted environment. This is reflected in the rcsults of measurements of the uptake of nicotine by active and passive smokers (US DHHS 1988). Smokeless Tobacco As noted above. the special Report of the Surgeon General. The Health Consequen- ces of Using Smokeless Tobacco, has shown that tobacco chewers and snuff dippers face an increased risk for cancer of the oral cavity (US DHHS 19Rhh). In the United States the four primary smokeless tobacco types are plug tobacco. loose leaf tobacco. twist tobacco, and snuff. The composition of processed, unadulterated tobacco has been discussed. Chewing tobacco and snuff are made with various flavor additives (LaVoie et al., in press). It is of special significance that the preparation of smokeless tobacco products, which en- tails curing, fermentation, and aging, occurs under conditions favoring the formation of tobacco-speci f ic N-nitrosamines (TSNAs) from nicotine and other tobacco alkaloids such as nomicotine, anatabine, and anabasine (Figure 15). Of the six identified TSNAs in smokeless tobacco. N'-nitrosonornicotine (NNN) and 4-(methylnitrosamino)-I-(3- pyridyl)-I-hutanone (NNK) are strong carrinogens in mice, rats, and hamsters, induc- ing benign and malignant tumors of the oral cavity, nasal cavity, esophagus, lung, liver, and pancreas (Hecht and Hoffmann 1988: Rivenson et al., in press). Table 10 presents chemical-analytical data for TSNAs in U.S. smokeless tobacco products (Hoffmann and Hecht 19RR). The concentrations of carcinogenic nittosamines in smokeless tohac- co exceed those in other consumer products by at least 2 orders of magnitude (US DH HS 19Rhh). During tobacco chewing and snuff dipping, additional amounts of car- cinogenic TSNAs are most likely also formed endogenously in the oral cavity (Hoff- mann and Hecht I9RR). Carcinogenic TSNAs have been regarded as a major factor for the association of snuff-dipping with oral cancer in humans (Craddock 19R3). Other carcinogens identified in smokeless tobacco are volatile nitrosamines (N- nitrosodimethylamine. 5215 ppb), N-nitmsomorpholine (54f1 pph), N-nitrcKodiethyl- amine (56,R0() pph). formaldehyde (57.0(X) pph), crotonaldchyde (52,4()<) ppb), and henz'(Xo)pyrenc (nt(1 pph), as well as traces of the ndioelement pcilonium-210 (Sr1.6 pCi/g) (t IS I)HHS 19R6; Hoffmann et al. 1997. Chamberlain, Schlovhauer, Chortyk 19RR). TABLE 9.-Sotne toxk and tumorltenk agenb In htd°°r MAroa'nents polluted by tobacco "noke IothNanl LoeKion Concentntior~ 30-,41pg Nhric oxide Wortioonr 17-270 µ6 Reuaw.ntr t10-320 pg Brs Caferair 2."R PR 6"10 µ6 Nilrogen dioxide woekroo- 40-190 Pg Renauraft i 2-116 pg Bxn 67-2Ix1 pg I Cafeterir ~ b-122 µg Rydroeency.eide Lh'intt>om 20-317 µ9 hbtie tlem 1 Benmie 23-50 ps rennddefiyde {,i.{n<rooms 30-120 µ6 ~ Acrokin PAlk plaxs 36o-S.tt00m . Acemne Prblic pUoet 4-I 1.3 ng 7 Phenols (vot.tik) N-NidaodimethYlami- CoffxAower ReArrrMrft public phoera . 0-240 ng . N-Nihowdiethrlamine Ra5mrrNt, PoaK PbM 0-200 ns 1-6 ps Nicaline P.blie t>Moes Rerlw.ants< worRroona Rddwrmt+ft public phm 3-to pg 1-13.tS pg 3.3-23.4 na fienso(a1pMne scxlRCE: MerrnrnWe NeeM. in pe+.. 8S89 TBSTS ~ `tl en

CHAPTER 4 TRENDS IN PUBLIC BELIEFS, ATTITUDES, AND OPINIONS ABOUT SMOKING 8689 TBSIS

It leading cauce% of cancer death in U.S. wonen, accounting for approximately equal nomher% of c:mcer deaths. Cigarette smoking is the major cause of Crnro. an etrect Ihat far oatwcieh% all other factnr.; .n"ing i% estimated to account for R21+Crcent of COPf) cM:uh.. (See Chapter 3.) The 1964 Rmirt of the Surgeon Generat aated that death rates from cerebrova.cular di.ca.r (.trokc 1 were incrcascd in cigarette snx+kers compared with nonsmokers. hut it drew no conclu.ion% concerning cuusality. In the current 1989 Repcxt, for the tirst time. cigarette cmoking i% cited as a cause of stroke, the third most common cause of ikath in the Unitcd St:uc.. Stopping smoking reduce% the risk of stroke. The effect nl .moking an pregnancy was briefly mentioned in the 1964 RReport. Many aadir% have .uh.cyucntly shown that cigarette smoking causes fetal growth retarda- tion and is a Prohahle cause of un.ucce..ful pregnancies. Tahlc 13 cunmiariics other important xmokinc associations with.cveral di.eases, in- cluding athero.clerotic aortic aneurysm, athero.clerotic peripheral vascular disease, and Ix•ptic ulcer disease: it also includes occupatitmal and alcohnl-reiated interactions with .nxskint: that increase the risk of cancer. finally, the rclxirt% of the Surgeon General have empha.ized the hcnefits of yuitting for zmokcr% of all agc.. CONCLUSIONS Part 1. Health Consequences I. The 1964 SSurgeon General's Report concluded that cigarette smoking increases overall mortality in men, causes lung and laryngeal cancer in men, and causes chronic hronchiti.. The Report also found significant associations between smok- ing and numerous other diseases. 2. Rcrxirt% of the Surgeon General since 1964 haveconcluded that smoking increases mortality amd morbidity in both men and women. f)isease associations identified a. cau.al since IW,4 include coronary heart disease, atherosclerotic peripheral va.cular dieeace, lung and laryngeal cancer in wornen, exal cancer, esophageal catx•cr, chronic obstructive pulmonary disease, intrauterine growth rrtardation, and low hirthweight hahics. 3. ('igarcttc .mok ing is now considered to he a prohable cause of un.uccessful Ixeg- nancice. increased infant ntortality, and peptic ulcer disease: to he a contributing factor for cancer of the hladder, pancrcas, and kidney: and to he associated with c:uxcr nf thc.avmach. 4. nccumulatinf; research has elucidated the interaction effects of cigarette smoking with certain ticcupational expnsurcs to increase the risk of cancer, with alcohol ingc.tion tn increase the risk of cancer, and with selected medications to produce advcr.c cffcct.. 5. A dccadc ago, the 1979 Report of the Surgeon General found smokeless tobacco to he a.a,ciatcd with oral cancer. In 1986. the Surgrnn General concluded that smokcics tohacco waa a cause nf this disease. 6. Research in the prcsent decade has established that involuntary smoking is a cause of disease, including lung cancer, in healthy nonsmokers, and that the children of parents who smoke have an increased frequency of respiratory infection% and symptoms. 7. In 1964. tobacco use was considered habituating. A substantial body of evidence accumulated since then, and summarized in the 1988 Surgeon General's Report. has established that cigarettes and other forms of tobacco are addicting. Given the prevalence of smoking, tobacco use is the Nation's most widespread form oG ~' drug dependency. R. Studies dating from the 1950s have consistently documented the benefits of smok- ing cessation for smokers in all age groups. 9. Recent evidence, including that presented in this 1989 Report of the Surgeon General, documents that cigarette smoking is a cause of cerebrovascular disease (stroke) and is associated with cancer of the uterine cervix. ~ i Part Ii. The Physicochemical Nature of Tobacco y I. The estimated number of compounds in tobacco smoke exceeds 4.0(10. including many that are pharmacologically active, toxic, mutagenic, and carcinogenic. , 2. Forty-three carcinogens have been identified in tobacco smoke. 1. Carcinogenic tobacco-specific nitrosamines are found in high concentrations in smokeless tobacco. I I E989 185t5 1 101 IfMI

% TABLE l3.-Summary of the principal effects of cigarette smoking Effect first discussed in Surgeon General's Reports Year first discussed in a Surgeon C',eneral's Repon: Current knowledge in 1989 N %D 00 Mortality and morbidity O.enll monaiity, increased in men 1961 Overall mortality incneaud in men and women %D r-t Co O.erall morbidity, increased Cardiovaacutar CHD, morn)ity increased in men 1967 1964 Overall nrorbidity increased A major cause of coronary heart disease in men and womas Ln .-i Cerebrovascular disease (stroke). mortality increased 1964 A cause of cerebrovaxular disease (stroke) ti'1 Atherosclerotic aortic aneurysm. mortality inueased 1967 Incn.ased mortality from atherosclerotic aortic aneurysm Atherosclerotic peripheral vascular disease, risk faaor 1971 A cause and nsost impottant risk factor for atherosclerotic peripheral vascular disease Cancer Lung canca, the major cause in men 1964 The major cause of lung cancer in men and women Laryngeal cancw, a cause in men 1964 The major cause of laryngeal cancer in men and women Oral cancer (lip), a cause (pipe smoking) 1964 A major cause of cancer of the oral cavity (lip. tongue. mouth. pharyna) Esophageal cancer, associated with 1964 A major cause of esophageal cancer Bladdercancer, associated with 1964 A contnbutory factor for bladder cancer Pancreatic canca, increased mortality 1967 A contributory factor for pancreatic cancer Renal cancer, increased mortality 19ti8 A contributory factor for renal cancer Gastric cancer, associated with 1982 An association with gastric cancer Cervical cancer, possible association with 1982 An association with cervical cancer TABLE 13.--Contlnued Effect first discussed in eon General's Reports Sur Year first discussed in a Surgeon General's Report Cunent knowledge in 1989 g PWmarry Chronic bronchitis, the major cause 1964 Thn major caufs of chtonic bronchitis Emphysema, increased mortality 1964 The major cause of emphysenu Woetew Luw-birth-weit,itt DabKs. associated with 19tS4 A cawe of intswsaine growth tetardatio. Utssstaaaful ptetpt.nc7.+saociated with 1980 A peob.bM eatm of unaaeeaatid progtuneia O1tar dfiefss Tob.ceo habit, sdated to psyctatogicd and social drive. 1964 Cigrerts smoking and other forttu of tob.oco ws ne addicting kM h Invotunatry smoking, irtiunt efFecs 1972 y nensmo A cars of diwaa including lung cascer, in healt Peptic ulcer diseass. associated w'id1 1964 A ptob.ble cause of peptic ulcer diseaas f Qccupatioeul insasetionsm adverse 1971 canotr Adverse occupational interactions that increi+e the risk o t Alcohol interactiom. advers 1971 caaoes Advens interactions with alcohol thal incnease the risk o Drug interacti.arum advass 1979 Ads'em drutImeracdom ' Nonmdignant orai disease, aswciated with 1969 tsears An uwciation with namnligtt.nt orai d Smokeless tobncco. associated with oral cartcu 1979 Smokdw tobnooo is a cause of onl oancat

FEMWLES 5 4 2 1 r 1965 ® Current smokers ® Former smokers I 1985 1985 FIGURE 3.-Populatlons of current and former cigarette smokers, men and women aged 60 years or more, United States, 1965 and 1985 SOUR(F.: F.aimaed frewnw"Midrd t.hrl.riew.. NHIS. I9M1t and 19113:.nA eaimae" of the teaidem ppolation.d the United Staea l.y.Ite rnl.ex,1965 atd 19115 (US B.ew dlhe Cenws 1974. 19A6). Accordingly, the period between 1965 and 1985 saw a marked increase in the num- ber of women smokers who reached the age of 60 years (Fgurcs 3 and 4). Moreover. the number of such women who started smoking in their teens increased by about ten- fold (Figure 4). Additional data on age of initiation are presented in Chapter 5. Overlapping Populations at Risk In 1965, a total of 71.3 million adults had a history of regular cigarette smoking, past or pre%ent. By 1 QR5, this count had increased to 94.4 million. These two populations overlapped. Among the adult population at risk in 1985, about 54.8 million were born before 1948. and therefore they were also aged I8 years or more in 1965. About 95 percent of the latter group began to smoke during 1965 or earlier (Harris 1983: un- 1+uMiched tabulations from the Curnetlt Population Survey 1985). This means that ahout 51.R million adults, who had ever smoked in 1995. had also been at risk in 1965. The overlap is depicted graphically in Figure 5, where the diagonal litles show the 1x1pu1atione common to both years. Among 44.1 million adult men with a hi.;tory of FIGURE 4.-Populatbns of inen and aonkn aged 60 years or mOe with a history of regular cigarette aeaking• classNkd by aRe started to smoke ~~,, Nmss 19t~s reRularly, United States,1965 and 1995 SOURCE: E+timMCdf^'mHuri.(14R)) t~ttletd.(195tiF.Honrnond(1966}.wtprbaflteA at the Ur:ad StNen by NR ~°«• ad 1915. wpubG+~hed t.ht.laion.. CPS 1903: ~ MM^~ d de rnid~+~ 0°a1~0^~ 1953 ad t9B5 (US awer of the Cn"'tts 1974•19l6). Jim lines cigarette snwking in 1965, a~~~ died Ixforel 1983 (standard error. 0.4 m'dlion). the remaining 13.3 million with a smoking history in 1965 (diagonal Likewise, among 27.2 million adult women lines and vertical lines combmed)• about 6.2 million died ~~r cigarcttertUiet lines). Not all of the dreedents, ~"~~' died as a conceq The horizontal lines in Figure 5 show the populations of adults at risk in 1985 who wen; not also at risk in 1965. The estimates are 22.6 million men and ~k'n Ilaf er women. These counts do not include persons who may have taken up 18 in 1965 and 1965 but died before 1985. Nor do they include smokers under age ars that in the two-dccadc period following the 1964 Surgeon 1985. Still, it appe 1 Ci arctte Ubeting and Advertising Act, some Getleral's Report and the 1965 Federa g 43 million Americans took up regular cigarette smoking, either tempnr1ri1 • Y or Per- manently. About two-thirds of them began to smoke by age I8. j ~ / 137 11fi T889 T8St ''S

younger men may reflect their increased use of filter-tipped and low-tar cigarette.,. Most currcntly smoking men aged 35 to 39 years in CPS-II, for example, were likely to have heen lifelong filter-tipped cigarette smokers. An even more striking crossover is shown for female current cigarette smokers in Figure 7. In particular, the age of crossover comes somewhat earlier. Among women cmokers aged 45 years or mexre, lung cancer death rates have increased fourfold to sevenfold. (There were no deaths and a small number of person-years of exposure at ages 75 or more in CPS-1.) By contrast, lung cancer death rates in the very youngest cohorts, aged 35 to 44 years, have declined by 35 to 55 percent. As in the case of men, the crossover appears to reflect differential trends in cigarette smoking among succes. sive cohorts of women. FE}rtiES t t I to4 .r t 36-3B 40-44 46-40 o CPS-I e CPS-u o-__~_ . r.- ~~- ~ . . . , , 60-IS4 t5ti-t90 00-t!4 (15-tIO 70-74 75-79 80-84 ME fiT ENt0.U$W F/l:I1RF. 7.-Age-spe.rifk death rates (IoA scale) for lung cancer, female current cigarette smokers aged i5-}t4 yqrs• 6-year followup of CPS-1(1959- 6S). compared with 4-year folkn.up of CPS-II (198L-tifi) iIHIRC7:: U,~„MiahcA iahla~i~na. AmerieM CwKe. Secie~r. Euimmea rMCVS-n aee {weliminry. Current Cigarette Strakers• Death Rates: Coronary Heart Diseaee Figure R shows the pmptxtional decline from CfS-I to CPS-11 in the age-adjusted CHD death ratcc ofcurrent smokers and nonsmoker:c. The relative declines are depicted 5889 185i5 separately for men and wornen, and for persons younger than 65, and 65 and olc}er. CHD death rates have declined in both cigarttte smokers and nonsmokers. For the hredominantly white, middle-class populations under study in CPS-1 and CpS-II, the merall decline among smokers and nonsmokers was greater than observed for the U.S. white population. Still, the declines in CHD tnortality rates among nonsmokers were notably greater than among current cigarette smokers. The disparity is seen at all ages, but appears somewhat greater among younger persons. In contrast to lung cancer (Figures 6,and 7), no crossover in age-incidence curves is observed. '11K increasing smoker-rion- smoker disparity at younger ages argues against a significant salutory effect of lifelong filter-tipped cigarette use. The possibility that changes in other coronary risk factors among cigarette smokers may explain their reduced decline in CHD rates needs further investigation. w Q 100 90 ~ 80 w o 70 Q 90 z .4 T 50 0 mFLES FEMPLES A(>M 35-84 ® Nonsmokers ® Smokers l r, htfk.ES FEMR.6S I ® HC4=D 85+ FIGURE g.-Percentage decline in aRe-adJusted death rates for CHD; 6-year fol- lowup of CPS-I (1959-65). compared with 4-year followup of CPS- ~ il(1982-A6) sot~RCY: U~,~uhu~ni~n+.Amerkr~C.ncer5oc~eiy. Eathnre.kxCTS•tl.epelimieary. 145 1.1.1

TABI,F, 1.-thtaiied computation nfsmoking-attribufabk lung cancer deaths among females, United States, 19RS fitlw+curc calcFiwy Prevatcnce Pl%1 Relative rick' r AaaiRned share s PR,) Case fraction /('x.) ('rrrent snwoken I-I0 per dayh 9.3 5.3 a 1.9 9.4 11-I9 per day 1•3 11.3 91.1 6.7 20 per day 9,3 14.2 93.0 24.0 21-.10 per day 3.2 20.4 95.1 11.9 231 per day 2.7 22.3 95.5 In.R Former amnken 0-2 year%` 5.0 1R.2 94.1 16.7 3-5 yeara 2.3 11.2 91.1 5.0 6-10 years 3.4 4.9 79.5 3.0 11-15 yeam 2.0 3.2 61-3 1.2 216 years 4.0 1.9 43.4 1.3 F..prnurc Prevalence C ~~ AnribtNd+k Attrihuu~k caK~wY p 1~F) ~ ~ ri~ deatlx ~ ,) a ('1F) A Ctment cmdces 27.R 62.7 57.7 22l(tt1 FvKmer amnkera 16.9 27.2 24.1 9,7n0 Cutrent and fermer amnkera 44.7 R9.9 ><1.R ~I.fN10 'RMin Ol aR!-MIN4[d AeNh tN!{, M11e 7! W ad/ortn1HM wN r1Hfnnn(d by diNA Uhn4Mdi7Jntln 10l/le aFt dianhNian Of wnnann yeam nf e.porwe.nw.~ nm.nr*era. "Numher n(ciRarnea amnked per day. an of tht Jw n(enmllment (SeyleoEer (q12). 'N.mher eI Yean r/qr.eA cintr lap ~ed reR.larly. mof 1he dale cif eaean1trr 15eykrMjer 10112). ~AnnAuwaMr de.rM A erpnl an..rAne a it anrilaMal.k riat and D eQrda 1R.Nt71"geanar dpdn rnonR.dvh reinak.in IOtS. S(H IRCI?. (:arfinket aeA SGellnum I 1911Rk NNIS IaRs, wiprMi.hed t.bWation.: NC11S. Diviaien of Vital CIa1NWa, VHIt, ynMMi.hrd. variahility, statistical confidence bounds for A can also be calculated. For the calcula- tion shown in Table 1, the estimated 95-percent confidence interval on a for all smokers was 72.1 to 99.6 percent. The corresponding confidence interval for D was 27.900 to 34.1(tt) ckaths. Only 2.6 percent of the variance of the logistic transformation of a was due to.amhling variahility of prevalence rates. 9L89 Z8St5 Uncertainties in Attributable Risk Aggregation Bias Versus Statistical Precision Sampling variation is not the sole sounce of uncertainty in estimates of attributable risk. The computations of Table I entail the assumption that the relative risks rt< depend only upon the specified indices of current and former smoke exposure. Thus, for former cigarette smokers in Table 1, the degree of risk after cessation of smoking is shown as depending only upon the length of cessation. Yet the magnitude of the residual risk also depends upon the extent of prior cigarette smoke exposure (Ilammond 1969. Lubin et al. 1984) and the reason for stopping (Kahn 1966). Alco,' some persons may have quit smoking after lung cancer had been diagnosed. As Table I shows, women who had stopped smoking for 16 or more years at the time of enroll- ment into CPS-11 had a subsequent 4-year relative risk of lung cancer equal to 1A. • Within this group of long-term quitters, however, those women who had previoysly •, smoked 21 more cigarettes daily had an estimated relative risk of 4.0 (Garfinkel •and Stellman 19R8). Likewise, for current smokers in Table 1, the degree of lung cancer risk is shown~as depending only upon the current number of cigarettes smoked per day. Yet the!risk depends critically upon the lifetime dosage of cigarette smoking, especially the dura- tion of cigarette use and the age of initiation of regular smoking (Brown and Kes~er ~, 1988; Doll and Peto 1978,1981; Peto 1986; US DHHS 1982). While the relative risk r was 22.3 for all women currently smoking 31 or more cigarettes daily (Table I), it was 18.9 for heavy smokers of IS to 30 years' duration and 38.R for heavy smokers of more than 40 years (Garfinkel and Stellman 198R). A more detailed, multidimensional breakdown of exposure levels may minimi7e er- mrs of classification, but such disaggregation also increases the sampling variability of the estimates. Conversely, increased aggregation of exposure levels will reduce sam- piing variability. Thus, if relative risk were assumed todepend only upon present smok- ing status (current versus fofiner), then the estimated attributable risk for female lung cancer deaths in 1995 would he 80 percent, with a confidence range of 77 to 83 per- cent. The confidence range of attributable deaths A would be narrowed to 29,7t1() to 32.(100. Age-Standardization The relative risks in Table I were estimated as a ratio of age-adjusted death rates, where the age ad.justment was performed by direct standardi7ation to the age distribu- tinn of nonsmokers' person-years at risk. In principle, if the relative risk is in fact age independent, then the estimate of relative risk in large samples should not be very scn- sitive to the choice of the standatd population (Anderson et al. 1980). In practice, however, the estimates can depend strongly upon the standard population. For thf il- lustrative calculation in Table I, the use of the entire population of CPS-11 woman-ycars at risk (rather than nonsmokers only) resulted in an attributable risk for lung cancer of 79 percent, with a confidence range of 75 to R2 percent (see Table 10). 1 +~, . 127

w Ir U 3: ~ m rr a_ t30 50 >I 40 tn ~ w ¢ m z 0 _j J S 30 20 10 M ' 1965 1 995 E~ 1985 smokers bpm after 1947 ® Poputattons common to both 1965 and 1985 ® Decedents by 198S 1985 M 1985 F1(:URE S.-Populations of adult men and women with a history of regttiar cigarette smokinR, United States,1965 and 19aS St N tRCf rcrimauvt fmm I larm 11 Vlt l/; ~.1~~~ y~~~ ~~, 1014{ aed 19AS; wirriqithed ladatinm. CPS IQN1. ~t eanmmn ot Ihe re.i.k.el Irrutatkmna nf the llniled yoex I,p spe.itiKe. to6S .nd 19R31US Rdrew of the Cew wa 11174. IORnI. Changts in the Cigarette Prndact The 1965 and 1995 population surveys did not elicit information on the type of cigarette smoked. tlowever, there was a decline in the average tar and nicotine yield of cigarcttcc, at least ac measured by the U.S. Federal Trade Commission (FTC) using sm<.kinle machincs undcr standardised conditions (Chapters 2 and 5). Data on ag- grcgatcciFarrttc.cdrsanJr.therpopulationsurveys(US ntIEW 1979: US DHHS 1990. 199 1; ('ha(•tcr 5) ;Ilco show that the proportion of persons smoking filter-tipped ciFa- rettt•% incrca.nl %ohstantially. Among entrants into CPS-il in 1982, tnone than 90 per- cent were filter-tipped cigarette smokers. In this gnaup, there was an average of IR ycar. (d fila•r-tipprd cigarette smoking prior to enrollment (Stellman and Gatfinkel 1'tx6). The mnittrity (.f these Ix•rame had smoked nonfilter cigarettes earlier in life. MRLES FEhifil_ES It rcmains problematic whether such changcs in cigarette manufacture and patterns of cigarette smoking have substantially reduced risks to cigarette smokers. There is considerable evidence that the actual reduction in the dangerous chemicals in cigarette cmoke is much smaller than implied by the FTC machine measurements (US DHHS 19R8a). While there is evidence that the long-term use of filter cigarettes and low-tar cigarctte, may somewhat reduce the risk of lung cancers, there ate considerably fewer data on a protective effect for other smoking-induced diseases (Alderson et al, 1985; Castelli et al. 1991 ; l lawthome and Fry 1978. Kaufman et al. 1993: Lee and Gatfinkel 199 1; Lubin et al. 19R4; Hammottd et al.1976; Wynder and Stellman 1979; US DHHS 199 1: Wilcox et al. 19RR; Stellman 1986a.b). - During the 1965-R5 period, numerous chemical tteatments and additives have been applied to cigarettes during tobacco curing and storage, sheet reconstitution, puffing, casing. and cigarette assembly. The chemicals include humectants, pesticides. Pavor- ings, plasticis.ers, ash adhecives, and other agents. Cigarette filters, plug wraps,•and tipping papers have evolved. The mix of domestic tobaccos has also chan¢ed, and oriental varieties have been added increasingly to American cigarette blends. The details of these product changes remain proprietary (US DHHS 1981). Other Changes In the Cigarette Stnoking Population The present comparison of populations at risk in 1965 and 1985 has been cbnfihed to sex, age, and history of tobacco use. Still. there may have been other changes in the characteristics of persons who smoke cigarettes. Surveys such as the NH1S have consistently shown a socioeeonomic gradient in cur- rent cigarette use, ac measured by education, occupation, and other characteristics (US DHEW 1979: US DHHS 1980; Novotny et al. 1988; US DHHS 1988a; Brackbill, Fnzier, Shilling 1988; Chapter 5). Thero is some evidence that socioeconomic dif- ferentials in smoking rates have widened. The proportionate decline in adult smoking rates between 1965 and 19g5 was highest for people who had graduated from college and lowest for those who had not completed high school (Chapter 5). Between 1970 and 1980, white-collar men and women showed propotliortatety greater declines in smoking rates than their blue-collar counterparts (US DHHS 1985). Among the factors that may influence the risks of cigarette smoking are: the coexis- tence of untreated hypertension; elevated serum cholesterol; consumption of oral con- traceptives; alcohol use; diabetes mellitus; and workplace exposure to other toxic and carcinogenic agents such as asbestos and radon daughters. With respect to these fac- tors, it needs to he determined whether the typical cigarette user of the 19R(ls differs from his or her counterpart of the 1960s. Cigarctte smokers have higher rates of alcohol use, are ntore sedentary, and are less likely to wear seat belts (Schoenborn and Benson 1988; Williamson et al. 1986). It is unknown whether these relationships have strengthened or weakened over the years. There is evidence in the American population of declines in dietary cholecterol, in dietary saturated fat as a percentage of total calories, and in serum cholesterol levels (Havlik and Fcinhcib 1979). The prevalence o` untrcated and inadequately treated hy- pertension has ala+declined (Havlik and Fcinleib 1979). However, detailed studies of Z889 iBSTS I I tN 09

TABLE L---~SurRerm (',eneral's Reperts on SlmoklnR and heaMh,1964i1l1 Year 19fS4 1967 196R 1969 1971 1972 Suhjeet/Hi(thliftMs Firu official n;port of the Fedetsl Gwemnent on smokm6 and hulth. Concluded that "Cigarette snwdunE is a health haml of sufficient importance in the United States to wanant.ppmpriate remedial action" Concluded that cigarette smokinR is a cause of lung cancer in men and a suspected cause of lung cancer in wumen. Identified many other eausal relationships and smokin6Ai¢ase assncininns (US PHS 1964). Confimrcd and stnengdiened concha<ions of 1964 Report. Suted that "The case for cigarette smoking as the principal cause of lung cancer is overwhehnin`." Frnmd that evidence "attothtly sultltesta that ciRarette smokinE can cause death frum comnary, hean disease." 1964 Report had described this relationship a an "unociMinn " Also eonehrded thaa "Cigarette smoking is the most importaM of the eau.es of chronic non-neoplastie Monehiopulmonary diseases in ahe (tnited States." Identified measurcs of morbidity associated with smoking (US PHS 196Ra). Updated Mformation presented in 1967 Report. Estimated smoking-related loss of life expectancy among young mt:n as A yean for "heavy" smokers (over 2 paeh per day) and 4 yean for "Ii6M" smokers (less than 112 pack per day) (US PHS 196Eb). Also appldnented 1967 Repat. Confimbd esociation between nutemal smoking and infant low birth weight. Identified evidence of increased incidence of prematurity. spnntanears abortion. stillMrth, and neonatal death (US PHS 1969). Reviewed entite fkld of anu+kin6 ad he.Nb, with emphuis en moa necent Iiteralure. Discussed new data indicating as.aeiations hetwren snaking and peripherat vaeeuly diseaaee athetosckrosis of the aona and coeonary arteries. ineeeused iincideece and severity of respir.bry infections. and increased mortality from caeMovascalar dixase aed nonsyphilitie sortic aneurysm. Concluded that smoking is asaeciaed with earkm of the oral cavity and esoplrRus. fouwd that "Maternal smoking during pregnancy e><erts a retarding influence on fetal growth" (US DHEW 1971). Es.mined e.idem,e on in.mmohtSieal eRaefa ot tobaceo and tobacco smoke. harmful constiturMs of tobacco smoke. and "public exposure to air pollution from toh.cco smnke." Found tobacco and tob.cco smnke antiRenic in hununs and animals; tnhaeco may impair polective rnechanisms of immune system: nammokers' exposure to tob.cco smoke may esacerlwe allergic symponn carbon maaaide in smoke-filkd naKm may harm health of persons with ehronic hatR or hean disease: toh.cco smoke contains hundmds of comprnmd.s. several of which have heen shown to act aa tarcinoRens, tumor initiatora, and tumor pronrolen. Idernified carfinn mppRide. nicotine. and tar as smoke constituents most likely to produce health hazards of smoking ((IS DHEW 1972).' PratetNed eridnrce on health effects of enokins pipes, ciRns. and "Gttk ciEns." Found mottality rates of pipe and ciltar smnkers higher than those of nnnemoken hut lower than those of ciRaretle smokers. Found that ciRarcne smoking Impairs exercise performance in healthy yramR men. Presented additional evidence on smokinR as risk facMr in peripheral vascular disease and pmhknts of pregnancy (US DHfiW 1973). I TABLE 1.--Contirtued Year 1974 1975 1976' 1977-7R 1979 19R0 1991 19R2 19R3 SobjeedHiRhliEhts Tenth Anniveraary Report. Reviewed ad strengthened evidence on major han.ards of smnkins. Reviewed evidence on association hetween smokinR and Nherosekrdic brain infarction and on synerEistic effect of smokinE and asbestoa exposure in causing lung cancer (US DHEW 1974). Updated infonnMion on health effects of Involuntary (passive) smokinR. Noted evidence linking parental smokins to Iwmchitis and rneumonia in' children during the fnrt yev of life (US DHEW 1975). Compiled xlected chapters from 1971-73 Reports (US DHEW 1976). Combined 2•year Report focused on smukinE-telated health problenn4unique to women. Cited studies showing that use of oral eanracepives prn}~ iates harmful effects of smokin6 on the cardiovascular system (US DHE197lI). Fifteenlh Mniverfry Report. Presentrd most cornprdtensive nwiew of health effects of smokin6 ever published. and first Surgeon General's Reptxi to carefully examine beh.vioral, pharmacokMic. and social factors influ~ncing smoking. Also fint Report to consider rok of adult and youth educlition in prwrwtin6 nonsmokin6. First Report to review health consequences of smokelesa tobacco. Many new sections. including one identifying stnoki+'S a "one of the prnnary causes of drn6 imeractions in humani"(US DHE1W I979a). Devoted to heddt canequabes of smokinR for women. Reviewed evidence that strensthened previous findings and permined new ones. Noted limjcctions that lung canca woukl surpass hm.st cancer as leading cause of cancer mortality in women. Identified trend toward increased smnking hy adokseent females (US DHHS 19A0a). EsNnined health eaesequencea of "dte changkq ciguette " i.e.. lower tar and nicotine ciEarettes. Concluded thr lower yield ci}tarettes reduced risk of lung cancer but found no conclusive evidence that they reduced risk of cardiovaculy disease. chronic obstructive pulmonary disease. and fetal danaRe. Noted possible risks from additives and their products of combustion. Discussed cotnperoatory snpkinR behaviors that might n'duce pxentisl risk reductions of lower yield cigarettes. Emphasi?ed that there is no safe cigarette and IhM any risk reduction associated with lower yield cigarettes would be small cotnpared with benefits of quittin6 smoking (US DHHS 199 1). Reviewed and extended underanndinlt of the health censequences of amrAinR as a eause or cont rihutory factor of numerous eaneers. Included first Surgeon General's Report consideration of emerginR epideminlnRic evidence of increased lung cancer risk in nonsmoking wives of smokinR hushandc. Did not find evidence at that time sufficient to conclude that relationship was causal. but l.bekd it "a possihk serious public health pmhlem." Discussed potential for lowtost smokinE cessation inlerventions (US DHHS 19R2/. Enwnieed health consequenees of smoking for cardiovascular disease. Concluded that cigarette smoking is one of three major indcpendent causes of coronary hent disease (CHD) and. given its prevalence. "shnuld he cansidend the me+d impixtant of the known mexlifiahle risk factors fnr C)If)." Discussed relMien.ships hetween smokinR and other forms of cardimascular diicaa (US DHHS 19R3). 9 i I

o Females, CPS-1 A Females. CPS-It o Mates. CPS-l1 o Males, CPS-1 FIGURE 9.-ARe-.pecitic death rates for COPD, mde and female current ciRarette smoker. axed 4S-S4 years: 6-year follovmp of CPC-1(19.59..- 65), compared with 4-year foltowup of CP4-11(198248/i) tfx IRCr: t/ep,Aliched 1aMsta1Nma. Amnit.~ Cmeer Grciety. EqimaK. r4xCPC.II an prrliminWy, Current Cigarette SmRkers' Death Rates: Chronic (Rntructive Pulmonary Disease Figure 9 gives corre%pem<fing changes in age-specific death rates for COPD. In this figure, the ages are grouped into 10-year rather than 5-year age ranges as in Figures 6 and 7. For male smoker-, there has been a reduction in COLD death rates for ages 45 to 74 y~ars. For fcmidc smakers over 55 years old, there has been about a twofold to threefold increase in C( )PD rates. F.stimated Relative Ricks from CPS-1 and CPS-11 For mcn and wtxnen, respectivcly. Tahlc..i and 5dcpict estimated relative risks in the 6-year follnwup nf CPS-I for a11-causc mOrtality and for 14 specific causes of death (15 cao.es for women, inchldinle cervical (-ancer). For men in Tabk 4, the ectimated relative risks for current and fomlercigarette smokers are given separately. For women in Table 5, the numbers of deaths and person-years of exposure among former smoker5 was kio small to give reliable death rates for many causes. Accordingly, in conform- ity with earlier reports of CPS-I mortality, the death rates for current smokers are com- pared with women with any history of regular cigarette use, whether past or present. For both men and women, the estimates in Tables 4 and 5 are in accord with earlier reports on CPS-1 mortality (Garfinkel I9ROb; Hammond 19Cvla,b, 1966, 1972: Ham- mond and Garfinkel 1909: Hammond and Seidman 1980). Among men. fonncr. smokers have lower mortality ratios. In both sexes, relative risks for CHD are higher' at younger ages. Both scxes, and to a greater extent, men, show elevated risks of other cardiovascular diseases including sttoke, hypertensive heart disease, and aortio aneurysm. In bnth sexes, smokers' death rates are higher for bronchitis and emphysema and for seven cancers including lung cancer. The relative risk of lung cancer among current smokers in CPS-I is about 11.3 for men and 2.7 for women. The results for CPS-11, given in Tables 6 and 7, show substantial changes in the mor S tality risk of cigarette smoking over two decades. The all-cause relative risk for mdn has increased from 1.9 in CPS-1 to 2.3 in CPS-11. For women, it has risen from 1.2 to 1.9. These increases in overall mortality are not an artifact of the method of age adjust: ment, because CPS-11 contained proportionately fewer person-years of exposure at tht youngest ages than CPS-1. i As reflected in Table 3 and Figure 8, the telative risks for CHD death have increased for both men and women. The relative risks for men, in particular, are consistent with those reported from recent case-control studies (Kaufman et al. 1993. Rosenberg et al. 19R5) and from the followup of the Multiple Risk Factor Intervention Trial (MRFIT) cohort, ac described in Chapter 2. The markedly elevated relative risks for younger women in Table 7 are consistent with those reported in a recent case-control study (Slone et al. 1978) and in a prospective study of 120.000 female nurses (Willett et;al. 1987). Such consistencies acrcxs epidemiologic studies---especial)y cohort and case- control studies reported during the 1980s-argue against any appreciable bias in the 4- year preliminary results of CPS-11 given in Tables 6 and 7. Tables 6 and 7 show consistently increased relative risks for cerebrovaccular lesions among both men and women, particularly in the younger age groups. Among women under 65 years old, the estimated relative risk of death from stroke is 4.8, with a 95- percent confidence range of 3.5 to 6.5. The observed increases in risk for current smokers are reduced in former smokers. The finding of an elevated risk of cerebrovascular disease among cigarette smokers ic not new. Elevated death rates frotll stroke were reported in CPS-1(Hammond 1966; Il:unnxxld and Garfinkel 1969) and am reproduced in Tables 4 and 5. The 1983 Sur- geon General's Report noted the association between stroke and cigarette use: no data on the effect of smoking cessation were available (US DHHS 1983). A recent prospec- tive study of R,((X) men of Japanese origin (Abbott et a1.19R6) showed an elevated risk of thromhoemholic and hemorrhagic strdces among cigarette smokers. While there was no clear trend of increasing risk with higher daily smoking rates, suhjects who quit smoking had reduced risks compared with continuing srnnkers. )n the prospective stndy of 12(),(X)) female nurses. CoIditz et al. (19RR) found a dose-recpnnse rclation.hip he- i I t I,I,, 9889 T8SZS 147

tive risk r when incidence of the disease is low (Cornfield 1951). Both types of studies provide estimates of the assigned share s. The estimate of relative risk r, derived from epidemiologic studies, is then applied to the population of interest. Let p denote the proportion of exposed persons in the sub- jcct px+pulation, estimated independently from survey data. Then the quantity j= pr/(P(r-I)+ I l is the fraction of all cases of the disease (in a given time interval) that occur among exposed persons in the subject population. This is sometimes called the "ca.se fraction" (Miettinen 1974). Moneover, if fraction jof all cases occurs among ex- posed persons, and if fraction s of such exposed cases is attributahle to the hazardous agent, then the fraction of all cases attributable to the agent is a =f.c. From the defini. tions of j and .c, the quantity a can he expressed as a= p(r-1) p(r-1)+l (1) This is Levin's measure of attributable risk, also termed etiologic fraction (Miettinen 1974), attributable fraction (CDC 1987b), and population-attributable risk (MacMahon and Pugh 1970). When A is expressed in percentage terms, it is often termed percent attributable risk or population-attributable risk percentage. Equation (1) shows how the attributable risk a depends upon both the relative risk r and the proportion exposed p. Thus, an agent may be significant in the causation of disease among exposed per:torts so that its relative risk r greatly exceeds I. Yet that agent may cause a small prttpottion of all caees of the disease because exposure rates p are low. Convet:sely, an agent that is widely prevalent (with large p) may contribute substantially to the total number of cases, even when its relative risk r is close to unity. As a consequence of equation (1), the logistic transformation of a is a b8 1) = logp+log(r I) (2) where log denotes the natural logarithm. Equation (2) provides a convenient method of decomposing the uncertainty in the attributable risk a into two compottents-uncer- tainty in the proportion exposed p and uncertainty in the relative risk r. Levin's measure of attributable risk can be generalized to cases where there are mul- tiple levels of exposure, multiple causative agents, or confounding or qratifying vari- ables, or when an agent can prevent a disease (Walter 1976; Miettinen 1974). In the case of multiple levels of exposun*-, it is convenient to let dk denote the incidence rate and rk = di,/db denote the relative risk for the k-th exposure level. Similarly, let pk denote the proportion of the subject population exposed at the k-th level. Then ert = (rt-I )/4 is the assigned share among cases exposed at the k-th level. Likewise, the quantity fk = pkrk/(T*n (rir-I) +Iwhere Ek deno(es.summation over exposure kvek, is the fraction of all cases occurring among persons exposed at the k-th level. The generalized formula for attributable risk becomes F.a fksk, which can he expressed aa U/rk (nrl) - a - EW~ (rk-I ) + I (3) Lct 1) denote the total number of ca.ses of disease in the population of interest in a given time interval. Then A = aD is the estimated number of cases in the interval that are attributable to the agent. The quantity A is sometimes called "attributable caees." When relative risks or exposure rates vary by age, sex, or other stratifying variables, then separate estimates of A can be made for each combination of variables. When there are multiple causative agents, attributable risks can be computed for each agent separately and for combined exposures. Thus, if agents X and Y both have a causal role in the development of a particular disease, then the relative rick for agent X may depend upon the presence or absence of exposure to agent Y. When X and Y act synergistically, some portion of the total risk attributable to X will reflect the combinej cnntribution of X and Y. For example, indoor exposure to radon has recently been esr' timated to account for about 13,3(101ung cancer deaths annually in the United States (Luhin and Boice 1988). Radon exposure and cigarette smoking interact synergistical~ ly in causing lung cancer (National Research Council 1988). Of the estimated I;.(1(10 deaths attributable to radon exposure, about 11.000 would be due to the combined ef- fect of smoking and radon, while about 2,(tt)0 would reflect radon exposure in nol- smokers (Lubin and Boice 1988). lllnstrative Calcnlation: Sttaking and L.ea Cancer In Women ~ Table I provides a detailed illustrative application of Levin's method to female deafhs frcxn lung cancer in the United States during 1985. The population of female smokers has been divided into ten exposure levels: five categories of current cigarette smokers hased on the number consumed per day; and five categories of fomtercigarette smoke4s hased on the length of time since quitting. Foreach exposure category, the upper panel shows the estimated prevalence pk. derived from the 1985 NHIS. Also given are e's- timates of relative risk rt derived from the 4-year followup (1982-86) of the second American Cancer Society prospective study (Garfinkel and Stellman 1988). At each exposure level, the upper panel also shows the atsigned share a and the case fraction ft. The computations are summariaed in the lower panel of Table 1. For both current and former smokers, as well as for all females at risk, the estimated prevalences p rep- resent the corresponding sums Ft pk over the prevalence rates pk in the individual sub- categories. The case fractions j likewise reptesent sums of individual fractions fk, while the attributable risks a are derived from the corresponding stnns F.k .ctA. Attributable deaths A are derived from the products aD, where D= 38.687 hmg cancer deaths among adult females in 1985. Table I shows that almost two-thirds of all female Itmgcancerdeaths occurred among women who currently smoke one pack or more daily or who have quit smoking within the last 5 years. Nine out of ten lung cartcer deaths occurred in women with any his- tnry of regular cigarette use. Cigarette smoking accounted for an estimated 82 percent of lung cancer deaths in wornen, or 31.600 deaths in 1985. About 9,3(tt) (or 29 percent ) nf the 31,fdtt) female lung cancer deaths that were caused by smoking occurred among Gxmer smokers. tioth the prevalence rates and the relative risks in Table I are subject to sampling variability. By a formula analogous to equation (2), a standard error for the kogictic transformation of a can he derived. Under the assumption that f) has no .ampling 17.1 SL89 i8SZS 1 125

-0 CONTENTS introduction ........................................ Data Sources .................................... Issues in Comparing Surveys ....................................... ___- - 175 175 177 --- -- Trends in Public Beliefs About the Health Effects of Smoking ............... Overview ....................................................... Is Cigarette Smoking Harmful to Smokers in General? ................... 179 179 179 Heavy Versus LightSmoking .................................1R1 Tar Yield ..................................................1R3 Duration of Smoking ........................................1R5 Does Cigarette Smoking Cause : ................................ Lung Cancer? .......................................... Heart Disease? .......................................... 185 185 188 Chronic Obstructive Pulmonary Disease? .................... 18lF~ OtherCancers? ......................................... What Are the Special Health Risks for Women? ................... Effects of Smoking on Pregnancy Outcome ................... Risk of Cardiovascular Disease Among Smokers 195~ 195 191 ' Who Use Oral Contraceptives ........................... 197 - Other Health Risks Related to Tobacco Use ...................... Involuntary (Passive) Smoking ............................. Is Smoking an Addiction? ................................. Interaction Between Smoking and Other Exposures ............. Smokeless Tobacco ...................................... Personal Health Risks for Smokers ................................... 2001 200 200 ! 202 202 202 How Harmfulls Smoking? ..................................t......204, Absolute Risk ....................................... I)' .....206 Relative Risk ...............................................206 Attributable Risk and Smoking-Attributable Moctaliry .............. 206 Comparative Risk ...........................................207 Knowledge Among Adolescents About the Health Risks of Smoking ....... 212 General Health Effects ....................................... 212 Personalized Risk ........................................... 215 Comparative Risk ........................................... 215 Addiction ................................................. 216 Smokeless Tobacco Use ...................................... 217 Constituents of Tobacco Smoke ..................................... 217 Health Benefits of Smoking Cessation ................................ 219 Discussion ...................................................... 219 Current Gaps in Public Beliefs About the Health Effects of Smoking .. 219 6689 IBSiS Factors Interfering With Changes in Knowledge .................. 227 The 1990 Health Ohjectives for the Nation ....................... 22.3 I 172

(COPD); and lung cancer. For COPD and lung cancer, in particular, there has been no discernible change in nonsmokers' death rates. The relatively small changes-less than 15 percent up or down-are all statistically insignif icant. The absence of significant change in nonsmokers' lung cancer rates confirrns and extends the ftndings of Doll and Peto (19R 1) and Garfinkel (1991). For COPD, the table presents the first information on trends in nonsmokers' death rates. It needs to he emphasized, however, that the statistical test for a change in lung can- cer or COf n rates is of relatively low power. For COPD, there are sufficient data to have detected an increase of 53 percent or more in males and an increase of 42 percent or more in females at the 0.05 level of significance. For lung cancer, increases of m(xe than 37 and 24 percent for males and females, rexpectively, were detectable as statisti- cally significant. In contract to lung cancer and COPD, Table ; shows a very marked decline in CHD death rates in nonsmokers. Over an approximate 20-year period, nonsmoken' age-- adjusted death rates dropped by 64 percent in men and 69 percent in women. The ob. served decline in nonsmokers' CI iD death rates is in keeping with the CHD decline in the general population. However, the magnitude of the decline is larger in the ACS subjects. Among U.S. white males, the age .adjusted death rate from CIiD (stand- ardi7ed to the 1965 population distribution) declined by 41 percent during 1965-85. For U.S. white females, the decline was 40 percent (NCI IS 1967 and unpublished; U.S. Bureau of the Census 1974. 1986). TABLE 3.-Age-adjusted annual death rates per 1/N/,1NN/ for CHD, COPD, and IunR cancer among males and females, aRed 35 years or more, who never smoked regttlarly, 6-year followup (1959-65) of CPti-1 compared with 4-year fitllowup (19R2-86) of CPS-11 Maka Diaa.e CPS-t cPS-IP" Females CPS•I cP5-tl•" ('11I) " 74S 270 479 153 42o ;41n--tl4r (7215-•773)A (2.Sl.:RII (467-49t) (14[-159) (Y)M) 9.3 R,7 4.0 5,6 Mrn1-502,527.Ir; (7•(1-12.9) (6.5-11.7) (4.5-7.0) 4w}-492. 44(i' I,anRcam•er 133 11.6 10.7 11.4 162 1fi1r; 1.2' (I2.5-19.1) (IO.R-17.0) (R a-11.9) (9.a-17„1) 'r.w Mwh (9'C.1 and (•P5-11, aEe rljddmrrw nf ralr" w„ perhnm.d hy direcl .landanhraliwm lu the aRr divirilMima of 1I C rraeknr whire nuka and Grnalra, rryrclivrl., in 1o"t 11 I S, p.n au n( Ihr (, ~.w 1 V 7 t1, "1 .. (•/K It. death .atn wrte reneerrA (nr rklared avcMainmrtw d caN.ra.d.k•ath. Anw.nv,4,OW lnnwn drMh. rhmnR I'pl± Rti in rnak s...mnken, rkarA crrt~ricMr. hal mM M•n rr'ctivrd dw 4.14) Lr Janr 10RR• Anr+nR t0.1A1 \nnwn.k.Nha in Iernak n.M,.rrw,krra, 1.411 ha.l n.M hrtn rrcrnn1 `('IK.I,...ImR, lnlrrnalnm.d /'Ia..rrirati,n rd hw•av.• trvrnlh Rrvkinn. ~NnmM,..n parrntlwas arr'r1 rrrrrM rnnlMlnM.r trnnval.. '('Ih II,.MhnR,hllennNMNITI('IM\I(N'MMnLI INInlhKrrl,nM1. S(IIIRI'1ItnM,M,.Iwrtrahdan..a.AorrNanl.uHrrG~u•IV, b889 TBSiS Current CiRarette Smokers' Death Rates: Lnng Cancer Figures 6 and 7, respectively, show changes in the age-specific lung cancer death rates of men and women who described themselves as regular cigarette smokers on the original questionnaire for each prospective study. 'I1+e death rates, depicted in each figure on a logarithmic scale, apply to all such current smokers. No adjustment has Aeen made for differences in the number of cigarettes smoked or duration of cigarette use. The age-incidence curves in both figures show a striking crossover effect. Aniong older male smokers, especially those aged 70 years or more, lung cancer death rates in CPS-11 exceed those in CPS-1 twofold to fourfold. By contrast, among younger male smokers, especially those less than 50 years old, CPS-11 death rates are about 30 to 40 percent lower. The observed crossoverphenomenon appears to be consistent with long- term changes in cigarette smoke exposure among successive cohorts. The incre se in lung cancer among older male smokers reflects their increased frequency of cig~rette uce and increased cigarette smoking in early life. 'ihe decline in lung cancer ilmorle 35-3G 40-44 t~W__000 4t5-4t7 ti0-64 t~-150 t70-t)4 (!t5-ti9 RI£ f1T EwMll4E'IT • - -~ 70-74 7ti-79 tj0-d4 0 CPS-I A CPS-11 FIGURE ti,--Age-Rpedfk death rates (InR sak) for lung cancer, male current cigarette sntoRers aged 35-R4 years:6-year followup of cPS-1(1954- (iS), MntpatYd with 4-year followup of CPS-11(1 QR1~-R6) St)URCF•: t)npMiahrd /ahnlatinn.. Amerierr Cancer Wirly. F.•ninnlta (m ('PC•11.we prliminary. 142 1 14,1

1 TARLF, 12.-Fdimated deaths (in thml.ands) attributabk to cigarette smoking, 10 selected cauac, males and femakt, United States, 19R5 Cau%e of death Maks Females CF1D. aRe <ht 34 11 (3(1-3Rf (9-12) CHD. age 2RS 44 26 ( 3(.-54) (20-34) Cc)rD 37 20 (35-39) 0 R-11) Cancer of lip, rxal cavity, and pharynx 5.1 1.6 (4.4-5.4) (1.2-2.0) Cancer of larynx 2.3 0.6 (1.6-2.7) ((1.4-0.7) Cancer of ear"altua 5.0 1.6 (4.(1-5.7) ( I . ~-1.9) Cancerofluns 76 10 (74-77) (29-32) Cancer of pancreaa 3.3 3.4 (2.1-5.0) (2.R-5.1) Cancer of hladder 3.1 1.1 (2.1-4.2) (0.6-1.9) Cancer of kidney 2.6 0.4 (1.R-3.S) (0.1-1.5) Cerebrovascular disease, alte <65 5.5 5.2 (1.9-7.0) (4J-6.2) Cere(xova.cular dicew, aRe 261 12 4.R (R-17) Ten cau.es 231 106 (220-242) (98-115) N(1TF: Canpned fmm Tahk 1 t rd uquMidcd uMlninna nr draha at aRea 20 yean cw mme try c.we fmm NC11C, 1995. Cinn of iedividrNcw.rs nar eol equal ielah tecawt nlrtwndinR. 'NumAr.a m/rreewht.ea oe vS-perceny anfiAerKt hwetvah. in 19R5 were 67,(tt10, compared with 30,0(10 in 1965. Even if the population had remained entirely stable during 1965 through 19R5, the lethality of cigarette use in American women would have doubled. Among men, the total of 231,000 emoking-induced deaths in 19R5 represented 41 percent of total deaths from the 10 caucec combined and 22 percent of all deaths among persons aged 20 years or mrm. Among wqnen, the total of 10fi.()(10 cm(>tc ing-induced deathc represented 25 percent of deaths from the 10 causes combined and I 1 percent of deaths from all deatha among pcrsrrnc aged 20 years or more. The axnputationc in Tahleti I() and 12 have omitted other causes of death that are likely to he aurihutahlc to cigarette urc. If the relative risks given in Tables 6 and 7 (ott Iw low v 0 w I+ALES 61) so 11w 8 1 40 m r+ 10 low 0 CI-p <tj5 CHO tj54 IXILD Co Li ng F7(:URE 10.-Fdimated ciRareNte-sntokinR-attribatabk deaths from C4iD. COPD, and lunt; cancer, men aged 20 years or more, United States, 1965 and 1985 i, Kdmkfn~-.M'hut.Mede.An in 19115 A.ve been correca:d fi+r populaiim Nire: rror the Irn vnarked 1"t , the e+wim. .n innr.aaehninR IVtiS-n5. O 34 32 FEM~ES 30 28 low 29 ' 24 /am 22 low 20 18 18 14 to" I 12 low taeelt 8 low 10 i e low 2 Itaee llI 0 Vr{J \u:J F1CURE 11.-Fstimated ci~arette-smokint;-attribntabk deaths from CHD, COPD, and 1nnR cancer. females aged 20 years or more. United States.1965 and 19R5 i N(T1F rv. thelMrc ma.keA I~M1i . rht e.~i~n.kr/ am*inR-annMnshk deadn in 19Rt have heen aweected fix I'MoIaNan iun.wMninR I~t>«. 159

f:rmr. in the Clasification of Causes of Death The cstimatiom of attributable ckaths A rcquires information on total deaths D. For the comlxilaliom in Table I, the latter yuantity was defined as deaths in 1995 whose un- derlyinF cause was primary lung cancer (International Classification of Diseases, Ninth Revision I I('1)-91, ('oxk 162). Dcaths from the larger class of Respiratory Cancers (1('f)-9 Ctxlcs I62-I65) were nM used hecause they include pleural mesotheliomas and secondary lung cancers. Slill, thc use of ICD-9 ('rKie 162 alone may not eliminate all en•ixc <d dcath certificati++n. In a review r+f +iver (.zOO thnrrcic cancer deaths in Min- nc.ota 1n•twccn 1979 and 1991. Lilicnfcld and Gunckrsnn (1986) iidentified fnur caees nf pleural malignant meuHhelirrna that had been classified as Ccxle 162.9. Morcover, it ic at Icast arguahlr that physicians in recent ycars have been reluctant to diagnose primary long cancer in the absence of a history nf cigarette smoking (McFarlane et al. 19R1.). While crrcmrs in di.ease classificaticm and death certification of lung cancer in 19115 may be relatively minnr, thc samc cannot he mid with avsurancc ahnut other discascs caused by cigarette u.e. Thus, deaths certified as being caused by CI ID (ICD-9 Codec 410-414) may not adequately reflect the lethal consequences of cigarette use on the cardiovascnlar system. Many deaths from Hypertensive Diecases (Cocks 401-4(14, in- cluding ilypcrtensivc Heart Disea.se, 402, and llypertcnsivc Disease. 404) may have been agFravated by cigarette use. Similary, deaths certified as being caused by COPD ( ICD-9 Crxks 490-492 and 496) may incompletely reflect the numbers of deaths from nnnnernplaxtic respiratory disease clue to smoking. Many cases of Influenza and Pneumonia (ICD-9 Codes 4R(1-4R7) may not have been lethal hut for the coexistence of cigarctte-induced lung damage. The major prmpcctivc studies of cigarette smoking and mortality that were initiated in the ly5(k relied upon the International Classification of Diseases, Seventh Revision (ICD-7) (i(ammond 1966; Dora 1959: Kahn 1966; Rogot 1974; Rogot and Murray 1990; DDoll and ilill 1956, 1964. 1966; Doll et al. 19R(1; Doll and Peto 1976). Coding conventicmc have changed considerably since ICD-7 was adopted in 1955 (Kkw 1975, 1992: Klehha and Scott 19R0). While ICD-7 Code 162 was reserved for lung cancer that was "specified as primary; ' a separate code 163 was allocated to lung can- cer. "ni,t specified as primary or secondary:' In practice, however, epidemiologists and vital .tatiaicians recognized that the great fraction of lung cancer deaths certified under ICD-7 ('ix(c 163 were primary and that deaths certified under the two codes were in fact indistingui.haMe. Accordingly, it was standard procedure to repnrt combined dc:rth. for Coxlr. 162 and 163-a practice adhered to in the analysis below. Still, the uxc of the combinedcategory 162-16i in ICD-7 may have intnxluced greater diagnos- tic uncertainty than the current use of Coc1e 162 in ICD-9. Pres•ino. P;stim:des nf Attributable Risk from Cigarette Smoking Many authox% havc cctimiqect tax ntnnhrr or proportion r,f deaths attributable to ci,earrttc u.c, cithrr from ;1 .inplc csimc. a group r+f causes, or all causes (Ravcnhnlt 1'N,.t. I9!t 1: Rice 0 :91. Irtxr,; Mclmo.h 11194: Whyte 1976: (lammcmd and Seidman 1990; Doll and Peto 1991; Garfinkel 19g0a; U.S. Office of Technology Assessment (US OTA) 1995; SSchultz 1986; Goldbaum et at. 1987; CDC 19R7b). Doll and Pcto (19R 1) estimated R3,()()0 smoking-attributable deaths from lung cancer in 1979. Rice and colleagues (1996. TTable 5) estimated 270.000 smoking-attributable deaths among U.S. adults in 1980. including 86.000 from CHD. 75.000 from lung cancer, and 14,()00 (mm "emphysema, chronic bronchitis." The Centers for Disease Control ( IyR7b) ec- iimated 315,0(10 smoking-attributable deaths for 1994. including 77,000 from CI1D, 9t,(xl(1 from lung cancer, and 51,000 from "chronic bronchitis, emphysema' comhined with "chronic airways obstruction." These studies differ with respect to specific causes of disease, the time period under consideration, the populations at risk, the sources of epidemiologic data, and the specific , methodology for estimation of risk. Thus, some researchers have directly applied Levin's measure of attributable risk, as defined in equations (1) and (3) (Rice et al. 1996; MMcIntosh 19R4; CDC 19R7b; Goldbaum et al. 1987; Whyte 1976). In doing sc~, they assumed that estimates of relative risk r, derived from particular epidemioingic %tudies, could he extrapolated to the population under consideration. By contrast, Hain- mcmd and Seidman (1980) and Garfinkel (19R0a) computed attributable risks direcily for the CPS-I study population. In an analysis of avoidable deaths from cancer, Doll and Peto (1991) employed ajiiF- ferent model. Let N denote the size of the population at risk, while D denotes the tOtal number of deaths from a specific cause. If do denotes the cause-specific death rate ~ among unexposed persons, then D-dnN is an estimate of the number of deaths At- ' tributahle to the exposure. To estimate attributabk cancer risks for the United States in 1978. Doll and Peto (19R 1) then assumed that the age- and sex-specific cancer mor- tality rates for nonsmokers do observed in CPS-1 during 1959-72 could he applied to nonsmokers in the general population in 1979. In support of such an assumption, they note that for men, nonsmokers' cancer rates in other prospective studies (Kahn 1966; f)+)1 and Peto 1976) closely matched those observed in CPS-1(Doll and Peto 198 1). Moreover. CPS-11ung cancer rates of nonsmoking women were similar to those of U.S. women in 1950, before their lung eattcer rates began to increase. Doll and Peto's method was employed by OTA (1985) to estimate attributable deaths from CHD (US OTA 19R5), For cancer, nonsmoker death rates in CPS-1 may well ap- proximate do for the U.S. population. But the same conclusion does not appear to be warranted for CHD (Sterling and Weinkam 19R7). In fact, the use of CPS-I nonsmoker death rates yielded an estimate of 142,OOt/ smoking-attributable deaths from CI1D in 1982. By contra.st, application of the Levin method gave an estimate of 91.(1()0 deaths (US OTA 19R5). Doll and Peto (1981) rejected the application of relative risks derived from CPS-1 to the U.S. population in 1978. Their central concem was that such relative risks had in- creased in the two decades since the start of CPS-1 in 1959. Among smokers aged 6(1 years or tnnre in 1965, a much smaller fraction had smoked regularly during early life. For older women smokers, in particular, only one in eight had begun to smoke regular- ly as a teenager. This proportion increased markedly in suhsequcnt decades (Charter 5). In view of the importance of quantity and duration of smoking in determining IunF cancer rick-and especially in view of the critical role of early-life smoking in the etiol- 8L89 IBStS I ltl tun

I TARLF 9.-Fstimated attributable risks for 10 selected causes of death from cigarette %mokinR, males and females. United States, 1965 , TABLE 10.-E stimated deaths (in thousands) attributable to cigarette smoking, ' ~ 10 selected causes, males and females, United States,1965 Cause nf dkath Makc' 414) Femaks" (1) CI II), aRe 3S-fr4 42 26 (40-45)c (2t-.V)) CIID.aFe ?6S (I 3.3 (9-14) (2.1-5.1) CnpD 94 67 (7'/• RR) (57-76) Cancer nf lip. eral cavitvl arnl ph,iryns 74 27 (S9-Rs) (12-51) Cancer nf Iarynx 94 47 (h1-94) (R-90) Cancer of ea,phague 57 14 (.W76) (6-29) Cancer of lung RIS 40 (92-RR) (31-5(1) Cancer of pancreaa 41 14 ( t()-53) (G-30) Cancer of h6xkkr 51 76 («.hIS) (20-56) Cancer of kidney 36 17 (19-56) (5-42) CerHnnv.scular di"se, age.1.5-(d 2R 29 (21-11+1 (22-33) Cerehrnvaccular disease, age 263 2.0 1.3 (0.f+-/i.ti) (0.2-6.5) 'rnr ~n.ks. awnrwnalwmK ha.ed an peevaknet nMCS in T.Ak 2 anA Rdai.e eAs fmmNe cunrrn ud kmner cipKne .nr*eR. with or wid+mn a bia4ry of pipe aad ciRa.mnkinR..kri.v.I fnam (7!C.1. % ~~. femaka, anriMn.Me riaka c~nrd frvnn pevaltnce alt, ia Talik 2 and Rlalive riaka Gw all femak amnkcn, raN anm1 ppr.enl. in Table S. 'Nwnhrn in paremAe.c, aR Vt.penel n aaridenee inlervala. In 1965, as Table 9 reveals, cigarette smoking was fespoffsible for 42 percent of CHD deaths among younger men and 26 percent of deaths among younger women. For COPb deaths at all "ages, the smoking-attributable risks were 84 percent for men and 67 percent for women. For lung cancer, the respective attributable risks were 96 per- ccnt and 40 percent for men and women. With the exception of deaths from stroke among younger pcrsons, attributable risks were markedly higher for men. Table 10 reports the cttrreslxmding cmoking-attributabk deaths, A, during the year 1965. Attributable (kathc wcrc comPlned by multiplying the attributable risk percent- ages in Table 9 hy the corre%lxal<ling rlu.e-specific death rates among persons aged 20 0689 T8StS Cause of death Males Femaks CHn. age <65 31 9.5 (4A-54~ (R.2-10.R) CI1D. age ?ISS 25 6.0 (20-30 (3.9-9.4)4 COPD 16 2.3 (15-t7) (2.0.2.7) Cancer of lip, oral cavity. and pharyna 3.6 0.4 (2.9-4.2) (0.2-0.R) Cancer of larynx 1.9 0.1 (1.4-2.2) (0.02-0.3) Cancer of eschfiaRuc 2.4 0.1 I, Cancer of lung 35 3.1 (34-36) (2.4-3.Rj 1 Cancer of pancreas 3.E 0.9 (2.R-a.9) (0.4-2.0) Cancer of bladder 3.0 1.0 ' (2.2-3.7) (0.5-1.5) Cancer of kidney 1.2 0.3 (0.7-1.9) (0.1-1.d) Cembrvvascular diseue, age <65 53 4.7 (4.2-7.2) ( 3.R-5.6) Cuebrovrcular disease, age 265 1.5 1.0 , (0.4..•t.1!) (0.2-5.9) Ten eau+a 1.-0 .10 (143-137) (26-34) N(7TF.: Conaned fMn T.hM 9 rd tabultlbna ddcMha at.da 20 yean or nwe hy ew.e far 1963 (NCHS 1967). Smms may nod cqud nwaN hecwne of ~owndin~. Numhera in parernhe.es.e 93-perent confidence Inlav.li 'When Ihe anriMnaMe riak euimree given in Nore a d T.Me 9weae areAA doe loul NribMaNe dewha far inak*'rcre 1 ie.nql (9ti.pncem conr~BnKe iMeeval. l s I(Mlf1 w 16A 111101. AppwxinaNely IwothMda of the R,pM1.dAitioeal Aealr were fmm CIID. years or more. For the 10 causes combined. cigarette smoking was responsible for 150.000 deaths among men and 30.000 deaths among womeo in 1965. Among (nen, CHD deaths made up 51 percent of smoking-attributable mortality for the 10 causes combined. This proportioft is consistent with the estimate of 45 percent reported by the 1964 Advisory Committee to the Surgeon General for excess mqrtality from all causes (US PHS 1964). Similarly, lung cancer accounted for 23 percent of the %moking-attriMltable mortality for the 10 causes combined-again consistent with the 155

tiated that smoking remains an important risk factor in the older age groups (]ajich, Ostfeld, Freeman 1984). TABLE 2.-Mortality ratios for aeketed cages In Swedish males,1964-197l. by type of Rtnolcing Type of anakins Cauv of death CiRele~ only Pipe only CiRan only Cancer of oral cavity and Iarynx 2.9 (R) 1.4(3) 0.6(l) (140-146. 141t• 161)~' Cancer ore%aphaRtn (150) 3.7(9) 3.6(6) 6.5(2) Cancer of liver and biliary 3.0(13) 1.7(5) 7.2(4) pns4Res(155-IS6) Cancer of pRncress (157) 3.3(28) 2.9(19) 1.0(1) Cancer of mrchea. bivndMM. and 7.4(77) 7.2 (39) 7.6(11) IunR (162) Cancer of bbdder (1RR) 4.2 (17) 4.0(16) 1.9(1) Ixhemie heart disew (410-414) 1.4R(399) 1.39 (366) 1.16(42) Aortic aneurysm (nonsyphitidc) 2.1(11) 2.101) 5.1(4) (441) 8 ~vechkia and empAysenu 3.3(18) 3.606) 1.3(1) (490-492) Peptic ulcer (Sl I-534) 2.0(11) 2.R(13) 4.00) Cirrfiosis of liver (571) 1.d(21) 0.7(4) 2.70) Suicide. accidan. and violknee 1.7(90) 0.9(35) 2.5(10) (ERn0--E999) All cMnei 1.43 (1,0631 1.29 (R66) 1.39(131) NOTF.: nerA rwn rrI diaed for spe a.A n~id~wce. Nerer I'll eaeMiRMe die ak~ence Vup. Nwnber of derM we Riven in prenlheaet 'Tlrc ~e~n p~rm d ~dreco ree4eA p d~y i~ 19R1, rw~drIteA re-ne soA n"nce. •vu ewiewed ur he 1n.7 ie ciRrene nn*en. 8.4 in pipe reokas. imd 1I3 in cipr u eolcen. Nrngrn in rarenthe+n we ICD•R coAa. iOURC'F.: Canwnun. PrnlrRee• Elhrd (10R7). fi+£89 18STS Lung Cancer lntroduction the most prominent conclusions of the 1964 Report was the determination one •'Cigarctte cmoking is causally related to lung cancer in menthe s e~6 that ensive ~po~ effect of far outweighs all other factors ~ ic ev~defor nce a« ailabk in h 1964 on smoking anQ in the same direction." The eT- og lung cancer was already extensive. Sharply~;~ increasing l ~~abledocumentationofanew the United States acro~c the 20thcentury pro epidemic. Clinical ohservations and early epidemiOlogic find'ngs suggested that tobac- ' co smoking was assexiated with lung cancer. but hypotheses related to air pollution, also extant. By 1964, however. the epidemiologic occupation. and other factors were tive studies, were conclucive: smot- data. derived from 29 rctrosPectlve and 7 Pro<Pec ing was causally related to cancer of the lung. Further support for this conclu%ion was obtained from animal studies showing that condensates of tobacco sMOke were car- cinogenic and from the demonstration that tobacco smoke contained carcinogens (US ikd through 1964 also provided additional insight DHHS 1982). The evidence compiled tobacco smoke. The risk of into quantitative aspects of respiratory carcinogerxs by lung cancer was shown to increase with the amount and duration of smoking and to' decline with cessation of smoking. voluminous evida+ce has continued to support ' in the 25 years since the 1964 Report• The new evidence has been the causal relationship between sn'+oking and lung cancer. sufficient to establish that smoking also causes 1~~~ n~i~SO d~~p~se prehensive epiclemiologic data have provided expa rclationships between smoking and lung cancer risk. Research has also been directed , ibility to tobacco smoke. New .~Dt now pmviding insight at environmental and host factors determining cu investigative techniques in molecular and ceu" by'e biology are crc moke. into the molecular mechanisms of careinoge tose-Response Relatiimships and prMlective The 1964 Report reviewed evidence from rctrospective epiclcmioloFic investigations that documented dose-1'eSDn^~ rclationships between and meacurcs of exposurc to tobacco smoke. This evidence was cited lung cancer risk rcla~~ h ~ of ~o~ung cancerdh ~~wb- by the 1964 Report in relation to the criterion ing causality. Investigation of dose-resPon IchavebeenappliCdtothecpidemiobgic cigarette has .equently bcen extendcd. Mathcmatical mode • t~cic The data to Fain hiok~gical imiFht into respfctirn+s designed to reduce tar and nicotine evolved sulntantially since 1,N,4 with modl ~I~tc, Studics yiclcls. Recent reccarch has addressed ^heh~ve examined lung cancerr icke at low dose of lung cancer and involuntary . g Icvcls (US DI I11S 19Rfia). % ce n lationchiit< of lung Abundant cpirkmiologic evidence h('a`h ~FrcC ~f i~ ac'^' and age at initiation cancer risk with cigarcttes smoked per day. 43 :hi A~

the clustering of cigarette smoking with other risk factors for CHD are unavailable. It remainc unc Icar whethcr the observed long-term declines in hypercholesterolemia and hypertension have been mcx+e or less pronounced in cigarette smokers than in non- smokerc. Thcrc is srxne evidence that cigarette smoking reduces therapeutic effective- ness of new pharmacologic and invasive treatments of CHD (Deanfield et al. 1994: C:alan et al. 1rtRR), pinal)y, in 1965. oral contrxeptives were just coming into widccprcad ucc. Ry 1995. oral contraccptivc usc was prevalent among both smokers and nomcmokvrc (Galdhium ct al. 19R7). Thoce Smokers Most at Risk in 1085 Were Also Smokers in 1965 In .um, hctwrcn 196.5 and 19R5, thcrc have been m;(jrsr changcs in the populations of cmnkcrs ;it risk for cigarcttc-rclatcd injury. Jn 1965, nxism men who smoked ciga- rettc% had also used cigars and pipcs. Ilowevcr, by 1985 the great majority smoked cigarettes exclusively. In 1965, about 40 percent of current smoker-, were women. By 1995. wwomen numbered almost half or current smokers. Moreover, the numbers of fonmer smoken increa.ced substantially in both sexe.c-- especially in men. In 1965, about one-quarter of all living men (self-respondents to NI IIS, age I R or older) with a history of regular cigarette use were fomxr srnokers. By 1985. fformer cmokers made up almost half of all living men age I R or older who ever smoked. Finally, the two-decade interval witnessed a substantial increase in the number of women smokers neaching the age of 60 years, with a tenfold rise in the population of older women who had begun to smoke as tcenagers. These changes in the population at risk have also been observed in other, nonrandcxn samples of the U.S. smoking populatirm, including a recent cnmpariton of the 1959 entrants into CPS-1 with the 19R2 entrants into CPS-11(Stellman and Garfinkel 1986). The percentage of mak smokers who smoked 20 or more cigarettes per day in CPS 11 (76 percent) was higher than in CPS-1(69 percent); the percentage of female smoken who smoked 20 or more cigarettes per day increased even more from CPS-1 to CPS-II (4i percent to 61 percent). Ammg the 94.4 million adults in 19R5 with a history of cigarette u.ce, about S 1.8 mil- lion smoked cigarettes as adults before 1966. The youngest of these persons is now in his or her late thirties. This grnup represents the vast majority of persons who arc now at risk for the fatal and nonfatal con%equcnces of cigarette smoking. Cancer Prevention Study I and Cancer Prevention Study 11 CPS-I. fomrcrly terrtxd the American Caneer Socicty 25-State study, began in Oc- tober 1959 arxl ended in October 1972. Over I million men and women, representing 3 percent of the population over the age of 45 ycars, wcre trcntitcd in 1,121 crnmties (Ilamrrxmd 19fr/a,h, 1966: Garfinkcl 1985). Illitcratc pcrsons, institutionalimd polndatione, itinerant workers, and illegal alicnc were not recruited. Mote than 97 per- cent of enmllecc were white. f'snmllnx nt was by family: an eligible family had to have one memher <wcr ar#• 45, Once a family was cliRihle. every family member over the ar.c trf 35 -wac acl;rd In L:ir:icilmtc. ,1c a rrcnh of familwixt.cd recnlitrnent, more than t three-quarters of CPS-1 subjects were married. As a consequence of the e)igibi lity rulesl . the age distribution of entrants peaked at 45-49 years. More than one-third of par- ticipants had at least some college education. CPS-11 was instituted in September 1982. The study, conducted in a1150 States, had the same enrollment plan and organiaational structure as CPS-1. Over 1.2 million per- sons were enrolled. As in CPS-1, subjects were predominantly white and more edu- cated than the general population. While 2 percent of CPS-1 participants were black, the proportion increased to 4 percent in CPS-11. Still, black persons were under- represented. Like CPS-1 participants. CPS-II enrollees were predominantly oZer 40 years of age. Unlike CPS-I, the mode of their age distribution was 50 to 59 years (Gar- finkel 1985, Stellman and Garfinkel 19g6). CPS-11 is planned to continue through 19RR. Preliminary resuhs of the first 4 yeara of followup (19R2-R6) an: available. For these 4 years, ascertainment of the fact of death among enrollees is thought to be virtually complete. However, ac of lulT 1988. the cause of death had not been ascertained for about 9 percent of male deaths;and 13 percent of female deaths. ~ Comparison of the 6-year followup (1959-65) of CPS-1 and the 4-year foRnwup of CPS-11 are reported below. For computation of relative risks, cause-specific death rates for CPS-1 males and females have been standardized to the age distributions bf man- years and woman-years of exposure during 1965-69. Relative risks in CP§-li were likewise computed as the ratios of age-adjusted death tate.c, where standardiza(ion was performed with respect to the age distributions of man- and woman-years of eIxposure during 19R2-86. For comparison of absolute death rates (as opposed to relative risks), the age1specific rates in both studies were standardized to the age distribution of U.S. resident white tnales and females in 1965. For CPS-It, absolute death rates have been corrected for underascertainment of causes of death. No such coneetion was made for CPS-I, where death certificate retrieval has been virtually complete. No attempt has been made to correct for possible noncomparability between ICD-7 (CPS-1) and ICD-9 (CPS-11). Studies of the transition between the Seventh and Eighth Revisions of the International Classification of Diseases have shown significant non- comparability (Kkbba 1975,19R2). Similar results have been reported for the transi- tion between the Eighth and Ninth Revisions (Kkbba and 5cott 1980). Comparison of the Seventh and Ninth Revisions, however, suggests that the combined changes have been self-cancelling (Personal communication. l. Kkbha to l. Harris, June 19RR). Roth CPS-1 and CPS-1I are mor'e representative of middle-clacs white Americans than the U.S. population as a whole. Sti)I, the two cohorts were derived from virtually iden- tical sampling schemes, and analysis of the entrants has shown similar demographic characteri-tics (Stellman and Garfinkel 1QR6). These consideratinnc enhance the validity of comparisons between the American Cancer Society studies. Nonsmokers' Death Rates Table 3 reports a comparison of the arc-adjusted death rate for the three leading cauces of dcath from cigarette smoking: ('I11); chronic ohctructive Pulmonary disease 141

TABLE 6.-Public beliefs about the health effects of smoking in relation to duration of smoking, 1964 How many cigarettes a day for how many years might make a cigarene smoker ngore likely to get lung cancer? (percentage indtcaung the following number of ye us-) 59 10-19 20-29 230 Don't know/ no aaruwer Smokers not mote likely to get lung c.uxer Curtent smoken t0 12 12 11 10 43 Former smokers 17 17 16 14 14 22 Neversmokers 17 16 10 13 19 24 'A•,ke9 only of that who undicated in drc pperiaq saney Queseioa ttLt wwkers an awn likely due aonamken to develop lung ancer. The denominaors for drae yaceMagas include all reipondenu. 'Regudless of nwnber of ciaainus per day. SOI;RCE: AU731961(USPHS 1969). TABLE 7.-Public beliefs about the health effects of smoking in relation to duration of smoking, 1986 How long would a person have to smoke (number) cigarettes' each day before it would affect eheir healtfi? (percentage indicating the following yean of smoking) <1 1-2 3-5 6-10 11-15 >1S Never Doftt ktsow Currentsmokers 23 1S 10 8 3 l0 0.6 30 Fwmer smokea 24 13 13 10 3 9 0.4 29 Neversmoke» 36 16 10 6 2 5 0.1 25 'TAe numEer of ciprersa med ie thia qupoo. vea tbe aumbet idsmlLd by de is.pasdnt (eme pevio...rvsy qne.om) ea ma.~hiaR -a pena. wwW C7.ve to.eoke betow i.wfd aKat the'v hnldL" (See Tabie 6). SOURCE AUTS 1986 (US DHHS. ie per).

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(ed.) f:'pidrnrinbr.~ir rrl AlrlrrrKrr nr, nr the Snah• of ('unrcr• und Other Chronic Dixratrs. National Cancer In.titutc %kxx+graph 1 y. U.S. Ihl.artnx:nt of Hcalth• FAlucatitm• and Welfare. Public Hcalth Scrvicc. National ('anccr In.tilutc. lamrary Ir". pp. 1-125. KANNF.I.• W.R.. SHl'RTI.F•FF. D. llte Framingtam Study. Cigarcttcs and the ckvck+jmxnt afinacrmincntclatKlir.~aHx~. (irr•irrtr•ic•.~ 2R('):t+l-6R.Fchnrary tU7~. Irx, 9989 I8StS ~ 107

. TARLF, 3.-Trends in public befiefs regardinA the relative hamrds of dilRerent cigarette brands,1970,1975,19A6 Plercentage of cunent amnken 1970 1979 19R6 Smne kinds of ciEarett~a are rmbahly mde Mzardous to health than rnhers Kind 1 aeinke prnhahly mtMe harsrAout,han othen' (6) (10) (1t) ,' EO & a P Kind I.mnke pmhahly ks.a harArdous than others' (25) (2.S) (21) o,s Kind I smoke probably about the vme at others,' (4) (14) (13) ' t)nn't know (2) (2) (2) .y SuMntal 47 51 43 tiu ~ Q go ~'o aN a AII ciFarettes are probably attout equally ho.ardous' 43 41 50 i 7 ~at ~ Cigmnea are probably not hvsrtlous to heahh at alt 4 5 2 1 ., Y 7 :• !9 t7nn't know or not stated if .ome are hasudous 6 4 3 ' S 0 ~ Tmal 100 H)0 1(1(1 C! r i C a`a sP if `nrc word "pmhaMy" was nM u.ed in the 1906 A(JTS. 'ttte wadft M the d.ee wevey . wn etherwiae aimitr. I S(HIRCF: AUTSa 1970, 1975, 19R(. (US thIF.W 1973,197(r: US DNHS, in pea.). I e ~ K Y o ~ o cx o P P ~ < P ~ K C069 TBSTS Although smokers and nonsmokers acknowledge the health risks from smoking, cer- tain types of smoking (such as light smoking or smoking low-tar cigarettes) or smok- ing for a limited period of time may be perceived as less hazardous. In general, there are few data to ac.cess the degree to which these beliefs are held. According to the AUTSs in 1970, 1975, and 1986, 45 to 50 percent of current smokers believed that "some kinds of cigarettes are probably more hazardous than others;" 40 to 50 percent believed that "all cigarettes are probably about equally hazardous," and 5 percent or kss believed that "cigarcttes are probably not hazardous to health at all" (Table 3). More specific data are reviewed below. Heavy Versus Light Smoking A large body of evidence has shown that light making, that is. l to 9 cigarettes per day, is associated with a significantly increased risk of overall morbidity and mortality frexn lung cancer, chronic obstructive pulmonary disease (COPD), heart disease, and other smoking-related diseases compared with never smoking (US DHEW 1979a; US DH11S IQR2, 198i, 1984), Between 1970 and 197R, national surveys conducted by the Roper Organization ad- dres.ced beliefs regarding the health risks of heavy versus light smoking (FTC 1981). Resp(xldents were asked how hazardous smoking is and were given three pos jible rcsixxlses: any amtxmt, only heavy smoking, and not hazardous. In 1970.45 pekent of reclxmdents considered only heavy smoking to be hazardous (Table 4: by 1978.31

1 Trends in Public Attitudes About Smoking and Smokers ................... 224 Involuntary Smoking as an Annoyance ............................... 224 Ncxnsmokert'Rights .............................................. 224 Actions When Smokers Light Up .................................... 227 Opinions of Teenagers ............................................ 227 Trends in Public Opinion Ahout Smoking Policies ....,.., _ 2zQ Overview ....................................................... 2.'10 Background ................................................ 2.10 Limitations of the Surveys in Assessing Public Opinion About Smoking Policies .................................... 230 Restrictions on Smoking ........................................... 2';ll General ...................................................230 Public Places ............................................... 232 Workplace ................................................. 232 Airplanes .................................................. 232 Restaurants ............................................. 2l5 OtherPlaces ....235 Restrictions on the Sale and Distn"bution of Ciganyttes ................... 235 Complete Ban on Sales ....................................... 235 LimitingSalestoMinors ..................................... D5 Banning Free Samples ....................................... 2i9 Policies Pertaining to Information and Education ....................... 239 Restrict or Prohibit Tobacco Advertising ......................... 2'19 Warning Labels for Cigarettes ................................. 241 Economic Policies ................................................ 241 Taxation .................................................. 241 Hiring .................................................... 241 Conclusions .......................................................244 Appendix .........................................................246 References ........................................................254 0069 I8SZS Introdnctbn This Chapter analyzes trends in public beliefs, attitudes, and opinions about smok= ing. It is divided into three sections. The first describes trends in public beliefs regard- ing the health effects of smoking, the second describes trends in public attitudes about smokers and smoking, and the third describes trends in public opinion about smoking policies. At the out.ut, it is important to define and clarify the important terms used in ihis Chapter. Terms such as knowledge, awareness, opinions, beliefs, and attitudes liave commonsense meanings to the lay petson, but more complex meanings to the social scientist. For example. Allport (1935) reviewed many definitions of attitude and con- structed his own comprehensive definition: "An attitude is a rnental or neural state of readiness, organized through experience, exerting a directive or dynamic influence upon the individual's response to all objects and situations with which it is relatw.'` Entire books have been devoted to the science of defining and measuring public atz titudes. opinions, and beliefs (e.g.. Oskamp 1977). ; For sections two and three of this Chapoer, which deal with attitudes and opinions, the commonplace understanding of these terms will suffice. For the first seclion, however, which covers beliefs about health effects, a tnore careful approach il war- ranted. This Section generally follows the construct described by Fishbein (1977), which embraces three levels of belief: ~~ 1. Level l(awareness): A person may believe that "dte Surgeon General has deter- mined that cigarette smoking is dangerous to health." 2. Level 2 (general acceptance): A person may believe that "cigmtte smoking is dangerous to health." 3. Level 3(personalined aeeeptanoe): A persott may believe that "my cigarette - smoking is dangerous to my heatth." Abat of the survey data ptesented in the first section address Ltvel 2 beliefs: At times, the term public knowledge is used to refer to public beliefs (Level 2 beliefs at the population level). There are few data regarding Level I beliefs; consequently, use of the terms awareness and public awareness is generally avoided. Data pertinent to Level 3 beliefs are available from a few surveys in three forms: (1) questions asking whether smoking "is harmful to yotrr health": (2) questions asking whether respondents are "concemed" about the effects of smoking on their health; and (3) questions asking whether respondents believe that they ate kss likely, as likely, or more likely than other people to be adversely affected by smoking. These levels of beliefs are discussed in more depth later in this Chapter. Data Sources The information presented in this Chapter is derived from three principal sources: 1. Nationally representative surveys conducted by the U.S. Public Health Strvice from 1964-g7, including the Adult Use of Tobacco Surveys (AUTSs) (1964, 1966, 1970, 1975, 19Mi) and the National Health Interview Surveys (NHISs) (19R5,19g7). The NHIS questions were part of the Health Promotion and Dis- 175

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Health Cnnsrqutncts 'y Smnkinjq for Wnmrn. A RrMtrt of the Surgeon General. U.S. Department of Health and I luman Services. Public Health Service. Office of the Aesistant Secretary for Health. Office on Smoking and Health. 19R0. U.S. DEPARTMENT OF HEALTH AND HUMAN SER VICE,S. The Health Constqutncss nf Smoking: The Changing CiRannt. A Rtpnrt of the Savgtnn General. U.S. DepartmerM of Health and Human Services. Public Health Service, Office of the Assistant Secretary for Health. Office on Smoking and Health. DHHS Publiealion No. (PHS) RI-5(1156, 19R1. U.S. DEPARTMENT OF HEALTH AND HUMAN SER V ICES. The Health Cnnsrqutncts nf Smoking: Cancer. A Rcrnrt nf tht SurRrnn General. U.S. D^partment of Health and Human Services. Public Health Service. Office on Smoking and Health. DHHS Publication No. (PHS) R2 :S()i79, 19R2. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. Tht Health Consequrnrrs of SmnkinR: Cardinra.rcu/ar Disease. A Rryrnrt nJthr Surgtnn General. U.S. Department of Health and Human Services, Public Health Service. Office on Smoking and Health. DHHS Publication No. (PIIS) R4-5(1204, 19R3. U.S. DF.PARTMENTOF HEALTH AND HUMAN SERVICES. The HralthCansequencts of Smoking: ChrnnirOhstructivtLungDistast. ARrpartajthtSurRtanGtntral. U.S. Depart- ment of Health and Human Services. Public Health Service. Office on Smaking and Health. DHHS Publication No. (PHS) RI-50205,19R4. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The HealthCnnsequsncesef Smoking: Cancer and Chronic LunR Disease in the Workplace. A Report of thc SurRrnn General. U.S. Department of Health and Human Services. Public Health Service. Office on Smoking and Health. DHHS Publication No. (PHS) RS :SI12(17, 19R5. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. Tht Health Cnnstquwncrs of Involuntary Smoking. A Report nf the Surgeon General. U.S. Department of Health and Human Services, Public Health Service. Centers for Disease Control. DHHS Publicaticxt No. (CDC) R7-R39R, 1996. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. Tht Health Consequences nf Smoking: Nicotine Addiction. A Rtpart of tht SurRton General. 19RR. U.S. Department of Health and Human Services, Public Health Service. Centers for Disease Control. Center for Health Promotion and Ednation. Office on Smoking and Health. DHHS Publication No. (CDC) RR-R406, 19RRa. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. Health, Unittd States.1987. U.S. Department of Health and Human Services. Public Health Service. Centers for Disease Centrml. National Center for Health Statistics. DHHS Publication No. (PHS) RR-1232,19RRb. U.S. DEPARTMENT OF HEALTH. EDUCATION. AND WELFARE. Smoking and Health. A Report nJthr Surgrnn Gtneral. U.S. Department of Halth. Education, and Welfare, Public Health Service. Office of the Assistant Sec•retary for Heahh. Office on Smoking and Health. DHEW Publication No. (PHS) 79-5tNkk4.1979. U.S. OFFICE OF TECHNOLOGY ASSESSMENT. SnakinR-Rtlatcd Otaths and Financial Cn.ct.c. Health Prt+gram, Office of Technokgy Assessment. U.S. Cemgress, September 19R5. U.S. PRFSICENT. F.rnnnmie Report of the President. Transmittrd to the Congress January 1987. WWashington. D.C.,19R7. U.S. PURLIC HF,ALTH SERVICE. Smoking and Health. Report of the Advisory Committee to the Surgeon Grm•rol nfthe Puhlic Health Servicr. U.S. Department of Halth. Education. and Welfare. Public Health Service, Center for Disease Control. PHS Publication No. 1103. 1964. WALTER, S.D. The estimation and interpretation of attributable risk in health resean:h. Rinmr•trit•s 12:R29-R49, December 1976. WHYTE, H.M. The relative importanoe of the nujor risk factors in atherosclerotic and other diseases. Australian and Ntw Ztalandlournal nJMtdicint 6(5):3R77-3393. October 1976. WILCOX. H.B., SCHOENBERG. J.B., MASON. TJ., BILL, J.S., STEMHAGEN. A. Smok- ing and lung cancer: Risk as function of cigarctte tar content. Preventive Medicine 17:261- 272. 19RR. WILLETT. W.C.,GREEN. A.. STAMPf'BR,MJ..SPEIZER.F.E..COLDiTZ,G.A.. ROSNER. B., MONSON. R.R., STASON. n w~ ~c•H6s~ a'~ ~~fand lnurnai of of coronary heart disea.se among ~ Medicine 117(21):13(13-1309, November 19,19R7. WILLIAMSON, D.F., FORMAN, M.R., BRADSTOCK. M.K., GENTRY, E., RINKIN. N.J• Behavioral Risk Factor Survey results for cigarette smoking and other health-rick behavicxa amcxtgU.S..vomen,19g1-19R3. (Abstract.) In: EpidendclntrlliRtnctServict35thAnnual Conference. U.S. Department of Health and Human Services. Public Health Service. 1986. WYNDER, E.L., STELLMAN, S.D. Impact of long-tenn filter cigarette usage on lung and larynx cancer risk: Acase-controlstudy.lournalnfthtNatianalCancrrlnstituts62(3):4~ 1- 477• March 1979. i I L689 T8SZS ~ 16° 16R

TABLE 4,-FStimated relative rid(s fer current and former smokers of ciRarettec, males aped i5 years or more, 6-rear (t959-65) foltowup of American Cancer Society 25-State study (CPS-i) UnAr•rlying cause nf /kath Current Vmdcersa pcxmer smnkerso AIICausea LRO 1 •3R (1.75-LRS>w (1.3 3-1.421a ('110, a(te 235 (420f LR3 1.42 ( I .76-I .91) (1.34--1.49) CHO. a(le 15-M° (420) 2.25 I,S6 (2.1t-2.39) (1.45-1.6R) CFID, age N,S (420) 1.39 1.27 (L.7(11.48) (1.17-1.37) flypertensive HeaA Diceace (44f!_441) 1.63 1.19 (1.36-1.96) (0.94-1.51) Cerehravascular Lesions. age 235 (33(~3.34) 1.37 0.96 (1.25-1.49) (O.RS-1.0R) Cerehrcrvascular Lesinna. aRe 3S.~G4 ( i IQ.3'1{) 1.79 1.02 (1 _S.S-2.0R) (0.R3-1.23) Cerchrovaacular Lesions, age 263 (31p..33•) 1.13 0.93 (1.02-1.30) (0.R0-1.0R) Anrtic Aneurysm, Nnn-Syphilitie (451) 4.11 2.40 (3.13-5.40) (1.73-3 l4) llker, Duneknal. Gaatric, and Jejun.I (.S4(1-342) 3•o6 1.49 (2.24-4.111) (0.98-2.27) Influenza and Pneumnnia (4R0--/R1, 490-493) I.R2 1.62 (1.45-2.27) (1.24-2.12) Braechitia and ~mphysema (.t(N1-J02, 527.1) R.R 1 10.20 (6.40-.12.13) (7.34-14.17) Cancer. Lip. Oral Cavity, and Pharynx (140-141t) 6.33 2.73 (3.60-11.13) ( I ,76-3.40) Cancer. EsophaEus (130) 3.62 1.28 (2.02-6.4R) (0.53-3.0R) Cancer. Pancreac (157) 2.34 1.10 (I.al-3.02) (0.92-I.A4) Cancer. l.arynx (161) 10.00 R.60 (3.51-21t.S1) (2•97-25.74) Cancer. Lung (11+2-I61) 11.35 4.96 (9.10-14.131 (,1.R6-6.3R) (':mcer. Kidncy ( IRO) 1.94 1.79 (1.2.4-2.76) (1.11-2.n7) Cancer. Rt.•wkkr• (lther ( Irinaryt7r((alu (191) 2.90 1.75 (2.01-4.19) (1.07-2.R7) N( )Tf Ilased wwln LrH2.6i2 nan-yean of tt[pnwre s/rwmR nrk ..A(ete. wM ntve. swwdtd trytulwrly. or whn +nr4eA / nly . iya.enn. Iwe.nN nr pat. Relative rixh., ealmatd with n•yKt•1 In mtw wMl never .nw.ked reEularly, h.w• Men Alm Ily .~alwl..ntixd M Ihe aRe di.hiMMinn nf all mwr-ytua nf e./aay,e. Relrn tn. lr.n•ne• ala.l.m~ ablx. /w tnn.llmeM /(kadr. 1-359-Manh IOfII). vNmnlw. in ra.rmlrvs are us P"i-rWnwlf-w/nw'e i/wervak awnpnkM nw the weumrlian IhM the Inprithn af RI}IIK rnk Maa MKm~IIY II/a/I11wwnl. `All /hva.e I laM•a r.tn w. lnn•mawmal (lataifiralinn nf fkMeaw. Stwenth Revi.inn. ~N'hw >'n aRe ronM ia rwcn. It n•Lv. In Ihe aRe at rmnllmcM in 1959. N fl'R( •F - (~npdd../w./ t.d.daM.r.. Amnwan (:*w rr G.w•eW. TABLE 5.-Fstimated relative risks for current ciprette smokers and for all, subjects with a history of retiular ciRarette smokifrye, females aRed 35 years or more, 6-year (1959-65) followup of American Cancer Snciety 25-State study (CPS-1) ltnderlyinRcau.e of death Ir101IetsCuntnt~ t Current and f4rrner Snnlhert All causea CHO. age 233 (420f CHD, ase 3S-44a (420) CHO. age 263 (420) HypeAensive HeaA Disease (440-4t3) CereMovascular I.esinns, age 233 (;'1)-334) Cerebrovascular Lesions, age 3'.5-64 (330-334) Cerehrovascular l.aions, age 26S (330-334) Aortic Atteurysm, Non-Syphilitic (451) Ulcer. Duodenal, Gaattic, ald Jejunal (340-342) In()uenza and Pneumnnia (4R0-481, 490-493) Bronchitis ad Emphyxma (S()0-302. 527.1) Cancer. Lip, Oral Caity, ald Pharynx (140-•14A) Cancer.Esophagus(150) Cancer,Pancreas(137) Cancer. Larynx (161) Cancer,LunR(162-163) Cancer. Cervix Uleri (171) Cancer. Kidney (1A0) Caneer, Bladder. Other Urinary OrRaes (1R1) 1.19 1 •x' 1.R0~ 11.06-1.35) (1.13- T ( .~69-2.1R) (U R 1-1.16) 4.64 00•-7.20) 1.37 (0.81-2.31) 0.91 (0.59-1.41) (7~9 -1.76) 96 (1.14-339) (1 02-3.69) 1.39 l L(14-1.A6) 3.1(1 (0.76-1 a.S2) 2.69 (2.14-3.37) 1.10 (0.R3-1.47) 1.43 (0.N9-2.31) 2.R7 (1.74-4.74) 1.80 (I59-2.01)' 1.09 (0.95-1.26) 3.67 (2.46-3.44), 1.52 1 (0.96--2.41) 0.96 (0.69-1.33) 5.85 (4.02-9.53) (IR9 2.15 -4.23), 1.3R (.07-1.7R) 1 3.10 (0.65-14.99) 2.59. 1.32 (LO2-1.71) 1.47 ((i v7-2.23) 2.31 I 1. d.S-3.671 NOTE: Raaed tryKwt ? t2t,91t9 wanae-yera deapwwe wawtR..hjeed who ne.er.nw+kcd eeRnlarly, nr whn amnked nnhr ciRMytea. (we.ent nr pad. Relative riaka. NtimMed with nNpeet 1n w/wnew wfin never amnked rrrnl:nly. havc heen din ctly aalwlnnliied ro the aRe dWnhutiat d dl wanamyean ef ta(IOUtre. 'Refes to ciRarene anwlkinR .tatoa wt enmRnunt (Och+6er IuSa-Mateh IQ60). "Nunher>< in p«enthe.a.re 9t.(Itrcem eowfwknce intervala, e~wt~ed I+n Me aawtKMial thN the lerarithm of relative riak waa nlwmally lhatriMned. ~~~~~ R~~ ' All di.ra.e amka refer In IntemMilwul ChwsificatirN eWhew an are r.ripe i. given. N rekn la the aRe M emnRmeM in 1959. S()URC'li: 1 InpuMnhal UhaIlNNma. Americnn ('wn~rr GK irty. I,1M L889 TBSTS 1 149

I'oacnti:rl Ri:r%cs in Applying thc Results of Prc..pi•ctivc Stodicc to thc Gcncral I'opularion Suhjcct. enrolled in tlrc CPS-11 prospective stntlv ccxtstitutcd over 1.5 percent of all Amcrican adult. agc 45and over (Stcllman,l3ollrlta, Garfinkcl 19RR). Still, tlhcy dif- fcrrd from Ihc U.S. pi+rulatinn in a numhcrnf wavx (Garftnkcl 1985: Stcllman and (3ar- finkrl Irt!tf+). CPS-II cntrhnt% were ntnrc highl' y cducatcd. The hlacl, and Ili.panic pol+ulation% were ondrrrrpre.rntcd• thiwch Ic.x.o than in CPS-I (Garfinkel I91%S). i1s in (-PS I, in-.titntion:Jiird and scrirnt.h• ill /x•r.ons, as well as illitcratc people who radd not complrtc :r qnr.tir+nnairc. were cxclndrd ((.cw and C7arfinkcl 19R4). In tx.th CI'.C-I and CPS-II. Ihr nwrrall mnrtalitv r:ttc% of the cnmllccti 1a11 suh%tantially fx•Inw th<+sc of the gcncral l I.S- pnpnlation (I l:tmmond IWO: Lew and Garfinkel I9RR). These crm.idcratiom rlo not hy Ihrm.clvr% inralitlatr tirc usc of CPS-11 to c.timate smnkinF-attrihutahlc rias for the entire Amcric:m IM+pul:ninn. The critical a%sumrtiom in T:thlc I above is whether the cstim;urd relative ri.k% rk---nM the ab.olutc death rates Jk-arc rcprrscntative ol-thc gcncral population. For (-I lf) and for all-causc nicxtality. (TS-I cuhjcctc who were reportedly well at the time of enrollment showed higher e%timated relative ri.ks of cigarette smoking than those suhjects whco said they were sick or who gave a recent history of cancer, heart disease, or stroke (Il:tmmomd and Garf inkcl 1969; lLew and Garfinkel 19RR). A.imilar elevation of relative riak in well subjects has been found for lung cancer in CPS-i1(Gar- finkel and Stcllman 1r)R)tl. Since initially well pcrsons hid lower disease ratee, the proportional effect of cigarrtte smoking appeared to be larger. While CPS-I and CPS- 11 excluded seriously ill and institutionalized persons, the magnitude of the resulting bias is unclear. In the 1990 U.S. Census, about 1.5 percent of the U.S. adult popula- tion wae institutionaliied. Amcxtg persons aged 65 years and over, the proportion wac 5.3 percent (U.S. Rurcau of the Census 19R6). Cigarctte smoking has been found to act synergistically with certain workplace ex- pocures (such as asheskx and ionizing r.-diation) in the development of lung cancer (US D11HS 19R5: Saracci 1997; National Research Council 19R8). Such interactions may also he present in the etiology of rnmneoplactic lung disease. Alcohol and tobacco likewise interact synergi.tically in the etiology of oral and esophageal cancer ((1S DIIFW 197Q). Moreover, cigarette smoking has been found to interact synergi-tical- ly with elevated scnrm cholesterol and elevated hlncxl pressttrc in enhancing the ri.k ~if CI(D (US D111IS 19Ra). Persons of lowcr saciocronomic status (SES) may hc more likely to receive such workplace expe.suRs, to consume alcohol heavily, or to havc tm- favt+rahle CHD risk factors. However, if the cffccts of cigarctte smoking arc multi- plicative, then exclucion of such persons fnNn Cf C-1 and CI'5-11 would not hias the es- timatcd relative risk% of discacc due to cigarette smoking. Conver.cly. if the effects of ciF:m•tte smnk ing are purcly additive, rather than synergistic, then the rxclu.ion of per- sons with clcvatrd hawlinc disease ratcs wcmtld bia% opwanl the extimatcd relative risks of diccasc due to smokin,r,. The caimatcd relative risks in Table I are specific to wrnncn and have hcen stand- ardircd fnr agc. Stand:rnli~atinn fi+r r~thcr ar:rtil'yinl• nr nmframdinF varihhlcc was ncN performed. In principlr, failure to conmrol fpr •urh vari:rtdcs could hias rnpward or downward the estimated relative risks due to cigttette use. As discussed in Chapter 2, eumemus attempts to control statistically forconfoundmg and strattfying variables have not materially altcred the estimated relative risks for ciganette-relat tdhedt~ has been In the illustrative computation of Table 1, no distinction among drawn. For both sexes, the prevalence of current cigarette use is higher for blacks than for whites. Conversely, sntaller fractions of black men and women am fom'er cigarette smokers (US DHHS 19RRb)• Black persons were undetrepresented in CPS-11, con- dituting only 4 percent of entrants (Stellmatt and Garfinke11986)• Hence• the relative f black women. Among the 38,687 r risks reported in Table I may not be accuKte o t) occurred in black adult female lung cancer deaths in 1985, a total of 3,392 (8 bSI~P ~n ~~n only women. Hypothetically, if the attributable risks a among whites, then the smokin8-attnbutabk lung cancer deaths in Table I would half those of he reduced from 31,600 to 30,300• in the initial year or ~ In prospective cohort studies, mortality rates tend to be reduced two of followup. This phenomenon of lower initial tnortali ;~urt cu~the relative ~ to exclude persons who are sick at the outset of,~uP (%2~) of CPS-11 subjects. ri%ks in Table I were derived from the 4-year r followup of CPS-11(1982-88) will d 7_ Accordingly it is possible that the planne ~ for ~ first 4 years• reveal scxnewhat lower relative risks than ~~~al characteristics• typically Conversely, measutrments of expusure less accurate as the duration of foi- e i nbtained at the start of a prospecttve study. becotn k• have been clas- , reported in Table 1, for examp k,wup increa,ces. The relative risks s~ing practices upon enrollment in 1982. sified according to the subjects 8a~e uit smoking by 1986• if many wome~ rclative n ks for "scu~rren~ inokers aretactually those of a mixture of then the teport current and former smokers. followup of CPS-11 is to in compared with In the analysis reported below• the 4-Yar son needs to be interpreted in light of ' the 6-year followup of CPS-L Such a can1~ imtion followup in prospective studies. potential biases arising from short- and IonB Uncertainties in Exposure ~ uncertainty in Potential errors in estimated exposure >~ Pk am a fuRh~ source the computation of attributable risk a. 1n the illustrative ~klelst~`if,~Tf~le to-face exposure rates were derived from the 1985 NHiS' ~I~ge ilian population of the United )K,usehold interview survey of the t>oniTMt~~lO^a m or misreport- States. Among the possible ertors in NHIS estimates are: unde ~ ng ~rcsp~~ ing of current cigarette use: inaccurate tecall of past cigare hiases due to exclusion of some persons not available for interview: and undenePrcsen- tation of certain population segments- These s°u*~ of unceKainty are discussed in Chapter 5. On the whole. NH1S-derived estintams of population smoking rates have hcen consistent with other face-to-face interview surveys (CDC 19R7a). LL89 T8STS 129 t 1 V

1 the broader categories of cardiovascular and nonneoplastic respiratory disease are ap- plied to deaths from hypertensive heart diseace, arteriosclerosis, aortic aneurysm, and influenza and pncumonia, then smoking-attributable deaths would increase to 256,(Nl0 among men and 126.000 among women. Inclusion of deaths among newborns and in- fants due to smok ing during pregnancy would add an additiona12,500 to the total (CDC 19R7b; Mclntcxh 19R4; Kleinman et al. 19RR); this does not include fetal loss due to smoking (Stein et al. 19R0). Inclusion of lung cancer deaths among nonsmokers due to environmental tobacco smoke (NRC 1986) would add 3.900 and inclusion of deaths from cigarette-cauced fires (Hall 1997) would add 1,700 to total attributable deaths. In- clusion of deaths etue to cervical cancer caused by smoking would add 1.500. Includ- ing these additional causes of death, the smoking-attributable mortality in 1985 is then e-,timatcd to he appmximately 390,000. Recent studies have also noted increased risks among smokers for hepatic cancer (Trichopoulos et al. 19R7), penile cancer (Hcllherg et al. 19R7), leukemia (Kinlen and Rogot 19RR), and anal cancer (Daling et al. 1987). Among all persons at risk during 1995. an estimated 52 million were also cigarette smokers in 1965. The remaining 42 million were new cigarette smokers. In 1985, only about 4.400 deaths occurred among the latter group, which consists of persons in their teens, twenties, and thirties. Thus, 99 percent of deaths attributable to cigarette use in 1985 occurred among people who started smoking in 1965 or earlier. These people started smoking before the release of the 1964 Surgeon General's Report and before TABLE 13.-Fstimated risks ot various adivities Activity or cause Annual fatalities per I million exposed percons Active snmkin6 Akohnl 7.IMN)' 541 Accident 275 Disease 266 Motor vehicles 197 Akuhnl-involved 95 Non-akohol-involved 92 Work 113 SwimminR 22 Pacsive cmokine 19 All other air pollutants~ 6 Foaxball 6 Ekchocution 2 LiRhtninR 0.5 DFS in cattlefeed 0.] nee sting 0.2 HasketM.ill 0.02 All causcs A,74n Alleancers 1.917 NO'rF.: Activein ae eot mw.allr aeMdve: dme are averlap. hnween c.KEories. Diferenee.ln rnaGties do nnt kM'ly 1mMKMk we difterentta in yean er life kw. •NamMr er Ar.rM Irr minim .mder..hn heRan +nwAcfnR Aerae 1965. "c.ncer eeat%% mty. S(xtRf'F.: Active aw*1M C/K •11; N/ ltt. 1911S.1a11j: U.S, awew af 11rc ClnMN (1974. 10RIt). Other activittas ~/ taa.ea. l l S Preai,knt f 19117). 160 £689 t8STS the 1Q65 Federal Cigarette Labeling and Advertising Act. For this grvup- the annual smoking-attributable fatality rate is about 7 deaths per 1.000 a~f `~ ~~ dent N S deaths per I million persons• As shown in the Economic Report precident 1987), this rate far exceeds the rates for other risks of death (Table 13). Co811611.5 1. Lung cancer death rates increased two- to fourfold among older male srnokers over the two decades bet""een the American Cancer Society'cancerCdeath ates for tion Studies (CPS-1,1959-65, and CPS-11,19R2-86). Lun hic period. younger male smokers fell about 30 to 40 percent during female smokers aged 2. Lung cancer death rates increased four-W,th v-I, while among cancer death rates 45 years or older in CPS-11 compared among younger women declined 35110 55 percent. 3. two-decade interval witnessed (COPDn fema~leesmokers a d-55 yelr~s chronic obstructive pulmonary '~ or older. ~•~~ death rates for lung cancer and COPD 4. There was no change in the age 1 who ~v~ smoked mgularly. between CPS-1 and CPS-11 among men and women 5. Overall death rates from coronary lteart disease (CHD) declined substantially be- CPS-i and CPS-l1. The decline in CHD mortality among nonsmokers, tween ~ than among curt ent cigarette srnokers. ,~ however, was notably grea accular lesions were 3.7 and 6. 1n CPS-11, the relative risks of death from cere ~ dcks of stroke were also 4.8 for men and women smokers under age 6 smokers- Along with the recently observed among older smokers and former 1 cu a causal role for these findings strvn8 stroke reported results of other studies, cigarette smoking in thmmboemboltc and ~~ag c rcent of 7. In 1985, smoking accounted for 87 percent of lung cancer deaths, 82 pe COPD deaths, 21 percent of CHD deaths, and 18 percent of stroke deaths. Among men and women less than 65 years of age. smoking accounted for more than 40 percent of CHD deaths. among American women be- 8, '1 he large increase in smoking-attributabte rrarta ~of their adoption of lifelong tween 1965 and 1985 was a direct conseq ars onward. cigarette smoking, especially from their teenage ye people who 9. In 1985,99 percent of smoking-attributable deaths occurred among grouP, the started smoking before the 1964 Surgeon C~netal's Report. annual smoking-attrilwtable fatality rate is about 7.~ deaths per 1 million per- sonc at risk. 10. For 10 causes of death, a total of 337,000 deaths wel attributable men 1lopercen 19R5. These rrpreunted 22 percent of all deaths among among women. lf other cardimtascular, neoplactic. and respiratory causes of death were ietluded-ac well ~~ths among newbTM^s and infants resulting fron maternal smoking, deaths frotn cigarette-causedlrM~ g nonsnx'kers co smoke-the total cancer deaths amun due to environnx smoking-attributable mortality was about 390.0M in 19R5. 161

I I The percentages of those correctly identifying this statement as false were 59 percent of black men, 76 percent of white men. 42 percent of black women, and 60 percent df white women. Those who considered the statement to be true may believe low-tar and -nicotine cigarettes to be less ha7srdous. 1 %t C 0 ~ a n T N r P P Co 0 0 r -O P = = N I I Y, s ls 9 a ff ~ ~ S069 IBSTS Duration of Smoking Overall mortality ratios for smokers compared with nonsmokers increase with the duration of smoking. Overall mortality rates among smokers are slightly above, the rates of nonsmokers for the first 5 to 15 years of smoking but then increase more rapid- ly as the years of smoking increase (US DHEW 1979a). Mortality ratios for lung can- cer, coronary heart disease (CHD), and COPD increase with decreasing age of initia- tion (US DHHS 1992. 1983. 11984). An increased risk of morbidity (e.g.. as meacGred by days of hospitali7ation, bed disability, and work lost) among smokers may pccur much earlier than increases in mortality ratios. ; The 1964 AUTS asked respondents. "How many cigarettes a day for how many years might make a cigarette smoker mone likely to get lung cancer?" Most of those iwho considered smoking to be a cause of lung cancer believed that smoking would inOease the risk of lung cancer only after at least 10 years of smoking (regardless of the num- ber of cigarettes smoked per day) (Table 6). The 1986 AUTS asked respondents. "How long would a person have to smoke (num- ber) of cigarettes each day before it would affect their (sic) health?" The number of cigarettes used in this question was the number identified by the respondent (in the pre- vious question) as that which "a perton would have to smoke before it would affect their (sic) health" (see Table 5). A majority of rtspondentc in all smoking categories believed that smoking 10 or fewer years would affect a person's health. A higher per- centage of never smokers (36 perant) than current smokers (23 percent) believed that smoking less than I year would affect a person's health. Correspondingly, a slightly higher percentage of current smokers (10 percent) than never smokers (5 percent) believed that health effects would occur only after at least 15 years of smoking (Table 7). The wording in these two questions front the 1964 and 1986 AUTSs is substantially different, making any comparison difficult. In particular, the 1986 question may have favored responses indicating a shorter duration of smoking by referring to general ef- fects on health (which could be interpreted as nothing more than a cough) whereas the 1964 question asked about the risk of lung cancer. Does Cigarette Smoking Cause: Lung Cancer? Lung cancer, first correlated with smoking tnore than 50 years ago. is the single largest contributor to the total cancer death rate (US DHHS 19R2). Lung cancer olone accounted for an estimated 139,000 (28 percent) of the estimated 494,0(X) total cancer deaths in the United States in 19RR (ACS 19RRa). It is estimated that cigarette smoking 1ec

TABLE 9.--Continued Survey Smoking cigaretces cwxs heart disease (percentage who agree by smokmg status) Current Former Never All All Year Reference smokers smokers smokers nonsmokers adults (0. NHIS' 1987 73 82 77 77 'Preliminary fira-quanee dau (anpebWishedk Yeaesnd pncenuq for all adulu ia 76 penww NOTE: Actual Questians: I-'_ Do y ou think the chances of gettinf coronary heert disease are the same for peopk who don't smoke ciptettes as they art for people who do smoke cigarettes? MTo would be mom likely to Yet it. people who don't smoke ciga/et9ea or people who do smoke cilafetaeaT 3. Ci`areete smoken an more likely to die from heaR diseafe than people who don't smoke cigarettes. (suongly apee. mildly apee. no opinion. mildly disapee. mongly diaapai 4-7. Do you think that cigarette smoking is oe is not one of the causes of hean disease? i. Do you think cigatette amoking definitely increases. probeWe increases. pwbebly does not, or deflnitely does nod increase a penon's chances of genina hean disease'' o. Do you think a person who smokes is any mom likely to get hean disease thaa a person who doesn't smoke? (much mom likely, somewhat mom likely, no. don't know)- 10. People have differing beliefs about the relationship between smoking and Ixahd Do you believe ci6artte smoking is rclated to.. hean diseaw° Percentages include, those who"ttrongly apee" or "mildly agne.' Percemages include those who believe that smokinj -defudtely" or'ptoE.Ely increases the risk. Percentages include those who believe smokers an "much mots likely" or "wmewhat mom likely" to get heart disease. TABLE 10.-Trends in public knowledge about smoking and emphysema or chronic bronchitis Percentage who agree by smoking status Survey Year Refetence Current Forme smokers smoker r Never s smokers All nonsmokers All adults Smoking is a cause of emphysema/chronic bronchitis 1. AUTS 1964 l:S DHEW 1969 42 60 55 56 50 2. AUTS 1966 US DHEW 1969 46 60 52 54 51 Smoking is a cause of emphysert n 3. NH1S 1983 NCHS 1986~ 89 94 91 92 91 4. AUTS 1986 US DHHS. in pfea 83 92 90 91 89 S. Gallup 1987 AL11987 75 91 90 85 6. NHIS' 1987 79 87 84 84 Smoking ia a cause of chronic blonc hida 7. AUTS 1966 US DHEW 1969 50 56 65 56 59 8. NHIS 1983 NCHS I98e 82 89 88 88 86 :.~:.

. 1964 Report's estimate of 16 percent of deaths from all causes. Among women, CHD deaths made up 52 percent and lung cancer 10 percent of the smoking-attributable mor- tality from the 10 causes combined. Table t 1 siows the estimated attributable risks a from cigarette smoking for the year 1995. For comparability with the 1965 calculations, the same 10 causes of death are considered. The computations are based upon the relative risks reported in CPS-11 and the prevalence rates reported in the 1985 NHIS. For tnen, the computations employed the relative risks for past and present smokers of cigarettes exclusively, as shown in Table 6. As Figure 2 indicates, the proportion of male smokers who used other forms TARLE 11. Fstimated attributable risks for 10 selected causes of death from cigarette smoking, males and femakc. United titates, 111115 CauW of death Maka Fernales CItD.aRe <65 45 41 (4n-Sn)• (34•-4E) CHD. aRe 2t,5 21 12 (17-26) (V-/S) COPD (t4 79 (7R4ta) (7}-g3) Cancer of lip. oral cavity, and pA.ryex 92 61 (79-97) (45-76) Canceroflarynx at E7 (57-93) (56-97) CancerofesophaRus 7a 75 (62-t(9) (57-a7) Cancer of IunR 90 79 (a><-92) (7S-a2) Cancer of p.rlcr~ett 29 ;L1 ( IS-41) (25-44) Cancer of Mackkr 47 77 (31-451) ((a-(St) Cancer of kidney 49 12 (i2-64) (.l-41) Cerehmva.cular Aikase, aRt <R5 tt (if.4SS) 55 (4S-fr5) Cerchawa%cu(ar diceace. alee NrS 24 6 (1 f. 13) (2-14) Nf nT: C.rrryrwrA rmm Tahk. 2. 6. and 7. fw aArh wwa wrkr Ri, lAe papnnians er e.nenl.eA knmer cipmeMe arw 4m in la1ti wrrr. ,rapn fi.rly. U.7 rd 21.4 Im itc„1. f•.K mre 61 or fikr. lIr pevalencer of currenl and fmeer eiR.ReM anw,kinR.,rRW rc.rwlivrlr. 19.4 anA t 1.1 percrnt. t'vw aduh wanee wwkr 65. tAe eewmyawidinR ,mrqra ..ert 10. 1 atil 16 tr4wcK Gw Mkdl w,wrKa ai ,y okkr. 12.6 mwl IV,6 pref NumMa in ryrrnllKVr..wc V{.,q ce I eonfMkmr inlervda. 156 1689 18StS of tobacco was too small to affect significantly the results for 1985. For women, rela- tive risks for current and former cigarette smokers were employed (Table 7). Comparison of Tables 9 and I 1 reveals significant incr+ea.ses in attributable risk from 1965-85. In 1985, smoking accounted for 21 percent of CHD deaths in older men, compared with 11 percent in 1965. The attributable risks for cancers of the lip, oral cavity and pharynx. ecophagus, and lung increased significantly. Changes in the attributable risk estimates for women are even more striking. Among younger women, smoking now accounts for an estimated 41 percent of CHD deatht and an estimated 55 percent of lethal strokes, compared with 26 and 28 percent, rcspeC- tively, in 1965. Among women of all ages, 79 percent of lung cancers are attributable to cigarette use (see Table 1). Overall, smoking accounted for 86.7 percent of all lung cancer deaths (95-percent confidence interval 84.9 to 88.4), 81.8 percent of all COPD deaths (95-percent c- fidence interval 78.3 to 85.i), and 21.5 percent of a)1 CHD deaths (95-percent c;-I fidence interval 19.4 to 23.4). In addition, smoking accounted for 18.0 percent of~all s stroke deaths (95-percent confidence interval 14.2 to 22.9). ~ Table 12 reports estimated smoking-attributable deaths for the 10 causes duridg 1985. Total deaths have increased to 231,000 for men and 106,000 for women. As ot)- posed to 1965, CH D in men now accounts for only one-third of the smoking-attributtible mortality from the 10 causes combined. The proportion of these attributable deaths d}te to lung cancer has increased to one-third. Likewise, among women, smoking-at- ~ tributabk CHD fatalities now account for one-third of the 10-cause total; the relative importance of smoking-induced cancer fatalities has also increased. The total 10-cause smoking-attributable mortality for 1985 was 337,000deaths, com- pared with 183.000 in 1965. A portion of the observed 196545 increase, however, was the result of population growth. In addition, there were increases in the proportion of elderly persons who would be more at risk for smoking-induced death. For men and w(xnen, respectively, Figures 10 and 11 show the results of acortection for population increase and population aging. In each figure, three quantities are shown for each of four categories of smoking-attributabk mortality: CHD deaths under age 65; CHD deaths aged 65 years or mone' COPD deaths: and lung cancer deaths. The first quan- tity is the estimated smoking-attributable deaths for 1965. The second bar shows smok- ing-attributable deaths for 1985. The third bar chows the estimated 1985 smoking-at- tributable deaths it the U.S. populations at each age had remained at 1965 levels. The latter quantities were computed as aD where a is the attributable risk given in Table I I and D is a population-corrected estimate of 1985 U.S. deaths. The latter quantity was computed by multiplying 1985 age-specific death rates by the populations at risk in 1965. Figures 10 and 1 I show that population growth and aging cannot explain the chan- ges in smoking-attributabk mortality between 1965 and 1985. In particu)ar, the marked increases in smoking-attributable deaths from lung cancer and COPD in women are systematic consequences of the American woman's adoption of lifelong cigarette smoking. from teenage years onward. ; For men, (x>{w)ation-corrected deaths due to smoking in 1995 wwere 165,(1()0. com- pared with 150.(1(10 in 1965. FFor women, population-corrected deaths due to %moking 157

00 e ~ 0 E ~ ~ 0 N V V S ~. i ok I A r ~ "oO E " ~ a i I 0 0. a o. a o a oe oe oe oe •! b069 TBSTS percent considered only heavy smoking to be hazardous. Corresponding increases,oc- cuned in those responding "any amount." , The 1986 AUTS posed a similar question but did not offer "not harmdous" as a pos- siMe m-pcmse (Table 4). It showed that most respondent.s, given the two choices of "any amount" or "only heavy smoking," chose the former (85, 81, and 72 percent of never, former, and curmnt smokers, respectively). When asked, "How many cigan:ttes a day do you think a person would have to smoke before it would affect their (sic) healah?", 49 percent of current smokers and 40 perCent of never smokers cited 10 or moi+e (Table 5), thus failing to recognize light smoking as a health risk. Twenty percent of current smokers cited 25 or more cigarettes as the min- imum number necessary for adverse health effects (Table 5), which is identical to the proportion of current smokers who indicated, in response to the prior question, that only heavy smoking is hazardous to health (Table 4). 1 1 Tar Yield Studies have shown that smoking filtered lower tar ciganates reduces the risk of /1ong cancer compared with smoking unfiltered higher tar cigarettes. However, there iis no conclusive evidence that the lower yield cigarettes are associated with reduced risk of overall mortality, cancers other than lung. COPD, or heart disease. Moreover, com4 pen.satory smoking behavior in response tolowernicotine intake might actually increase the intake of tobacco smoke toxins In some individuals (US DHHS 1981). Very few surveys have as.sessed the perceived harmfulness of low-tar ciganettes ver- sus high-tar cigarettes or never smoking. In the 1980 Roper Survey (FTC 1981), respondents were presented with the following false statement: "It has been proven that smoking low-tar, how-nicotine cigarettes does not significantly increase a person's Msk of disease twet that of a nonstnoker." Nine percent of smokers said they "kpow it's true," 27 percent said they "think it's true," and 32 percent said they did not know if it was true or not. The complicated wording of this question and use of the word "proven" make interpretation of these results difficult. Different results may have been obtained using a question such as, "Do you believe that smoking low-tar cigarettes is or is not harmful to health?" The 19R0 Roper survey also asked respondents their beliefs about the following state- ment: "Even if a woman smokes low tar, low nicotine cigarettes during pregnancy. she still significantly incrcme.s her risk of losing the baby before or during birth." Forty- three percent of all respondents and 37 percent of smokers said they "know it's true" or "think it's true" (unpublished data. FfC). The 1987 NHIS asked respondents if they believed that "People who smoke low tar cigarettes are Iess likely to get cancer than people who smoke high tar and nicotine cigarettes." A total of 30 pereeM agreed with the statement whereas 50 percent dis- agreed (year-end data). Folsom and associates (1988) surveyed 1,252 blacks (aged 35 to 74 years) and.1;870 whites in the metrcpolitan Minneapolis/St. Paul area during 1985-86. Respondents were presented with the following statement: "If'tar' and nicotine were removed from cigarettes, there would be no other chemicals in tobacco smoke that cause disease." 191 I

causes approximately 90percent of lung cancer deaths in men and 80 percent in women (see Chapter 3). Surveys have addressed public knowledge about the relationship between smoking and lung cancer since 1954. In 1954, fewer than half of adults (41 percent) thought that srnoking is one of the causes of lung cancer (Table 8). Since that time, public knowledge of the association between smoking and lung cancer has increased steadi- ly. By 1964. a majority of adults (66 percent) believed that smoking causes lung can- cer, surveys in 19R5, 19R6. and 1997 showed that this proportion had increased to he- tween 87 and 95 percent. Heart Disease? The 1964 Report of the Surgeon General's Advisory Committee identified an associa- tion between smoking and CHD, although it did not consider the available data to be sufficient to estahtish a causal relationship (US PHS 1964). Since that time, evidence from numerous investigations has. established cigarette smoking ac the most important modifiable risk factor for CHD in the United States (US DHHS 1983). Cigarette smok- ing increases the risk of death from CHD approximately threefold in persons less than 65 years old and is responsible for 40 to 45 percent of CHD deaths in this age group (Chapter 3). Public beliefs that smoking is associated with the risk of CHD have steadily increased since 1964, when fewer than hatfof adults (40 percent) thought that smokers were more likely than nonsmokers to develop heart disease (Table 9). Surveys in 19R5, 1986, and 1987 showed that 77 to 90 percent of adults believed that smnking increases the risk of developing heart disease. Each of these rccent surveys showed that current smokers were less likely to have this belief than former and ttever smokers. In 1986, current smokers were less likely to acknowledge a relationship between smoking and heart disease (71 percent) than were former smokers (84 percent) and never smokers (80 percent). Chronic Obstructive Pulmonary Disease? The 1964 Report of the Surgeon General's Advisory Committee identified cigarette smoking a.c the most important cause of chronic bronchitis (US PHS 1964). Tcday, cigarette smoking has been identified as the majoreause of chronic bronchitis and em- phy.cema in the United States. Eighty to eighty-five percent of deaths from COPD are attributed to cigarette smoking (Chapter 3; also see US DHHS 19R4). Since 1964, the public belief that smoking is associated with an increased risk of COPD has increased. In 1964, half of adults (50 percent) thought that smokers were more likely to get chronic bronchitis and emphysema (Table 10). By 1986, most adults thought that cigarette smokers were more likely than nonsmokers to develop chronic bronchitis (R 1 percent) and emphysema (89 percent). The preliminary first-quarter 19R7 NHIS estimates were similar. ln three surveys that asked identical questions regarding emphysema and chronic bronchitis (NlllSs 1985 and 1997. AUTS 19R6), there were consistent slightly higher prMxxtions who believed that smoking is associated with emphysema compared with chronic bronchitis. ln 19116. smokers were less likely to acknowledge an ac.cociation between smoking and chronic hrc.richitic (73 percent) than were kimner smokers (84 percent) and never ~ R 4 S 2 9 9 9 = 10b ^ o P ~ O. f~ F~ T T P P P 3 ' ~ {SQY lTQJ• J y > ? 0. ' v V v 7 7 O C~7 f~7 U V x a ~ ~ ~ ~ ~ ~ a a o~ u 5< v ~ u o u ° i 1R9

deaths from cigarette-related fires (Consumer Product Safety Commission 1997; Bot- kin 19RR) are not discussed, nor are the morbidity consequences of cigarette smoking (()S DHF.W 1Q79; Rice et al. 1996). A Twenty-Year Perspcetive: 1965-SS The two-decadc intcrval, 1965-1995, was selected primarily for reasons of data availability. The year 1995 was the most recent one for which complete, nationwide, cause-specific mortality statistics were available from the National Center for Health Statictics (NCI IS). Moreover, in both 1965 and 1995, questions on cigarette use were appenclcd to the National llcalth Interview Survey (NHIS), a nationally representative, face-ko-face interview survey that has been conducted annually by NCHS (Massey et a1., 1987; NCIIS 19R6). In particular, 19R5 was the most recent full year for which complete population-weighted data from the N141S were available (see Chapter 5). In addition, the years 1965 and 1995 represented the approximate midpoints of two large-scale prospective surveys of smoking and mortality among men and women in the United States, both sponsored by the American Cancer Society. In the first of these two prospective studies (Garfinkel 198(la,b, 19R1: Hammond 1961, 1964a,b, 1966, 196R,1969,1972; Hammond and Garfinkel 1961,1964,1966,196R,1969, 1975; Ham- mondet al. 1976; Hammond and Seidman 19R(1; Lew and Garfinkel 19R4, 19RR), about I million persons were followed from 1959 through 1972. In the second study (Gar- finkel 19R5: Stellman and Garfinkel 1996; Stellman, Boffetta, Garfinkel 19R8), about 1.2 million participants were followed from 19R2 through 199R. The two studies will he referred to, respectively. as "Cancer Prevention Study 1(CPS-1)" and "Cancer Prevention Study 11 (CPS-11)." In particular, this Chapter will present unpublished, preliminary results from the 4-year followup (19R2-96) of CpS-II. The theory, mathematics, limitations, and other methodological issues concerning the calculations af smoking-attributable mortality are described in the next section. The results of the analysis follow thereafter. Readcrs interested primarily in those results may proceed directly to the section entitled "Populations at Risk: 1965 and 19R5•" The Concept of AttriMttabk Rkk In 1953, Levin estimated that 62 to 92 percent of all male lung cancers were "at- tributable to cigarette smoking" (Levin 1953), Levin's computatinns addressed the general problem: Now many cases of a disease in a given.populaticm can he explained by the presence of a particular hazardous agent or a particular personal trait? Put dif- fcrently, how many cases would have been avoided but for the presence of the agent or the trait? (Doll and Pcto 199 1). In principle, the answer requires an experiment whereby di%ease rates are measured before and after the complete elimination of the has.ardous agent or particular trait from the population of interest. Since this type of cxpcriment is usually impractical, the most widely used apprnach is to estimate dicease rates in rcpxesentative sampie populations of exposed and unctft,.ed pcrsoms. The results are then extrapolated to the population of interest. The phrase "cases attributable to agent A" is often used interchangeably with "cases caused by agent A." The latter term is meaningful so long as it is recognized that "caused" refers to an entire population rather than to any single, predetermined mern- her of the population. Thus, the scientific validity of an estimate that 1,(1(1(1 lives would be saved by the removal of some hazardous agent does not hinge upon naming the names of the people to be saved. The population-based notion of causation is especially important for chronic diseases with multiple causes. Agent A. for exampk, may promote or enhance the disease caus- ing effect of agent B. A case-by-case analysis of afflicted individuals may never iden- tify agent A as the primary cause in a single instance. Yet its elimination might sub- stantially reduce disease incidence in the population under study. Moreover, the concept of attributable risk generally requires a timeframe. In an as- sessment of the effects of removing a hazardous agent, a researcher could ask how many cases of a specific disease could be avoided in a specified time period. such as { year. When the disease has multiple causes. this quantity may differ from the number Qf cates of the discase that may eventually be avoided. By specifying a timeframe,;the re- searcher inquires not whether such cases could be completely prevented, but whether their premature occurrence could be avoided. For many diseases, death rates ate ntore accessible and reliable than disea$e rates. Accordingly, computations of "attributable deaths" from a disease have been used in place of "attributable cases" of the disease. Because death from one cause or itnotlher is inevitable, such computations necessarily refer to a specific time period during which premature mortality may have been prevented. Mathematics of Attribatabk Risk Let dt and da resfiectively denote the incidence rates (in terms of new cases per unit time) of a particular disease among two sample cohorts-one exposed to a hatardous agent, the other unexposed. The two samples are assumed not to differ materially in any other respect, so that both would experience disease incidence do in the absence of exposure. Accordingly, the difference dt-do measures the increase in disease in- cidence, or absolute risk, due to the agent. Moreover. the unitless ratio r= d tldo, termed the relative risk, measures the degree to which the hazardous exposure multiplies the baseline incidence rate. It is often employed as a measure of the epidemiologic and biological significance of an observed association between an agent and a particular disease (Lilienfeld and Lilienfeld 1980: US DHEW 1979). In the exposed cohort, the proportion of disease case% attributable to the hazardous agent is thus equal to s=(dt-A)/dt (which equals (r-I )tr. This quantity has been variously termed the assigned share or probability of causation or attributable propor- tion of risk armx+g the exposed (Bond 1981; Oftedal. Magnus. Hvinden 1969; Black and Lilienfeld 1984; National Research Council 1994: Cox 1987). For some hazardous agents. such as cigarette smoke, the disease incidence rates di and dt- and the relative risk rhave been estimated dirrctly from prospective longitudinal studies of exposed and unexposed cohons• Alternatively, retrospective case-contrrl studies do not provide estimates of dt and dn but yield a close approximation to the. rela- VL89 iBStS 123 122

60 0 ¢ 20 T 0 J 10 J .r F MFlLES 1985 1885 ® Current smokers, less than 25 per day ® Current smokers, 25 or nqre per day ® Former smokers. 5 years or less ® Former smokers. more than 5 years FEMALES IIIIIIIIIIIIIIIIIi 1985 ® 1985 FI(: URE 1.-Populatiens nf current and former ciRarette smnkers, adult men and women, United States,1965 and 1985 Chl tRCrF.timatnl Imro unruM~ala.l taMn4yiana, NIIISa 1961 rd I9Rk andeetimNCS of the rtaithM rt"lati"wnn( nK I tmted Stme. hv ,rr and.ca, twi'; am/ I4net (I1S parr•ar nf rtw Cen.w /974. 1'M6). Figure 2 chowc a marked change over two decades in the forms of tobacco used by men. In 1065.5.2 million men (9 percent) had a history of ever smoking pipes or cigars, hot not cigarettes. In 1995. the number using n(xlcigarctte tobacco dropped to 2.7 mit- lilm or 3 rcrcent of the men. In 1965, 29 million men had a history of ever smoking cigarette, arni other forms of tohacco, about two-thirds of all cigarette smokerc. Ry 1995. tthe numhcr had dropped to 5.6 million, only I in 10 of all cigarette smokers. Older ( bhorts of ('iRarefte Smokers Figurcc z and 4 fncuc on pere,mc aged 60 years and rner, who suffer the highest in- cilIC/1Ce ratCC rif .moking-rrl:ltcd di.cascc. For IIN,S and II1RS, rc.pectively, these /:rouh% of older rcrcon% were hl>'rn hcGxc 19Ofi and before 1926. Among older men, as %hl.wn in Fi1Y1rC 3. the (wo-(IC( :hdc interval witnessed a 1 i!,-percent incrrase in the num- IK•r 1l1 Itamwr cir:lrenc .m„I,er., /1m1mp older wrNnen, the number of current smokers (!0 eo 50 ~ 40 30 J J .... 20 1: 10 0 MFILES I ........` 1 t395 1985 ® Never smoked regularly ® Noncigarette tobacco only ® Cigarettes onty ® Cigarettes and other tobacco 1 t365 1985 t FIGURE 2.-Populatinns of adult men and women clamified by history of tobpc- co u.se, United States,1965 and 1985 VN tRCF.: FminnKef rrnT unruMidKd ulwlalw.n. NNISx 1965 atwl 1911S: anhMi.lkd IdatMrtNw. CPS 19Rt; and r.- timanr. nr ~Ae re.nknt Irhwlalinni o( the Unired Slau+lry a(!e ud.r>t. 19f:S rd I9Rt (US Breew ot the Cetnva 1914. 19MS). dnuhled, while the number of former smokers increased sixfold. Between 1965 and 1985. the population of older women with a history of regular cigarette use. pact or present,incrcased ovcrthreefold. The NHISs for 1965 and 19R5 did not ask about the age of initiation of cigarette use. Ilowever, this information is available from other sources. For 1985, tahuL•lticms of the age of onset of regular cigarette use were ma/k from the Current Population Survey. Ah(xtt 69 percent of older men with a history of cigarette usc. past or present, began to cmoke before age 20 (Figure 4). Among older w(xnen, the proportion was 39 percent. For 1965, thrce "arcca of information provide the age of smoking initiation amcmg cohcxts horn before 19(K,: the NHISs of 197R-lt() (Harris 19Ri), the Current 1 col+ula- tinn Survey of 1955 (ilmncrcl el al. 1956), and the initial 1959 questionnaire to CPS- I(Ilammnnd 1966. Appendix tahles). For okkr men with a history of cigarette use, about 60 percent started .moking before age 20 (range. 56 to 62 percent). For older w(mlcn smakcr., about 12 pcrecnt started in ttx ir teenagc years (range. 9 tM I S percent). t.t I I11s

tween cigarette use and risk of stroke. They also noted a slight increase in risk among former cigarette smokers, especially for the first 2 years after cessation. The prelimi- nary results from CPS-11, reported in Tables 6 and 7, further support a causal role for cigarette smoking in stroke. The preliminary results of CPS-11 al.so show significantly higher relative risks for cancers of thc I ip, oral cavity and pharynx, esophagus, and lung, as compared with CPS- 1. The computed relative risk for lung cancer death has increased to 22 in men and 12 in women. While the relative risks for COPD death have not changed significantly among men, there is a trend toward increasing risk among women. The available data from CPS-11 do not permit identification of specific mortality risks for hypertensive heart disease, aortic aneurysm, and influen~.a and pneum(mia, as in CPS-1. liowever, among broader categories of cardiovascular and nonneoplastic respiratory dicease, in- creased risks are likewise found in CPS-11. Endocrine and Sex-Related Cancers in Women A protective effect of smoking on cancer of the endometrium has been suggested in a recent case-control study (Lesko et al. 1985). For CPS-I, the relative risk for cancers of the uterine corpus (ICD-7 Codes 172-174) among current smokers was 0.94 (95-per- cent confidence interval, 0.57 to 1.53). Preliminary results forCPS-II suggest a reduced relative risk for endometrial cancer (ICD-9 Code 182). Recent data on a possible protective effect of smoking for breast cancer have been contradictory (See Chapter 2; Rosenberg et al. 1984). For CPS-I, the relative risk for breast cancer (ICD-7 Code 170) among current smokers was 0.88 (95-percent con- fidcnce interval, 0.77 to 1.01), while the relative risk among former smokers was 1.20 (q5-percent confidence interval, 1.15 to 1.35). Preliminary data from CPS-11 have likewise been contradictory. An increased risk of cervical cancer among cigarntte smokers has been reported in case-control studies (t,aVecchia et al. 1986; Nischan, Ebeling. Schindler 1988). For CPS-1, the relative risk for celvical cancer (ICD-7 Code 171) was 1.10 (95-percent con- fidence interval, 0.83 to 1.47). Data from CPS-1I show a twofold increase in cervical cancer mortality among current smokers (relative risk 2.14, 95-percent confidence in- terval 1.06 to 430). Summary The relative risks for current smokers for selected comparable disease categories causally related to smoking in CPS-I and CPS-11 are summari>'ed and listed side by side in Table 8. These comparisions show substantial increases in the risk of death due to smoking for most of the disease categories listed between the years 1959 and 1965 and 1992 and 1996. Statistically significant increases in relative risks occurred in those dis- case categories for which 95-percent confidence limits around the estimated relative risks do not overlap between CPS-I and CPS-II. Compared with men during this period. women experienced greater increases in the relative risks of cerebrovascular Iesions (aRes 35 to 64 yearc). COPD. laryngeal camcer, and lung cancer. TABLE 8.-Summary of estimated relative risks for current ciRarette smokers, ~ major disease cateRories causally related to cigarettes, maks and females aged 35 years and older, CPS-ll (1959-65) and CPS-11 (1982,-86) Mala Females Underlying cause nf dealh' CPS-1 CPS-11 CPS-1 CPS-II CttD. age 2.15 1.t{3 1.94 1.40 1.70 , ('HD. aEe 15-154 2.25 2.E1b 1.91 3.nn" Ceretxnvaacular W. ions. atte 215 1.37 2.24° 1.19 10 Certtxovtaulv Lesions. 1.79 3.67` 1.92 40 ~ aRe 33-64 I COPD 9.91 9.65 s.tl9 10.47 ~ Corcer. Lip. Oral Ca.iAy. and Pfiarynx 6.33 27.4% 1.96 5.59 i Cancer. Ewphasu 3.62 7.60 1.94 10.25" Cancer PancMa+ 2.34 2.14 1.39 2.23 Cancer. Laryna 10.00 10.43 3.e1 17.79 Cancer. Lung 11.33 22.3e 2.69 11.94" 'See Tahk.4-7 ta ImanNiaml CluslantIea eIt>Ifere e°dh. bOS.percem coeriAence imen.b do na o.eMp te~weee CYS-1 rd CrS-n. SOURCE: Tabks 4-7. Smokins-Attributable Mortality in the United States,196S and 1985 Table 9 reports the att>;butabk risks a from cigarette smoking during the year 1965. Ten causes of death are considered: CHD, CUPD, cerebrovascular dlsea.se• and can- cers of seven sites. The computations are based upon the age-adjusted relative risks reported in CPS-1 and the prevalence rates reported in the 1965 NHIS. For men, the age-adjusted relative risks among present and past cigarette smokers with a history of pipe or cigar use were slightly lower then t comparison and inwTabk4 the f ciga- rettes rettes exclusively. Whik the latter tue reported for ,~ were used in the attributable risk computations. In 1965, a.s shown in Figure 2, about two-thirds of men with a history of regular cigarette smoking were also exposed to pipe or cigar smoke. (As noted in Note b of Table 9 below, the use of relative risks derived from the death rates of men who smoked cigarettes exclusively resulted in about a 5- percent increase in attributable deaths for 1965.) For women, the computation of at- tributable risks in 1965 did not distinguish between current and fotmer smokers. 6889 t85tS 1 It3 ts2

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Na- tional Cancer Institute. 1966. pp. 205-26R. DOLL. R.. PETO. R. Mortality in relation to smoking: 20 years' observations on male British doctors. British Medicallnnrnal2:1525-15i6, December 25, 1976. DOLL, R.. PETO. R. Cigarette smoking and bronchial carcinoma: Dose and time rclatiorjships among regular and lifelong non-smokers. Journal of EpideminloRy and Cnmmunirol/talth 32(4): .102-31 i, c)ecemher 1978. ( DOLL. R.. PETO. R. The causes of cancer Quantitative estimates of avoidable risks pf can- cer in the United States today. Journal of the National Cancer Instinoe 66(6):1191-I 3(>Ft, June 198 1. DORN,H.F. Tobaccoconsumptionamdmortalityfromeancerandotherdiseases. PuhlisHealth Reports 74:581-593, 1959. GALAN. K.M., DF.LIGONUL, U., KERN. M.J.,CHAITMAN, B.R., VANDnRMAELs M~G. Increased frcquency of rcstenosis in patientscontinuingtosmokecigarettes after percutAnedus transluminal coronary angioplasty. American Journal of Cardiology 61:260-26Z, 19RR. GARFINKEL, L. Cancer mortality i0 nonsmokers: Prospective study by the American Cancer Society. Journal njthe National Cancer Institute 65( 5): I 169- I 173, November 19g0a. GARFINKEL,1.. Cardiovascular mortdiry and cigarette smoking. In: Ramstrnm, L.M. (ed.) Tht Smnking Epidemic. A Matter of Worldivide Concern. PrortrdinRs ojThr Fourth World Canjirtnce on Smoking and Health. Stockholm: Almqvist and W iksel I Intemationa1,19R()b, pp. 41-44. GARFINKEL, L. Titne tnends In hmg eancer mortality.mong nonsmokers and a note cxt pas- sive smoking. Journal njtheNatianal Cancer lnstitaMt66(6):1(K+1-I(k56. June 198 1. GARFINKEL,1.. Selection, follow-up and analysis in the American Cancer Society Prnspec- tive studies. In: Garfinkel. L. Ochs. 0.. Mushin•ski, M. (eds.) Selertinn. h'.dlnw•-up, and Analvci.c in ProsnretivtStadies: A Workshnp. NCI Monograph 67. National Cancer Institute. NIH Publication No. R5-2713,1985. pp. 49-52. GARFINKEL. L.. STELLMAN. S.D. Smoking and lung cancer in women. Conccr Rr.cearch, December 19RR. GOLDBAUM. G.M., KENDRICK,I.S., HOGELIN, G.C.. GENTRY. E.M., BEHAVIORAL RISK FACTORS SURVEYS GROUP. The relative impact of smoking and oral contracep- tive use on women in the United States. Journal of Ameriran Mediral Association 25R( I U):1339-I i42, September 11,19g7. HAENS7.EL, W., SHIMKIN, M.B., MILLER. H.P., MILMORE, B.K., CONOVF.R. A.G. Tnhacc•n Smnking Patterns in the United Statts, Public Health Monograph 45. U.S. Public Health Service. 1956. HALL,I.R.1R. ExPected ehanges in fire (lamages from rcducing cigarette ignition prc#xnsity. In: Rryxrrr No. 3, Technical Studv Group. Ciganttt Sa/rtv Art of 19R4. Quincy. Mas- sachusetts: National Fire Protection Association. Fire Analysis Division. 19R7. I L, I 1(,:

like a drug addiction." Of current smokers. 79.6 answered "yes" to the question, "Do you think you are addicted to cigarettes?" (Canadian Gallup 1996) IInteraction Between SntnkinR and Other Exposures The 1985 Surgeons General's Report (US DHHS 1985) reviewed evidence regard- ing the interaction between smoking and a variety of occupational exposures in caus- ing disease. With respect to the interaction between smoking and aslxstos, the Relxxt conc luded that these two exposurcs act synergistically tc increase the risk of lung can- cer. The risk of lung cancer in cigarette-smoking asbestos workers is more than fif- tyfold the risk in noncmokers who have not been exposed to asbestos. Few data are avaitahk on public knowledge of these interactions. The 1980 Roper survey (unpublished data, FTC) asked respondents about their belief concerning the following statement: "If you smoke and have worked with asbestos you are at least 50 times more likely to get lung cancer than if you have done neither." Seventy-four per- cent of respondents (and 69 percent of smokers) said that they "know it's true" or "think it's true." Smokeless Tobacco Smokeless tobacco (ST) use leads to increased risk of oral cancer and nicotine ad- diction (US DHHS 1986c). No data are available to assess trends in public knowledge of the health risks of ST use. In the 1986 AUTS, 78 percent of adults thought that the use of chewing tobacco is harmful in any way to a person's health. Similarly, 73 percent thought that the use of snuff is harmful to a person's health. Current smokers were less likely to know about the health effects of using chewing tobacco and snuff (71 and 66 petcent, respective- ly) compared with former smokers (79 and 75 percent, respectively) and never smokers (81 and 76 percent. respectively). According to the 1987 NHIS (preliminary first-qwuter estimates), 82 percent of adults thought that a relationship exists between chewing tobacco use and mouth and throat cancer. Seventy-seven percent thought that snuff use is related to these cancers (unpublished data, National Cancer Institute). Peramal Health Risks for Smokers There have been few attempts to determine smokers' beliefs regarding their own per- sonal risk. Several Gallup surveys conducted between 1977 and 1987 asked tespon- dents, "Do you think cigarette smoking is or is not harmful to your health?" (Table 14). Data are available for current smokers for the years 1981 and 1985. The prnpcxtion of current smokers answering in the affirmative increased from RO percent in 1981 to 90 percent in 19R5. These data, at first glance, suggest that a high percentage of smokers a O ~ N ~ ~ I -0 IR ~ R r I z ab p V V V 7~ ..: eJ r+ + ~; `c " fiiT69 t8SiS I mi ~

a a ~ z I; ~ C : S 3 e a ~ a ~ ~ " ~ ~ ~ 0 C I . a ~ 'a a E a ~ u o ~ g m ~ %E 3;. 2 Y a g~ c I -1 a o. .5 " z „ y a a ~z s g ~A g E$ ~d ~~g~ ~tt ~~aa ~ ~ ~a $~~~," g ~~ ,€~'' 5ts5s ~ -6 g~ i ~I~ ~ Y 7{ _~1 g y O;Y~y 3y t~Jiy~~~ T3d'~g~ `~~~...'a~$s"' ~~.1;5LIi ~j ..~~~ MMy w,. C~~i.~Y~~'•'p~ 'Y~wC; E~ ~ga., i i._E.~€-4i V1W nW 0 smokers (83 percent). Similarly, smokers were less likely to acknowledge an assecia-' ~ tion between smoking and emphysema (85 percent) than were former smokers (92 per- cent) and never smokers (90 percent). Similar patterns were seen in the eariier turveys. Other Cancers? Laryngeal and esophageal carteer. By 1964, srrwking was identified as a cause of laryngeal cancer in men; an association between smoking and cancer of the esophagus was also noted, although the data wen; not considered sufficient to establish a causal relationship at that time (US PHS 1964). An estimated 75 to 90 percent of laryngeal and esophageal cancer deaths are attributed to smoking, and smokers have mortality rates from these diseases that are approximately 8 to 18 times higher than those of never cmokers (Chapter 3). Since 1977, public beliefs that smoking inerea.ses the risk of developing cancer of the larynx and esophagus have not changed substantially (Table 11). In 1977,79 percent of adults reported that smoking is one of the causes of throat cancer. In 1985, 80 r- cent of adults thought that smoking increases a person's risk of developing esopharal cancer and RR perccnt thought that smoking increases the risk of acquiring larybgeal cancer. Use of different wording to describe the cancer site (throat, laryrtgeal, esophageal, "mouth and throat") makes oomparisons among these surveys difficutt. In 1986, curtent smokers were less likely to acknowledge a relationship betv4een smoking and laryngeal cancer (82 percent) than were former smokers (91 perccnt) or never smokers (91 percent). Similar pattems were seen in the earlier surveys and ip thp preliminary 1997 NHIS data (Table 11). 1 1 Bladder cancer The 1964 Report of the Surgeon Creneral's Advisory Committee identified an a.ssociation between smoking and cancer of the bladder, although the evidence was not considered sufficient toestablish acausal relationship (US PHS 1964). Thirty-seven to forty-seven percent of bladder cancer deaths ate now attributable to smoking (Chapter 3). Few data are available on public knowledge about the association between smoking and cancer of the bladder. The 1979 Chilton Survey (Chilton 1980) showed that 25 percent of adult respondents (29 to 31 years of age) believed that "cancer of the hlad- der (has) been found to be associated with cigarette smoking." In the 1985 NHIS, 36 percent of adults thought that cigarette smoking definitely or probably increases a person's risk of developing bladder cancer. In the 1986 AUTS, 33 percent of adults thought that smokers are more likely than nonsmokers to develop bladder cancer. Cur- rent smcAcers were less likely to acknowledge this relationship (25 percent), than were former (32 percent) and never smokers (38 percent). What Are the Special Health Risks for Women? TM special health risks for women include effects of smoking on pregnancy out- cnme, increased risk of cardiovascular disease (CVD) among smokers who use oral contraceptives, and increased risk of cervical cancer in women who smnke (Chapters 2 and 3). Data exist on public beliefs regarding the first two of these three categories of risk. h 194 0169 iBSZS 193

. Rcferences ARROTT. R.h.. YIN. Y.. REED. D.M.. YANO. K. Ri.k of stmke in male cigarette cmnkcrc. NrN /'n~l~rn,llnrn,url n/ Mrrlir•inr 315(12):717-720. September 19. 19R6. ARLIN. R.J. CiFarrnc .m(king and quality of spcrm. ILctter.) New Yor•L Stutr Journal n/ Mr,Gr inr x(H?): 109. Fchnrary 19R6. ARI I-7.F.11). II.A.H.. (1101. N.W.. MAINI. K.K.. HSU. P: H.. NELSON. N.A. Relative role nf GK•Inrc a..rK iatcd w ith cerebral infarctirnr and ccrchral hcmrxrhagc. A matched pair cace- cnntml .tudy. .Crr,.kr RI 11: I(M,-112.1anuary-Fchmary 1977. ADAMS. l.l).. ()'MINRA-AbAMS. K.1..1(OFFMANN. D. Toxic and carcinogenic agent% in nndilutcd main.nc:mi .mr+kc anrl .irM.trcam .mnkc of diffcrent typcc of cigarettes. Car- , 7nncr7/r'ri ~ X0029 . 7{ I. I r)1(7. ALJ)f:RSnN. M.R.. I F•.f:.I'.N.. WANG. R. Ricksnl'IunFcancer.chronic hnmchitic. i.chacmic hcarl di.ca.c. :nxl.trnl.c in relation to typc nf cigarctlc ..nnkcd. Jnrrrrrrd,r/ lilrirlrrninl,rcr unrl ('rnrnnrrnrn llrvrlr/r ]')141:2Rh-291. fkccmhcr Irrx5. RAII.AR. 1.('.. SMITII. F•..M. Pn+grcs again.l cancer? NrM• F.n,chrnd Jrntrnrrl nf Mrrlirinr ?1•Ir I1)):1226-12z2. May R. 1986. RA IR 1).1).D.. W IL('( )Y. A.1. Cigarette .moking a.ax•iated with delayed conccption. Inrn•nal n/ Hrr Anrrrirun Mrvli.rd Ac.rrN•iolinn 253(2(1):2979-291ii, 1995. RBARON. 1.A.. RYI:RS. T.. GREENBERG. E.R.. CUMMINGS. K.M.. SWANSON. M. ('iFarcnc .mr+king in w(xnen with carxcr% of the hrcacl and reproductive organs. Journal n/ Nrni,nnd Cunrrr• Inc)irnrr 77( i):677-6R0. ScptcmhCr 1996. RFARr). ('.M.. ANNEGERS. J.F.. WOOLNER. L.R.. KURLAND. L.T. Rnxmchngenic car- cinnm:r in OIm.rcd Cnrmly. 1935-1979. Crrnrrr 55:2f126-2(1.1(1. 19R5• BEHRMAN. R.li.. VAIIGIIN. V.C. (cdc.) NrLanr'aTerrMwrk rrfPrdiarrir•s.Thirteenth F.tlitinn. 1'hil:uk Iphia: W.R. Sannrlcn. 19R7. BGI.L. B.A.. SYMON. L. Smoking and tuhanchnnid haemorrhage. Rrili.dr Mrdir•al.lrnrrnal 1(h1hi):577-57R• March ;. 1979. RENOWITZ. N.L. ('Iinical pharmacology af nicelinc. Annrml Rrrirn•rrfMrdirinr 37:21-22. 19lt6. RFST. F.W.R.. JnSlf:. G.H.. WALKER. C.B. A Canadian study of monality in relation to .mak mc hahitc. A rrcliminary report. CunarliunJrnrrrkrl nfPnhlir I/ralrh 52:99-106. March IrK+1. lil.( )T. W.1.. MCLAII(7H1-IN.1.K.. WINN. D.M.. AUSTIN. D.F..GRF.ENRERG. R.S.. PRF.S- T()N-MARTIN. S•. BERNSTEIN. L. SCHOENBERG. 1.R.. S?F.MIIAGEN. A.. FRAI rM1:N1.1.F. 1R. Snr+king and drinking in rrlation to oral pharyngeal canccr. Currrr•r Resr,rr, h JR: t'R2 - t2R7. Junc I. 19RR. RONITA. R. ('irarcnc .mr+king. hypertcn.irrn and the risk of .uharachnnid hemorrhage: A pnMrlatirurh:r.cd ca•c-craurnl study. Sn•„Jr, 17:R11-Ili5. 19)((+. R()N1TA. R.. S('RA(:(i• R.. STEWART. A..IACKSON. R.. REAGLEHOLF,. R. Cigarrtlc .mrrLing :nxl ri.k nf premature sln.l,c in men and women. Rrili.dr Medical .Jnrn•rrrd 29t(65 tX):(,--R•.lulv 1996. Itk IN 1 ()N. I..A.. S('I IAIRI:R.C.. HAENS7.EL. W..STOLLEY. P..LEHMAN. H.F.. LF.VINF. R..SAVIf/..h.A. ('rpnrcllc.nN+kingarnlinvacivcccrvicalcanccr. Jrnrr•nrdn/Yhr•.4nrrrirrm Mr•dn,d :1 r+,ti irlli.rn :«r _ i/: i_(r5-{?h9. 1')R6. RRI%MAN. R.. RAKIX R.R.. I:I.KINS. R.. IIARTMANN. W.H. Carcnxana of Inng in frxrr .il.linc~. (,mr rr ?rN I I I:NW1(-_(15 i, Nrwcmhcr 1967. ItRt 1%S. 1.1) .( G1RS(1N. R. Ri.k% nf lonc canccr in .nrr+kcrc wMr .witch to filtcr cigan•ttc.. arnrri, nrr.l,rnrn,d r~l Pnhlr, llr,drlr SK(17t1:1 trN~.-IJ(/.1, 19(iR. RROWNSON. R.C.. RF.IF.1.S.. KEEFE. T.1.. FERGUSON. S.W.. PRITZL.I.A. Rick factnrs for adcnrxarcnKrma nf the lung. Mrrriranlnnrnal njEpidemiolney 125(1):25-A4.lanuary 1997. RR(INNEMANN. K.D.. HOFFMANN. D. The pH of tobacco atrwrke. Frrnd and Cn.tnrrrir:c Tn.rir•nla•tv 12:115-124. February 1974. RUFFLER. P.A.. COOPER. S.P.. STINNE7T. S.. CONTANT. C.. SHIRTS. S.. HARDY. R.1.. AGU. V.. GEIIAN. B.. BURAU. K. Air pollution and lung cancer mortality in Harric Coun- ty. Texac. 1979-19R 1. AnMrirrm Journal nf Elridrnrirrln•rty 12i1(4):6R t-699. October 19Rlf„ RLIRROWS. B.. KNUDSON. R.1.. CLINE. M.G.. LEBOWI7Z. M.D. Quantitative rclatiori- .hips between cigarette smoking and venlilatory function. American Rr+•irw• rrjRrspirtnni.+• !)i crrr.cr 115:195-2O5. 1977. ('ARSTf•.NSI:N.1.M.. PF.RSHAGEN. G.. EKLUND. G. Mortality in relation to cigarette and pipe cnn+king: 16 ycars' ohservation of 25.(I(0 Swedish men. Jrnrrrrol njEpidrrninln•qc rnrd (•rnnnrnnirc llr•nlrlr 41:16(t-172. 19R7. CAl ILEY. J.A.. GUTAI.I.P.. SANDLER. R.B.. LAPORTE. R.E.. KULLER. L.. SASHIN. lp. ' Thc rclatir+nchip of endogcnous estrogen to bone density and bone area in nomral prxtmcnopaucal wnmen. Anrrrironlnrrrnel njElridrmlrrlngy I24(5):752-761. 19R6. CP.1)F.RLOF. R.. FRIBERG. L.. HRUBEC. Z.. LORICH. U. The Relationship nf Snlnkirrg and Cnnrr Srk-ird C'm uriablrs In Mrrrralilv and Canr•rr Mrn•Mdih•. A Trn Year Fnllnw•-rrp irr ;o Pr„Iruhilirr Sonrplr (,( t c•(/(/I) Srr•rdixh Snhjtr9s Age 18-69. Porr 112. Stockholm. Sweden: Karolincka Inaitute. Department of Enviromnental Hygiene. 1975. ! CENTERS FOR DISEASE CONTROL. Smoking-attrilwtabk mortality and year- nf potential lifclrxt-UnitcdStates.19R4. Mnr•hidin•andMm•ralirrWreklrRr/x+rl:i6(42):69.1-b97.O~- i k+hcr .1(1. 1997. CHAMBERLAIN. W.1.. SCHLOTLHAUER. W.S.. CHORTYK.O.T. Chemical composition of nonsmoking tobacco products. hnrrnnl nf Agric•nllnral and Frxrd Chrmiarr+• 16(1):413-50. t 9RR. CHIIRCH. D.F.. PRYOR. W.A. Free-radical chemistry of cigarette smoke and its toxicologi- c:d implications. F.rn•Lvnmrrnrrrl Hralrh Prr,ryxrNrrS 64:111-126. December 1985. CLARKE. E.A.. HATCHER.1.. MCKEOWN-EYSSEN.G.E.. ET AL. Cervical dycpla%ia: As- .nciatiorr with cexual hehavior, smoking. and oral contraceptive use? Anrrric•anlnnrnul l~f Oh.rrrrrir•.c unrl (ivnrr•nlrrer I51(5):612-616. March 1. 1995. cOt.n1T7.. G.A.. RONITA. R.. STAMPFER. MJ.. W ILLE7T. W.C.. ROSNER. B.. SPEIZER. P.E.. I IENNl:KF.N9. C.N. Cigmdte.nltrkh+#ltnd rick of atroke in n(irldk-dged wanen. Nrw• F.nClurrd.Jrnonul nrMrrlirinr 3113(151:917-941. April 14. 1911R. COi.DlT7.. G.A.. StAMPFER. M.1.. WILLE?T. W.C. Diet and lung cancer. A review nf the cpidcmiologic evidence in humans. Arrhir•ra nf Internal Mrrlir irrr 147:157-I6(). January 1987. C()MMITTEE TO STUDY THE PREVENTION OF LOW BIRTHWEK;HT. Preventing Low Rirthwcight. Wa.hinFtrxt. D.C.: National Academy Press. 1985. ('(x)K. D.( i.. POCOCK. 5.1.. SHAPER. A.G.. KUSSICK. SJ. Giving up smoking and the ri.k nl'Inan attack.. A report from The British Regional Heart Study.l.rmr•rr 2(RS20):1 i7(,-1390. hrccnrlxr 1 i• 19xh. ('RAI)fNX'K. V.M. Nitrn.aminec and human cancer. Proof of an acxocialicm! Narnrr 1fKN 5')JJ 1:(+tR. fRYCmhcr 15. 1910. f RIQUI. M.11.. FRONEK. A.. KLAUBER. M.R.. BARRETT-CONNOR. E.. GARRIEI.. S.W. Pcriphcr:d artcrial dicca.c in large vesels is epickmiologically dic(inct from.m:dl vc..cl di%- ca.c. 1 Ab.tr,n•t. )('1 l) FriJrrrrinl.!t r Nrn :r/rYlrr• 37:67. January 1995. 35989 t8StS ~ I(), In~

TABLE 12.-Trends in public knowledge about the special health risks for women who smoke Percentage who agree by smoking sanu' N Suney Yeat Current smokers Fonner smokers \ever All smokers nonsmokers All adults .-a ON Smoking during peifwwy incRases the chances of premature birth W 1. AUTS L %HIS 19" 1985 (all) 25 64 43 71 34 73 70 V-4 1 NHIS 1985 (men) 64 00 ~ L %410 1983(womea) 76 ~ Smoking during pregnancy increases the chanca of stiHbirsh 1n 3. MUs 1983 (all) 37 67 72 66 3. NHIS ' 1983 (men) 63 MIS 3. \ 1985 (womea) 68 Smoking during pregmncy increases the chaeces of miscartia8e 4. `WS 1985 (all) 66 73 79 74 4. `M 1983 (men) n 4. NHI3 1983 (women) 75 Smoking during preguncy incnasea rhs chances of havin8 a!ow-birth-weigAt baby 5. NHIS 1983(aU) 74 82 83 go 5. NM 1985 (men) ' 74 5. \ MiS 1985 (women) 85 A woman taking birth control pills is mom likely to have a stroke if she smokes ' 6. N M 1983(all) 39 67 64 65 62 6. YHIS 1983 (men) 48 ' 57 54 53 52 6. ` H1S 1983 (women) 70 80 72 74 72 TABLE 12.-Continued Percentage who agree by smoking status Current Fomw Yever ~~n All Survey Year smolcers smokas smokers adults A woman who ukes birth conaot pills fuNrcr increases her risk of getting a tsart aaack if she also sewkes 64 7. Roper 1980(women) Smoki{ a prtgnrn wortun may ham the baby 83 90 93 ~ 8 1987 'Dau fat 196i i.chde all daYa (US DHEW 1969). lAs far 19{3..6os Fa: et al. (19{7) md NCIiS (1966) aod iedudft odr mo.e people l{ ro u yan d ye. Rapsr dra fat 1980.e 60e dr FTC (19t116 'Pretiomsry tirnyrrsr dra (a~blssrA~ YeraM paoiataM tbr a0 adrb +{9 pwe.a Ivarti Aemd awstiorr b.biw dr..am..~e do eat smoio. (.rondy a0.., milmy a0w..o aqimo.. eildy afay.4 auo.{!) di..w>~ 1. Womea wAo saoks duein{ PR~arcy ne mae likely ro Irrt pse ~. ~y em oa deMiid7 oat inaow dto drooea of peenuoee bNTs 2. Doa ci{areas saakin{ dunn{ PRO>a°cy d~7 ~' P1O~r . 3. . . . d soub'ut>1f 4. ... of miaearei.wT' s. ... cf ww bittlmviglr of mo s.~bm.T' 6. If a womr nks biA aoaad pW. ia sEe mon liiuly ro have a sudps if sh :maka dta. if sba dor ao1 smobt 7. A womr rbe nkM bi11111ooeud piW Ilutlminqpus ber riak af gqon{ a hwt auaek if s6o a4o amda (kaow i'a ae., doe't kww if i's mie, diok i's doeL diet it's oot mne, beow i'a not avs)! {. smoking by a pe{nmt varm- may baee ase baby. (w-dy aoes. agres. diaa°s' fe'O1ey dis•ve)r •~ap. iucsree dron who"suon<ly apes' e<"esiW) ~' •Paoenm8o isdude dtor wbo believe Ihst smoking "defieidy*a-pabaWiacmmtAe rht iPetcenu{e includes dro.ewho'9mow it'f aw" ar "ttink it's aaa' "Penx+eage indude dMe who"ueoe{ly, aV.i ar'agrea' 3

(Aher Health Risks Related to Tobacco Use Involuntary (Passivt) SmnrEing In 1964. the health effects of environmental•tobacco smoke (ETS) exposure were nnt established. Taday. ETS has been identified as a cause of disease, including lung can- cer, in healthy nonsmokers. In addition, compared with the children of nonsmoking Irarents, children of parents who smoke have an increased frequency of respiratory in- fections and slightly lower rates of increase in lung function as the lungs mature (US DHHS I9Rba). From the available data, it appears that the public is more likely to believe that there are health ri-k% from ETS exposure. The percentage of adults who thought that smok- ing is hazardous to nonsmokers' health increased from 46 percent to 58 percent be- tween 1974 and 1978 (Table 13). By 1986 (AUTS), 81 percent of adults thought that tobacco amoke is harmful for nonsmokers who live or work with smokers. Similarly, in 1987 (ACS I 9RRh), R I pencent thought that people's smoke is harmful to others near- by. The 1996 and 1997 surveys used wording corresponding to Level 2 (general ac- ceptance) beliefs. The 1987 NH1S used wording corresponding to Level 3 (personal- ized acceptance) beliefs, but nevertheless obtained the same proportion (81 percent) (Table 13). In the I 9R6 AUTS, former and never smokers were more likely to consider ETS to be generally harmful to health (g2 and 87 pereent, respectively), compared with cur- rent smokers (69 percent). Similar patterns were seen in the 1987 NHiS and 1988 Gal- lup survey. In the 1996 AUTS. when nonsmokers were asked whether they considered ETS to be harmful to their health, 69 peroent responded that they thought so (62 per- cent of former smokers and 74 peteettt of never smokers). Is SmnkinR an AAdiNion? In 1964, the Surgeon General's Advisory Committee eame to the following con- clusion, based on the evidence available at that time: "71te tobacco habit should be characterized as an habituation rather than an addiction " The Advisory Committee's Repcxt, however, did note that tobacco use is "reinforced and perpetuated by the phar- macologic actions of nicotine on the central nervous system" (US PHS 1964). The 1979 Surgeon General's Report called smoking "the prototypical subctance-abuse de- pendency" (US DHEW 1979a). The 1988 Surgeon General's Report reafTrnned that conclusion and provided a detailed review of the evidence (US DHHS 198R). Only limited data are available to assess public knowledge of the addictive nature of tobacco use. In a 1979 survey conducted by the Roper Organization, 50 percent of adults (57 percent of smokers) considered smoking a habit. 29 percent (22 percent of smokers) thought it an addiction, and 17 percent (15 percent of smoken) believed it to he both (Roper 197R). In a 1996 Gallup poll of 1.046 adults IR years and older conducted in Canada by hoxisehold interviews, 76.5 percent of rcspotxkntc considered "cigarette smoking to he 2txi E169 18SZS I h Y ~ a © a n o $ ad N i A .. I I s 0 I~ ~ • .~s ~ d _: 4 A 4 vS ' I 201 /

1 riculum Program during the 19R()-R 1 school year. Respcxtldents were asked to select the three major risk factors for CVD from a list of nine. The percentage responses for these risk factors were: high blood pressure. 25 pemcent; overweight. 22 percent: stress/tension/worry,14percent;ciRarttttsmokinR,13pereettt;heredity/familyhistory, 7 percent; eating too much cholesterol (fat). 7 pereent; not enough rest/working loo hard. 6 percent; not enough exercise, 4 percent; and diabetes. 2 percent. From 1982-86. Becker and Levine (19R7) surveyed 90 adults with no known CHD who were siblings of patients hospitalized for recently documented CHD. Patients and siblings were all less than 60 years old. The siblingt were randomized into an assess- ment group (interviewed within 2 weeks of the index patient's discharge and again 4 months later) and a control group (received only one interview at 4-month followup). Participants were asked in an open-ended question to name factors thought to cause or he associated with CHD. Smoking was identified by 81 percent of the control group (after strrss, 91 percent) and was the risk factor most often cited by the assessment group (97 percent). Folsom and others (1988) conducted two surveys in the metropolitan Minneapolis/St. Paul area during 19R5-86. One survey sampled blacks aged 35 to 74 years, while the other sampled a primarily white population. Subjects were asked the open-ended ques- tion, "What do you think are the most important causesof cardiovasculardiseases (heart attack or stroke)?" The percentage of blacks (total sample sine=1,252) who identified smoking as one of the most important causes of CVD was 32 pencent; stre.ss/worry (54 percent) and improper diet (45 percent) ranked higher. Atnong whites (total sample size=1.870), smoking and improperdiet were both ranked highest (54 percent). In a survey conducted in 1987 by the Gallup Organization for ACS. 90 percent of adults reported that smoking cigarettes contributes to a higher risk of cancer. Lower percentages reported that a highercaneerrisk is as.sociated with suntan and sunburn (73 percent), alcohol (34 percent), high-fat diet (33 percent), and smoked and nitrite-cured meats (31 percent) (ACS 1988b). For the studies reviewed above on comparative risk, data stratified by smoking status were available only from the 1986 AUTS. Knowledge Among AdoksceMs About the Health Rhks otStnoking Because most regular cigarette smokers begin to sn~oke before age 21 (Chapter 5), it is important to consider teenagers' knowledge about the health effects of smoking. This knowledge can he addressed in the following categories: (I) general health effects of smoking. (2) personalized risk of smoking-related diseases, (3) risks of smoking com- pared with other health ricks, (4) beliefs about addiction, and (5) health effects of ST use. General Ncalth Effects Since 1975. beliefs among adolescents that cigarette smoking is harmful have in- creased. National data on knowledge of high school seniors about the health risks of smoking arc available from the Monitoring the Future Project (sponsored by the Na- 213

8069 TBSTS 8 TABLE 8.-Continued Cigarttu smoking causes lung cancer (percentage who agree by smoking status) Survey Year Re(erenoe Current smokers Former smokers ~evet smokers All nonsmokers All adults 11. 1983 NCHS 1986a 92 96 96 96 95 12. AUTS 1986 US DHiS, in ptess 85 94 95 93 92 13. Gallup 1987 ALA 1987 75 90 94 8'1 14. NHQSe 1987 83 92 92 89 'PeReatages include thoae wAo bdisve that smoking "derudtely' ar 'ptobeWy' ineteata t)te ri1t. a.Vr.npaWiswd dat,i. `RNiwinary Mtqurter dats (rap.bWA.di Year.ed paaatap far aY ae.Ma is 89 peeat %O7E Actwl questioes: 1-3. Do you think that cipteee smoking is or is nwt one of the cauww of lus4 caooel! (yee. is a cauK no. is eot a cauaK no opinioa) 4-S. Mould you say tAat cigannse smoking is definitely. probably. probably not or de8nitely not a major cauae of lung canca. or dut you have no opinion eittsa way?' 6-100. Do you tbink dat cigeeae smoking is or is not one of tAe caawe of lung cancer? (yea, is a cause; no, is ooc t+ cause; no opinion) lung 11. Teil pte if you ddnk ciga.ne snwking deruutely increaaa. probably incteasa, probably does not. or deMitely doea not innease a penon's chances of gescng the following pteElenr ..g caaoacr 12. t]b you think a petsoa who smokee is any mae likely to get lung cancer mas a penao who doeea't smoke? (mucA mae likdy, somewhat mote likely. no. don't know)t 13. Do yw dtink smoking is a cause of lung cancer? (yeae, no. dpn't know) 14. ptopk have differing belie(G a(+ow dte relationship between smoking ard Aea& Do you believe cigarette smoking is rtlated to ... lung cancer? . Peoentago include dtose who say smoking is "deflnioely" or .'pmbebly" a majar cause ot lung cancer. ••Pamragp include dfose who believe smoking "defeitely" or "ptobebly" inneasea the risk ~Paoesagea include those who believe snakers an 'mucA mae likely' or "sotoewhae mose likely" to get lung cancer. TABLE 9: Trends in pubiic knowledge about smoking and heart diseate Smoking cigarettes causes heuc diseue (percentage who agree by smoking status) Survey Year Reten:nce Curtent smokers Former smokers Never smokers All nonsmokers All adults 1. AUTS 1964 US DHEW 1969 32 31 44 46 40 2. AtIfS 1966 US DHEW 1969 33 33 43 47 42 3. AUTS 1966 US DHEW 1969 46 63 38 60 54 4. Gallup 1969 Gallup 1981 3. Gallup 1977 Gallup 1981 68 6. Gallup 1978 Gallup 1978 63 72 68 7. Gallup 1981 Gallup 1981 59 82 74 8. NHlS 1983 NCHS 1988 88 93 92 92 90 9. AUTS 1986 US DFHS, in pn:ss 71 84 80 81 78 4

perceive a personalized risk from smoking. However, nonsmokers were asked to respond to the question, implying that the wording may not he understood by sane rcspondents as referring to truly personalized health risks. Wording such as, "Do you think that your cigarette smoking is or is not harmful to your health?" might elicit dif- ferentresptxrses. The 1987 NHIS (unpublished data, National Cancer Institute) showed that 55 per- cent of current smokers answered "yes" to the question. "Do you believe your smok- ing has affected your health in any way?" The principle reason this percentage is sub- stantially lower than that obtained by the 1985 Gallup survey (90 percent) is probably that the former was likely to he understood as referring to overt symptoms or disease, while the latter was likely to be understood as referring to the risk of harm. Another approach to measure perceptions of personalized risk has been to ask smokers whether they are "ccxrcerned" about the effects of smoking on their health. It appears that smokers are more likely today to be concemed that smoking is harmful to their own health. In 1964.50 percent of current smokers were concerned about the pos- sible effects of smoking on their own health (Table 1 S); this proportion increased to 73 percent by 1986. However, in 1986, only 18 pereent of smokers were very concerned about the effects of smoking on their health: 56 percent of smokers were only fairly or slightly concerned; and 24 percent were not at all concerned. From 197(1-86, the percentage of smokers who were very concerned about the pos- sible effects of smoking on their health decreased from 29 to 18 percent, while the per- centage who were only slightly concerned increased from 19 to 34 percent. This redistribution within the population of smokers having any concern may have occurred because a much greater propottion of those who were very concerned may have quit smoking during this period; therefore, they would not have been included in subsequent surveys. A third approach to assess personalined risk, or anore comectly, the absence of per- sonalized risk, is to ask smokers if they believe themselves to be at lower risk than other smokers. In 1986, 21 percent of adults thought that the cigarettes they smoked were less hazardous than other cigarettes (Table 3). Other data pertaining to perceptions of personalined risk from ETS and from smok- ing among 3dolescents appear in the sections on Involuntary Smoking (above) and Adolescent Knowledge (below). How Harmful 1s SmokingT The data presented above reveal that a vast majority of adults agree that smoking is ha7ardous to health and correctly recogni7t the conditions that are associated with smoking. I:owever, these data do not address the depth of the public's understanding regarding thc ab%olute risk of smoking, the relative risks of smoking, the population- attributable risk of smoking, and the risk of smoking in comparison with other risks. A monc in-depth understanding of the risks of smoking may he much more important in promoting hchavioml change than the mcm superficial beliefs measured by the data prescnted ahnve. Unfortunately, only limited data are available to addrcss the public's in-depth underst:mding of the risks of smoking. A a ~ ~ a A ~ 0 u ~ W ~ V 4 R h o: 0 .e = a a A = iC A °- S i I I ST69 T85ZS .os 204

LZ69 T85T5 TABLE 2a.-Trends in attitudes about smoking and s:nokers among high school seniors. 1981-56, .%tonitoring the Future Project, National Institute on Drug Abuse like he's TRYL*iG to appear mature and sophisticated insecure conforming runged.tough.independent cool. calm. in control mature. sophisticated like she's TRYIING to appear maturc and sophisticated insecure conforming independent and liberated mature. sophisticated cool. calm. in control TABLE 24.-Continued In my opinion. when a guy my age is smoking a cigarette. it makes him look ... (percentage who agree) 1981 1986 61 63 42 44 zs 21 9 10 6 6 3 3 In my opinion. when a girl my age is smoking a cigarette. it makes her look ... (percentage who agree) 1981 1986 65 65 47 50 27 22 I1 10 7 s 6 5 ou agree or disagree ... Do y (percenuge who agree) 1981 1986 66 71 I prefer to dau people who don't smoke 69 66 Smoking is a dirty habi[ 57 59 I think tbat becoming a smoket rcf llects poor judPnent 45 Is=,* dsfike being neat people who are smokin{ 38 37 I pessomlly don't mind being atomsd peopk who ars smokitt{ 16 16 The hatmful eKeuts of cigartoea have been eaag8"11ed 3 2 Smoken kaow taw to enjoy life mote ttm nommottais ~ NO1E: PoaibM rtsponses induded apes. mostly apee. d<saper. moMly disa0ae• nithlt. Ptroutta=a inctude thae who "agni °r "mestly a0v& SOURC& 1droMOa. BacAmr. O'Malley (l9l2);BacbmU&JobrsoE-O'Malky 11987). :-.~-. ....:

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Jrnrrmrl r~f nc~ Nntinnal Conctr /n.airare 711 Z):473-479, Sep- Icmhcr 19R1. HA V I.IK. R.J.. FEINLf:IR, M. (cds.) Prrx•rtdin.es njthrGmjcrcnrcon the Dcrlinc inCnronary llrart ni.cease Mnrtedin•. 1).S. Department of Hcalth. Educatirm, and Wclliire, National In- stitutes of Ilcalth. DI(I'.W Puhlication No. (NIl1) 79-161t1, 1979. HAWTIIORNf:, V.M.. FRY. J.S. SmnkinF and health: The a%snciation between smoking be- havaNir- total mortality, anrl cardinrespirhtrny discasc in wc.t central Scotland. Journal of I•:p6lrntirrln.ci• nn.l Cmm"nmitv llrahh .i2:2r+(1_2M1I+, I')1R, HELLRERG, D., VALENTIN. l., EKLUND, T., STAFFAN, N. Penile cancer. Is there an epidemiological role for smoking and sexual behaviour? British Medical Journal 29S(6609):13U6-1308, November 21. 1987. 1NTERNATIONAL C'LASSIFICATK)N OF DISEASES. International Classtficarion nf Dis- ' rases, Seventh Revision (ICD-7). INTERNATIONAL CLASSIFICATION OF DISEASES. IntenwtianalClassificatinn ef Dis- taas, Ninth Revision (1CD-9). KAHN. 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950 N N N 2 > P~ t- ^ Y e ~ i Y 0 ~ ~ ~ A 0 €S -S ~ o . r Y ~ o TE`o wegEa O o ~7 e gY = ~ w3 Tro ~ o s e ~ o u ~"-5 e ~ . O _ rS O '~ b A 10 ~ y C_ ~ ~ " " ,A a ~ 0 >i " at: E ~ ,o Q n 0 ~ W ~ r ~ M :4 :3 r Y t V ~ 0 7 = _ '_° ~ A e°o 'A ~ v Y ~ £Z69 iBSiS rclevant-10 percent in 1985 did not believe that smoking is harmful to health. In 19R6, 15 percent did not think that a person who smokes is more likely than a person who does not smoke to get lung canoer. Similar proportions of smokers did not believe that smokers are more likely to get heart disease (29 percettt), chronic bronchitis (277 per- cent), emphysema (15 percent), and laryngeal cancer (18 percent). These percentages correspond to R million to 15 million adult smokers in the United States. Another gap exists in the public's understanding of the special health risks of women who smoke. Compared with 1964, in 1985 smokers were more than twice as likely to recognize smoking as a cause of premature delivery. However, in 1985, 24 percent of all women (smokers and nonsmokers combined) 18 to 44 years of age did not'recog- nize the risk of prematurity; 15 percent did not recognize the risk of low hirthweight; 25 percent did not recognize the risk of miscarriage; and 32 percent did not recognize the risk of stillbirth (Table 12; Fox et al. 19R7). The fact that in 19145 10 percettt of smokers did not indicate that smoking is fiarmful to health (Table 2), despite all efforts designed to impart such information (~. hapters 6-R), suggests that this group of smokers may resist accepting any informatiob,on the health effects of smoking. This finding has important implications for smokiog con- trol efforts and for setting public health objectives. It implies that other techniques be- sides providing information (e.g., policy incentives-see Chapter 7) are necessary to persuade sottte smokers to quit. It also suggests that it is unrealistic to set a goal abOve 90 percent of smokers for public knowledge about any health effect of smoking. * Another gap in public knowledge involves teenagers. Youth may understand that smoking is generally harmful to health, but many may not appreciate the addictive na- ture of smoking or may deny a personal susceptibility (Leventhal. Glynn. Pleming 19R7). In addition, data from one study (US DHHS 1986c) suggest that many ST users ae not aware of the health effects and addictiveness of the product. Fishbein (1977) described three different ways in which individuals may be inf,orntted of a given piece of information: (1) they may become aware that the information ex- ists; (2) they may accept the information in genetal; or (3) they may accept the infor- tnation at a personaliaed level. These three ways of being informed cottespond to three levels of belief mentioned at the beginning of this Chapter. Level I(awareness), Level 2 (general acceptance), and Leve13 (personalized acceptance). Persons may have knowledge or beliefs at one level, but not at another. For example, some smokers may be aware of the Surgeon General's Reports and accept the general fact that smoking is dangetous, but do not believe that they will be harmed by smok- ing. The data presented in this Report support this concept. Whereas in 1975 ap- proximately 90 percent of smokers believed that smoking is harmful to health (Table 2), in 1986 only 75 percent were concerned about the effects of smoking on their health (Table 15). The recognition of a general risk but disbelief in a personal risk may result from sevcral factors, including a belief that using low-tarcigarettes (see Table 3), smok- ing fewer cigarettes daily (see Table 5), or having certain genetic factors eliminates the personal risk. In order to make a fully informed decision, a person should have complete and ac- cttrate l..evel 3 beliefs atxntt the outcomes of each alternative action (Fishhein 1977). The personalis.ation (perception of the personal relevance) of abstract infonnaticxt has -Wt

o.: nNhdckq {boul the bwril naNn a/ ni{ pawal papubtlon, how impbtdnt Is K rotaauai,..W a Uum.t a ta. 10 I"ro«oeob 9 a f 6 5 4 3IM6_r%"0' 1 F-" Na smWa 9.78(.09) )-.--r iAlar ss»DMb aM tM nnr n hant saf 9.16 (.12) F---~1 New Crns af4r onnkrp 9.031.18) ~-.-~ Hrw smoka aASctam m Mm. 6.53 (.17) lM wlMra Gnnknp wa0u Is d aCCaptiDM QuiWy 8.41 (.17) F-F-~ 11aN hNeW. nwho, ntiqlbatf 6.31(.16) F-~-1 t~urda~ reqwlAy 8.201.16) 1-«--~ orrrl aloala moaKaar 6.15 (.t9) E-.-t Not Mt bo mudl er 7 62 (.15) t.-..-~ K«n cws. w nconnwwsa w«ytr 7.71 (.15) f-t---i f4caM aQvla trom Ooctor on twen Wits. T.67 (.22) M---.-~ Mar. daod prMn r.aalnq Lu+wYy 7.62 (.21) /---~---~ Inlwnt pwt hae pinnn lar kw+q k!a 7.62 (.26) f-..-...~ rak, sip"a caMra >xr.a 7.58(.18) F--r-i Fst enppA IiD~I 7.41(.17) 1---~--1 Get srouph calarn (/or warmn) 7.2a (.19) F--.-~ Nm q1t loo IAuqI q1plK1re1 7.15 (.19) liw wMn air b aaapfa0b 7.12 (.22) F---~-/ GM wlapll vftmi/d m0 mirw* 7.12 (.22) 1----F-~ Not al !oe mudl sodkm 7 04 (.19) Naf qt too muce supr 6.90 (.19) F--~-~ GN l•6 iaurf slNp 6.71 ( 20) F---9 i Eri breakflst CLIy 6.16 (.25) OAnk no akdal 3.15 (.23) F----~~--~ FIGURE 2.-Experts' rating of 24 health and safety factors %G7E: Shown abovs is ehs mue importanoe ndn4 faeack facwr Siven by 103 expens usinj a 1 io 10 scak. Given in pa,tndfesn is tM uandrd etror a( die meat AR ieditaWe of tAe rariabiliqq ol individud r.onp a,ound each meae is Qaphi- c ally duplaysd a a b.,d or r.np oauiam,ga( t Nw amda,d enw.alu.a SOIRCl: Hamstl9s3). -Public knowledge about the harmfulness ot cigarette smoking compared with other risks,1986 T?1BLE 17. Percenu wtb disa Peccenn`e who a~ee ~ s Fom+er smokers Nevet smoken Current smokets Fortner Nevet s smoken ers mok 63 54 63 f ci{an~s ~~~n~ to health thas 32 21 20 40 ~toderate use o derate use of akoholic beveca{ea. 37 33 34 mo cl{uem is lesa hactnful to hw* dM un0k'Oj kin 43 38 57 { Smo 41 54 mariju~ 30 29 "m 49 58 6{ oputioa ia a Qere* beea ^* th° cipre i 26 52 r p A Smokin{ cigamta ia ku dan{ecau d+•° drivia{ wimaa a 36 23 59 69 71 seat beit. 31 19 is Smokin{ ia leaa lunntul dun bein{ 20 Pa" 0' se who dis.Os iaclua. mo.. + eo ss°°d7 ~~ °r f0sw~+&&F-• t d w a's0'Oe• lr.~ Pet`'Ute, a ,i0'iE: Pleri+P o( di°r rho apes iodrds Ibon to r'nontl7 ave: SGI; RCE: AUTS 1966(US DHHS. in prM). 1J

KAPI.AN. (;.A.. SF.FMAN•T.E..COIIF.N• R.D.• KNItDSF.N• l..P.•('iURALNIK.1. Mortality :nrnmy thc clrkrly in the Alamcda Cuunty Staly: Rchaviar:d arwl ckmryer.rphic rick LK•1ors. Amrr rr rrn .l..unntl.•/'PrrMrt• Ilrnldr 7701: J(17-t I 2. March 19X7. KAt II MAN. 11 W.,11f_LMRICH• S.P.• ROS(:NRf:RG. L.. MIFTTINFN• O.S., SHAPIRO. S. Nicrninr an,l carhrm mrxurxitk crmtcnt nf cigarcttc smnl.c arnl the rick nf mytxanlial infarc- tirai in yrxm•c mrn. New F.n~land.lnnrnrd n/ Mrdrrrnr ~(Mt(R1:4(19 d l s. Fchruary 24.19143. KI:I.I.F.RMANN. (;., CIlAR1.F:S• R.S.. I.IIYTf-'.N-11[:LI.FRMAN, M. Aryl hydrocarbon hwlm,tyla.c inJucihitity arKt MrmcM+gcnic carcirxMtra. New F.n,¢lenrl Jnrrrrrnl n(Mrdh rrtr 2X9:q1.1 - yiX• Ir/7i• KFLSFY.1.1... I)W YI.R• T.. I It7LFORD• T.R.. RRACKF.N, M.R. Maternal smnking and con- }rnitalmailfirrma/1rrnC: AnCflhll•minloglcal%IIHIV. JllHrnallrfr/yllrnnrilir¢\•anrlCrmrnrrtnlh• llrrrltlr i?;I11? 1f17• 197x, KI:MP. Il.r.• KRONMAL. R.A.. VI.IFTSTRA. R.F... FRYE. R.L.. 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The Nati/mal Institutec of Hcalth Intermit- tcnl Pocitive-Pressure Breathing Trial: Pathology studics. (I. Correlation hctwelen mor- phologic findings• clinical findings, and evidence of expirattrry air-flow trbstructicm. American Rrt•rrN• nJRtspiralary Di.ctasr 1.12:94Cr953, 19R5. NAKAYAMA. T.. KODAMA. M., NAGATA. C. Generation of hydrogen pemxide and cuper- nxidc anion radical from cigarette stnoke. Gann: Japanese Jurrrnal n/ C'ant•rr Rccr•urr•h 75(2):95-98. February 19R4. NATIONAL ACADEMY OF SCIENCES. Dirt.Nu/rrlrtnrandCanrtr. Wachingttxt. D.C.: Na- ti/mal Academy Press. 191112. NATIONAL CENTER FOR HEALTH STATISTICS. Health. United Srrrrrs. /9•Yh. U.S. Department of Health and Human Services. Public Health Service. National Center for Health Statistics. DIIIIS Publication No. (PHS) R7-1232, December 19R6. NATIONAL INSTITUTES OF HEALTH. NATIONAL INSTITUTE FOR ENVIRnNMFN- TAL HEALTH SCIENCES. Airbome pollutants and respiratory cancer reproductive and developmental toxicology. Enr•irrmmtatal Health Prr•.yxrtrrea 70. December 19x6. NATIONAL RESEARCH COUNCIL U.S. COMMITI'EE ON MEDICAL AND RIOLOGIC EFhI:CTS OF ENVIRONMENTAL POLLUTANTS. Carlr.nr Mnna.lfdr. Wa•hington. D.C.: National Academy P1ess. 1977. NATION Al. RESEARCH COUNCIL Fm'rrtmrntnlnl Tnlxn rtr Smrr(r. Mraarrrrr•¢ F. ~IHrsurrs and A.«r.l.crnc llrrrldr Efltcrs. Washington. D.C.: National Academy Press• 1986. NATIONAI. RFSF.ARCII COUNCIL. llralrlr Rrsks tr/Rodnn tnrd lhlrtr Irrrrrmdh I)r/rrr.crrrrl Alplur-l:'nrrrrr•r.c. RF.IR Ilr. Washington. D.C.: National Acatlcmy Prccc• 19xR. L989 T8SI5

I creases the risk of having a low-birth-weight baby (Table 12). The percentage who knew of the interactive effects of smoking and oral contraceptive use on CVD was also below thc 199(1 goal. No data exist to asses< progress toward achieving the fifth objec- tive. Trends In Pubtk Attitudes About Smoking and Smokers This Section de.crihec trcnd% in public attitudes about smoking in general and about cmokere. Involuntary Smoking as an Annoyance Since 1964, the population has become increasingly annoyed by exposun; to ETS. In 1964. less than half of adults (46 percent) thought that it was annoying to he near a percon smokin)g cigarettes (Table 22). Identical questions asked in surveys conducted in 1964. 1966, 1970, and 1975 reveal an increase in the proportion of adults who were annoyed by being near a person who is smoking (from 20 to 35 percent among smokets and from 64 to 77 percent among nonsmokers). By 1986. 42 percent of smokers and 80 percent of nonsmokers reported that they were annoyed by the smoke from another per.uin's cigarette. The 1987 NHIS (preliminary first-quarter data) obtained results similar to those of the 1996 AUTS. Nonsmokers' Rights Acconding to Gallup stnveys, the pnoportiort of adults who feel that smokers should refrain from cmoking in the presence of nonsmokers increased slightly between 1983 and 1987. In 1993.69 percent of adults thought that smokers should refrain from arrok- ing in the presence of others (Table 23). By 19g7, 77 percent of adults (64 percent of smokers and 96 percent of nonsmokers) thought that smoken should refrain from smok- ing in front of otherc. In the 1997 Gallup survey, respondents were asked where smokers should refrain from smoking when nonsmokers are present. The proportions who believed that smokers should not smoke in the presence of nonsmokers were 62 percent with respect to public places. ?4 percent with respect to work, and 19 petcent with respect to the home (ALA 19R7). In a 1987 survey conducted for AMA, respondents were asked, "Which do you fcel is a more important individual right, the right of smokers to smoke anywhere, or the right of nonsmokers to a smoke-free environment?" Three-quarters of respondents (76 percent) thought that nonsmokers had the right to a smoke-free environment (49 per- cent of smokers and 86 percent of nonsmokers). compared with 10 percent who thnugla that smokers had the right to smoke anywhere (25 percent of smokers and 5 perccnt nf non%ou ,kcr.) (liarvey and Shubat 19R7). SZ69 18515 2?4 ~ 0 E © w O C y _o eE 0 V Y O 7.E LLN ~~ E < < < < oG < I. rtot- F 4 225

N 1n 'D 00 GO a0 I Actinns When Smokers LiRht Up Surveys conducted by the Roper Organis.ation in 1974,1976, and 1978 (Roper 1978) iccessed actions of smokers when they are indoors with other people and want a ciEarette, and actions of nonsmokers in response. Although these questions technical- q pertain to smoking behavior, the subject of the next chapter, they are indicators of ittitudes toward smok ing. Smokers were asked, "Do you light up a cigarette without really thinking about it, or do you look around and then decide whether it's okay, or do you ask if others would ~ mind, or do you just not smoke?" In 1978, a total of 57 percent either looked around md then decided (27 percent), or asked others (26 petcent), or did not smoke (4 per- , crnt). Slightly lower total percentages for these three actions were reported in 1976 (55 percent) and 1974 (53 percent). The 1987 NHIS indicated that 21 percent of smokers would light up in a public place, while 26 percent would look around first, 15 percent would ask others, and 31 percent would refrain from smoking. ( A total of 58 percent of nonsmokers in 1979 said that when someone is smoking in-i ftirs, they either ask the smoker to stop smoking (6 percettt), indicate disapproval; without saying so (10 percent), or try to move away (42 percent). In both 1974 and , 1976, the total percentage for these three actions was 53 pencent; other pos.sible respon- , ses were: "doesn't matter." "enjoy it," "it depends," "and "don't know: ' According td the 1987 NH1S, fewer than 5 percent of nonsmokers would ask a smoker in public not M %moke (preliminary first-quarter data). , , Opinions of Ttaettagers According to recent surveys from the Monitoring the Future Project, most high school crnicm think that smokers their age ane trying to appear mature and sophisticated, and ahcwt half of teenagers think that smoking makes them look insecure (Table 24). Only 5 to t0 percent of respondents thought that smokers look eool, calm, in control; rugged: tough, ittdependent; or mature and suphisticated. Most teenagers prefer to date pec>Ede who do not smoke. Most also consider smoking a dirty habit and think that becoming a smoker reflects poor judgment. In 1986. 45 percent of teenagers strongly disliked hcing near people who were smoking white 37 petcent did not mind bein around people who were smoking. There appears to have been little change in these~ttitudcs from 1981-86 `s In summary, smokers and nonsmokers, adults and teenagers alike, generally believe that smokers should refrain from smoking in the presence of others and that it is annoy- ing to he near a person who is smoking. In addition, teenagers are tnore likely to as- uciate smoking and smokers with negative attributes than positive ones. 226 9Z69 T85I5 I 227

Trends In Public Opinion About SnakinR Policies Overview Background This Section describes trends in public opinion about smoking policies. Public opinion information is helpful to legislators, public health officials, and other policymakers who often wish to know the degree of public support for an issue unckr consideration. The results presented in this Section are taken primarily from public opinion polls spnnscxed by a variety of private health organizations (Appendix). This Section u-,es the categori7ation of policies employed in Chapter 7, including the following categories: (1) smoking restrictions, (2) restrictions on the sale and distribu- tion of cigarettes. (i) policies pertaining to information and education, and (4) econcxnic policies. Each section reviews trends in public opinion toward the policy and briefly describes the current status of opinions toward the policy with respect to the smoking status of the respondents. Limitations of the Surveys in Assessing Public Opinion About Smoking Policies Assessing trends in public opinion regarding smoking policies is more difficult in some ways than assessing trends in public knowledge regarding the health effects of smoking. For instance, surveys that ask about public opinion often refer to the "cur- rent" situation. However, the "current" situation may change from year to year and from survey to survey. For exampk, in 1964,52 pencerH of adults thought that smok- ing should be allowed in fewer places than it was at that tinte. By 1975, 70 percent of adults thought that smoking should be allowed in fewer places than it was at that tinx. However, the "current" situation changed from 1964-75, making the survey results dif- ficult to compare. Because smoking was already allowed in fewer places by 1975, the results of the 1975 survey reveal even gnetter support for limitations on smoking than indicated by the difference in pen,entages. Restrictions on SmokinR General Between 1964 and 1975, aduits increasingly favored restrictions on smoking. In 1964. about half (52 percent) thought that smoking should he allowed in fewer places than it was at that time, compared with 70 percent by 1975 (Table 25). Comparable questions have not been asked to assess more recent tttnds since 1975. However, in 1986. 50 percent of adults disagreed that there were already enough restrictions on where peoplc can smoke. a 8 3 F a a~ I ~y 7E ~ ~ „ n ~ n, 2 2 2 2 ~ 1 2 ~R nG P .Y, .~.+ v r+ ~ F Z ~ h ~ st r 0 n M ~ ~ ~ ~ 9 t I 8Z69 TBSTS ' 231 1. 210

case Prevention Supplement in 1985 and the Cancer Control Supplement in 1997. The surveys for 1964-75 used, for the most part, the same methods and questionnaire wording. Different methods and questionnaires were used in sub- .equent survcy.. 2. Naticmally representative surveys conducted by private organizations, such as Gallup and Roper, and sponsored by various organizations. 3. National surveys of population.cuhRroup.c or local surveys. These surveys were usa1, for the most part, only when nationally representative data were unavail- able. Data from these surveys are presented in several tables throughout this Chapter, each of which addresses heliefsoropinions about a particularsmoking-rclated scientific fact or policy. When one of the primary data sources (e.g., the AUTS) is not included in a tahle, it is because the relevant question was not asked in the survey or survey year or because the data were not available. Preliminary first-quarter estimates from the Cancer Control Supplement to the 1997 NHIS arc provided in some tables (unpublished data, National Cancer Institute). These data are unweighted. When availahle, year-end weighted data are cited: in all cases, these figures are very similar to the first-quarter estimates. The surveys used in this Chapter and in Chapter 5 are described in the Appendix to this Chapter. Table I provides basic information about the survey methodology. The amounts of information provided for the different surveys vary because certain TABLE 1.-MetMMobRy of surveys strrrer Survey fnre Snnple sis,e Age (yeart) Response rate (%) Mcxk' AUTS 1964 NNational Analyett 5.794 221 76 P AttTS ItMr. NatinnalAnatvalaA 5.768 72 P Th AIITS 1970 (ltikon 5.M10 221 P(W) T(vl%) Al1TS 1975 Rtqtr1a7R Chilton Roper 12dq10 2 SII T(96'1F) IM4'.Tr`) P NHI.S 1oRS Crncuc Rurtau 33.6.'t0 21>t 90 r AIITC 14R8 AMA 1oRri AMA tyR7 Wcc(an Kane. Parsnns Kane. Parutc 13.0.11 I,S(10 1 S(tt1 217 74 T T T MTt't 1a7t-R7 lIniveraitYnfMichipn IR 0 'V. /e+mnal inatvKw; T, telrpMww uwervKw: V..rlr-aAm/niqered queatMrwwee. % Nmwr.t.vwlrnt. t.. /rr...n:d ~nlrnirwa. ~ NmtN'kplwuwMrnr•M.NIa. AMnniNVmR tIr Future 1`nrye~1. aurv'v r.f hirA acMml aninra. T069 TBSiS methodological details were available for some surveys but not for others. Additional, information on the methodology of these surveys has been published elsewhere (Mas- scy et al. 1987). lssues In ComparinR Surveys When assessing trends from different surveys conducted at different times by dif-: fercnt organizations, it is important to consider the following caveats. The response trn, each specific question depends upon multiple factors, including the mode of data col- Icction (e.g., in person versus telephone), the sociodemographic representativeness of the sample, the exact wording of the question (e.g.. bold, direct-sounding questions ver- cuc comervative-sounding statements), the type of response allowed or requested (e.g., open- versus closed-ended questions), the order of questions within the survey, and the4 content and nature of the rest of the survey (e.g., a survey specifically addressing smok, ing versus another of a general topic). Even minor changes in the survey methods dr questionnaire wording may lead to markedly discrepant results for a specific questioo. Additional precautions exist when interpreting surveys that assess public knowledge; When asked a knowledge question, resporKknts may attempt to answer it "correctlX' in order to please the interviewer. The Health Promotion and Disease Prevention Sup- plement to the 1985 NHIS sheds light on this question. In this survey (NCHS 19R6), recptxtdent.c were asked whether smoking increases the risk of developing cataracts and gall bladder disease-two conditions not associated with smoking. The extent to which these types of questions (sometimes called "red herrings") are answered in the affirm= ative (and thus incorrectly) may reflect the respondents' general tendency to respond in the affirmative. More than 95 ptacent of respondents reported that smoking causes emphysema, chronic bronchitis, and laryngeal, esophageal, and lung cancer: howevrrr, I 1 percent and 16 percent reported that smoking causes gallstones and cataract.c, respec- tively. The responses indicating a connection between smoking and cataracts or gall bladder disease may represent misinformed beliefs or a bias from attempting to answer knowledge questions "correctly." There are other possible explanations, however. For instance, these responses (as well as other "correct" tesponses) may represent inferen- ces that respondents have made, in some cases regarding questions they have never thought about. In these cases, some persons may be inclined to infer a connection he- Iwecn a known risk behavior and any disease outcome. In the case of questions about public knowledge (e.g.. "Do you think that smoking is or is not a cause of lung cancer?"), the "don't know" response should be included in the denominator when calculating the pmportion of the population that believes a par- ticular fact. This process was used for calculating unpublished data presented below. When two surveys produce unexpected or discrepant results, a close inspection of the methods often explains the fmdings. Two examples involve surveys of public opinion about smoking policies. In one case. two separate national surveys conducted in 1996 regarding support for a ban on cigarette advertising provided apparently dis- crepant results (American Medical Association (AMA)19R6), A careful review of tlie questionnaire wording revealed marked differences in the remarks made just prior to cnch question. In a survey conducted for AMA, respondents were first infomned about 177

TARLF, 20.-Beliefs ahout the health effects otsmokekss tobacco (.CT) use among 399 junior and senior hiRh school students (percentage who agree) in 16 States,1986 Uxn Nc.w.en Junior hiRh acfaol (N = 76) High school (N : 214) Ncwwsers (N = 109) ST use can br harmful no 92 97 Rick fmm ST uce Ncw or aliRht 57 42 32 Moderate to great 43 St; 6R Regular ST use may lead to 33 s 5 mouth cancer Gum and mouth rmbtents aenons 64 41 33 usen are very rare ST u.e increa.es risk of tooth 24 11 16 stains. wear, and loss Snuff does not contain nicotine 33 20 32 Regular ST use is not addictive 25 1s to ST use is much more safe than at tet 59 ciRaretten N(TTF.: ST u.er dernord .a fallow.: haa dipped or che.cd exwe Arn IfN/ time.. eyuenttr wen d.ily ew at ksa thice drva per week. dirtinR M kaew tMee tinr% en d.y% ef ..e. Ne.w.rr deffeed a falbw.: hn ne.er dipped a chewed. er haa mly iried in .!ew fimea nr ~n,xe th.n a few time. (M fe.ee M.n Idl times. scnIRt•r•: US IHntctloartid). ZZ69 1851S Health Benefits of Smoking Cessation The overall mortality ratio of former smokers (compared with never smcikers) declines with increasing years of abatinence. According to data reviewed in the 1979 Surgeon General's Report (US DHEW 1979a) from the U.S. Veterans Study and the British Doctors Study, overall mortality rates of former smokers are similar to those of never smokers 15 years after quitting (US DHEW 1979a). W ith respect to lung cancer mortality, the increased risk diminishes substantially by 5 to 9 years after quiiting' but remains above the risk of never smokers for many rnore years except for those with fewer than 30 years of cigarette smoking (Chapter 2). A reduction in CHD mortality occurs within the first few years after cessation (US DHHS 1983). The risk of COPD mortality decreases eventually after smoking cessation but does not decline to equal that of never smokers, even after 20 years of cessation (US DHHS 1984). In the 1986 AUTS, respondents were asked how long it takes before former }mokers' chances of developing a disease return to normal. Slightly more than half heI ieved that the risks return to normal within 5 years (Table 21). Results were similar wheq stratified by smoking status. The 1987 NHIS included questions regarding the health benefits of quitting in terms of specific disease risks. These data were not available for inclusion in this!Report. Discussion 4 It has been 25 yeArs since the release of the first Surgeon General's Report on smok- ing and health. During that time, a major public health effort has been made to educate the public regarding the health consequences of smoking (see Chapters 6-8). Public knowledge of the health risks of smoking has improved as a result o,f this mas- sive public health education campaign. The belief that smoking is harmful to health has increased since 1964. In 1964, a majority of adults acknowkdged the geneFal health ri.sk of smoking and believed that smoking is a majorcause of lung cancer, but a minority believed that smoking inrneates the risk of COPD, heart disea,se, and premature birth. By the mid-1980s. a substantial majority of adults (including nonsmokers and smokers) recognized the general health risks of smoking and believed that smoking increases the risk of lung cancer, COPD, and heart disease, and prematurity, low birthweight, mis- carriage, and stillbirths. Knowledge of the risks of exposure to ETS has also increased markedly since 1974; in fact, this high level of belief preceded the release of the 1986 Surgeon General's Report on the health consequences of involuntary smoking. Current Gaps in Public Beliefs About the Health Effects of Smoking Despite the growing level of public knowledge noted above, a substantial number of Americans are still uninformed about or do not believe the health rinks of smoking. These gaps in knowledge or beliefs are more evident when one considers the propor- tion of adults who do not acknowledge certain health risks rather than the proportion who do. For example, among smokers-for whom this information is particularly 'tQ 1 210

Public Places Table 26 presents data from five surveys conducted since 1978 that asked about opinions regarding restrictions on smoking in public places. Differences in the word- ing of the questions make comparisons among the surveys difficult. Two surveys solicited opinions about three mutually exclusive options (total ban on smoking, separate sections for smokers and nonsmokers, and no rcstrictions at all), two surveys asked for an opinion only about a total ban, and the fifth asked for an opinion only ahout "no smokinR ' sections. The 1979 Gallup survey and the 19R7 Harris survey both presented three opions. The proportion of respondents favoring either a total smoking ban or separate secti<xn was 84 percent in both. However, the percentage favoring a total ban increased from 16 to 23 percent. The 1987 and 1998 Gallup surveys showed that the percentage favor- ing a total ban was 55 and 60 percent, respectively (69 and 75 percent of nonsmokers, respectively); the option of separate sections was not presented in these surveys (Table 26). Workplace Questions used to assess opinions tegarding smoking restrictions in the workplace have varied from year to year. It is not poa.sible, thettforo, to identify a clear trend, but the public has consistently shown support for policies that limit smoking in the workplace. In 1966. 92 percent of adults thought that an employer had a right to tell employees when or where they can smoke while on the job (US DHEW 1969). In 1975, 78 per- cent of adults thought that management had the right to pmhihit smoking in a place of business (US DHEW 1976). By 1985. 87 petcent of adults thought that companies should have a policy on smoking (80 percent of current stnokers, 92 percent of non- smokers). Most adults (79 percent) pnefentd as.signing certain areas for smoking and nonsmoking as opposed to totally banning smoking at work (8 percent) (Gallup 19R5). Airplanes Since 1978. it appears that more adults favor restticting smoking on airline flights. In a 1978 Gallup survey. 43 perceM of adults thought a smoking ban should he imposed on commercial airline flights (Table 27). A 1987 AMA survey reported that 67 per- cent of adults thought that cigarette smoking should not be allowed on commercial air- line flights. A 19R7 survey conducted by the American Association for Respiraa,ry Care (AARC) of 33.242 airline passengers in 39 states and 89 airports in the United States yielded similar results (AARC 1987) (Table 27). AccordinF to the 19R6 AUTS. 61 percent of respondents (R2 percent of never smokcrs. 69 percent of former smokers, and 14 percent of current smokers) ask to he seated in the no-smoking sections of airplanes, restaurants, and other public places when given a choice (CDC 19RR). I I ~ "I I a oi a O ~~pp (p. ~~O. P P P P P $a h n „ $ ~ ~ $ yw u V ~ •r{~ r+ + v' M .1 j / I 213 212 6Z69 t85tS

Condnsbns I. In the 19.5(k. 40 to 50 percent of adults believed that cigarette smoking is a cause of lung cancer. By 1986, this proportion had increased to 92 percent (including 85 percent of current smokers). 2. Between 1964 and 1986, the proportion of adults who believed that cigarette smok ing increases the risk of heart disease rose from 40 to 78 percent. A similar increase occurred among smokers, from 32 to 71 percent. 3. The proportion of adults who believed that cigarette smoking increases the risk of emphysema and chronic bronchitis rose from 50 pen:ent in 1964 to R 1 percent (chronic bronchitis) and 89 percent (emphysema) in 1986. These proportions in- creased among current smokers from 42 percent in 1964 to 73 percent (chronic bronchitis) and 95 percent (emphysema) in 1986. 4. ikspite these impressive gains in public knowledge, substantial numbers of smokers are still unaware of or do not accept important health risks of smoking. For example, the proportions of smokers in 1996 who did not believe that smok- ing increases the risk of developing lung cancer, heart disease, chronic bronchitis. and emphysema were 15 percent, 29 pen:ent, 27 percent, and 15 percent, rcspec- tively. These percentages correspond to between 8 and 15 million adult smokers in the United States. 5. In 1985. substantial pencentages of women of childbearing age did not believe that smoking during pregnancy increases the risk of stillbirth (32 percent), mis- carriage (25 percent), premature birth (24 pen;ent), and having a low-birth-weight baby (15 percent). Of women in this age group. 28 percent did not believe that women taking birth control pills have a higher risk of stroke if they smoke. 6. Some smokers today do not recognize their own personal risk from smoking or they minimize it. In 1996. only I R percent of smokers were "very concerned" about the effects of smoking on their health, and 24 percent were not at all con- cerned. 7. In 1996. about half of current smokers and 40 percent of never smokers incorrect- ly bclieved that a person would have to smoke 10 or more cigarettes per day before it would affect his or her health. R. A national survey conducted in 1993 by Louis Harris and Associates found that the public underestimates the health risks of smoking compared with many other health risks. 9. Many smokers underestimate the population impact of smoking. In 1997,29 per- cent of smokers (and 16 percent of the general population) disagreed with the statement. "Mcxt deaths from lung cancer are caused by cigarette smoking." 1(1. The proportion of high school seniors who believe that smoking a pack or mrxe of cigarctte- per day causes great risk of harm increased from 51 percent in 1975 to fih percent in 1986. I I. In 19xh. about three-quarters of adults believed that using chewing tobacco or snuff is harmful to hcalth. 12. The social acceptability of smoking in public is declining, as measured by thc proportion of adults who find it annoying to he near a person smoking cigarettes. l'his proportion increased fram 46 percent in I'K.4 to 69 percent in 1986. 13. A majority of the public favors policies restricting smoking in public places and, workcites. prohibiting the sale of cigarettes to mirwrs, and increasing the cigarette tax to fund the medicare program. Recent surveys indicate that about half the public supports a ban on cigarette advertising. S£69 TBSTS I i

the AMA's support of a policy to ban advertising-67 percent subscquently responded that they were in favorof such a ban. In contrast, in a survey conducted for the American Cancer Society (ACS), the American Heart Association (AHA). and the American LunR A.c,cociation (ALA). respondents were first informed that "some people feel that as long as cigarettes are legal, cigarette advertising should he permitted. Others feel that cigarette advertising should not he permitted." Thirty-three percent subscquently rcslxxWed that cigarette companies should not he permitted to advertise in newcpapM and magazines. There are at least three reasons these questions might be expected to evoke different responses. Firs;t, the wording prior to each question may have biased the respexndents- one to align with the sponsoring agency's policy and the other to consider the legal im- plications of such a ban. Second, the first survey asked whether cigarette advertising should he hanned while the second asked whether cigarette advertising should be per. mitteA. To the extent that some respondents may have a general inclination to answer in the affirrnative, such wording differences could influence the results. Third. the wc„+d "ban" may have negative connotations for some tesixxtdents. Two national surveys (including one sponsored by AMA) conducted 1 year later, which provided no intro- ductory comments, found that 49 percent of adults (Gallup 19R7a) and 55 percent of adults (Harvey and Shubat 1997) wwere in favor of a ban on tobacco advertising (see Table 31). A second example involves two surveys conducted in Michigan in 1986 regarding public opinion on smoking in public places (Peristadt and Holmes 1987). A survey sponsored by the affiliates of ALA and AHA in Michigan revealed that 82 percent of adults favored restrictions on smoking in public places. In contra.st, a survey conducted 2 months later and sponsored by the Michigan Tobacco and Candy Distributors and Vendors Association indicated that 82 percent of the public thought the legislature should refrain from further legislation restricting smoking. After assessing the survey methods and questionnaires, the Michigan Department of Public Health concluded that markedly different questionnaire wording and survey methods accounted for the dis- crepant results. To assist in the interpretation of the data presented in this Report, data sources are described in Table I and in the Appendix to this Chapter, and the exact (or appmximate) question wording and response choices m provided as a footnote to each table when available. Response choices, when obvious, are often omitted (e.g., simple yes-no questions). Althoughthesamequestionwordingmayheusedindiffemntsurveys,other factore may have important effects on the responses. The reader should therefore in- terpret with caution observed diffetences and trends presented in this Chapter because many of the potential factors that may affect rcsponses are not known. Z069 185I5 Trends in Public Beliefs About the Health EReds of Smoking Overview The health consequences of smoking are well documented and widely acknowledged in the scientific literature (see Chapter 2 in this Report). In 1964, the Surgeon General's Advisory Committee on Smoking and Health, after an extensive review of the litera- ture, reported that cigarette smoking was causally associated with lung and laryngeal cancer in men, was the most important caase of chronic bronchitis, and was associated with esophageal cancer, bladder cancer, coronary artery disease, emphysema. peptic ulcer, and Iow-birth-weight babies (US PHS 1964). During the 25-year period since 1964, subsequent reports of the Surgeon General have updated and extended the findings of the Advisory Committee. The purpos.1 of, this Section is to determine the extent to which this information has been disseminited to and accepted by the U.S. public. Public knowledge of the health risks of smdking' can be considered under three broad categories: whether smoking is harmful to health in general and whether smokers perceive themselves to be at risk from smoking, as rvell as the magnitude of risk from smoking and how this compares to other health risksI . `Se- cause health concerns and risks among adolescents differ from those of adults, we have i addressed surveys of their knowledge under a separate heading. For each specific known health risk noted, the section below includes: (1) a desCrip= tion of the known medical or scientific facts; that is, a brief summary of the informa- tion known about the health risk (see Chapter 2 for a more detailed description of the information about health risks), (2) a report on the trends in the public's knowledge of this fact (if available), and (3) a brief description of the current status of knowledge with respect to smoking status. This Section concludes with a sumtnary of the impor- tant gains in knowledge, the gaps that remain. the factors that may promote or interfere with change, and the relationship between these trends and the 1990 Health Objectives for the Nation. In a few cases, published sttWms have analyzed public knowledge or beliefs by wciodemographic groupings (NCHS 1988; Folsom et at. 19RR; Fox et al. 1987; Shopland and Brown 19R7; Dolecek et al. 19R6). Because these analyses were avail- able only occasionally. and because some of these studies did not control for smoking ctatus, sociodemographic correlation data are not presented below. Because smoking rates and socioeccmexnic status are inversely correlated (Chapter 5). differences in public knowledge or beliefs according to smoking status may reflect differences in socioeconcmtic status. Is CiAarette Smoking Harmfbi to Stnokers In (',enerai? In 1964. RI percent of adults strongly or mildly agreed that smoking is harmful to health (Table 2). An identical series of questicxts asked in the AU'1'Ss from 1964-75 demonstrated an increase in this belief to 90 percent of adults. Public knowlcdlee on this question increased during this period among current smokers (70 to R 1 percent), as well asamong never smokers (R9 to 95 percent). 172 1 179

~i! ~ 8 c 00 7. E a ~ ib&loa m O D a M e~ ao G Y Y oE a n } Z H 0` ~ P -0 a ~+ $ ,•, ~ ~ ~ ~ P a ~ 7 y V V 0 Z 7 P r ee 2 2 2 T P P O~ P O. p~ 7 ~ ~ N ~ F N V V V i '!. -C z Efjecn of SnrokinR on Pregnancy Outcome In 1964, knowledge of the health consequences of smoking during pregnancy most- ly concerned the increa.ced ri.ck of low-birth-weight babies (US PHS 1964). Con-, sidcrable evidence has accumulated since that time. In the 1980 Surgeon General's Report, smoking was identified as an importsnt cause of premature births, miscarriages, and stillbirths, as well as low-birth-weight babies (US DHHS 1980). From the data available, it appcaus that the public has become more knowledgeable about the effects of smoking on premature births. In 1966, 34 petcent of adults ofall ages thought that women who smoke during pregnancy are more likely to have prcina- ture babies than women who do not smoke (Table 12). Fox and coworkers (19R7) published data on beliefs about the risks of smoking during pregnancy among perscms 18 to 44 years of age. By 1985, 70 percent of adults aged 18 to 44 years thought that smoking during pregnancy definitely or probably increases the chances of premature birth. I , Only recent data are available on public knowledge of the effects of smoking on spon= taneous abortion (miscarriage), stillbitth, and low birthweight (Table 12). In 1983, 80'' percent of adults (aged 18 to 44 years) thought that smoking during pregnancy definite- ly or probably increases the risk of having a low-birth-weight baby; 74 pement of adplts thought that smoking definitely or probably increases the risk of miscarriage; at~d~ 66 percent of adults thought that smoking during pregnancy definitely or probably in- creases the risk of stillbirth. The 1987 NHIS showed that 89 percent of respondents~ believed that smoking during pregnancy "may" harm the baby. The 1966, 1985, lind~ 1987 surveys each showed that current smokers wene less likely than nonsmokers to believe that smoking increases the risk of adverse pregnancy outcomes. The FTC (1981) reviewed data from a 1979 Chilton survey and a 1980 Roper survey on public beliefs concerning the effects of smoking during pregnancy. Ri.ck of Cardiovascular Disease Among Smokers Who Use Oral Contractptivcs ' In 1964, the interactive effect of smoking and oral conttaceptive nse on the risk of CVD had not been established. The 1977/1978 Surgeon General's Report cited nxent studies showing that oral contraoeptive use potentiates the harmful effects of smoking on the cardiovascular system (US DREW 1978). Since 1978, the package incerts for oral conttaceptives have described this risk for users (see Chapter 7). It is now known that oral contraceptives or cigarettes, when used akxte, increase the risk of heart attacks twofold; however, when used in combination, the increased risk is tenfold (US DHHS 19R0). Smoking and oral contraceptive use also appear to interact synergistically to greatly increase the risk of subanrchnoid hemorrhage (US DHHS 1983). No trend data are available on the knowledge of health risks from the combined use of cigarettes and oral contraceptives. In.1985, 62 peroent of adults aged 18 to 44 years believed that a woman who both takes oral contraceptives and smokes is more likely to have a stmke (Table 12). Nonsmokers wer+e only slightly more likely than smokers to believe this (65 vs. 59 percent). Women were much nwte likely to believe this than were men (72 vs. 52 percent). In 1980.64 percent of women believed that a woman who takes birth control pills further increases her risk of getting a heart attack if she also smcdces. 1169 Z8Si5 197

ogy of smoking-induced cancers (Peto 19R6)--it waa highly likely that the relative risks for smokinle-induced cancers would have increased since the early 1960s. (See also IMII et al. 19Rf1.) Acccmdingly, there may he serious biases in the application of relative risks from 19riA.c prospective epidemiologic studies to 19Rf)C populations. Such potential biases constitute the most serious criticism of prior studies of smoking-attributable deaths. Updated epidemiologic evidence for the 19R(k is needed to address this criticism. Populations At Rlsk• 1965 and 1985 Table 2 and Figurec 1 through 5 describe the populations at risk in 1965 and 19R5. White Table 2 reports the percentagcs of snxikers, the figures show the absolute num- bers of U.S. resident adults in each smoking category foreach year. Children and young adults under age I R, who may also suffer adverse effects from cigarette use, are ex- cluded from Table 2 and the figures. In both 1965 and 19R5, n:slxmdents to the NHIS were asked,'•Have you smoked at least 100 cigarettes in your entire life?" Those who answered affirmatively were then asked how much they smoked currently or, if they were not current smokers, when they TABLE 2.-Prevalence of cigarette smnkinR, permns aged 18 years or more, United States, 1965 and 1911,5 19rr3' (%) 1905` (9F) Maks ('urrcm amnkeRc 33.4 32.7 Fowner smnhers 202 29.1 Never arnnked mRularly 25.8 32.9 Fnn.k+ CurteM amnkerac 74.t 27.s Former amrtlcerx 9.1 17.t Never unoked reRutarly 57.R 55.4 N(YTF.: P.ev.k.wle eaimawa r.. IqSS rd IORt Iwve hcew Afowur +qndwdimd ro Ihe qte di.Mbwionm of the U.S. red.km ".latinna in e. h ye.r. ie.peclively (11.s. nwew of Ihe Coea.. 1974, IaIK). •Raaed ury+n ~z.ft7 t.eu•mqrunr. b Me r~.rellr SmnhinR Suryilemrnl hr the IOM1S NNie.ul tle.hh 4uerview suney. Sra.wlarvl crnva n. ~ rr, n.a ~~ rrr m.ka, o. l h, 0.2 ferctn~ fiv ftnuk.. tnclw~itm nf ~~,a22 r1Ai~iMql pm.y reyrvva n•avhm in the fnl/nwinE taimalec: nyk ewrenl .nnken, 51.0 PeftTrot: nyk f„mer y,u*c M. 19.11 pncent fernak c.r.enr amnkera. t ~ R~~: ~ fe.n.k ri.nrt amnkera. 7.7 paeerM. r'na.eA ufw.n 12.f1tv.vlf n•., - w,.t •aothe CiR.rene SnwdinR %upriIenoe.M to Me IVIIS Nalinnal Heahh Inierview Sur.ey tuiwlanl e.nw. n 1~.cr,a r.. nuUe., ll, t~ fnr femaka. ' In t~N~t, cwxn~ anw.ier. u.clwlM all repr.rkvwa wM. n:ry.ad 0 eMrenl uwMnr wnudeeA trr day, indudinR'ku than I pe. Aav.- In I"a, ,ir+aw.n"ert inchwkA.N Myr.wlrMa whn rAawemd affineall.ely In die quemiem'De y-tv ..M-ke m.w?' . d Int.wh Iahta.ll'dlt,rhreM" +.y'never.nM+4..IrrRularlv"incturlrQfwv.Rnwit nfrequwkkM.: (1)tMwewhe rnwr.r.l ncealivelc i.s thr qurup.n 91ave y.w r+. cr .ml ked al lre.l I/MlciprrNn tu yew ad (2) fhne a'hn .nawerr•d allinnahvelv 1MN.knitrl r-ve..nM.kinF.iranyka rc*nl.+rlv. In a4/1S.nA 1995. rr.trclively, Rmur I aarrMli fnr IF1 per. rM ad 007 LyierN ,q all royr.n.k~x. m thc cawR..rv "nrver qo..hayl Rplxtt ' last smoked regularly. While the NH1S for 1965 permitted proxy respondents, the es- timates in both years have been derived from self-respondents only (see Note h of Table 2). Tahk 2 shows the percentage distribution among adult men and women in three categories: current smokers, former smokera, and those who never smoked regularly: Between 1965 and 1985. the proportions of current smokers declined and the propor- tions of former smokers increased. The most marked change was the decline in the prevalence of current cigarette use among adult men. In Figure I, the responses have been further divided into four categories: current smokers of fewer than 25 cigarettes daily; current smokers of 25 or more cigarettes daily: former smokers who quit within the last 5 years; and former smokers who stopped for more than 5 years. The weighted proportions in each category, tabulated by age and sex, were then multiplied by the corresponding estimates of the U.S. resident pnpulation (U.S. Bureau of the Census 1974, 1986). 4 In 1965, there were an estimated 53.7 million adult current cigarette smokers (stano- ard error. 0.2 million), which reprtsented about 43 percent of all U.S. residents aged I R years or more. By 1985. there were an estimated 53.5 mil l ion adult current smokerx, comprising 30 percent of U.S. adults. While the total number of current sfmokers stayed about the same. there was a shift in their distribution by sex. The number of adult male current stnokers declined from 31.7 million (53.4 percent) in 1965 to 29.2 million (32.7 percent) in 1405. while adult female smokers increased from 22.0 million (34.1 pef- i cent) to 25.3 million (27.5 percent) (Figure 1). In 1965, about 2R percent of adult male smokers who were nonproxy respondents to the NHIS consumed 25 or more cigarettes per day (Figure 1). By 1985. this proportion had risen to 32 percent. For women, the proportions of heavier current smokers rose from 14 percent of nonproxy respondents in 1965 to 21 percent of smokers in 1995. The true population prevalence of smoking 25 or more cigarettes per day in 1965 is somewhat uncertain because theeliminationof proxy respondents may make the sample nonrepresentative. As shown in Chapter 5, however, there was no significant change in the proportion of heavy smokets between 1974 and 19g5. By contra.ct, the numbers of former amokers increased substantially between 1965 and 1985. Thus, in 1965, there were about 17.6 million adult former smokers (12.4 million men and 5.2 million women). By 1995, this number had risen to 40.9 million (25.2 million men and 15.7 million women). There was an increase in the proportion of former smokers who had stopped for more than 5 years (from 49 to 63 percent of male former smokers, and from 41 to 57 percent of female fonmer smokers) (Figure 1). Cigarette Smoking and Other Forms of Tobacco Use Figure 2 shows the 1965 and 1985 adult populations broken down according to the type of tobacco used. In 1965, the NHIS included questions on cigar and pipe sfnok- ing as well as cigarette use. The 19R5 questionnains inquired only about cigarctte smok- ing, However, questions about all forms of tobacco use, including smokeless tobacco, were included on a supplement to the 19R5 Cwrent Population Survey, perfimncd by the U.S. Bureau of the Census (see Chapter 5). 112 / 1 111

fiE69 I8STS TABLE 32.-Trends in public opinion concerning cigarette warning iabels Percentage who agree by smoking status Current Former Never All Survey Year Reference smokers smokers smokers nonsmokers All adults Cigarette advertising should NOT be reouued to cartY a warning statement I• AUTS 1964 US DHEW 1969 38 2. AUTS 1964 27 19 21 28 Ciguette packages should NOT be required to carry a warning stmment US DHEW 1969 42 27 21 22 30 Cigarette advertising SHOULD BE required to carry a warning sutement 3 AU r3 1970 US DIi>EY 1973 83 • 90 91 91 88 \pM- Actuat qutaoons: I. Cigarette advatising or commeteiau should not be tequind to carty a waming statement to the effect that smoking may be harmful to healtA. (suoagly agree. mildly apee, no opieioe. onldly disagree. strongly disagme) 2. Cigatetts manufacturers should nw be tequued to put an the outside package a waming latal lilu "Cigruene smoking is danaerau to heatth." (snongty apee, mitdty apee. no opinion. muWly disagtce. stsonSly disapeq 3. Cigarette advertising or commncials should be required to carty a warning statement to the effect that smoking may be harmful to healft* Petcentaaea include ttwn who ••suon6ly app" or °ntildly apoe.' TABLE 33.-Trends in public opinion about increasing cigarette taxes ' Taxes on cigarettes should be increased (percentage who agree by smoking status) Survey Year Reference 1. AUTS 1964 US DHEW 1969 2. Roper 1970 Roper 1978 3. Roper 1972 Roper1978 4. Roper 1974 Roper 1978 S. Roper 1976 Roper1978 6. Gallup 1977 Gallup 1981 7. Roper 1978 Roper 1978 a• Gallup 1978 Gallup 1978 9. Gallup 1981 Gallup 1981 10. AMA 1987 Harvey and Shubet 1987 NOTE: .a.tual auestione: Current smokers Former smokers Never smokers All nonsmokers All adults 14 33 44 42 30 20 46 36 13 44 32 14 42 31 12 46 33 39 16 50 38 45 57 45 23 59 46 75 so 79 1. Tues on cigarettes should be much higher than they aro now. (strongly apse. mildly agree, no opinion. mildly disapa, sttongly diupee) :-5. 7. The tu on cigarenea should be sharply increased to reduce their sale. (apee• disapee. don't know) 6. 9. Do you think federal and state ta ea on ciguetsea shouW or should not be incteaaed? g. Do you think the present 8«nWpack Federal tax on cijucttes should or should not be increased? I0. Would you favor or oppose an increase in the tu on tobacco pmducts if the money from the innesn war to Medicare? . Petcentages include those who'suonfly agtee' or"mildly agtea'

TARI,F 6.-F,stimated relative risks for current and former sfnekers of cie:Ircltcs. makc aAed 35 years or nMre.4-vear (1992,-86) fo(Irlw'up of American Cancer Cnciety SQ-State study (CPS-ti) l ImkrlyinR cauce nfrkath Curtent anw+keraa Fornrcr arrNrkelc' All t•:wcec 2.34 (2.26-2.43)t' N5, ( t-1.61)h ('lll).aFc>l5(4In-4141' 1.94 1.41 (1,1U1..2.08) (I.3t-1,50) C'11f). apc 15 64'1(41(1-414) 2.91 1.75 ( 2.49-.1.1 R) 11.55-1,99) ('l lf)• are ?65 (410-414) 1.62 1.29 (1.4R-1.77) (1.2f,-I.'(It) Other Hean niKace` ( WO-.tqR, 401-405. 41S 417.420 4211 I,RS 1.32 (I,1R-1.4R) Cerchrova.cular I.e\inrrs. are 215 (4 t(1 4t9) 2.24 1.29 (I.RR-2.67) (1.I(1-(.51) Cerchmvascular I.ecinns• age 34-M (4:1441R) 3.67 1.39 (Q91-2.(17) Cerchmvascular I.e\innc, aEe N.S (430-4 tR) 1.94 1.27 Other Circulatory Diceacer(440-IIR) (I.SR-2.zR) 4.06 ( I.Iq-1.V1) 2.33 ( 3.(MI-5.33) (I.RI-3.n1) (Y)Ph 090-492 4961 . 9,65 9.75 (7.(10-11.30) (CrAR- I 1.R0) (hher Rec 'rau.ry ()ice,•ISeR(010-4112, 99 1 IS6 490 ax9,i) . (1.52-2.61) 11.25-1.95) Cancer. l.ip. Oral C„vity. l'harynx (140-149) 274R 9.90 (9•96-75.93) ( i.15-24_S9) Cancer. Fcr>pllaRuc (150) 7.69 S.R t (3.91-15,17) ( 3.(12-11.25) ('arner. r.lm rca. (157) 2.14 1.12 (1.h2-2.R2) (o.W1.45) (:mcer, 1aryns (1h1) 10.4R 5.24 (},61 • :1f1,4•1) (I.N3-1499) ('ancer• l .une 1 I t.2) 22.16 936 (17.77-2R.13) (7.4 3-11.77) Canl cr. Kidney 1 I 99) 2.95 1,(05 (1 V2-4,S4) 11.31 -2.90) Canter. Rlackkv (Nhrr Urinary C>-Rans ( IRR) 2.R6 1.90 (1.R5-4.44) (1.2R-2.R2) N(/l I~ 1lrhmimrv e.limateh, hsarl ury.n I•4V I,791 man~ yean nf espx,dre mxmR male auhircla whn nrver.rmkrrl rl'KrA:nlv, rr wMr ~nxrl.rrl.nllv cr/arrllr., PNr'~ M~ri.l Relalivr riska, e•limated wnh reywct In mrn whr. Mver snxAnl .mrxtary, have Irrn clmt IN .I.wrlanhnr) to the are rkrtrfhMmn nl all man.yean nl raryxnrc. 'Nrlr•r. u.. q-aretle "xdinR .lalus M rnnrlhnrnr (.SepN'mM I91121. '.Nunrlr•r. m I.arenthrw~ ,1rr• Q{ lrenrM Crwlfirkncr Infrrvalt. pyn(ruerf fM11he a"wmtMinn that the InRarirhm nf rrLrh.e u~- wxa nrwmallv.Mlnhntnl Alt .hva.e r rrk. rru•r to IrMmalirnal ( IaavlfKNirm r41);.eava. Nin,h RevisiMl. nWtr-w.m a" r.'xrr,• r. rrv- ~1 rrlem In111e are at ermdlmelN in 1'tlt! 'ImIrxw•.Ilvry•nru.rce 1h•an hr.~:w•IJ(11 .d1t11. r6ehxlP\AIYIx Arw•xr, .m.Mrr Cvl.hlhlx',arxl(wiKralAnrrin.eknNia14411441). 'I14 4MM, IntI1N•n/.r .m.I PrN•rmxnx•I I.ItNI 497(, \r rl Itl-1~. ('nlrrldr.lx.l l.d+rl.xxm~. Anw•rx;m( :xm•~rGriyv. TARLF, 7-F;stimated relative risks for current and former ciRarette sm(-lcers. females aged 15 years or more. 4-year (19R2-86) folMwup of American Cancer Society 511-State study (CPS-11) llmkrlyinR cause of death Current snaken' FnrrrKr tmnkere Altcauses 1.9(1 h 11.R2-1.9R) I.t2 ( I .27- ( .171h CIID,age 235 (410-410 1.7R (1.62-1.97) 13) (1.19-1.44) e 35-M 11(410-A 14) a CHD 3.n0 1I4l g , (2.50-3.39) CHD, age 265 (410-414) 1.6(1 (1.42-I.Rl1) 1.29 (1.16-1.43) " 1.69 1.16 4( 11odier-dOHS 41ad1~420429) (1.44-1.99) (L Cerehrosvascular Lesions, age 235 I.R4 56••2.161 (1 1.06 lo xR-I:~'h ( 4 311•-4?R) . age 35-64 lar Lesions h 4.80 1,41 94 0 11) 2 , rovLScu Cere (41(" 1R) (3.52-6.54) - ( . . Cemhrovascular Lesions, age 263 1.47 (1.19-I.RI) 1.01 (0.R3-1124) (4MI-4lR) Other Circulatory Diseaser (44(1-448) 11.00 (2.20-4.0R) 1.34 (0v5 -1.9K-) C()pD (490A92,496) (0.47 (7.7111-14,09) jS0..t3-9.301 DisseascR i t h 2.1% 1.}R R4 I 4 orY ra er Resp Ot (01(1-(112.41(04R9 493- (1.60-2.97) ) . - l L11 Phuynx l Cavit Li O 5.59 2.RR S 26) 7 y. ra Cancer. p. (14(1-149) (3,13-9.91) • - (1.S Cancer, Esophalnn ( I SO) 10.23 (4.94-21.27) 3.16 (1.45-.6.113) Cancer. Pancteaa (157) 2.3 (1. 7-3.OR) 179 (1,37-2.301 Cancer, Larynx (161) 17.78 (3.45-91.74) II.RR (2.46-57.34) 94 11 4.69 Cth+cer, LunE (162) . (9.99-14.26) (3.R6-S.70) 14 2 1.94 Cancer, Cervix Uteri (180) . 11d16-4 70) 97-3.R7) 41 1 1.16 Cancer. Kidney ( IR9) . (0.R6-2.30) (0.72-1.R7) Cancer. Rladder, (Aher Urinary (kgans (1 RR) 2.SR (I.31-S.OR) I.RS (1.(M1-.1.42) Mr1fR: Aelirninary euknales. Mved qqn 2 41R.9(19 wanan'yers ef eapacwe anw+n~ kmak wAjccra who never umlked 1'!puM who NlNlked mlly ellUlON. Qre~eM M~l1. Relative risk{, eatimared with eeslect in wmnen who Mversmnkid n.yrolary, Mve hetn direcdy aandardired In the age distrihutinn of all wnman- yean of ec"ure. 'Rekn In ciFarene qrmiulR uans at enmlhnenl(Selrlemher 1992). ''Numhen in prrnlhe.es are 9S.perteM eonfidente inMCrvah, cnnqMt:d an the asswrqtMn that the hrprilhm of relative riak was mremally diariMMed. ' All Ai%ra.e cndea /ekr In tnlemaliwwrl C1aarNieMiar of Diqeaqen, Ninth Reviiien. "When an alte ran)te is Riven. it refen in the Ke at enndlment in 19R2. hnclwks llypertenaive Ikan Duease (4111-4)1). /IncMeks Arwuc Aneurm. Nnn•SyphiMic. and Genrnl Anerilnekruaia 14" 11. hMlurki Inllurnra and PeKwrrmia (411M1497). S(N IR('E: C InpnMi~IrA ulwlalitm. American Cancer Sa'itty. 8889 iBSIS Iqt 1S)

CONTENTS Eb69 t8STS Introduction .......................................................263 Part 1. Changes in Smoking Behavior .................................. 263 Trends in Cigarette Smoking ....................................... 263 Introduction ............................................... 263 Nature and Quality of Data ................................... 2tj4 Excise Tax and Saks Data ................................ 264 Self-Reported Survey Data ................................ 264 Validity of Self-Reported Survey Data ....................... 265- Correlation Between Self-Reported Survey Data and Sales Data ........................................... 265 Trends in Cigarette Sales ..................................... 207 Trends in Smoking Prevalence Among Adults .................... 367 Cigarette Smoking by Sex, Raoe (Whites and Blacks), and Educationitl Attainment (National Health Interview Surveys: 1965-l17) .... 267 Adult Use of Tobacco Surveys: 196446 .................... 211 Cigarette Smoking Among Different Oocupstional Groups ......Z72 Special Populations: Hispanics ............................ 274 Special Populations: American Indians and Alaskan Natives ..... 274 i Special Populations: Asian Americans ...................... 275 Special Populations: Pregnant Women ...................... 275 Special Populations: Military Personnel ..................... 276 State-Specific Smoking Prevalence ......................... 278 Behavioral Risk Factor Surveillance System: 19g2-87 ...... 278 Current Population Survey: 1995 ....................... 27Q BRFS and CPS Comparison ........................... 291 Summary ..............................................2R4 Trends in Quitting ...........................................2R5 Introduction ............................................2R5 Trends in the Proportion of Smokers Quitting (Quit Ratio) (NHIS) 286 Smoking Continuum (AUTS) .............................. 286 Summary of Trends in Quitting ............................ 292 Trends in the Proportion of Smokers Who Are Heavy Smoker:e ....... 292 Trends in the Initiation of Smoking ............................. 296 Age of Initiation ........................................ 296 Prevalence in 20- to 24-Year Age Group ..................... 300 Trends in Adolescent Smoking ................................. 02 NIDA High School Seniors Surveys on Drug Use. 1976-87 ...... 302 1987 National Adolescent Student Health Survey .............. 306 US DHEW Teenage Smoking Surveys. 1968-79 ............... 307 NIDA National Household Surveys on Drug Abuse, 1979-85 .... 312 Summary ..............................................3t3 Changes in the Types of Cigarettes Smoked ...................... 313 Filtered Cigarettes ........................................ 31.3 261

through 9. Surveys are filled out in class by students under a teacher's supervision. The topics addressed are totated so that the same survey is repeated every 4 years. The Spring 1996 survey covered safety and health (Weekly Reader 1986). Of an estimated 400.000 student responses for grades 2 through 6. 128,000 were randomly chosen for analysis. Although the respondents do not represent a randomly selected sample, results pertaining to tobacco are presented here because of the large sample sin and the paucity of data available for young children. The survey included the following question: "Many people say the following things an; harmful for kids to do, How harmful do you think each is for kids your age? (very harmful, somewhat harmful, not harmful)... oveneating, eating junk food, listening to very loud music, smoking, chewing tobacco, staying up late, failing to get enough ex- ercice." Grade-specific results for students in grades 4 through 6 showed that smoking (90 to 95 percent) and chewing tobacco (80 to 90 percent) were much more likely to be perceived as "very hartnful"compared with the otherchoices, all of which were con- sidered to be "very harmful" by less than 40 percent of respondents (except for loud music, among fourth graders-70 percent). However, these results should be inter- preted with caution because of the possibility of sampling bias and the leading nature of the question. Addiction Of particular concern are teenagers who ate unaware of the addictive nature of cigarette smoking, and who, therefore, may be tempted to "experiment" with smoking. In the 1974 and 1979 DHEW Teenage Smoking Surveys (US DHEW 1976b, 1979b), about one-quarter of the teenagers agreed with the statement,'Teenagers who smoke regularly can quit for good any time they like." About 60 percent agreed that "It's okay for teenagers to experiment with cigantttes if they quit before it becomes a habit." In the 1979 survey, teenagers were acked, "What would you say is the pos.cibility that 5 years from now you will he a cigarette smokeft." Fifty percent of the current regular smokers (48 percent of boys and 52 percent of girls) answered "definitely not" or "probably not." These findings suggest that a large proportion of new smokers are un- aware of or underestimate the addictive nature of smoking. In 1975. S6 percent of girls aged 13 to 17 yeats and 62 percent of young women aged 18 to 35 years thought that smoking was as addictive as illegal drugs (US DHEW 1975a). In the study by Leventhal. Glynn, and Fleming (1987) of 895 students in grades 2 through 12 in Milwaukee. WI, subjects were asked how hard it is for heavy smokers and for light smokers to quit smoking, and how heavy and light smokers feel when they quit. Answers were used to construct a "knowledge of addiction" scale. The inves- tiFators found that young people who smoke or who have smoking family members have lower "knowledge of addiction" scores. The authors speculate that these in- dividuals may he "defending against the thought that either they or a parent has an un- controllable problem." Information on teenage beliefs concerning the addictiveness of ST use is discussed below. ZZ69 I85tS Smokeless Tobacco Use In 1985, the Office of the Inspector General, Department of Health and Human Ser- vices, surveyed a nonrandom sample of 399 students in I 1 juniorhigh or middle schools and 20 high schools in 16 States regarding ST use (US DHHS 1986d). ST users were oversampkd based on identification of users and nonueers by school officials. The sample was composed of 290 current ST users (73 percent) and 109 nonusers (27 per- cent). Eighty percent of junior high school users and 92 percent of high schookusers acknowledged that dipping snuff and chewing tobacco can be harmful to a petccm's health (Table 20). When asked about the extent of physical harm that may result from ST use, however, about half of users believed that there is no risk or only slight risk from regular use. One-third of junior high school users and only 5 percent of high school users thought that ST use may lead to mouth cancer. There was poor under- standing of the effects of ST use on gum and dental conditions. One-quarter of junior high school users believed that regular ST use is not addictive, and more than one-tliird did not know that snuff contains nicotine. In summary. these findings suggest that u.c~rs are substantially uninformed about the health effects and addictiveness of smbkeless tobacco use. However, the degree to which these results can be generalized national-11 ly is limited by the nonrepresentative nature of the sample. 1 Data from the Monitoring the Future Project showed that in 1986, a total of 59 per- cent of high school seniors believed that regular ST use poses a great (26 percent) or moderate (33 percent) risk of harm, compared with 36 percent who believed that'ST use poses slight (28 percent) or no (8 percent) risk (Bachman, lohnston, O'Malley 1987). Constituents of Tobacco Smoke The estimated number of known compounds in tobacco smoke exceeds 4,Q(10, in- cluding some that are pharmacologically active• toxic, mutagenic, carcinogenic, and antigenic (Chapter 2). One of these is carbon rnonoxide, whose presence in cigarette smi>tce is cited in one of the four health warnings rotated on cigarette packages and ad- vertisements since 1985 (Chapter 7). In a 1979 survey conducted by Chilton Recearch Services for the Federal Trade Com- mission (FTC 1981), respondents were acked, "Does cigarette smoke contain carbon monoxide?" Fifty-one percxnt of teenagers (aged 13-1 R) either did not know (21 per- cent) or said "no' (29 percent): 45 percent of adults (aged 29-31) either did not know (26 percent) or said "no" (19 peteettt). In a 1980 Roper survey (FTC 1981).53 pacent of all respondents and 56 percent of smokers did not know or believe that "Cigarette smoke contains carbon monoxide, which is a dangerous gas." In the 1996 AUTS, 62 percent of current smokers answered "yes" to the question, "As far as you know, does ciganette stm6ke contain carbon monoxick?" Thirtcen per- cent said "no," and 25 percent did not know. Former and never smokers were not asked this question. 216 217

\EUR,\T11. r B.. hU\.rER. Nt.. nRTll. D.. PEM F.G. Tran.-!'-htdrmtcotinine a. a main mctafxrlite in urine of .mokcrt. hurrnuri.rnal arf hh rt .r/ f)r t re/rrni.mul ,rnd F.rn irvmrNrrnul Hrrr/tG 59: I1r''_'(n I. 19x7. NIEBI RG. P.. \I:\RKS. J.S.. N1CL.aRE\. N.M.. REMINGTON. P.L. The fetal tobacco t, ndrnmc. /.nu ru+l .4 the.inrerir rra lfrflif fll.1, vN iuNnn ?i•i, 2(/1:'99x-?y99, \1at ?J-i 1, 14Xa. ~II \\OI II~FR. D.E. Cigarette .mnAing. lunc inllammatinn. and the (Ictclnpmcnt of em- ph%.cma .l.rnrrr.+l ../ l.rdNnur.n t frrrd C/iqif (ol tlrJif inr 1(1:1 5-'7. 1999. NIF.\\Y)CIIM:R. 1) E.. KLEMERM.aN. 1.. RICE. D.R. PathoMgic chamw% in the I+criphcral arrttat. nt tfwn!! cit!arcttc .makcr.. \ru F•rr.l,nr,l.l..nrnul../ l/rvb, rrrr '91f 14;r:75t.-7ix, 1471. \t-)R\1.\\. V. (-h:mect in.mn{,c chcmi•tr% of mfxkm (tat cigarcttet. Rrfrnt.irA(+rurt in l..ltirr , n St irn, r• X.11 I-177. 1992. NOW.\K.1.. \ICRR.-\Y.1.1.. O.aTES.).A.. FIT7GF:R.ILD. G.A. Rirxhcmical ct iclcnce of a chrnnic ahnnnnahtt in platelet and ta.cular furclinn in hcalthy indi,idual. ttho.mnhe ciparctte%. Cirf nlr+tirrrr 76(1 I:I+-1 J. Jul% 1997. f001. W L.. F.LSTON. R.C.. CHEN. V.W.. B;\ILEY-WIL.SO\. 1.E.. ROTHSCHILD. H. In- crea.cel familial n.k for lung cancer. Jnurrrul rr/thr \'a+i.raol Cmrrrr /rrvinur 7f+t? 1:'-17-,,, Fchnrar\ 14Xh. P.>TH,\K. D.R.. S.\\tET. J.\1.. HL'\1BLF.. C.G.. SKIPPER. R.J. Determinant% nf lung cancer risk in ciparette tmnbert in \ett \1e\icn. Jrrnrrrnl rr/ Nrr Aulinnr+lCun, rr /rrtrirnrr 7t3t J/:597- h(/J. .\rnl 14Xf,• PE.1RSf)\. T.A. Coronan arteriograpM- in the .tud% of the epideminlog~ nf coronan anen cli.eate. FlrirlnNinln,•ir Rrrirrr, 6: IJ(t-IG6. 1994. PFRSII.\GF.\.G.. HRLBEC.7..SVE\SSO\.C. Pa..ite%mokingandlun¢cancerinSaedi.h tt rnncn. .I nrrri, nrr .Arnrnul rr/ F.Pirle•rrrinl.rer L'tr I 1: t 7-_'1. Januan 1997. PETITTI. D.R.. \\'I\f;ERD.1.. PELLE(iRI\'. F.. R.aNICH.aR.a\. S. Ritk o(,a.culardi+ca.e in tt,t,ncn: Smohinc. oral crxnraceptite.. noncontr.•tccptitc e.troncn.. and other factnr.. /onrrarl.r( rhr .anrrri, urr .Ntdif nl.a ~„a iutinrl ?1?t I I r: I I S(L-I 1 SJ. September I J. 1979. PETO. R. Ot cr, ictt of cancer time-trend .tudie% in relation to chance% in cigarctte manuf.•te- ture. In: 7arid>•c. D G.. Peto. R. /ed../ T.Ixu r.,: :1 .Nujr.r /nrrrrunwnrrrl Hrdlth llu:urd. L\RC Sciemrfic Puhlicatitm. No. 7J. Lton. France: International Acenet for Re.earch on Cancer. 14xf,, pp. ? 1 1-„(r PETO. R.. rX)LI.. R. Ke, rnne acklre..: The control of lung eancer. In: \1i~ell. \1.. Cnrrea. P. fcd.. r l.rur; Crnn rr (-urrtr, (+nr/ Prrt-rrninn. Pr.N rrdirret .rrdrr Irrlrrnuri.rnul Lrmt Cum , r•r I/qGrlr (.rnJrr rrn r. \et, (hlcan.. Lnuiaana. \larch 3-5. 1984. pp. 1-19. Pf:TO. R.. Ix)1-L. R.. Bl ('KLEY.I.D.. SPORN. M.B. Can dictar, hcta-carotcne materiall, rcduccc;unccrratc0 .\umrrMarch 19. 1991. PET(). R.. SI'E17ER. F.E.. COCIIR.\\E. A.L.. MOORE. F.. FLF.TCHER. C.M.. TINKER. C.\1.. HIGGI~S. I.T.T.. GRAY. R.G.. RICH.\RDS. S.\1.. (iILLIL.a\D. 1.. \OR\LaN- S\111 H. B. The rclrt;mcc in adult% af air-Ilna nh.tnKtion. hut not nf muw. h, prr.ecrctron. tm mortalit, frnm chronic lunr tli.ca.c. Rc~ultt fn,m _(1 tcar. uf pm.ptYti,c nh.cnation. Irnr rir urr Rr•f rr n../ Rr y,irrrr.rrr I)itro,r 1?Xr Zt:~41-ift l. Scpt~mhcr 19x 1• PII-LSRI RY. FI (•.. BRI(iHT. ('.C.. O'('O\\OR. K.1.. IRISH. F.W. Tar and nicntinc in ciparcttc •mn{,c l.rnrnul a/ hr a„r,r irninrr n/'ONif iul:lrruAti(ul (Yrrnritr, 32(3 1:d5X_16:. \1at 1969. Pn\1REF1\. P.. Dl \CAN. l; .\\'F.ISSFFLD. L.. \\':1LLACF.. R.B.. BARNES. R.. IIEISS. ti..FKF.L1 ~1).L.-(~..('Rlql L V.11..1OH\SO~.~..CN:\\11iLF~S.L.E. Thca..nt•iatinn ,dd~.lilwrPrntcirxrma,tithamptnm.anfl.it'n.fd~riPlxr:d:frhri:ddi.ca.c: ThcLipidRr- .rart•h ('linrc. ('rn..•ram I'trtalt•ntc Stuft%. !'nr nl,+n, rr 71tSu~hkmcnr I r:l-I(Nr. 14196. POOLING PROJECT RESEARCH GROUP. Relationship of blood pressure. serum chnle.terol. mokin¢ hahit. relathe Ueight. and ECG aMtonnalitie< to irkidence of maior coronart et ent.. Final report of the Pooling Project. Jrrnrrerl rrlChrrNrif Di.tt•nnrc z I t.t c`1 t 1- t(K,. .alxil 197R. R.1. REl'NOLDS TOB.aCCO COMPANY. C/lrnnt dl UlHl81f11r1t1t'UI S/II/I/rS fNl Nr1, Ci t,+rrrrr PrwNrlrrc Tlrfn Hrfrr lnsrrfltl rN Burn Tfr/+uct•e). \\'incton-Sa1em. North Carolina: R.1. Re, nold. Tobacco Compant. 19RR. R.\NT.aK.aLLIO. P.. KOIRANEN. M. Neurological handieaps among children,t ho.e mr,thera .mnled during pregnanc%. Pr•rtrnrit•r Mrtlit-inr ati:597-bqfi. 1987. R.\l T.aHARlI . P.\L. PRINEAS. R.J.. EIFLER. \\'.1.. FURBERG. C.D.. NE.aTO". 1.D:. CRO\\•. R.S.. ST.a\1LER.1.. Cl•TLER. J..i. Progno•tic s alue of eserci<e electmcardioeratn in men at his:h ri.k of future coronary heart disease: Multiple Risk Factor Inten ention Tri:d e\Ix ricnce. Mnrnul rrl thr .Arrrrr•irtln Cf+llr4r fN C,Irdinlrrtrc RI I r 1-IR. luly 19R6. RI\"ENSON. .\.. HOFFMANN. D.. PROKOPCZI'K. B..AM1X. S.. HECHT. S.S. .> ctud. of tobacco carcinogene, i. XLII. Induction of lung and pancreas tutnorn in F344 ratc M tohtt( cn-.pecific and arcca-deri, ed N-nitro%amines. C.nrrrr Rrvwrh. in precs. ROGERS. R.L.. MEYER. 1.S.. SHAW. T.G.. MORTEL K.F.. H.>RDENBERG.I.P. Z.>Ib. R.R. Cigarette smoking tlerrea.e% cerebral blood tlo.• suggesting increased risk for troke. Jnu+,rul fif Ir,r.anlrritfnl I/rdif u/.accrKiurirrn'-S(1t'(11.^_79G-'R(1(1. Nocember 25.1993. ; ROGERS. R.L.. MEYER. J.S.. JUDD. B.\S'.. MORTEL. K.F. ABdemion from cigarette .mol:- ing iml+ro,e, cerebral perfution among ekkrly chronic smokers. Jnnr•nal frl rrrr .amrritlfm l/rditu/.atsrH ifrrinn 35~t_'l)r_'97(1-=971. .Mav :4-s1. 1995. RONXES'IK. P.K.. GUNDERSEN. T.. ABRA.aS1SEN. A.M. Effect of smoking hahit< ar~d ~ timolol treatment on nxtrtalitt and reinfarction in patients surviving acute m%ocardial infarc- tion. Rr•irislr Heart Jrnr•nul SJt?/:1 3J-1 39. August 1910. ROSENBERG. L. Ca.e-comrol.tudiecof risk factors form.ocardial infaretion among ttorrnrn. In: Eaker. E.D.. Packard. B.. Wenger. \.K.. Clarkson. T.B.. Tyroler. H..>. led..t Cr,r,rnur., Hrur•r Diirusr in It rNrrru. PrrK rrdirrs•. rN'un \'.LH. tl'rarlshrN+. 1910. pp. 7(1-77. ROSENBERG. L.. MILLER. D.R.. KAMAN. D.W.. HELNtRICH. S.P.. \'A\ DE CARR. S.. STOLLEY. P.D.. SHAPIRO. S. ML•oeardial infarction in ttomtn under i0 %ears t+f ace. ./nurrra/.ff r/rr.lnrrritfulllrtlitdf.~~aKiurirNr:V1t'_(1r.-'R01 'R(1G.\oteml+er'_S.19Rz. ' RI'SH. D.. CASS.a\O. P. Relationship of cigarctte anoking and social class to birth ,t eight and perinatal m0rtality amcN+g all births in Britain. April 5-I I. 197(1. JrNU•nul nf•Fhidrmi.d- .rcr unJ C•Nnrnwrirc Health =7:_19-:«. 19R3. S.aCCO. R.L.. WOLF. P.A.. BH.iRI'CHA. N.E.. \tEEKS. S.L.. KANNEL. \\'.B.. CH.>RETTE. L.1.. NICN.aNI.aR.A• P.M.. PALMER. E.P.. D'.aGOST1NO. R. Suharachrnvid antl intr.•tcerchrd ht•mtxrhage: Natural hiaca.. Prognnsis. and prnur•i,e t:x•tor• in the FraminehamStudc. ~rrn./r+er?Jt7r.RJ7-R~a.July 19Ra. S.\LONEN.1.T.. Pl SKA. P.. Tl'OMILEHTO.1.. HOMAX. K. Relation of blood pressure. .rnmt lipid.. and .nud.ing tto the risk of cerclxal stroke: A longitudinal ctud% in Ea•tcm Fin- Icuxl. Sn,,Ar I?t?ri'_7-zti, \1a% -lune 1982. S.a\IET. ).\l.. Hl•\1BLE.C.G.. P.aTHAK. D.R. Per.onal and family hi.torm ofrr•pir:non di.- ca.e cmd lung cancer risk. .anlrrirrrn Rrt•irN• rN Rr.qririnfN;r Di.crfrtr 1344 ?ra6h-J'•11, Scp- tcmhrr 19Rh. S:\\IET.1. \I.. Ht' MRLE. C.G.. SKIPPER. B.E.. PATHAK. D.R. Hi.tory of re•idetxe and lulle cancer risk in \c,t \le\it•a. .arnt•riturrJrNrrnuffr/'FPiflrlnirdnt)• 1'_St{r`n>tt-;tl I. ItrX7. S:\\SET.1.\l.. NI:\RBt Rl'. \I.C.. SPE\GLER. J.D. Health effect. :mtI tntrcc• of intloi,r air pollution. Pan 1. .-Imrr if url Rrtiru af Rry'in+rnr, Di.ruxr 1?b: I a'(6-•I 5lt.`I. I't`17. 8989 T8SIS f ,,. 1 r 11

I TARI,F, 19.-Perceived harmfulness of drugs among high school seniors,19R(S, Monitoring the Future Project, National lnstitute on DruA Abuse effects of cigarettes have been exaggerated" (see Table 24; Bachman, Johnst8n, O'Malley 1987) (data stratified by smoking status were not published). 1 k+w nnkh do you think /tevtpk ry"k hmmins ~ffifteh'". (Phr. Kally or in other ways). if Ihey... (rercentalte of pet~tle resltttndinR) Great riak try one or tw) Arinks of an akoholic heveraRe (hex., wine. liquor)? try maripnna (rnt, Rrna) once or twice? take one or two drinkx nearly every dayl smnke marijuana occasionally? try aml4wtaminea (uppers. pep 011%. hetmies) sIwed) once or twice? try harhianates (dnwnen. Rrxdhalla. reda. yelMwa. etc.) once or twice? u.a .mokekm tebaeen rmul.rh (ehewtnR tnAsete, ploR. dlDpMtR tnbacco, uwm? try cocaine once or twice? have five or mexe drinks once or twice each weekend? try 4CD once or twice? try heroin (smack, htxme) once or twice? take cocaine occasionally stndce one or ewtar paek. of ctRarettes per dq? take amphetamines regularly? take barhiturates regularly? take Gror or rive drinka nearly every day? take heroin occasionally? vnnke marijuana regularly? take cocaine regularly? take LSD regularly? take heroin regularly? N(tTF,: P*.iMe Rary.ne. ind.d[d `r~e.t ri.k. nw+derNe riel,.IiRht ~ia, m+ri.k. dnn't knmv. C()t tRCt? Raclnnan. J..hnatan, p'Malky (1aa7). tional Institute on Drug Abuse) forevery yearsince 1975. Although nearly all teenagers recognize scxnc risk of harm from smoking, the proportion who think that smoking a pack or more a day causes great risk of harm increased from 51 percent in 1975 to 67 percent by 19R5 (Table IR). A 1975 survey (US DHEW 1975s) of teenagers who smoked revealed that many thought that the dangers of smoking were esa1egerated for their age group (52 percent of girls; 54 percent of hoys); that there was too much talk alx'iut things that were bad for them (43 percent of girls: 4R percent of hoys); and that air pollution was just as im- portant a cause of lung cancer as cigarcttes (67 percent of girls; 51 percent of boys). In 1996. cxdy 1(6 percent of high sctuxol .eniors agreed with the statement, "The harmful Personalized Risk In a survey of 895 students in grades 2 through 12 in 134 public schools in Milwaukee. W I, during the 1979-80 academic year. Leventhal. Glynn, and Fleming (1987) assessed the degree to which the students personalized the health risk from smokin$i When asked. "Do you think that smoking can injure or hurt the body?", 9R percent Answered affirmatively and were able to accurately name one or tttore body part.s,that are adversely affected by smoking. A aubsample of 622 subjects (smokers and non- smokers) was asked whether they "would be less likely, about as likely, or more like- ly to get sick from smoking than other people." Those answering "less likely" ac- counted for 47 percent of the smokers but only 36 percent of the nonsmokers, k percent of those who intended to become adult smokers versus 36 percent of those vyho djd not intend to become adult smokers, and 41 percent of those from smoking families versus 28 percent of those from nonsmoking families. These findings suggest that,-although children and adolescents recognize smoking as harmful, they may not personalize the risk. This failure to personalize the perception of risk may play a role in tl(e initiation of smoking. Some teenagers may minimize ordeny their personal risk because of a beli4f tFjat cer- tain smoking patterns are safe. In the 1974 and 1979 Teenage Smoking Surveys con- ducted by the Department of Health, Education, and Welfare (US DHEW 1976b, 1979b), about one-quarter of teenagers agreed with the statement. "There's nothing wrong with smoking cigarettes if you don't smoke too many." Ahout one-third agreed with the statement, "Cigarette smoking is harmful only if a person inhaler: " Comparative Risk In the 1979 Chilton Survey (Chilton 1980), teenagers were asked which of the fol- lowing caused the most deaths during the past year. traffic accidents, fires, cigarette smoking, or drug overdose. Traffic accidents were cited by 44 percent of teenagers, followed by drug overdose (21 pereent), cigarette smoking (19 percent), and fires (6 percent). The High School Seniots Survey inchxks questions about the risks associated with using a variety of licit and illicit drugs at different levels of intake. ln 1996.66 percent of high school seniors thought that smoking one or more packs of cigarettes per day causes great risk of harming oneself. More students saw great risk in the regular use of marijuana, cocaine. LSD, and heroin (Table 19). In contrast, more teenagers saw great risk in regular smoking compared with trying amphetamines, trarhiturates, cocaine, or LSD; in trying or using occasionally marijuana or cocaine: or in trying al- cohol, having one to two drinks per day, or having five or nxore drinks one tx two times per week. The Weekly Reader magazine includes a survey twice a year in the periodical, which is distributed throughout the country to nwre than 10 million children in grades 2 21S

.. . Absolute Risk Absolute risks can be described by the proportion of those exposed to a given risk factor who will actually die or develop the particular condition, or by the reduction in life expectancy caused by exposure. As many as one-third of heavy smokers aged 35 years will die before age 85 of diseases caused by their smoking (Mattson, Pollack, Cul- len 19R7), and 30-year-old smokers will shorten their lives an average of 6 to 8 yean if they smoke a pack a day (US DHEW 1979a). From 1970-78, the proportion of adults who believed that smoking a pack of ciga- rettes a day made a great deal of difference in longevity increased slightly from 42 to 50 percent (FTC 199 1). However, most adults underestimate the impact of smoking on longevity, according to a 19R0 Roper survey. In this survey. 30 percent of the population and 41 percent of smokers did not know that a typical 30-year-old smoker shortened his life expectancy at all by smoking (FTC 1981). Among those who did know that smoking reduces one's life expectancy, many underestimated the degree to which this is true. On average, nonsmokers underestimated the loss in life expectancy by about 2 years and smokers underestimated it by more than 4 years. Relative Risk Relative risk describes the risk of dying or developing disease for a person exposed to a particular risk factor compared with sorneotte not exposed. For example, mak smokers are 22 times mote likely and female smokers are 12 times more likely to develop lung cancer compared with nonsmokers of the same sex (Chapter 3). In the 1980 Roper study, m%pondents were asked if smokers were specifically 10 times more likely to die from lung cancer (the estimated relative risk derived from the data available at that titne); 23 peroent of the general population and 39 pe:rcent of smokers did not believe this statement. Some of this lack of belief may be due to the use of a specific figure. However, using more general temts, 16 peroent of adults and 25 percent of smokers did not think that smokers were "many times" more likely than nonsmokers to develop lung cancer (F'TC 1981). Attributable Risk and Smoking-Attributabk Mortality Attributable risk refers to that pnopcxtion of a disease that can be "attributed" to (or is caused by) a particular risk factor, such as smoking. For example, smoking accotmts for about 80 to 90 percertt of lung cancer deaths and 80 to 95 percent of deaths frcxn COPD (Chapter 3). Much of the information regarding the public's understanding of the magnitude of the risks of smoking comes from the Roper survey conducted in 1980. In this survey, 43 percent of adults and 49 pereent of smokers did not know that smoking causes nwrn of the cases of lung cancer and 22 percent of adults and 27 petcent of smokers did not know that smoking even causes many cases of lung cancer (FTC 1981). In the 1987 NHIS (unpublished data, National Cancer Institute), 28 percent (preliminary 6rst- quarter estimate) of smokers and 16 percent (year-end figure) of the general population disagreed with the statement, "Moat deaths from hmg cancer ate caused by cigarette smoking." Attributable risk figures can be used to calculate smoking-attributabk mortality. 7* 1979 Surgeon General's Report (US DHEW 1979a, p. ii) attributed approximately 350.000 deaths each year to cigarette smoking. In 1985, an estimated 390.000 deaths in the United States were attributable to smoking (Chapter 3). In the 1979 Chilton sur- vey, adults aged 29 to 31 years were asked: "In the United States, two million people die each year. About how many of these deaths are probably related to cigarette sn~k- ing?" The responses offered by the interviewer, along with the peteentages choScn, were: 10,000 deaths, 22 percent; 50,000,16 penxnt:100,000,16 pt:rcent: 300,000,17 percent; don't know, 31 percent (Chilton 1980). Comparative Risk S ' The risk of dying from smoking qn be compared with the risk of dying from pthen behavioral risk factors, such as living under stress, eating high-cholesterol foods, or drinking heavily. The public's perception of these comparative risks was assessed by Roper surveys from 1970-78 (Table 16). In 1970, living under a lot of tension lsnd stress and not getting regular exercise were considered by more adults to make aireat deal of difference in longevity than was smoking a peck of cigarettes daily. In con"st, fewer adults considered regularly eating food high in chotesterol. consuming three oi four drinks of liquor a day, or being 201b overweight to have an effect on longevity. In 1978, only stress was considered by more adults to make a great deal of difference on longevity. In 1983, Louis Harris and Associates conducted a national telephone survey of 1,254 randomly selected adults for PreveaNon magazine (Harris 1983). Respondents; were a.eked to rank 24 health and safety factors on a 1-to-10 (low-to-high) scale of impor- tance. A sample of 103 health experts (medical school chairtnen of prevedtive medicine, public health school deans, government ofFicials, journal editors, and others) was also interviewed and was asked to make the same rankings. All of the public's mean rankings were in the top half of the scate; thus, none of the factors were seen as trivial in importance. "Not smoking" was ranked near the middle, below "keeping water quality acceptable; '"having smoke detectors in the home," "taking steps to con- trol stress," and "getting enough vitamins and minerals" (Figure 1). In contra,ct, the panel of experts ranked "not smoking" at the top of the list (Figure 2). The 1986 AUTS asked five que.ctionscomparing the perceived risk ofcigarette smok- ing with the perceived risk of drinking alcoholic beverages, smoking marijuana, being exposed to air pollution, driving without a seat belt, and being 20 lb overweight (Table 17). In each of the comparisons, never smokers were more likely to disagree than to agree that cigarette smoking is less hartnful than the other risks. Only in the case of marijuana smoking are the percentages of those agreeing and disagreeing similar. On the other hand, current smokers wete mone likely to agnx than to ditagree that cigarette smoking is less dangerous than tnarijuana smoking and air pollution. ; Dolecek and coworkers (1986) surveyed 973 adults in Chicago from a sample of family members of students who participated in AHA's Chicago Heart Health Cur- I ^^~ 1 207

- - - - - - T- - s- - - - - - - - A _uyA ~ :yNTa-1~~s u a ~ a.+ v u ''~ - ~ 3i N a ~' 0 ~ ~ a O b O iw iw b '? tw iv O v» e.. u a i.+ ;o i iw a~. a O .. N N N - N '+~ 4W 'M 'J 'J 'J ~ a a a a a• u u~ a• r. a a yya ~a a v y - a~ N ' ' ' ' : b ! ~ N IN bbb : S-b1N~? j 0J. iJ T N a r ~ O ~ • N Q ~ 1.~ N 41 N N V t.a. J1 « ~O O ]9 /J :Jk NN 0~ u taw R>; . = + • • + . tj °: S ''t ~4 ~, '~t TABLE 3. Trends in smoking prevalence ( 9G), ,NRISs, United State3,1965-0'7, adults aged 20 yeus and older ii Sex Race Educational level Year Overal! population Maks Females Leu than HiBh So~ high school x~ college VYhites Bbdts gteduate gradwte College gr+dwte 1963' 40.4 50.2 31.9 40.0 43.0 1966 40.7 50.8 32.0 40.4 42.9 363 41.1 42.5 33.7 1970 37.0 44.3 30.8 36.5 44.4 34.8 38.3 36.7 28.1 1974 36.9 43.4 31.4 36.1 "0 36.5 37.6 36.9 283 1976 36.1 42.1 31.3 33.6 41.2 35.8 37.8 36.4 27.4 1977 35.6 40.9 31.4 34.9 4d.i 35.8 38.4 33.2 23.6 1978 34.0 39.0 29b 33.6 38.2 333 363 32.7 23.8 1979 33.5 38.4 29.2 332 36.8 34.9 35.4 33.3 23.4 1980 33.3 38.3 29.0 32.9 371 33.3 35.7 31.2 24.6 1983 31.8 35.5 28.7 31.4 X6 34.7 35.6 30.0 19.9 1983 30.4 33.2 211.0 29.9 36.0 33.7 34.2 28.1 18.4 1987b 29.1 31.7 26.8 28.8 34,0 35.7 33.1 26.1 16.3 Trend i nformatios 1 196S-8.S) Changee /yat -0.30 -0.84 -0.21 -0.30 -0.39 -0.06 -0.32 -0.70 -0.76 Statdud ertar 0.03 0.04 0.03 0.03 0.08 0.03 0.05 0.07 0.0e R2 0.97 0.98 0.81 0.97 0.74 NA4 0.87 0.94 0.93 'For 1963. ddata stratifled by education Went not availabla "Provisiaul data only. `In pacem3{e points. 4'Rie.lope of the reyossion line was not significantly diffaau rtoa apo, ataking t4c Iticomputadotia~ppepeirt--

TABLE 28.-Trends in public opinion about restrictions on smoking In restaurants Smoking should be banned (or limited) in restaurants' I percentage who agree by smoking sutus) Current Former Ne.er All Survey Year Reference smokers smokers smokers nonsmokers All adults 1. Roper 1976 Roper1978 22(37) 2. Roper 1978 Roper1978 23(73) 3. Gallup 1983 ALA 1987 12(74) 19(71) 16(65) 19(69) 3. Gallup 1987 ALA 1987 7(79) 19(74) 23(71) 17(74) 'Percenuges repteseot dtose who favor a total smohing b.L P1dopKagp N pare,myxt teptesent thoee who favor setting aside csrnia areaa fw smoti.g, NOTE: Actwl questiatc 1-2. Should smoking be pemltted oNy in sap.rate sxtimr or showld it be psmtioed anywhen... in eaong pl.cea? 3.i. What ia your opinion eegatding smoking in dteas public pl.w ... restauatw? (fet aside cataik taeas. totally bm smoking, or no nestrictiona) ~ M 41 sD TABLE 29.-Trends in public opinion about banning the sale of cigarettes Percentage who agree by smokln status Survey Year Gurrent Refete+xe smokers Never Fotmer smokers smokers All nonsmokers All adults 7Ae se11in8 o[ ciltatettes SHOULD BE stopped comGletslY 44 38 1. AUTS 1970 US DtEW 1973 27 36 48 15 2. Roper 1970 Roperl978 13 3. Roper 1972 Roperl978 12 1974 Roper 1978 12 4. Roper 5. Roper 1976 Roper 1978 16 6. Roper 1978 Ropet1978 19 Gallup 7 1977 Gallup 1981 23 19 . Gallup S 1978 Gallup1978 1I 26 20 . 9. Gallup 1981 Gallup 1961 10 The seUing of citatettes stauld NOT be stopped comDkul]t 70 EW 1969 83 74 57 61 10. AUTS 1964 H US D 75 1 l. Gallup 1978 Gallup 1978 ~O'iE: Actual quesuatc taiWly agtee• o0 opioias. wWly d~0~' strongly ~O«) 1. lAe selling or cigarettes shouW be stopped cempletely. (f°°^gly aP°~ don't ttww) . disagtee e . (aIro ale of all ciguenes h e s :~ A law should be pwed against t . 7-9. Do you think the sale of Ngauetus should or should not be bwxd completely? 10. The selling of c;arones should not be stopped completely. 11. Cigarctte sales should &M be bawed completely. .Percenta8es include those who "strongly aFas' a"mtidly agta6'

I been shown to be an important aspect of behavior change in general (Mahoney 1974) and of health-related behavior change in particular (Ben-Sira 19R2; Schinke and Gilchrist 1984). Factors Interfering With Changes in Knowledge There is a vast body of literature pertaining to the acquisition of knowledge and the process of learning. Research in this area has identified many factorc that enhance or interfere with this acquisition. The brief discussion below does not attempt to provide a comprehensive review of this literature, but rather attempts to idcntify a few of the tnore salient factors that may impede the development of accurate beliefs about the health risks of smoking. ?lte importance of beliefs in determining smnking behavior is discussed in Part 11 of Chapter 5 (sections on Cognition and Decisionmaking). Informing the public about the health risks of smoking is difficult to accomplish. Risk assessment is a complex discipline, not fully ttnderstood by its practitioners, much less the lay public (Slovic 19R6). Risk judgments are influenced by the memorability of past events: as a result, any factor that makes a risk memorable-such as a recent dis- aster or heavy media coverage-seriously distorts the perception of risk. Risks from dramatic and sensational causes of death, such as injuries, homicides, and natural dis- astets, tend to be greatly overestimated. Risks from undramatic causes, such as bronchitis, emphysema, or cattcer, which take one life at a time and which may be more common in nonfatal form, tend to be underestimated (Slovic 1986). News media coverage of health risks has been found to be biased in the same direction, thus con- tributing to the difficulties of obtaining pnoper perspective on risks (Slovic 1986). The fact that perceptions of risk are often inaccurate may indicate the need for wam- ings and educational programs. Such programs, however, face the obstacle that infor- mation based on probability is likely to have less impact on recipients than information based on certainty. For example, the data presented herein indicate that the majority of smokers believe that smoking increases the chance of getting lung cancer. However, not all smokers develop lung catteer, and on occasion, a well-publicized case of lung cancer occurs in an individual who never smoked. These "exceptions" may provide smokers with a rationale tocontinue smoking despite their abstract belief of risk. In addition to their difficulty with understanding risks, smokers may deny pet•sonal risk with respect to health effects of smoking and addiction. Some smokers incorrect- ly believe that while smoking may be ha7ardous to others, it is not hayardous to them- selves because of the particular type of cigarette they smoke, the amount they smoke. or their family history of disease. Persons who are exposed to a health risk, such as snx>hers, may attempt to reduce the anxiety generated in the face of that risk by deny- ing the existence or magnitude of the ri.sk, thus making the risk seem so small that it can be safely ignored (Slovic 19R6). Teenagers pose a special challenge for imbuing knowledge of the health risks of smoking. As mentioned above and as shown in Table IR, the majority of high school scniors do believe that smnking is generally harmful. However, the fact that the health risks are in the distant future for teenage smokers may make it difficult for them to fully appreciate those ricks. In other words, this lag may reduce teenagers' likelihood to ,tinsfcxm Level 2 beliefs to Leve13 beliefs. 7bis is one teason smoking prevention ef- forts now tend to emphasine social influence approaches and to deemphasize com-' tmmication of the long-term health risks of smoking (Chapter 6). Although empirical evidence is spar:se, tobacco industry activities in the form of ad- rertising and protttotion, public relations. atd lobbying may interfere with public beliefs md personalized acceptance of the health risks of smoking. Because most individuals may not understand how smoking causes the disease with which it is as.wciated, many persotts may be vulnerable to information that attempts to cast doubt on such relat ion `, ships. These industry activities are reviewed in Chapters 6 and 7. 11u 1990 Health Objectives for the Nation ln 1980, the U.S. Public Health Service established the 1990 Health Objectives for the Nation (US DHHS 1980). A mid-course review of progress toward meeting thesc{ objectives was publishnd in 19g6 (US DHHS 19R6b). These objectives included fiv,e goals for public knowledge of the health consequences of smoking: ; Objective 1: By 1990, the share of the adult population aware that smoking is one of tha ~ major risk factors for heart disease should be increased to at lesst 95 percent. Objective 2: By 1990. at least 90 pettxttt of the adult population should he aware that smnk- ing is a major cause of lung cancer, as well as multiple other cancers including IarynRea4 esophageal, bladder. and other types. Objective 3: By 1990, at least 85 pettxtrt of the adult population should be aware of the special risk of developing and worsening chronic obstructive lung disease, including bronchitis and emphysema. among smokers. Objective 4: By 1990, at least 85 petoent of women should be aware otthe special health risks for women who smoke, including the effect on outcomes of pregnancy and the excess risk of CVD with oral contraceptive use. Objective 5: By 1990. at least 65 petsent of 12-year-olds should be able to identify smok- ing cigarettes with increwed risks of serious disease of the heart and lungs. For the purposes of these objectives, the tetm aware was not defined and no distinc- tion was made between Level 1, Leve12, and Leve13 beliefs (see above). Progress toward meeting the first two objectives cannot be assessed reliably because they refer to smoking as "one of the major risk factors" for heart disease and "a major cause" of lung cancer and other cancers. On the other hand, tttost surveys have assessed public beliefs about whether smoking ittcreases the risk of or "is related to" heart dis- ease or lung cancer (Tables 8 and 9). As mentioned above, such wording changes can markedly affect results of surveys assessing public beliefs. The third objective appears to have been met in the case of emphysema and nearly met in the case of chronic bronchitis (Table 10). In 1985, the percentages of adults 1 R to 44 years of age who acknowledged the various effects of maternal smoking on the fetus were generally 10 to 20 percentage points below the goals listed in the fourth ob- jective, except that 85 percent of women believed that smoking during pregnancy in- bZ69 t85tS 223

nALA(;FR, N.A. PICKLE. L.W.. MASON. T.J., CORREA, P., FONTHAM. E.. STFM- I IAGI•.N• A.. lil If11.F.R. P.A.. '/.IF(;LER. R.Q, FRAI IMF:NI,1.F. JR. The rcl:uir»t of pa.. .ivc.mnkint Ir+Iunccant-cr. Canrrr•Rr+rurr Ir46(9):JRfIR-4RI I. ScPtcnihcr IrMih• f)ALRFY. W F.• NF.7Tf:SH[:IM. D.. GRIESF.MER. R.. CATON. 1.E., (;(iERIN• MR ('hnmK inhalalic+n nl'ci~arcoc.mnkc by F3J4 rhts. Jo<rrnol n/ tlrr Nalirnrrd ('arrrr lrruirrnr lat2r.ixs_i~cx.l'chroary 1990. DF:ANFIF.Lh. 1.F.. SFIF.A, M.i., WILSON• R.A.. IIORLOCK, P.. DF:LANDSIIf•.Rf, C.M.• SFI.WYN. A.I'. Dirccl cffccts or smnking rm thc heart: Silent ischemic di.torhnrK•cc „f curom:vy IL+w. .lmrrin,nJnurrerdn/Cnrdinln,~rS7(1;):I(A)t-I(I(14•May 1, I9M. DEANIJ.. WRIGHT, C., KRIKLER, S., RIBF•IRO, P.• Ft7X, K. Cigarette cmokinF arw) the Ircamu•m rd' :mLina with F+mPr,molol, :ncnnlnl• and nifedipinc. Nrn F.ng6unrl.lnrrr•nnl nf Afrrlrrrnr.1tlM 1t1;9% 1-954. April 12. 19R4• IX X'K FRY• I). W.. tiPE17F.R, F.F:.. FERRIS, B.G. JR., WARE,I.H., LOUIS, T.A., SPIRO• A. IIL ('mnul:ni. c:md rc~cr.ihlc cl'fcct. nf lifctinK .mnking nn simplc tr.tc nf lung furn•titm in adull.. Anrr rn mr Rr rlrn n/'Rr%lrirulnr r/)i.ccu.st I 37::xf. 292, 1999. f)(1L1., R.. CiR AY• R., IIAFNF.R• B.• PFT()• R. Mortality in rclation to.moking: 22 ycar.'r+h. ccrvatinn% rai fcmalr British dnclnrn. Rrnich Mrdicallnnr•aul 2xf1(h219/:967-971, April 5. 19Rf1. DOLL• R.• HILL. A.B. Lung cancer and nthercauces of death in relation to smoking. A.ecrnwl rcpnrt on the mnrt:dity nf British dockxs. Rr•ilish Mtdirrd Jnnrnal 2:1071-I Ox 1• Novcmlx r I. 1956. DOLL. R.. PETO. R. Cigarette smoking and bronchial carcinoma: Dnse and time relatirm.hipc among regular smokera and lifelong nrxr-smdcers. /nnrrrnln~Elrirlrminbr,~r und Cmm~nmin 1/ru1Nr 72t41: i0i-t 1.1. December 1979. DDOLL. R.. PFT(). R. The causes or cancer Quantitative estimates of avoidable ricks or can- ccr in the llnitcd States today. Journal nf Ihr Nauinnal Canrer lrr.oliltur (+6(6):1191-1 311R• June 1991. DDOLL. R.. PFTO, R. EJrrrn nn Hralih nf E.tposnrt In Ashr.sa+t, London: Her Majesty's Statitxxry Office, 19RS• DORN. H.F. The mcwtality of smokers and nonsmokers. 1959. nUBE, M.F•, GREEN, C.R. MethcxF- of ecdlectinn of smoke for analytical pur)xxes. Recent Adcanrrs ir, Tnhurrn Science: Frn•naninrr• Ana/l:ti.r. anrl Cnntl>rrsilian (oTnlxrr•rn Smote R:42-1(12, I9R2, DUNN•1.E.JR.•LINDEN,G..BRESLOW.L, Lungcancermextalityexperienceofinenincer- tain nccupations in California. American Jnnrnall jPpMic• Health SO(10):147S-14R7• Oc- tober Iol+(1. FLWOOD• 1.M., PEARSON,1•C.G-, SKFPPEN, D.H•, IACKSON, S•M. Alcohol, srnoking, so- cial and nccupatinnal factom in the aetiology of cancer of the oral cavity, pharynx and larynx . /rrrrrnrqinnal Jnurnal n/Cam'er i4:6(l.'i~ 12. 19R4• ER IKSSON, S. Pulmonary emphysema and alPhat-antidypain deficiency. Ar•la Mrdir•u Sran- dmo+•ir•u 175:197-205, 1964. ER NSTF'R: V.L., BUSH, T.L„ HUGGINS, G.R•, HULKA, B.S., KELSEY, J.L„ SCHOTTEN- FFI .I)• D. Rcnefitc ar+d risks of rrM-opausal estrngcn and/rx pn.gcstin hormone use. Prrcrn- Iirr Afr•dirinr 17:2(11-223, 19RR• FFDFRAI• TRADE COMMISSION. Rrpnrl nr Cnn,erts,o Pnr.a,anl In the Federal Ci,cnrrnr l.,lr<•lin,c nnrl Adt•rr•ri.tin,e Ar7 jnr N,r Year 1981. Fcdenl Trade Commission, July 1914. FEDERAL TRADF: COMMI.SSION• ••Tar,•• Nir•nlinr and Crrr•lwnr Mnnn.virlc n/rhr SmrrEt (/ 207 1 „rirrir.% nj l)nnrr.crir Ci,¢arrllrs. Federal TrKk Commission. January 1995. S989 TBSZS ffRA, T.. ARROUD• R.T.. RICHTER. A.. JOHAL. S.S. Acute effect of smoking on ela.- ' t:+%clike c.tcrasc crctivity and immunologic neutrophil elastase kvels in hronch(mlvcol:u lavage fluid. Anu•rirnn Review r!(Rrxpirutnr' v nisraxr 131(4):56R-S73. April 1996. fll'7.GI:RALD• (i.A.. OATES. 1.A.. NOWAK. J. Cigarette smoking and hemoaauc function. ,1 nrrrir on llrurl.lnurnr,I 11 5:267-27I , 19RR. fLf.TC'HFR, C.. PETO, R.. TINKER. C.. SPEI?.ER, F.E. The Nalnrtd Hislnr.r n(Clrrnnir Rrnnrhili% rrrrrl Enqrhv.crrna. Oxkxd: Oxford University Phess, 1976. GALAN• K.M.• DF.LIGON(JL. U.. KERN. M,1.. CHAITMAN, B.R.. VANDORMAEL. M.G. Incrca.eJ frcyuency nf restenosis in patients cont inu ing to smoke cigarettes after perctnanStws tranauminal corrmary angir+(+lasty. American Jrnn•nal af Car•dinln,¢y 6):26(-261. 19R1t; GAO. Y.T.. BLOT. W.1., 7.HENG, W.. F.RSHOW, A.G., HSU. C.W.. LF.VIN, L., 7_HANG, R., FRAUMENI. 1.F. Lung cancer among Chine.e wrxnen. Inrernolinnul Journal n/Cnnr•rrr• 40(5):04-M19. November 15. 19R7. GLOVFR. M.V•, KURER, M.T.. WARREN. S.E.. VIEWEG. W.V.R. Myocardial infarction heGm age 36: Ri.k factor and artiographie analysis. American Journal n( Crrrdinfn,q.c 49(7):)fi11(1-16()3• May 1992. G(1FFMAN, T.E., HASSINGER. D.D.. MULVIHILL. J.J. Familial respiratory tract c4ncer! (1t+pcxlunilies for research and prevention. Journal of the American Medical As.rrH•iarinn 247(7):)t12O-1(l2z,FeMuary 19, 19R2. GORDIS. L.. 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Restaurants 3 In four surveys, conducted between 1976 and 1987, approximately 20 percent of a.spondents favored a total ban on smoking in testaurants (Table 28). In contrast, most adult.s are in favor of limiting smoking in rataunmts. A 1976 Roper poll indicated that 57 percent believed smoking should be testricted to certain areas in restaunutts, while 22 percent favored a total ban on smoking. In a 1987 Gallup survey conducted for ALA. 74 percent of adults thought that certain areas should be set aside for smoking and 17 percent thought that smoking should be banned completely (ALA 1987; Gallup 1987a). As mentioned above. 61 pencent of tespondettts to the 1986 AUTS choose no-smok- ing sections of restaurants and other public places when given a choice (CDC 19R8). In a survey conducted by the Gallup Organization for the National Restaurant Associa- tion in 1987.adultswemaskedaboutvariousopinionsnegatdingsmokingintestaurants: ( 61 pen;ent overall said that they prefer to sit in a no-smoking section (83 percent of never smokers. 65 percent of former smokers, and 20 ptrcent of current smokers) (Gal- hip 1987b). 4a ~ g~ Ii A I t Other Places A Gallup survey conducted for the ALA in 1983 showed that 54 percent of adults favored setting aside certain areas for smoking in hotels and motels and 12 percent favored a total smoking ban. In a similar survey in 1987, these percentages were 67 percent and 10 pen:ent, respectively, and were slightly higher for nonsmokers than for cunent smokers (Gallup 1988a). Restrictions on tlte Sak and Dbttibatiat of CtRarettes v 9 Compkte Ban on Sales The qtte,sttons used to as.xss opinion regarding the outright ban of cigarette sales have varied considerably in wording. In 1964, respondents were asked if they agreed that "The selling of ciganettes should not be stopped completely." In 1970, respondents were asked if they agreed that "T1te selling of cigarettes should he stopped compkte- ly " Despite these differences, the responses consistently indicated little sympathy for this most stringent policy: approximately 30 percent of adults supported a ban in 1964. compared with 20 percent in 1981 (Table 29). Limiting Sales to Minors Most adults favor limiting cigarette sales to minors. In 1964, only 9 percent of adults thought that sales of cigarettes to people under a certain age should not be against the law. In 1970, 88 percent thought that such sales should be against the law (Table 30). 0£69 185T5 235

repmsent an accurate cros.s-section of high school seniors throughout the coterminous United States. The first stage involves the use of 74 primary sampling units developed by the University of Michigan Survey Research Center for u.se in its nationwide inter- view surveys. The second sampling stage involves choice of a single high school from most geographic areas (more than one is chosen in major metropolitan areas). The pmb- ability of selection of any school is propextional to the size of the senior class. When a sampled school is unwilling to participate, a replacement school is selected from the same geographic area. Response rate of schools has been from 66 to 80 percent throughout the survey period. Up to 400 seniors are surveyed from each school. In schools with more than 400 seniors, a random sampling system convenient for the school (provided it results in an unbiased sample) is used to choose the 400 students to be interviewed. Most schools use the classroom as the basis for this selection. The total number of students inter- viewed each year has been between 15,700 and 19.000. The student response rate has varied from 77 percent to 84 percent throughout the survey period. The questionnaire administration in each school is carried out by local Survey Re- search Center representatives and their assistants following standardized procedures detailed in a project manual. Questionnaires ate generally delivered in clas.srcxims during normal class periods, although in some instances larger groups are used. Be- cause of the range of topics, five different questionnaire forms are used in the survey. These are distributed to participants in an ordered sequt:nce to produce identical sub- samples. All five forms contain core data on demographics and some drug use (about one-third of the form); all other questrons are asked on subsamples of the total respon- dents. Basic questions on cigarette usage have been included in the core for all years. Followup surveys by mail are conducted annually using representative subsamples from each of the previously participating clas.ses, that is, the classes of 1976 through 1987. Thus, long-term panel data are collected on individuals, and analyses aimed at separating secular, age, and cohort effects are possible. (See O'Malley, Bachman. Johnston 19RR.) NIDA National Household Surveys on Drug Abuse NIDA conducted household surveys on drug use in 1979.1992. and 1985. Data were obtained from a stratified random sample of 8,000 U.S. households; approximately 2,000 in-pcrson interviews were conducted with respondents in the 12- to 17-ycar-old age group. Questioms included whether any cigarettes were smoked within 30 days as well as within the previous year. Roper Survey. 1978 This survey was conducted for the Tobacco Institute via face-to-face interviewing with 2,511 suhjcctc. Other methodological details an: unavailable. 6E69 IBSIS Roper Survey. 19R0 The 19R0 Roper Survey used face-to-face interviews to test a nationally neprb- sentative sample of 2,000 adults for knowledge about the health hazards of smoking. The study was commissioned by the FTC and was conducted in November 19R0: The total sample was split into two halves, and one set of questions was varied between the two. Thus, the sample size for several of the questions on the health effects of smok- ing was approximately half the total sample size. ' US DHEW Teenage Smoking Surveys In 1968, 1970. 1972, 1974, and 1979, random samples of teenagert aged 12 to 18 years were surveyed by telephone in December-January (US DHEW 1972. 1976b. 1979b). The first stage of the 3-stage sampling plan involved grouping and sele~ting telephone exchanges and was designed to eliminate geographic bias. Withip the selected exchanges, equal numbers of random-digit-dialed telephone numbers ;were generated and contacted. Household enumeration was undertaken with an adult respon- dent and, if more than one person aged between 12 and 18 years lived in the house, ran- dntn selection was used to choose the study participant. ! In 1968. the sample size was 4,931, 89 percent of whom were interviewed by telephone. The other I 1 percent lived in nontekphone households and were intervieweb in their homes. As exclusion of the nontekphone households did not substantially af- fect prevalence estimates, later surveys did not include household interviewing of non- telephone households. The sample size in 1970 was 2.640; in 1972, it was 2,790; in 1974. it was 2,553; and in 1979, it was 2.639. In 1979, a followup survey was also un- dertaken on 1.194 (46.g percent) of the 1974 tespondents. Approximately 12.000 households were contacted in 1979, from which 2.639 people aged 12 to 18 years were interviewed. In no survey was there any attempt to validate the smoking status ihdi- cated. 253

1 U.S. DEPARTMENT OF HEALTH. EDUCATION. AND WELFARE. Use ojTirharco. Prar. rirr.c. Attitudes. KnrnvlydKr, and Brlirf.r. United Sla/rs-FoU 1964 and Spring 1966. U.S. Department of Health. F.ducatinn. and Welfare. Public Health Service, National Ckaringhnu.e fcx Smoking and Health. July 1969. 11.S.DF.PARTMf•.NTOFHEALTH.EDUCATION,ANDWELFARE. TrrnaKrSma4ing: Na- rional Patrrrn.c ojCiRarenr Smr>kinK. Ages 12 Thrnngh 18. in 1W and 1970. U.S. DepaA- ment of Flealth. F.clucation, and Welfare. Health Services and Mental Health Administraliun, National Ckaringhouse for Smoking and Health. DHEW Publication No. (HSM) 72-75(1R, 1972. U.S. DEPARTMENT OF HEALTH. EDUCATION. AND WELFARE. Adult Use af Tnhacro, 1970. U.S. Department of Health. Education, and Welfare. Public Health Service. Center for Disease Control. National Clearinghouce for Smoking and Health. June 1973. U.S. DEPARTMENT OF HEALTH. EDUCATION. AND WELFARE. CiKarrrrr Smnking Among TrrnaRrrs and Young Women. U.S. DepartmeM of Health, Educaticxt, and Welfare. Public Health Service, Akohol, Drug Ahuse, and Mental Health Administration. National In- stitute of Drug Abusc. DHEW Publication No. (NIH) 77-1201, 197Sa. U.S. I)EPARTMF.NT OF HEALTH. EDUCATION. AND WELFARE. The Health Con.cr- qurnrrs of Smoking. 1975. U.S. Department of Health. F.ducation. and Welfare. Public Health Service. Center for Disease Control. HEW Publication No. (CDC) 77-R704, 1975h. U.S. DEPARTMENT OF HEALTH. EDUCATION. AND WELFARE. Adult Use of Tirhoc- ra--1973. (1.S. Department of Fkahh. Education, and Welfare. Public Health Service. Cen- ter for Disease Control. National Clearin(Chouse for Smoking and Health, 1976a. U.S. DEPARTMENT OF HEALTH. EDUCATION. AND WELFARE. Ternagr SmrnQing: Na- ri+mal Patterns of CiRarrnr SnokinK, Ages 12 ThrnwKh 18. in 1972 and 1974. U S. Depart- ment of Health. Education, and Welfare. Public Health Service, National Institutes of Health. DHEW Publication No. (NIH) 76-931, 1976b. U.S. DEPARTMENT OF HEALTH. EDUCATION. AND WELFARE. The Health Catia- qrrncrs nfSmeking,1977-1978. U.S. Dep.ritnt:nt of Health, Education, and Welfare. Public Health Service. Office of the Asaistant Secretary for Health. Office on Smoking and Health. DHEW Publication No. (PHS) 79 :S(xK+S, 1978. U.S. DEPARTMENT OF HEALTH. EDUCATION, AND WELFARE. Smoking and Health. A Report of rhr Curgron General. U.S. Deprartment of Health. Education, and Welfare. Public Health Service. Office of the A.aistant Secretary for Health. Office on Smoking and Health. DHEW Publication No. (PHS) 79-St106fi, 1979a. U.S. DEPARTMENT OF HEALTI), EDUCATION, AND WELFARE. TrrnaRr Smo4ing: IrA- mrdiarr and Long-Term Patterns. U.S. Deparbtxnt of Health. Education, and Welfare. Na- ticxtal Institute of Education, November 1979b. U.S. PUBLIC HEALTH SERVICE. SmnkieKandHe+alrh. RrportofrheAdriaoryCmmmrinrr to the Srrgrnn General oJdlr Prhlir• Hral/h Srrvice. U.S. Departtnent of Halth. Educatinn. and Welfare. Public Health Service, Center for Disease Control. PHS Publication No. 1103. 1964. U.S. PUBLIC HEALTH SERVICE. TheHral/bCan.aqawncr.raJSmatirtK. 19rf9SWplrmrnr rn the 1967 Pnhlir Health Service Rnirw. U.S. Department of Health. F.ducatian, and Wel- fare, Public Health Service. P11S Publication No. IFi9G-2 (Sulilpkment), 1969. WEEKLY READER. Safetyandhealthsettion. In: WrrklyRrodrrNrtrinnal SurvrynnSafnr and Health. Midclletc+wn, Gmnecticut: Field PuMicatiorn, 1996. ZV69 ZBStS CHAPTER 5 CHANGES IN SMOKING BEHAVIOR AND KNOWLEDGE ABOUT DETERMINANTS i ~co ?Sq

7 Appendix Description or Primarv Data Sources for Chapters 4 and S Adult Use of Tobacco Survey, 1964 This was the first AIITS sponsored by the U.S. Public Health Service. The survey was conducted by National Analysts, Inc., under contract with the National Clearin- ghouse for Smoking and Ncalth in the fall of 1964. The data for this survey were col- lected using area probability sampling tcchniqnes and stratifying by the type of popula- tion and geographic area. Approximately 5,794 adults 21 years and older were interviewed in person. The response rate was 76 percent. Detailed methods have been puhli.hed el.cwhere (US DHI;W 1969h). Adult Use of Tobacco Survey. 1966 This was the second AUTS sponsored by the U.S. Public Health Service. The sur- vey was conducted by two research firms: National Analyst.s, lnc., and Opinion Re- search Corporation, under contract with the National Clearinghouse for Smoking and Health in the spring of 1966. The data were collected using area probability sampling techniques and stratifying by the type of population and geographic area. The 1964 AUTS questionnaire was used with minor changes. Approximately 5.768 adults were interviewed. Interviews were primarily in person, although telephone interviews were used for nonrespondents. The response rate was 72 percent. Detailed methods have been published elsewhere (US DHEW 1969b). Adult Use of Tobacco Survey, 1970 This was the third AUTS sponsored by the U.S. Public Health Service. The survey was conducted by Chilton Research Services under contract with the National Clearin- ghouse for Smoking and Health in the spring of 1970. The data were collected from a probability sample of households in the contiguous United States. Approximately 5,2tu1 individuals were surveyed; 91 percent were interviewed by telephone and 9 per- cent, from nontclcphone households, were interviewed face to face. Of the total num- bcr of respnndcnt., 44 percent were male and 56 percent were fcmale; all were at least 21 years old. The methods have been described elsewhere in detail (US DHEW 1977). Adult Use of Tobacco Survey. 1975 This was the fourth AUTS sponsored by the U.S. Public Health Service. The survey was conducted by Chilton Rescarch Scrviccs undcr contrict with the National Clcarin- lehousc for Smoking and lleaith in 1975. The data were collected from a probability sample of telephone numbers in the contiguous United States, with n scparatc survey 9E69 IBSIS of nontelephone households. Approximately 12,000 individuals were surveyed. The methods have been described elsewhere in detail (US DHEW 1976). Adult Use of Tobacco Survey, 1996 lIn 1986. 113.031 members of the civilian, noninstitutionalized population of the United States 17 years of age and older were surveyed by telephone on their smokino history, attitudes, and beliefs (CDC 1986). A 2-stage sampling procedure was used within a computer-assisted telephone inter- view format. The first stage involved selecting a random sample of telephone exchan- ges within the United States. The sampling procedure wac balanced for the number of telephones within the exchange. Clusters of between 10 and 15 households within each exchange were contacted using random-digit dialing. Households were enumerateb and smoking status of inembers ascertained. Up to 27 callbacks were made to oMa~n a total of 36,405 households, with a response rate of 85.5 percent. ~ A further stratified random sampling procedure was used to provide an approximate equal proportion of respondent.s in each smoking category (current, former, never). Th6 stratification variable was the number of smokers in the household. Up to 10 callbaaks were made to interview the selected respottdent, with a response rate of 86.9 percent. The overall response rate from the two stages of sampling was 74.3 percent (85.5 per- cent times 86.9 percent). Quality control procedures in the survey involved 26 hours of survey-specific train- ing and practice for interviewers and a silent monitoring of 10 percent of all interviews by supervisory staff. Data obtained were weighted to reflect the U.S. population in 2 stages. A base weight was calculated, which was the product of the weighting for cluster (completed screeners within cluster), household (telephone numbers within household), and person (to account for selection based on smoking status). Poststratification weighting was then undertaken for tegion, education, race, sex, and age. American Medical Association,19g6.1987 The data were gathered in tekphotte interviews with approximately 1,500adults, con- ducted during May-June 19lt6 and January-February 19g7. The surveys were con- ducted by Kane. Parsons and Associates of New York City. The samples were generated by Survey Sampling. Inc. (Wes". Connecticut) using a multistage prob- ability method to provide a random sample of all residential telephones in the United States. Sampling error was an estimated plus or minus 2.5 percentage points at the 95- percent confidence level (Harvey and Shubat 19g6, 1987). Behavioral Risk Factor Surveillance System Between 19R1 and 19R:i. the U.S. Centers for Disease Control (CDC) collaborated with 29 State health ckparttnents (including the District of Columbia) to conduct one- time random-digit-dialed telephone surveys of adults I R years of age and older. Stand- I

V TARI,F 4.-Trends in snmking prevalence (%), AUTS velrnrs NHiS %.-yt•- AtTt'S' Faimued NHIS, Diftcrcnce (NHIS-A(1TS) 1964 440.3 40.4 0.1 19615 42.2 39.4 -2.R 1970 ;t14.2 37.4 1.2 1975 )l.x 34.9 1.1 19R6 26.5 29.4 2.9 'Fm .11 w.vfy yers, incNdn /ey.rdrMa.reet 21 yern wd elder eecrq 1aIlA. vvMc# inclrwkn rc.pm/erM..wA 17 ytaa and older. All d.ts weiRMed. Nnchwka na/r.Wenu .ped 20 ytaa rW alder. Vd.n rea eaA yea re de(erP wud Ay eidnl.daieE e.pecud prevaknce vahuea Aavd un repe..ian rnly.it ban T.Me 3. Slri IR(f: (Nf.ce nn Sm.M inR .nd Hahh (US D11F. W 1 VtiO. t97.'%L 1976: (DC 19a7.). Unlike the NHIS, for which data ane collected during an in-person household inter- view. AUTSs collected data via telephone interviews in 1970, 1975, and 1986. The three AUTSs conducted since 1970 all produced prevalence estimates below those es- timated (by regression analysis) from the NHISs (Table 4). The largest difference be- tween the two surveys is 2.9 percentage points in 1986. The 95-percent confidence limits around the NH1S projection for 1986 an: 27.8 to 31.7 compared with limits of 25.R to 27.3 frnm the 1986 AUTS; thus, the difference in estimates between the two surveys is statistically significant. A difference in sampling modalities is among the moct likely explanations for this discrepancy in prevalence eqimates. A similar find- ing has been noted in State-specific prevalence estimate.e (see below). Telephone sur- veys have a small sampling bias by excluding households lacking telephones and may have a greater nonrespcxlse bias because of generally lower response rates compared with household surveys (CDC 1987a). Cigarette Smoking Among Different Occupational Cmups Ni I1S data have been published on smoking prevalence by occupation for the years 1970. 1978-80 combined, and 1985 (Table 5). There is a consistent pattern of higher smok ing rates among blue-collar and service workers than among white-collar workers for all these survey years. For example. in 1985, the prevalence of smoking among blue-collar and white-collar workers was 40 and 28 percent, respectively. This dif- ference was greater among males (14 percentage points) than among females (6 per- ccntage points). Detailed data on smoking prevalence. percentage of fomler s.mokers. quilting attempts, and age of initiation within specific occupational categories for 1'178- R(/ were published in the 1985 Surgecm General's Repcxt (US DHHS 19R5), Weinkam and Sterling (1997) also provided a detailed analysis of smoking by occupation using the 1970 and 1979-R0 NI tIS data. Novotny. Warner. and colleagues (1999) pperformed multivariate logistic regression analyses on (lata from the 1995 NI IIS (ages 25 to 64 years) to examine the indepcncknt '7) r a I P b a F ~ 8 5 I tr 0 o a ., o ~ eo .~ .n ad f1 .-1 N\ N .-i - au n o~ a o, - rf " e ++ A q O n A a $ n n h 0 ~ = a > ~ Z a` 1, hI_' W rl m ~ O $A a ~ ~ V V Y k :J F ~ I ~ ~ 6V69 i8STS f 273 :.! I

35 30 25 . w° 20 c 1S 0 n 10 5 0 1974 1975 1976 1977 1978 FIGURE 1.-Percentalte of current snaken snaking 225 cigarettes per day, adults aged 20 years and older, United States,1974-R5 SqIIRCF: UnpuMishcd dau, ( Wice nn SGm*inR and {kahh. 40 30 1974 1975 1976 1977 1978 1979 1980 1981 1982 1983 1984 1985 YEARS J While Malea -~ Black Malee • Wh1/e Females -e- Blaek Females FIGURE 2.-Percentalte of current smokers smuking a25 cigareftes per da,r, by race and gender, adults aged 20 years and older. United States,1974-- 85 294 0969 TBSTS a k a P ae N O~ O! ~O ~O O ~ : O e~ ~G G f f a O, O? M O! - r ~O p y w1 ~I1 A1 O .~ fVN e, . .h~. .„.. - N ... h f`j - ~n r ~ r O~C V1 !'~ ~ ~ h a ,r~ e, ~ ry er, a O O N ~ f - ~ O O; O, r} R~ r1 ~i O~ O ~n ~6 eb M n o v; w~-, o N ~ 1 2QS 1

TABLF.1i.--Continned TABLE A.-.SmokinK prevaknce rates according to region of the rnantry, census division, and State, adults sKcd 20 years and older, by gender and education, United Ctates, CPS,198S Fifucatinn Averall Maks Fenuks 512 years >12- 7<am UnNed Ctates 29.5 32.9 26.5 35.4 22.2 Nnrtheast ReRlnn 2R.9 31.3 26.9 34.5 22.1 New England Divisinn 29.3 3t1.6 2R.6 36.3 22.5 Maine .10..1 iI.R 29.1 37.0 17.3 New Hampchire 30.7 35.2 26.7 37.4 21.0 Vetmnnt 30.7 31.R 29.7 37.7 21.4 Maasachusetts 28.2 29.4 2R.1 35.0 22.9 Rhode Island 34.4 35.9 33.3 39.9 26.3 Connecticut 29.6 30.9 285 36.3 23.1 Mid-Atlantic Divisicn 29.7 31.6 26.2 34.0 22.0 New York 28.7 31.4 26.3 34.1 22.3 New lersey 27.9 31.0 25.2 33.6 21.7 Pennsylvania 29.3 32.3 26.6 34.0 21.7 Nnrth Central ReRlon 30.2 32.4 2R.1 36.2 22.2 East North Central Division 31.0 33.0 29.3 37.5 22.5 t7hin 32.2 34.4 30.3 38.6 22.0 Indiana 32.8 35.7 30.1 38.4 23.8 Illim+is 29.7 31.3 263 35.0 22.7 Michigan 34.0 34.4 33.7 40.9 24.7 Wiscnnsin 26.3 27.6 2.5.2 32.6 17.9 West Nn.th Central Divisinn 21.1 31.1 25.4 33.1 21.7 Minnt•-Ada 23.7 30.0 27.4 34.6 21.6 Iowa 28.1 33.0 23.7 31.11 22.2 Missnuri 27.7 31.1 24.6 32.0 21.4 North f>akda 26.4 2R.3 24.7 31.3 21.8 Sauth Dakma 28.6 30.7 26.R 34.3 21.0 NeMacka 24.9 26.6 23.6 29.2 19.4 Kan.as 30.2 34.6 26.6 37.1 23.1 CGwfh ReRMm 31.2 36.4 26.R 36.5 23.3 Gwth Atlantic Divisinn 31.3 36.3 27.1 .16.6 24.0 Delaware 31.9 34.9 29.1 39.1 19.0 Maryland 29.7 ?I.S 2R.1 36.3 20.1 bS69 18STS Educadon e 12 >12 oraan Mdes f+emaks , years years District of Columbia 31.4 34.2 29.3 3R.5 24.2 Virginia 32.7 37.8 28.5 33.5 26.3 West Virginia 34.0 3R.6 30.0 3R.1 22:9 North Carolina 31.6 39.7 24.6 37.0 24.0 South Carolina 27.1 34.2 21.5 31.7 18.4 Georgia 31.9 38.5 26.5 36.4 25.1 ' Fkxida 31.7 33.5 29.4 36.11 25.4 F,st Scuth Central Division 31.9 37.6 26.9 37.3 21i R Kentucky 35.3 37.9 33.4 40.2 ZIl.S Tennec.m 30.8 36.6 26.0 39.6 08.4 ' AlaMma 30.6 39.5 233 35.3 23.6 Missis.sippi 31.1 3R.R 24.9 34.9 25.3 West South Central Division 30.6 35.3 26.3 35.9 ?2.R Arkansas 31.3 37.2 26.5 34.11 25.0 Louisiana 29.1 35.4 23.9 34.1 21.1 ~ Oklahom. 33.0 35.7 30.4 41.5 22.7 Terw 30.6 35.3 26.3 35.9 24.R West ReRteM 26.3 29.3 23.9 32.9 20.9 Mountain Division 27.2 30.1 24.6 34.7 20.2 Montana 25.9 26.1 25.9 32.2 19.3 Id.ho 24.1 26.6 21.7 29.6 17.8 WyuminR 31.7 31.9 31.9 40.9 21.0 Colorado 28.6 30.6 26.9 37.9 21.9 New Mexico 28.5 32.6 24.3 32.9 24.4 Arizaa 29.5 34.3 25.3 37.4 21.5 Utah 14.1 13.2 10.2 22.5 R.0 Nevada 35.7 37.6 33.9 39.0 31.4 Pacific Division 26.3 29.0 22.7 32.0 21.1 Washington 29.6 29.9 27.4 36.1 21.8 Oregon 27.1 26.8 27.5 34.7 21.2 California 25.6 29.9 22.5 2R.3 20.8 Alaska 34.3 40.9 28.0 41.1 27.2 Hawaii 27.6 30.7 24.7 30.6 24.9 N(11E: phtcewtaRee ae ade adjuMed b Ihe rohl U.S. ooO.Iatioe. SOURCF.: Offke on SmnkM6.d Iktaldt, rnpiMl+hM data. 2R3

S969 18SiS TABLE 20.-Smoking status (%) of high school seniors by sex, race, and educational plans, United States, 1975-87 Dailysmoken C.ess than daily smokers Sex Race Plans for higher education Sex Rxe Plans for higher education Year M F W B Yes Yo M F W B Yes No 1975 27 26 10 10 1976 28 28 29 26 21 37 10 10 10 13 10 10 1977 28 30 28 25 20 38 10 10 9 11 10 9 1973 26 29 27 22 18 36 9 10 9 9 9 9 1979 22 28 26 19 17 35 9 9 9 9 9 9 1930 88 24 22 16 14 31 8 10 9 10 9 10 1981 18 22 20 13 13 30 8 10 9 9 9 9 1982 I8 24 23 12 13 30 9 9 9 9 9 9 1983 19 23 22 12 14 30 9 10 9 9 l0 9 1984 16 21 20 8 11 29 10 11 11 9 11 11 1983 17 21 20 II 13 31 10 11 11 8 10 li 1986 17 20 21 8 12 29 11 1l 12 7 11 10 1987 16 20 20 8 14 30 11 II 12 6 11 11 TABLE 20.-C ontinued Never smokers i Previous smoken. not u+ last month Race on °++nLfor hi8her educu S~--e=-~ _ °luu for higher educraioa Race Yes No Sex M F w g Yes No w B Year 1975 yl 38 F 36 9 5 24 24 28 25 7s 24 31 19 19 1976 38 36 37 37 36 49 41 33 24 23 23 26 29 30 31 20 977 39 35 26 24 23 1 42 33 20 40 38 38 40 23 26 30 32 1978 39 41 42 37 27 30 34 23 1979 42 33 5 44 37 30 28 29 24 1980 43 39 40 4 45 38 31 27 29 33 33 1981 43 41 41 43 43 37 32 28 29 36 33 24 9 40 43 29 34 34 24 982 41 3 31 28 1 3 43 38 24 1983 41 40 40 4 42 38 33 29 29 40 35 1984 41 39 40 42 36 33 30 30 39 36 24 38 42 41 44 37 25 1983 39 39 34 31 30 39 37 7 25 1986 38 38 38 41 35 35 31 30 43 3 1987 38 38 38 41 39 ra 5ocial Rcara~d~ Univeniry a( Wcldfa l~ Tsble 19 ta ciunoorl SOUR~ Irwinuc - ~ ~ ~ ---

TABLE 16.-Trends in public knowledge about the health risks of smoking compared to other risk3,1970-78 It makes a great deal of difference in longevity if a person ... (percentage who agree by )ear) Question lives under a lot of tension and saeu doesn't get regular eseteise smokes a pack of cigarettes a day regularly eats a lot of food with high cholesterol drinks 3 or 4 highbal(s a day is :0 pounds overweight SOI;RCE; Roper(1971), 1970 1972 1974 1976 69 72 74 76 74 49 38 38 33 34 42 42 44 45 50 31 34 38 39 43 29 34 33 37 39 23 26 25 24 24 0.: In halping paopla In 9anaral to liva a long and haa-thy ufa, how would you rata the Importancw of ... Of Low Of Utmost Importanca 10mpoR~np9 8 7 8 5 4 3.004 •~ -40- Never drivinq a}tar drinkinq 9.25 (.05) -~+ KMpn9 atr Qua6ty a0apU11316 9.11 (.05) ~.. Kapinp wanr quality accaptabb 9.95 (•05) .410- Haviny smoW datoqms in homa 8.89 (•06) 5 -.0- ) K.epirq doas a raooam»ndaa w.ipfr 8.540 -0• Havirq Wood pnaawta nadinp arrraly e.51(.06) -i• Takwq stpa q contrd tow 8.38 (•06) -0- f3•Itlrq «taqh vitanwr, mwt•nlt 8.37 (.00) -40-- ExKOifMq t•quWM S•32(•0b) -4>~+ Not artqkinp 8.25 (.06) -~ Havhq fAatdri, ntatfws, nai¢fbots l.1e (.06) t IN,ar;IF+q pana han paru+ls tor lon0 wa e. t e(.0e) .•. FiaoMv~q advfa hom do~7or on hWlh nabila 8.13 (•0a) ...qp. Not sa0r+p too mudt aotlYirn a 10 (.06) t G.tanv 7•e howa ar..p e.04l.0et I ~~.. Eatirp Maqh AbM 7.96 (.06) -.0- wNrhtp aaabb ag RM One in bont wg 7.09 (.07) _,&.. Not a" 1u0 muCA tat 7.0e (.07) -4j... Gatdnp anapb cakJue 7.84 (.06) _0- Not aapnp too much xgar 7.81 (.07) _•_ EatlrqbrWdaatdaily 7.61 (.06) Not yattlnp too aRtcN dotastarol 7.42 (.07) --W_ pAnMinq aloohol modKaLaly 6.53 (.Oi) __*_ fhinkinp no aloWwl 6.42 (.0!) FIGURE 1.-Adult public's rating of 24 health and safety factors ..OTE; Shown abovs is the mean imporuntx noag for each f+W pveo by I.234 adults using a I to 10 uak. Givm in Qatenthexs is the swtdatd enor of tAe meaa The 95-pensat confidenoe imetvd traud each mein is gnpRiallr displ+yed as a bud or range coniisdng of : two scandrd ertor •duea SOURCE: Hams (1903) 1978

Low-Tar. Low-Nicotine Cigarettes .......................... 313 Mcnthol Cigatettes ......................................i17 Cigarette Length ........................................ 317 Summary and Comment ................................... 1R Other Tyl+es of T„hacco Use ....................................... 319 Smokeless Tohacco Use ..................................... 319 Cigar and Pipe Smoking .....................................322 Part II. Changes in Knowledge About the Determinants of Smoking Behavior , 329 Introduction: Historical and Conceptual Overview ...................... 329 1964 Surgeon General's Report ................................ 329 1979 Surgeon Gencral's Rcport ................................ i Current V icws .............................................. DDevelopment of Smoking ........................................... 331 31 Pharmacologic Processes and Conditioning ...................... 333 Cognition and Decisionmaking ................................ 3;5 Personal Characteristics and Social Context ...................... ;.16 Personal Characteristics .................................. 336 Peer and FamilyInFluences ................................33f, Cigarette Marketing .....................................338 Summary .................................................. 339 Regular Smoking .................................................. Un Pharmacologic Processes and Conditioning ....................... qp Nicotine Addiction ....................................... 40 Mechanisms of Nicotine Action ............................ 342 Conditioning and Smoking ................................ 343 Cognition and Decisionmaking ................................ 344 Personal Characteristics and Social Context ...................... 345 Personal Characteristics ................................... 45 SocialContextlnnuences .................................3a7 Summary ..................................................34g Cessation and Relapse ............................................. 349 Pharmacologic Processes and Conditioning ........................ 49 Cognition and Decisiontrtaking ................................ ISO Expectancy-Value Models ................................. 50 Self-Efficacy and Smoking ................................351 Outcome Expectations ................................... 352 Personal Characteristics and Social Context ...................... 353 Personal Characteristics .................................. 353 Social Context Influences ................................. 3.91 Summary ................................................... 55 Summary of Changes in Knowledge About Determinants of Smoking Behavior35ti ccxtclosions : . .-. . . : . . . : . . . . . . : : . -.--. .-- : . . .. . . : . .-. iSi Appcndix ..................3 9 9 Rcfcrenccs -- ......................................................... . 361 INTRODUC77ON This Chapter n;views two majoraspects of smoking behavior since rclease of the first Surgeon General's Report on smoking and health in 1964: (1) changes in smoking be- havior in the United States (Part 1) and (2) changes in our knowledge about the deter- minants of smoking during this period (Part Ii). During the past 25 years, the prevalence of cigarette smoking has declined in virtual- ly every major sociodenwgraphic group, including men and women, adults and adoles- ~ cents, blacks and whites, and persons with and without college education. This decline has been particularly evident among men, in whom the prevalence of smoking declined fnxtt 50 percent in 1965 to 32 percent in 19g7. The first part of this Chapter analyzes trends in smoking prevalence, cessation, and initiation, and examines smoking patterns amcxtg different sociodemographic groups and other special populations. These analyses are based, for the most part, on cross-sectional population-based data collected ; periodically since 1964. At the same time, our knowledge about dtatrminants of smoking has increased sub=, stantially. Physiological, behavioral, and social factors that may influence the initia- tion and maintenance of smoking have been extensively researched. Many important predictors of initiation, quitting, and relapse have been identified. The development ofl this body of knowledge is reviewed in the second p®ut of this Chapter. Information reviewed in that part of the Chapter is primarily derived from research studies and in- , tervention trials that employ smaller sarttple sizes than the population-based surveys used in Part 1. These studies, however. usually collect tnat detailed information and . often obtain longitudinal followup data. PART I. CHANGES IN SMOKING BEHAVIOR Trends hi Cigarette Snakhig Introduction Accurate information on tends in smoking pnevakttce in the major sociodemographic groups in the United States is of interest to public health officials, policymakers, researchers, clinicians, and news media. These data ate important for estimating the magnitude of the problem of smoking and for targeting public health in- terventions to those at highest risk of smoking. Accurate data on trends in smoking (including initiation and quitting) ate necessary to be able to project future smoking pattetns. Accurate projections must be available, in tum, to set appropriate but realistic goals for key future years (e.g.,1990. 2000). This Section analys.es trends in smoking prevalence, quitting, and initiation during the past quarter century. Data on smoking prevalence in the 1940s and 1950s from Gallup sur- veys and the Current Population Survey have been cited elsewhere (CDC 191S7a; US DHHS 19gR, Appendix A). bb69 T8StS ±~,, 261

i ard methods and questionnaires were used to a,ssess the prevalence of personal health practices and bchaviors related to the leading causes of death, including cigarette smok- ing. Beginning in 19R4, the surveys evolved into an ongoing surveillance system when States began collecting data throughout the year. For each State, approximately 1,200 (range 6(10-1.(100) interviews are completed each year. The raw data are weighted to the age, race, and sex distribution for each State from the 1980 Census. This weight- ing accounts for the underrtpresentation of inen. whites, and younger persons (18-24 years of agc). A detailed review of the survey design and methods of analyzing the data has been published (Remington et al. 1988). Chilton Survey. 1979 This survey was conducted by Chilton Research Services (Radnor, PA) for the FTC from December 21, 1978 through February 4,1979. A tandorn-digit-dialing procedure was used to collect interviews from 1,211 teenagers aged 13 to 18 years and from 407 adults aged 29 to 31 years in a national probability sample of telephone households. The 1.618 completed interviews represented 81 percent of the number of usable household telephone numbers (Chilton 1980). Current Population Surveys The U.S. Bureau of the Census regularly collecta information as part of its Current Population Survey (CPS). Households are selected for survey via a sampling proce- dure designed to accurately refkct the U.S. population, and information is collected in person during a home vi.cit. In 1955.1966.1967.1969. and 1985, the CPS included a supplement that asked questions on current smoking practices. For 1985. 114.342 in- dividuals, 16 years and older, were surveyed on smoking and smokeless tobacco use. Approximately 55 percent of the sampleconsisted of self-nespondents while the remain- ing 45 percent were proxy respondents. The 1985 CPS sample was initially selecled from the 1980 census files with coverage in all 50 states and the District of Columbia. This sampling methodology allows for State-specific analysis of smoking practices. The estimation procedure used in this survey involves the inflation of the weighted sample tesults to independent estimates of the total civilian, noninstitutional popula- ticxt of the United States by age, race, sex, and Hi.tpanicJnon-Hispanic categories. These , independent est imates are based on statistics on births, deaths, immigrat ion, and emigra- tion, ac well as statictics on the strength of the Armed Forces. Based on the use of a special weighting algorithm developed by the Bureau of the Census, the CPS household sample estimates are considered to be rcptesentatitve of the United States. However. one potential problem with the CPS is the effect of proxy repcxts on sample estimate,- of smoking status. This may result in an underreporting bias. Gallup Surveys Gatlup surveys are conducted using personal (face-to-face) or telephone interviews. L£69 Z851S Personal surveys. The design of the sample for personal surveys is that of a repli- cated area probability sample down to the block level in the case of urban areas and to segments of townships in the case of rural areas. After the Nation has been stratified geographically and by size of community accord- ing to information derived from the tnost trcent census, more than 350 different sam- pling locations are selected on a mathematically random basis from within cities, towns, and counties that have in turn been selected on a mathematically rardan basis. ` The interviewers are given no leeway in selecting the areas in which they are to con- duct their interviews. Each interviewer is given a map on whicha specific starting point is marked. and is instructed to contact households according to a predetermined travel pattern. At each occupied dwelling unit, the interviewer selects respondents by follow- ing a systematic procedure. This procedure is repeated until the assigned number of interviews has been completed. { Telephone surveys. The national Gallup telephone samples at'e based on the~4trt1 probability sample used for personal surveys. In each of the sampling locations selr;cted (as described above for personal surveys), a set of telephone exchanges that falls within the geographic boundaries of the sampling location is first identified. Listed telephpne numbers in these exchanges are selected randomly and used as "seed numbers" for ran- domly generating telephone numbers. The result of this procedure is a sample of listed and unlisted telephone numbers assigned to households within telephone exchanges serving the sampling locations. The final sample of numbers thus reflects the stratifica- tion and selection of sampling locations. After the survey data have been collected and proeatsed. each respondent is assigned a weight so that the demographic characteristics of the total weighted sample of respon- dents matches the latest estimates of the demographic characteristics of the appropriate adult population available from the U.S. Census Bureau. Telephone surveys are weighted to match the characteristics of the adult population living in households, with access to a telephone. The weighting of personal interview data includes a factor to improve the representation of the kinds of people who are kss likely to be found at home. The procedures described above are designed to produce samples approximat- ing the adult civilian population (18 and older) living in private households (excluding those in prisons, hospitals, hotels, and religious and educational institutions. and those living on reservations or military bases)-and in the case of telephone surveys, households with access to a telephone (Gallup 1987a). Lieberman Research Inc.. 1986 The study was based on tekphotte interviews in a nationwide sample of 1.025 per- ccros 18 years of age and older in the contiguous United States (Alaska and Hawaii were not included). A random-digit-dialed sample was used. Interviews were conducted fmm June 26 through July 10.1986. The study was jointly sponsored by the American Cancer Society, the American Heart Association, and the American Lung Associatdon; neither interviewers nor respondents were aware of the sponsors. 749

TABLE 23.-Cigarette smoking among teenage females, United States, 1968-79 Age - 12-IS }ears - 15-16 ~eus . 1'-19 %ears Total Smoking status Year Y % N g, V % N ~ %,'e% ersmokedor 1968 919 97.9 532 84.4 462 73.0 1.933 86.8 experimentedonly 1970 536 95.0 312 81.5 264 70.0 1.112 84.0 1972 569 93.3 312 77.0 277 66.7 1.158 81.7 1974 495 90.2 250 69.3 228 62.1 973 76.2 1979 514 92.3 319 81.8 239 63.9 1.072 81.2 Former smoker 1968 7 0.7 25 3.8 38 6.0 70 3.1 1970 8 1.4 IS 3.9 22 5.8 45 3.4 1972 11 1.8 26 6.4 30 7.2 67 4.7 1974 26 4.7 33 9.1 42 11.4 101 7.9 1979 19 3.4 23 5.9 34 9.1 76 5.8 Current occasional 1968 7 0.7 14 2.1 IS 2.4 36 1.6 smoker 1970 3 0.5 I 0.3 5 1.3 9 0.7 1972 0 0.0 1 0.2 3 0.7 4 0.3 1974 1 0.2 5 1.4 2 0.5 8 0.6 1979 tp m 0 0.0 2 0.5 3 0.8 5 0.4 ~ 60 u'1 ri tn TABLE 23.-Continued A n 7 18 Total 15-16 years yea - 1 Smokingstann Yar t 2-t4 yean N % N ~ N q6 N 9i 4 8 Curtent regular 1968 6 0.6 63 9.6 1 l8 18.6 22 8 187 158 . 11.9 smoker 1970 17 3.0 55 14.4 86 . 25 3 18b 13.3 :972 17 2.8 66 163 l03 . 195 15 3 1974 27 4.9 73 20.2 1 8 95 98 25.9 26.2 168 . 12.7 1979 24 4.3 46 . 1 100 633 100 2.226 100 Total 1968 939 100 654 100 1 324 100 1970 564 l00 383 100 377 . 417 1 100 1972 597 l00 405 100 415 100 . 277 1 100 1974 549 100 361 100 367 100 . 1 321 100 1979 557 100 390 100 374 100 , SOURCE: US DHEw Tan.p Smoking Surveyf. 1961. 1970. 1972.1974• 1979(US DHEW 1979b).

~ 0 E 0 ~ g ~ VI ~ V y 0 X ~ b e ~ n ~ n~O v~ a v1 v% A n n n .o v~i r h n ~ Warning Labels for Cigarettes Recent data are not available on public opinion about rvarning labels. However, from 1964-70, support for these appeared to increase. In 1964.28 percent of adults thought that cigarette advertising orcommercials should not be required to carry a warning state- ment to the effect that smoking may be harmful to health; in 1970. 88 percent thought that cigarette advertising or commercials should be required to carry such a warning statement (Table 32). Several surveys have assessed opinions regarding the need to strengthen the then ex- isting health warning on packages and/or advertisements (e.g., Roper 1978). Some of these surveys tested specifically worded warnings that had been produced as an alter- native to the existing warning. Because these data over time are difficult to compare and were most relevant at the time of the survey, they are not presented here. Survey data from Lieberman Research, Inc. (1986) pertaining to recall of warning ( statements are presented in Chapter 7. Ernnomk Policies Taxation V M ~ 5 C : c $ C a ~ 0 A N Vi A N N N N A O R~~ 16 V v E 0 r ae R ~8 8 a ~ 3 " Y ~ O P p -'" ~ n B ~ a 000 $' 2 1 V V ;- ~ v ~ t a 0 a 7 y7 V U V'...~i V < t7 ~iS IfifIfi ,~O Y c g ~ <~~ ~ a C ~ ~ ~ s~~~~~~ ~~ ~ V i P P P P O~ P P P P ~ P 5 I C Y V i ~ w Y ..d ~ - ~ > > y , ' ~ ~ ~ iiii . " ~- Z '~~~g~~Sa~ ~~ ~'~.~ ~~8~~~~ ~_ ~f. 1 r ~a ~ ~ v V lj ~ S~ ~ V V C 7 < 'C o~S ~r~ [ F ~{ ~i -i .ri ~d e~ eo o _° ~r4 S'-z .ie=lL°s Questions regarding taxation of cigaeteea ate refererteed to the taxation kvel at the ~ time of the interview. This level varies with time, so it is difficult to delineate trends in opinion regarding taxation. Neverthekas, national surveys indicate an increase in ' public acceptance of increased cigarette taxation (Table 33). In 1964, 30 percent of adults thought that taxes on cigarettes should be much higher than they were at the time of the interview. Similar questions asked in 1977 and 1981 ', revealed an increase in this pnoportion to 39 and 46 percent, tespectively (Gallup 1981) (Table 33). In 1987.79 percent of adults (75 percent of smokers and 80 percent of non- smokers) favored an increase in the tax on tobacco pnoducts if the money from the in- crease went to medicare (Harvey and Shubat 1987). These recent data are of particular interest in light of the prevailing sentiment opposing increases in taxes in general. Hiring A minority of adults feel that employers should be allowed to refuse to hire cigarette smokers. In the 1978 Roper survey, 22 peteent of adults thought that an employer has the right to refuse to hire sontecxte who smokes cigarettes. In a 1986 survey (Lieher- man Research 19R6), 21 percent of adults (27 percent of nonsmokers. 7 percent of cur- rent smokers) believed that employers should be allowed to turn down job applicants who smoke. CE69 18919 ~ ~r~ 1 241

TABLE 22.-Cigarette smoking among teenage malea, United States, 1968-79 Age 12-14 years I S-I6 yean 17-18 years Total Smoking sanu Year N 9i N Rr N 'b Y 5b Never smoked or 1968 876 93.1 w 75.2 344 54.7 1,683 77.0 experimentedonly 1970 512 90.5 268 70.5 178 48.1 958 72.8 1972 533 91.1 273 68.3 211 54.4 1.017 74.1 1974 496 90.7 253 69.5 202 55.3 951 74.5 1979 327 92.8 284 75.3 234 68.1 1.065 80.8 Fomxr smoker 1968 25 2.7 34 3.3 71 11.3 130 5.9 1970 21 3.7 33 9.2 52 14.1 108 8.2 1972 20 3.4 50 123 56 14.4 126 9.2 1974 28 5.1 43 12.4 44 12.1 111 9.2 1979 23 4.0 38 10.1 46 12.3 107 8.1 Currentoccasional 1968 13 1.4 14 2.3 24 3.8 31 2.3 smoker 1970 1 0.2 3 0.8 2 0.5 6 0.5 1972 5 0.9 6 1.5 4 1.0 15 1.1 1974 0 0.0 0 0.0 6 1.6 6 0.5 1979 t- 0 0.0 4 1.1 1 0.3 5 0.4 %0 r-4 (p tr VA Ln TABLE 22.-Continued Age eats 16 IS 17-I8 yean Total 12-14 years y - Smoking status Year N `li N 9G N ~b V q6 Curtentn:gular 1968 27 2.9 105 17.0 190 30.2 322 244 14.7 18 3 smoker 1970 32 5.7 74 19.5 138 37.3 . 15 7 1972 27 4.6 71 17.8 117 30.2 213 . 1974 23 4.2 66 18.1 113 31.0 202 15.8 7 0 1979 1i 3.2 31 13.5 72 19.3 141 1 . 100 Total 1968 941 100 618 100 629 100 2.188 100 1970 566 100 380 100 370 100 1.316 1972 SSS 100 400 100 388 100 1.373 100 1974 547 100 364 100 365 100 1,276 100 0 1979 568 t00 377 100 373 100 1.318 10 SOLRCE US DHEW Teedp Sasokiag Saneys.1969.1970. 1972, 1974,1979 (US DF(EW 1979U),

TARLF 7.---,Shte-specHk amokinR prewdence (•X,), geh.v{ard Risk Fadcr Curveiilance System, adults aRed lR rears and nlder,19ltZ-tC7 Stne 19R2 19114 19RS 19" 19A7 Alahama 31 zs 27 Alaska 36 34 Aritona 32 29 26 24 26 Arkanaaa 27 Califomia 29 26 26 23 21 Colorado 34 Connecticut 27 Delawae 31 District ofColumbia 33 3>< 26 27 24 Florida 32 27 28 29 GeorRu 29 37 29 27 23 Hawaii 25 23 Idaho 25 24 23 21 Illinoia 34 26 29 26 Indiana 33 2s 32 27 29 lowa 30 Kan..a 22 Kentucky 37 29 35 32 Maine 211 Marylyd 23 Ma.syehucetts 27 25 Michigan 31 Minne.Ma 27 28 25 24 Missouri 26 29 Montana 26 29 25 23 22 Neh.aaka 23 New Hampshirc 29 New ler.ey 32 New Mexico 29 26 21 New York 31 27 23 Nnrnh Carolina 311 31 27 27 26 North Dakota 2R 26 26 24 Ohio >n 29 29 29 27 ES69 tBStS TARI.F, 7.--Con/inued State 191t2 19144 19115 1986 1987 1'ennsylvania 34 Rhtxk taland 31 29 39 South Carolina 26 29 27 4.25 South Dakota 25 Tennes%ee 32 32 29 2R 2R Texa% 30 Utah 16 16 IS IS Virginia 34 ~ Washington ; 24 West Virginia 32 33 27 29 29' Wiwomm 27 25 26 26 Minimum 22 16 16 18 I S Maximum 33 3E 32 35 ~ 32 Median 37 29 27 26 24i Number of Sutes' 27 19 22 26 1 29~ 'Mclwk" dhe Diarict d Calwnbia. N(7ft;: No das were availahk for A2 followfa~ 1tMee LA. MS. NV. OK. OR. VT. aed WY. SoURCE: COC (19MS.,h.19RN.wquMkhed daa). RRFS and CPS Cnntparison In 1985. both the BRFS and the CPS collected State-s{>ecific information on adult smoking prevalence. Among the 22 States (including the District of Columbia) where comparisons can be made, the CPS (an in-person household survey) estimated higher smoking prevalence in 13 States and lower prevalence in 8 States than the BRFS (a telephone survey). ?1The median diffetence in smoking prevalence between the CPS and , 2Ro 1 281

Smoking prevalence rates among enlisted personnel (ranks E1-9) are at least twice the rat" among commissioned officers in each'curvey year (Table 6). In I9RR, for in- stance. smoking prevalence estimates ranged fnim 47 percent for the lowest ranks of enli-,tcd personnel (E 1-3), to 20 percent for the higher ranks of commissioned ofrccrs ((>'3-O 10). The proportion of smokers smoking a pack or more a day was 55 pcrcent: there was no consi%tent association between this proportion and military rank (US DOD 1 yRR). Cronan and Conway (19R7) collected smoking information from 6R7 recruits entcr- ing the Navy and from 1,357 Navy servicemen stationed aboard ships in the San Diego arca. The prevalence of sm~king was 27.6 percent among recruits and 49.R percent among shipboard men. The investigators concluded that the Navy is not attracting a higher than expected percentage of smokers from the U.S. population, but that many men start to smoke after they enter the Navy. Reasons for higher smoking rates among military personnel include the inexpensive price of cigarettes in military facilities, peer pressure hightened by conditions of group living, strcss, boredom, and lack of other forms of recreaticxt (Cronan and Conway 19R7; Blake 1985). In addition, there has been a historical connection between ciga- rettes and the military: cigarettes have been a part of the K-rations and C-rations provided to soldiers and sailors, and cigarette advertisements on radio and in the print media during World War II commonly featured military themes (Blake 19R5). Cigarette advertising continues to appear in military-oriented publications (Davis 1987). In September 1988. Philip Morris Tobacco Company began to publish a month- ly newsletter,"Mil itary Smoker," which features articles opposing restrictions on smok- ing and on cigarette sales in military facilities: readers are urged to call a toll-free "Military Smoker" hotline telephone number (Philip Mortis 19RR). Recent DOD initiatives to reduce smoking among military personnel are described in Chapter 6. State-Specific Smoking Prevalence Rebarioral Risk Fartnr Surveillanrt System: 1982-87 The Behavioral Risk Factor Surveillance System (BRFS) has prvvided State-specific smoking prevalence estimates for adults I R years of age and older for about half of the States since 19R2 (Table 7). Data are collected through random-digit-dialed telephone ZS69 18SiS '7R I interviews. Since 1984. the number of States participating in this surveillance system has increased steadily. For reporting States, median prevalence declined from 37 per- cent in 1982 to 24 percent in 19R7. This decline exceeded the decline mixnof prevalence in the NHIS (Table 3), probably because of the nonrepre• States included in the BRFS in different years. In 1987, prevalence ranged from 15 percent in Utah to 32 percent in Kentucky. Current Population Survey: 1985 In 19R5, the Current Population Survey (CPS), a population-ba.eed. in-person household survey of rnore than 114,000 adult Atnericaesd conducted by the U.S. Bureau of the Census, collected information about smoking and sttwkeless tobacco use. About ( 45 percent of interviews •were conducted'uith proxy respondents. The survey estimated I adult smoking prevalence (20 years of age and older) at 29.5 percent. Table 8 prre.sents , estimates of prevalence of cigarette smoking according to tegton of the counoY' cen- ; sus divisions, and States. Among the nine census divisions, prevalence was lowest in c the Pacific (26.3 percent) and Mountain (27.2 percent) divisions and was highest in the! East South Central (31.R percent) and South Atlantic (31.3 percent) divisions. Overall gender-specific prevaknoe was reported as 32.9 percent for males and 26.5 1 percent for females. Prevalence of smoking attang males exceeded that among females in all States except Oregon and W ing(where the ~a~erates among men and ' Y~ f-~ alence women were either very similar or the same). Overall eduaition-spe~ Pfe" was 35.4 percent for persons with 12 or less yeats of education (high school diplorna or less) and 22.2 percent for persons with 13 or more yars of education (some college with 13 or more years of education reported lowa smok- ' or more education). Persons ing prevalence rates than those with 12 yrws or less edncation in a1150 States by a range of 20.2 percentage points in Tennessee to 5.7 percentage points in Hawaii. 279 ;s ;

TABLE 11.-Smoking continuum by sex and education, percentage of ever smokers, United States,1986 Sex Education Males M Females t`b) 5l 1 yeats lRr) 12 years (%) 13-13 yeats (`4) 216 yean (40) Smoking contiauus Smoken who never oried tc 8.3 (8.3P 9.1 (9.1) 9.8 (9.8) 9.5 (9.5) 7.7 (7.7) 5.7 (3.7) quit ( l0)' Smokers who never tried to 9.1 (17.4) 9.6 (18.7) 9.8 (19.6) 9.3 (19.0) 10.9 (18.6) 3.7 (11.4) quit (9) Smokers not quitting in the last 213 (38.9) 23.9 (41.7) 23.9 (43.5) 22.5 (41.3) 22.5 (41.1) 17.7 (29.1) year(8) Smolws quitting 1-6 days in 3.4 (42.3) 4.6 (46.3) 4.4 (47.9) 4.9 (46.4) 2.6 (43.7) 1.3 (30;6) the lut year (7) Smokers quitting 7 or moae 6.3 (48.8) 8.6 (34.9) 7.4 (SS.3) 7.9 (34.3) 8.6 (52.3) S.0 (3J.6) days in the last year (6) Ex-smokers 0-3 mondu (3) 6.8 (33.6) 3.2 (60.1) 6.6 (61.9) 5.4 (39.7) 6.0 (38.3) 7.0 (42.6) Ex-smokers 3-12 mondts (4) 3.6 (39.2) 4.3 (64.4) 3.4 (63.3) 4.1 (63.8) 4.7 (63.0) 3.7 (46.3) Ex-smokea I-S yeats (3) 10.9 (70.1) 10.7 (75.1) 7.8 (73.1) 10.7 (74.3) 12.8 (73.8) 14.0 (60.3) Ex-smokars 23 years(2) 30.1 (100) 23.1 (100) 27.2 (100) 25.3 (100) 24.4 (100) 39.2 (100) 'CaoeB«y on d+e srtwkinj conunuum (see Tabl. 10 ror defSnunau). •Yumben in paanlwa ate cumulaeive pacentapa. 5O(:RCE: ALTS 19b6(US D1iH3. in pew a). TABLE 12.-Smoking continuum by race and age, percentage of ever smokers, United States, 1986 Race Age Whites Blacks 18-24 yean 23--44 years 45-64 years 263 years lR+) M (96) (96) M (5b) SmokingcaoNauus Smokery who never med 8.7 (8.7P 8.6 (8.6) 9.1 (9.1) 6.9 (6.9) 8.3 (8.3) 7.4 (7.4) to quit (l0)' Smokers who rieva pied 8.9 (17.6) 12.3 (20.9) 18.4 (27.3) 10.6 (173) 7.3 (15.8) 3.6 (11.0) to quit (9) Smokers not quitting in dle laat 22.2 (39.8) 22.2 (43.1) 16 3(43.8) 26.4 (43.9) 21.6 (37.4) 14.3 (23 3) year(8) Smokers quittin81-6 days in 3.6 (43.4) 6.9 (50.0) 7.2 (31.0) 4.4 (483) 3.2 (40.6) 2 l(27.6) the last year (7) Smokers quitting 7 or more 7.0 (50.4) 10.7 (60.7) 19.3 (70.3) 8.6 (36.9) 4.7 (s3.3) 2.0 (29.6) days in tNe lat yer (6) 6 2(S i 3) 8.2 (37.8) Ex-smoktrs 0-3 montfti (3) 3.9 (36.3) 7.S (68.2) 7.2 (77•S) 5.8 (62.7) Ex-smokets 3-12 tnoatn (4) 4.0 (60.3) 3.3 (71.5) 9.0 (86.3) 4.3 (67.0) 3.2 (54.7) 2.3 (40.3) Ex-smokers 1-5 yean (3) 10.8 (71.1) 9.4 (80.9) 10.3 (96.8) 11.4 (78.9) 9.9 (64.6) 10.1 (30.4) Ex-smokers 2S years (2) 28.8 (100) 19.0 (100) 3.0 (l00) 20.6 (100) 35.6 (100) 49.7 (100) 'Cuesory on dta smoking cancnuum (sx Tabls 10 faa deAnitior)6 Nunben in patenttteus ats cumutauve paceualpw. SO(: RCE: A<,TS 1996 (US DIIH3. is praaa. a). I

S.A\IfT. 1.\L. T.\GER. LR.. SPEI7FR. F.E. The rclatitMt.hip hita.rn rc.Piratrn. ilhk., irt chrlJhrxxl and chmnic uir-11t,a rlh.trurtit.n in aduhlMx,tl. .anrrrirun Rr•rirrr rr/ Rryrirrnrvt /)nr•rr,r• 1?7t J r: S(IR- 52i. ,\lail It)R}, S.a\ IET. J.\1.. \\.IGGI\ S. C.L.. lll \IRLE. C.G.. P:\THAK. D.R. Cirarcne.mohim_ arxl lune cancer in \e„ \lrsirr.. .lnrrrrrurr Rrrirrr rp Rr•,/+ir•ulrrrr /1r.r•rr,r 137:1 1 111 - 1 1 1?• It/;tR• ` S>\ DLFR. R.R.. SLIAIF.\ D.a•(-.\C•,1•.\PORTF.• R.E..CAL LE1'.1.:\.. SCIIR:\\t\1. \L\1.. R.\RRFS1. M.L.. KRISK:\. A.\I. Pt,.unenal,:nr.al ht>fx J.n.it, and mil{, con.mnlaian in cl,ildhrMxl :md atkdc.c,•tx.. .Inrrr•nrrrr.Innrrud nl ('lirrital.\nn•ilirm a`:?7f1-?7J• :\tu,_u.l IrrR:. S:\R \CCI. R. TI>< intrr:Ktirxr af tnh;K•co .nN,hin,• and Mhar :r;entN in cancer rtiolo,•,. /./,hlrrnirrlncir Rr rir'u ~ q:l73-1111• 1111(7. I.M.. 11.1Lf:1'. \.1.. H(N4\I:\\N, D.• WY\DfR. F.1... Hf:LLRF.RG. I).. \ II.SSO\. ti. Crt.-:nrttc .nud,ine arxl ncrry.la.i:r r,f the utcrirx ra n is: Smnl r rtql•titu~ m. in crr.ical rnuru.. .\rn rn,lrnrrl.l.rrrrn,rln, tfrrlirrrrr s1_15/:;I5 -3 1h.lanuarv 3 I. I')R5. SCfI.>RDEI\• J.1.. ('hrrnir,rll, indm rd hirrh rl~/rr r,. \c„ Yorh:.\1arc.l DrrlJ.er. It)R3. SCHOTTF•.NFELU. 1). Epidentitdr,t% pf carkcr rd' the c•rsphaLu•. .G•rrrinur, in r)rrr.rlntr I II-'/:V?-I(KI• Jtrnr 1rrX1. SEPKOVIC. D.W.. H:\LEY. N.J.. FIOFFMANN. D. Elimination fnnn Ihc Mxh ol'toh:x•cr, product. hs, .mokcr\ and pa..i,e .nN,hrrs. Jrntrwnl n/•tbr Arnrrir-rm rL/rdirrd.t,arr iurinrr 3SIN71:R(it. Au,nuct 1996. SKILLRI ID. D.\I.. OfTORD. K.P.. MILLER. R.O. Higher risk of lung cancer in chnxtic oh.tructive puhnr,nary di.ease. A pn..pecti,a matched• ctrnnrolled.Itkl%•. .Innul, rr/ Inrrr•- rrr,l.tfrr/ir inr 1014.3 1:5(/ i-5(17. OcN,hCr 19tt6. SLONE. D.. SI1.\PIRO. S.. KAUFMAN. D.W. ROSENBERG. L.. MIETTINEN.O.S.. STnL- LEY. P.D. Ri./, ol' mrocardial infarctit,n in rclation to current and discontinucd usc nf nral crnuraceplives. Nrtr Fn,eGwrd lnrn•nul rrf,Nrdicinr 3(/5:J'(1--f?J• August 21. I9R 1. SONTAG. S..GRAHAM. D.Y.. RF.LSITO. A.- WF.ISS,1.. FARLEY. A..GRUNT. R..COLfF.N. N.. KINNEAR. D.. DAV1S. W.. ARCHAMBAULT. A.. ACHORD. l.. THAYER. W.. (ill: LIFS. R.. SIhIROV. J.. SARESIN. S.M.. DYCK. W.. FLF.SHLER. B.. CLEATOR. L. WENGER.1.. OPEKUN. A.1R. CimetiJine• cigarctle smnking. arxl recurrence otdurxle,al ulcer. Nrir Fu,clund./rqrrnrd ry'!Nrtfir inr 31 I I I 11:(iR9_49i, ."emher 13. 19RJ. SOWERS. M.. WALLACE. R.B.. LEMKE. J.H. axrelates of forcann hntx mas% amnne anmcn during maximal hcme mineraliration. Prrt•rmireMrdirinr 1J:5R5-5`X+. 1t)R5• SPENGLER.I.D.. SEXTON. K. Itukx,r air pollution: A public health pcrspr-ctire. Sr•irrrr•r 121(Jh()51:9-17. July I. 1993. STAMLER. J.. WENTWORTH. D.N.. NEATON.I.D.. MRFIT RESEARCH GROUP. Mid- dle-aged American men at very low ri.k of ce,rnnary death: 6-year findings on the 356.222 scrcenecs of the Multiple Risk Factor Intervention Trial (MRFIT). Paper prc.entcd at the Tenth World Ccmgrcs% of Cardiology. Wa.hingu,n, D.C.. September I9tt(,. STEDMA N. R.L. The chemical eomposilion of tnhaccc+and tobacco smokc. Clrrrnir al Rrriru:, 6R1? 1: I5 i_?(17. A f,ril 19(,R. STEIN. 7... KI.INF.. J.. L.EVIN, R., SUSSER. M.. WARRURTON. D. F.pidemiah,cic .nnlies ofcnvirnnmcntal cspr,.urrs. In: Rcrg.G.G.. Maille. D.D. (eds./ Mru.tnrrrrrrnrr,jRi.,(,, 19R(1• p. 17(1• STUART-HARRIS.C.H. Theepidemit+kogyandevnhninnofchrnnichmnchitis. Rriti.alr./mnr- nal.,/'Tnhrrrnl.nb urrd ni.rrrrct.r n/'drr Clrrst JR( =1:169-17R.1tdy 1954. STUART-HARRIS.C.H. Chrnnichrrnx•hilis• (Partl.) Ahwrat•tse/'ll'nrldMrrlirinrJ'(')1:(*d9- Ir(i9. 19611ta. STl1ART-HARRIS• C.LI. Chrnmic hmnchitis. (Part II.1 :Ihstrrrr•tt n/' It'nr•hl .1frJirinr J20(11:7t7-751. 11161th. SI IARF7.. L.. RARRETT-CONNOR. E. Interrcticxt hetween cigarette smoking and diahetcs mcllitum in the prediction of death attributed In cardiova%cular Ji.ca.c. .Irrrrrir fur.lrrrrr nrrl rrl, F./rirlrminln,c. 12(N5070-675- 19R4. Sl!I.LIVAN.I.M.. ZWAAG. R.V.. LEMP. G.F.. HI:GHES.I.P.. MADDOCK. V.. KROET7.. F.W.. RAMANATHAN. K.R.. MIRVIS. D.M. Postmenopausal estrtipen usc :uxl cororiar. ;nhcrrnclero.i.. rlnmrls.rflmernal Medicine I(ht:i5R-i6t. March 19RR. TAIIA. A.. RAL.L• K.P. ILLINGWORTH. R.D. Smoking and wharachnoid hacmnrrhagc. .Inrn71rrl rrf rlu• Ra,vd Snt itty nf Mtrlirinr 75(5):172-i35, May 19R2. ~ TANAKA. H.. IIEDA. Y.. HAYASHI. M.. DATE. C.. RABA. T.. YAMASHITA.IL. SLK1)I. II.. TANAKA. Y.. OWADA. K.. DETELS. R. Risk factors for cerebral hcmorrh:tgc antl cerebral infarction in a lapanese rural community. Srrnkr 1 3:62-73• 19R3. T( )Kl1HATA. G.K.. LILIENFELD. A.M. Familial aggregation of lung cancer in humans..hnn - nul nj tlrr Nurinrrul Cant rr I rrstiturr 3(1:2R9-312• 1963a. TUKUFIATA. G.K.. LILIENFEL.D. A.M. Familial aggregation of lung cancer among ho.Pit•d P:nient.. Prdrlit lleullhRrl+rn•t.a 7R:277-2Ri. I963h. l!.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. Thr HralrlrCnnvqrrrnr f:. rrf, .SarnCirr,l (r,r• R'nnrrn. A Rrlrnrt nf tbt Snrtr•nt (;rrttral. U.S. Dcpartment of Hcaltfr; arn1 I Iuman Scrvices. Public Health Service.Offrce of the Assistant Secretary for Health. Otfice on Smoking and Health. 1980. 13.5. DF.PAR1 MENT OF HEALTH AND HUMAN SERVICES. The Health CnncrqranS•rk rpf SnrnAin,p. The Clurn,ocirr,k. Ci,cm•rtte: A Report nf drt Srrreenn General. U.S. Department of llcalth and lluman Scrvices. Public Health Service. Office of the Assistant Sccretary, for' I Icalth. ()fficc tm Smoking and Health. DHHS Publication No. IPHS/ R I-5()I5/+. 1981.1 . L;.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The HtalNrCnn.crqrrr•nr-rc nf Cmnkin,e: Crnrrrr•. A Rr/rrrr•r njrht Sar•teonGtneral. U.S. Department of Health ancl Human Services. Public Health Service. Office on Smoking and Health. DHHS Publicatitm No. (PHS) R2-50179, 19R2. 11.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. Tlre Healtlr C'nnaqnerrr•rs rrf Srnnkin,c: Ctrdim asrnlar picrast. A Rt/rnrt nf llre Snrqtnn General. U.S. Department of Health and Human Services. Public Health Service. Office on Smoking and Hcatth. DHHS Publication No. (PHS) Rd-5t12(14• 19lt3• U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. Tht HtalthConcrqnent•rs nf Snrnkirr,e: Clrrnnir Obarrorti,Y Leng Di.aast. A Rtpnrt nJtht Snretnrr Gtnrr•al. U.S. Depan- ment of Health and Human Services. Public Health Service. Office on Smoking and Hcalth. DHHS Publication No. (PHS) A4-5f1205. 19R4. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The HtalthCnnsrqnrru•ca of Smr,Rin,e: Canr tr anrl Clrrnnir Lnne Disease in the Workplace. A Relrtrrr rrf rht Sur.eenn General. U.S. Department of Health and Human Services. Public Health Service. Of/ice on Smnking and Hcalth. DHHS Publication No. (PHS) 85-502(17• 19R5. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Health Cnnstqnrnt•rs nf Irn•nlrmtm.t• Srrrnlin,q. A Report nf the Sarqrnn General. U.S. Department of Health and Human Serviccs. Public Health Service. Centers kx Disease Control. DHHS Puhlication No. (C DC) R7-R t9R. 19R6a. l/•S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Health C.rn.,rr/nemr'rrf Usin,q Smr,krlraTrdrarrn. ARejrrn7afthaAdriinrrCantminrrtnthtSrnrerarrGrrrrrrrl. U.S. Department of Health and Human Services. Public Health Service. National Inaitutes of Hcalth. NIII Publication No. fKi-2R74,19R6b. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. The Healrh C'nrrcrqnrnr'rs rrf Smnkirre: Nit ntinr Adrlirlinn. A Rrjrrrrt njrlrr Snreenn Gt•rrrral• 1yRR. U.S. Dcpartmrnt nf Hcalah arxl Human Services. Public Health Service. Centers for Disease Cnnarnl. ('cntrr frx 6989 18STS ' 113 tl t~

c ~ V a A < 91 .CE o` C t~ 7 E 0 L 3 0 9 oC a ~ .~ 13 s ~ © I i I s ~ 0 '~ N a & 0 a e v c ~ a i 2 1 9 01 F- W J m ~ I >~V.. h F - ~ j 6 0 I Banning Free Samples In a 1986 survey conducted by Liebemun Research, Inc. (1986) (New York City) for ACS. AHA, and ALA. 61 percent of adults said that the distribution of free cigarette .amplrs should not he pcrmitted (67 percent of nonsmokers, 48 percent of smokers) (Table 30). Policies Pertaining to Information and Education Restrict or Prohibit Tobacco Advertising Since 1964, several surveys have investigated public opinion regarding a cigarette advertising ban, with marked differences in the wording of questions. Taken together, { they do not seem to indicate any trend in public opinion (Table 31). However, separate; examination of surveys using identical questions over time indicate increasing support for an advertising ban. A series of identical questions from the AUTSs from 1964 and 1975 showed an increase in support for a complete ban between 1964 and 1970. In: 1964, 36 percent of adults thought that cigarette advertising should be stopped CMT pletely. This increased to 61 percent in 1970 and 56 petcent in 1975 (Table 31). Sup- port for an advertising ban may have increased by 1970 because Congress had already, banned cigarette advertising on television and radio in 1969 (effective on January 2,1 1971) (see Chapter 7). Another series of identical questions used in Gallup sutveys after the broadca.ct advertising ban showed an increase in the propation of the public' favoring a cigarette advertising ban, from 36 percent in 1977 to 43 percent in 1981 to 49 percent in 1987 to 55 percent in 1988. Since 1975, surveys have provided conflicting results regarding public support for a complete ban, most likely as a result of differences in the wording of questions. In the two Gallup surveys conducted in 1977 and 1981, support for a complett ban on' rigerette advertising increased from 36 to 43 percent (Gallup 1987a). In a 1985 Gal- lop survey, adults wer~e asked which atnemt:M best described the respondent's opinion mgarding cigarette adverti.cing: "Iltere should be a total ban on cigarette advertising." "Ihere should be a curb on some types or fornta of cigarette advettising." "There should be no ban whatsoeveron cigarette advertising in newspapets, magazines, or billboard.c." 11The public was divided in their reaponsat: about a third favored each option (32, 36, and 31 peroent, respectively) (Gallup 1985). As mentioned at the beginning of this Cltapter, two tsttrveys conducted in 1986 reported different results. One, conducted by AMA, mported that almost two-thirds of adults favored such a ban whereas another, sponsored by ACS, AHA, and ALA. rcported that only one-third of Americans supported such a ban for newspapers and magazines (see the earlier discussion of these discrepant results). Four morc rtcent sur- veys, conducted in 1987 and 1999, rrevealed that about half of adults favor a complete ban on advertising (Table 31). Z£69 i8S1S '1R 4 219 V

the BRPS was +1.8 percentage points. This pattern is similar to that observed in com- pariscros between the in-person NHIS and the telephone AUTS (see above). Summ.ry A numberof national and State-based stnveys provide information on cigarette smok- ing. These surveys have varying methodologies and response rates. The data of highest quality (large sample sis.e, high respnnse rate) are from the NHIS, and this source also has the best series of data for analyzing trends in smoking prevalence since 1965. Trend analysis demonstrates that smoking prevalence among adults overall is declining by 0.50 percentage points per year and this rate of decline has been consistent since 1965. If this rate of change continues for the next few years, overall prevalence will be 27 to 28 percent in 1990, which is higher than the 1990 Health Objective for the Nation (less than 25 percent) (US DI IHS 1980a; see Chapter 1). Although there are differences be- tween whites and blacks in smoking prevalence, the rate of change within each race has been similar in recent years. The decline has been much higher in men than in women and much higher in the more educated than in the less educated. The consistency of the trends in these smoking prevalence data contrasts with the lack of year-to-year consistency in the consumption (excise tax) data presented in an earlier section. Given that both data sets report cigarette usage in the population, reasons for this difference need to be addressed. Each data set has its advantages. Ex- cise tax data have the advantage of being an objective measure of manufactured- cigarette sales and are not subject to que.stions of validity that must be addressed with self-reported smoking from survey data. On the other hand, survey data provide infor- mation on smoking behavior in specific subpopulations within society. Cigarette sales data, and trend analyses of these data, reflect both the number of people who smoke and the number of cigarettes each smoker consumes (plus a wastage and stock error term). On the other hand, trend analyses of self-reported smoking prevalence reflect only the number of people who smoke. Antismoking interventions may affect an individual's smoking status or daily cigarette consumption. For example, worksite smoking restrictions may induce some smokers to quit, wheteas others who continue to smoke may smoke fewer cigarettes per day because of fewer opportunities to smoke. Similarly, increases in cigarette price (e.g., mediated by increased excise taxation) may induce price-sensitive smokers to quit or to reduce daily consumption. While consumption data are often used as a mom sensitive index of the relative im- pact of differing antismoking strategies, the primary goal of these strategies is a change in smoking prevalence. Smokers who reduce their daily cigarette consumption will reduce their health risks, but to a lesser extent compared with quitting entirely (see Chapters 2 and 3). SS69 T8SiS Trends In Quitting Introduction As the 1988 Surgeon General's Report documented (US DHHS 1988), cigarettes and other forms of tobacco are addicting. This addiction, including both pharmacologic and behavioral components, helps to explain the difficulty that most smokers ex= perience in quitting and then maintaining abstinence. Smokers can be on a quitting cycle in which they are abstinent for a while, followed by a relapse to smoking for a period of time, after which they may quit again, and so on. Given this pattern, no single' statistic can fully describe trends in quitting activity. Three interrelated statistics are: 1. Percenrageofforertrsmokers. Thepereentageofthepopulationwhoareformer smokers has been used as one indicator of quitting activity. For example, thel total number of living persons who have quit smoking is often cited and is cat- culated by mul:iplying the proportion of the population who are former smokers by the size of the population. This figure, as calculated from the 1986 AUTS, is 43.2 million adults 17 years of age and older. However, the prevalence of fomter smokers is of limited value ih assessing quitting activity because it doqs not take into account the number of people in the population who have ever smoked, because it does not include former smokers who have died, and be-, cause of marked differences in the initiation of smoking between males and' females in different birth cohorts (Hatris 1983; Warner and Murt 1982). 2. Quit ratio. This statistic is defined as the proportion of people who have ever smoked who are foirmer smokers at a specific point in time; that is, the number of former smokers divided by the number of ever smokers (Pierce et al. 1987). Thus, this statistic is to quitting activity what smoking prevalence is to smoking activity. Both statistics consider the size of the population undertaking a be-, havior as a proportion of those who could undertake that behavior. However, the quit ratio does not provide all the information needed when describing quitting activity. It does not distinguish between a person who has been a former smoker for 3 days and a person who has been off cigarettes for 10 years. It does not distinguish between a current smoker who has just relapsed after 6 years of abstinence and a current smoker who has never tried to quit. In addition, the quit ratio does not reflect the magnitude of smoking prcvalence: for example, a group in which 10 percent are curn:nt smokers and 10 percent are former smokers has the same quit ratio as a group in which 30 percent are current smokers and 30 percent are former smokers. 1. The smoking continuum. This is a 10-category index of the total population derived frrxn the smoking status variable (curtsnt, former, or never smoker) and timing and duration of quit attempts. This index is particularly relevant for describing which segments of the population are trying to quit. Trends in the quit ratio using NHIS data and an analysis of the smoking continuum ; using data from the 1986 AUTS are presented below. i 1144 1 791

, calculate estimates of the prevalence of smoking in any particular time perloa. However, it is possible to use these data sources to examine general pattems of smnk. ing during preFnancy. In genenl, women in the bwest age and socioeconomic categories have the highest likelihood of smoking during pregnancy. The earliest data available to examine these patterns are from the Collaboratilve Perinatal Study (Niswander and Gordon 1972), which included women who obtained prenatal care at selected university centers in the early 1960s. White women were nRne likely to smoke than black women (53 percent versus 43 percent), and among smokeR, whites smoked more cigarettes per day than blacks. (By comparison, the national prevalence of smoking among women 25 to 44 years of age was 44 percent in 1965 (NCHS 19RRc). The National Survey of Family Growth (NSFG) collected data in 1982 on the s(nok- ing behavior of w(xnen, 15 to 44 years of age, during their most recent pregnancy, regardless of when the pregnancy occurred (NCHS 1988b). Of these women, 32 per- cent smoked during the pregnancy. Women who were aged 15 to 19 years when pleg- nant, who had less than 12 years of education, who were at 149 percent or less of pover. ty level, or who were unmarried had the highest smoking rates. In the 1985 NHIS, questions related to smoking were asked of women aged I R to 44 years who had given birth within the past 5 years (NCHS 19RRb). Of these women, 32 percent reported having smoked during the 12 months preceding the birth: 21 percent of smokers reported quitting smoking and 36 percent reported reducing the number of cigarettes smoked after learning they were pregnant. Women under 25 years of aRe, with low income, of black race, unmarried, or unemployed were more likely to smoke than others. These sarne groups of women were less likely to quit smoking or to reduce the number of cigarettes smoked. The 1990 Health Objectives for the Nation (US DHHS 1980a) state that'"Ihe Ixolxx- tion of women who smoke during pregnancy should be no greater than one-half the proportion of women overall who smoke." At the time of the midcourse review of the objectives (US DHHS 1986), no data were available to evaluate progress directly. Ac- cording to the 1985 NHIS, approximately 31 percettt of women aged 18 to 44 years smoked cigarettes in 19R5 (31.7 percent of 18- to 29-year-olds and 31.2 percent of 3(1- to 44-year-olds) (NCHS 1988c). In the same survey, as mentioned above, 32 percent of women who had given birth in the preceding 5 years reported smoking in the 12 months preceding the birth, 21 petcent of whom reportedly quit after leaming they were pregnant. This indirect evidence seems to indicate that the smoking prevalence among pregnant women was much more than half the prevalence among nonpregnant w(xnen in the early 19ROs. Unless major changes in smoking behavior occurred in the latter half of the decade, the 1990 objective will not he met. Analysis of data from the Be- havioral Risk Factor Surveillance System supports this conclusion (Williamson et al., in press). Special Populations: Military Personnel In 1980. 1992. 19R5, and 19RR, the Department of Defense (DOD) perfomxd worldwide surveys of alcohol and n(xlmedical drug use among military personnel. 276 a 111ese surveys assessed cigarctte smoking among persomlel by asking. "During the past ical day?" t ri yp ng a packs of cigarettes did you usually smoke du w man h y o 30 days, (The 19R0 survey question used the phrase "in one day"). Thero were five possible , 4 t less than b u tecpnnses: 3 or more packs; 2 or mtxe. but less than 3 packa: I or more, Sample s 30 da s . y t 2 packs: less than I pack, but smoked some: did not smoke in the pa ating artici i ll p ons p at sines ranged from 15,(1(1() to 21.000. The number of military insta rep- nall ti y o in the surveys ranged from 58 to 81. The surveyed population was pnopor rital statu i F, ty, ma fesentative of all DOD active duty members for sex• rsce/ethnic education, and age (Herhold 1987: US DOD 1987,1988). : er- m 53 f dil p ro y Overall smoking prevalence among military personnel declined stea valence «nt in 1982 to 46 percent in 1985 to 42 percent in 1988 (Table 6). These pre oung les or ll y ma figures. although declining, are considerably higher than among a reflect ma ri y ty males in the general population (Tables 3 and 18). This dispa nel and the general pop' ~ s(,ci(+economic differences between military person er rdrts aft on g though one study suggests that smoking initiation may often occur am idual mil di i n v n entering the military (see below). The 198R estimates for the 44 e A p rmy. branches were: Air Force, 37 percent; Marine Corps• 42 percent: and Navy, 45 percent (US DOD 1988). { TABLF. 6.-Prevaknce of c'Pr*MsmokieR amonR U.S. miRtary pe+'w'n'~.19l00, 19R2,1985, and 1988 Pe.eematte of eunent tmdce(s' ` 1985 19RR 19R0 19R2 1 Rank' (N=15.016) (N=21.412) (N:17.32R) ) (N=1 R.67, ta ) 55 56 47 47 - 6 FA 55 55 52 45 - E7-9 56 61 56 4R 40 M wlrl 19 01-03 01-02 24 25 17 Ot 23 24 Is 21 20 04-010 0t-06 27 28 Tnmal 52 53 46 42 Aadanw,kedciR.reneadwinFArcpwlf/dqa• w1-411eca~rel~*iaW^tricer.(01-n1m. "In a.cemlinR nek. fm,n enlnrcA f~~l (E I-911o wran.r,t r4tl~~+t rPIfI11111nNY ~la1a (rtly a1p~k'd rM /M1/Ml1+^^^•^ •)• S(N 1R(1:: 11eA.+ld /19%71: US 1%)) (191t6.19R7.19RR1. ZS69 18STS 277

PERCENTAGE OF EVER SMOKERS 1001 60 40 20 BEFORE AGE 14 0 1910- 1915- 1920- 1925- 1930- 1935- 1940- 1945- 1950- 1914 1919 /924 1929 1934 1939 1944 1949 1954 YEAR OF BIRTH FIG(IRE 3.-AKe by which maies sfarfed snakinK, by birth coh(Wt CQ( IR('f NNICa VM-R), awnhin[d (wqsMklwA data. pRKe an«jog mW lkahh). PERCENTAGE OF EVER SMOKERS 100r --- - BEFORE AGE 21 0 BEFORE AGE 1e BEFORt AGE 1B BEFORE AGE 14 1910- 1915- 1920- 1925- 1930- 1935- 1940- 1945- 1950- 1914 1919 1924 1929 1934 1939 1944 1949 1964 YEAR OF BIRTH FIrURF, 4.-Age by which kmahmdarfed smokinR. by birth c(-hnrt SOUR('h NIUS4IV )R RO. 4'9WnAienllw410MidKr1 ANg. (NIKY mSnw4mp rwl (kdlM. £969 18S1S BEFORE ApE 21 fi _f1 BEFORE AGE 18 -yr BEFORE AGE 18 E N N M 144 ~,~, + w~ ~ ww ~ E IL ~p .n N O O~'1 O; ~'? „ M n e v o~•~, s~ a e ey O ? :4 -0 e .~ en v+ vl - a ~ o c 00 v1 N w} Y1 ~fO 1~p~ O~ r N~vO1 ~` ~ t~ ° e r ~ r Y e~ r~i M°en° °N° N q o 0 vf N a t N A 1t O IO r} rT p~ a0 P ~Il r1 Yf ~p Pf ~ O ~ .j n e~f ~ wf w~ ~+f en wf ~ C C ~ ~ ^ ~'$ q c o M .•, n o! „1 a.r n r-t o a o ~ ^ yl ~ 1p M O r y + d ~ ~ M f+1 a o ~ ~ o 0 0~p~ ~ vl ~ ~ 00 e+t ~+1 N ~ q O O - ~p ~ e0 n h p. P P O~ P a U ~ F V1 0~ n z(x) ~n t

tained from cigarette tax data. This ratio has been relatively stable recently, varying from 0.73 in 1974 to 0.69 in 1976 with a mean of 0.72 (Tahle I). A Ieaet-squares rcgrcs. sion analysis was used to identify any trend. The slope of the regneseion line was nM significantly different from wro (p=O.g5), countering the hypothesis that self-reponed data are increasingly underestimating actual cigarette consumption. These results sug- gest that national surveys provide a reliable estimate of U.S. smoking trends. The reasons for the consistent difference between cigarette consumption based on excise tax data versus self-reported data are unckar, olte possible explanation would be a sys- tematic bias from "rounding down" of self-reported daily consumption to the nearest multiple of a half-pack (see Table 14 and related discussion and Ko7lowski 1986). TABLE 1.-F:stimates of cigaMte cortwmptine in the United States, baoed on cigarette excive taxes and seU-reprlrt, 1974-11,5 Year F,xciw taRes (lallinns) Self-reporled (Aillioro) Fmcyion 1974 5oq.o 434.9 0.73 1976 613.5 424.4 0.69 1979 616.0 438.4 0.71 1979 621.5 441.2 0.71 19Rt1 631.3 439.1 0.73 19R3 600.0 467.8 0.79 I9a5 594.0 414.4 0.70 NOTE: F.timnrA hy fie U.S. neorlme~t er ApkyMme. SeH reponeA cr.rw~plia~ incl.de rinu*dcaw.npom fo. duhs 1 NNIS. NCNS) anA euinwtd ealomqmko for a&*WrM1 (NMymd HCOWWdsrwr an oM Atow. NIDA). SOUR(1:: HrzianAMe~ efd., ie prep. The difference in the findings reported by Hatziandteu et al. (in press) and Warner (1978) may relate to differences in methodology. For exampk, Warner used data from the 1964, 1966, 1970, and 1975 Adult Use of Tobacco Surveys (AUTSs). He found that the major decrease in the consumption ratiooccunrd between 1966 and 1970. This may have occurred because the 1964 and 1966 AUTSs wen- in-person surveys, whereas the 1970 and 1975 AUTSs were telephone surveys. As ntentioned above, telephone surveys generally provide slightly lower estimates of stnoking prevalence than in-per- son surveys. On the other hand. Hatziandreu et al. (in press) used only in-per.oxl inter- view data (NHIS) for adults, and the NIDA Household Interview Survey on Drug Use for adolescents. The consumption ratios obtained by Warner for 1964 and 1966 (0.73 and 0.72, respectively) using in-person survey data were similar to the mean ratio (0.72) reported by Hatziandreu et al. for the period 1974--85. In addition, the 1974 in-person estimate was 0.73 (Hatziandreu et al., in press), whereas the 1975 telephone estimate was 0.64 (Warner 1978). This difference provides further evidence that the decrease in the consumption ratio reported by Warner was an artifact of the change in the AUTS methodology. 9b69 18SLS Trends In Cigarette Sales Total cigarette consumption in the United States (a= estimated by sales data) increased dcadily from 1900 until 1981, when an estimated total of 640 billion cigarettes were cmoked (Table 2). Since 1981, there has been a steady decline in consumption despite increasing population size. The number of cigarettes smoked in 1987 is estimated at 574 billion. ` ' These figures refer to manufactured cigarettes and do not include roll-your-own! cigarettes. Roll-your-own cigarettes have accounted for a declining proportion of total cigarettes consumed through the 20th century. By 1950. the estimated per capita con- sumption of roll-your-own cigarettes was 126, or 3.4 percent of total cigarettes con- sumed; in 1987. these figures were 23 and 0.7 percent, respectively (USDA, un- published data). 4 Cigarette consumption data are divided by the population of adults 18 years of age : and older to give an estimate of adult per capita consumption. This estimate representi the average number of cigarettes sold per adult in the population, not per smoker. It should be noted that trends in adult per capita consumption an; somewhat biased be- ; cause there has been a trend over time for more people to start smoking regularly under'age 18 (see section below on Trends in the Initiation of Smoking). Per capita consumption of manufactured cigarettes increased dramatically from its, kvel of 54 cigan:ttes in 1900 to 4,171 cigasttes in 1960 (Table 2). From 1960-73. this' figure remained relatively stable (compared with the previous rates of change) at about 4.0(10 cigarettes per year. Since 1973, there has been a yearly decline in per capita con- su ' mption. From 1973-87, this figure fell trtore than 23 percent to 3.196 cigarettes per year. Although there has been a decline in every one of the,ee 15 yeats, the rate of decline has varied. From 1974-79, the magnitude of the yearly change increased rapid- Iyuntil it reached a 2-percent deirease per year. in the 10 years since 1979, this decrease has fluctuated with a mean of 2.4 percent per year (standard deviation (S.D.) = 1.9). The large drop from 1982-83 (7.2 percent) was more than two atattdard deviations above the mean and is thought to be related, to a significant degsee, to the March 1983 increase in the Federal cigarette excise tax from 8 cents per pack to 16 cents per pack (see Chaper 7). Trends in cigarette sales ate also presatted in Chapter 8 (Figure 3). Trends in Smoking Prevalence Ammta Adolts Cigarette Smoking by Sex. Race (Whites and Blacks), and Educational Attainment (National Health Interview Surveys: 1965-87) Table 3 presents smoking prevalence from NHIS data forthe years 1965,1966,1970, 1974, 1976-80 inclusive, 1983, and 1985, and preliminary data for 1987. These data are prcsentcd for the total adult population (aged 20 years and older) and by sex. race (whites and blacks). and educational attainment. They differ slightly from estimates published by NCHS (NCHS 1988c) because the data presented here are adjusted to the ;+i,i. 261

Changes in measures of smoking behavior (e.g., prevalence, quitting, initiation), like any quantitative variables, can be calculated as absolute or relative changes. Forchan- ges in percentages, the absolute change would be in percentage points; the relative (per. cent) change would be calculated by subtracting the "new" percentage from the base percentage, dividing the difference by the ba.se pereentage, and multiplying the quntient by 1()0. Each measure of change has advantages and disadvantages. Throughout Pan I of this Chapter, changes in smoking prevalence, quitting, and initiation are described primarily in terms of absolute changes. Nature and Quality of Data A number of sources of information provide insight into smoking behavior in the United States. These sources fall into two main categories: those based on excise taxa- tion of cigarettes and those based on population surveys of self-reported smoking. Excise Tax and Sales Data The Econehnic Resean:h Service of the U.S. Depanntent of Agricultune (USDA) has estimated total and adult per capita consumption of cigarettes for a number of years. These estimates are based on data from the Bureau of Alcohol, Tobacco and Fin:amn.s (Department of Tr+easury), the Bureau of Commerce (Department of Commerce), the Tobacco Institute, and other private and industry sounxa. The Tobacco Institute n-ports the number of packs of ciganttes on which State taxes are paid: the Bureau of Alcohol. Tohaeco and Firearms neports the number of cigarettes on which Federal taxes are paid: and the Bureau of Cormnetre n:ports the number of cigarettes imported into the United States. Both Federal and State taxes are excise taxes collected at the wholesale level (on removals) and ate not standard sale.s taxes. The estimated level of consumption is based on both Federal and State taxes on n-movals, as well as on import.s, and is adjusted forestimated inventory changes. Adult per capita consumption is customarily calculated in the United States by dividing total consumption by the total estimated population IS years of age and older. (The World 1Icalth Organization (1988) has published per capita cigarette consumption figures for countries throughout the world based on the population 15 years of age and older.) Self-Reported Survey Data A number of different data sources are available to assess national trends in smoking during the past 25 years. These surveys differ on the basis of sample size, method of data collection (telephone interview ventus face-to-face household interview versus questionnaire administered in school), population (adults versus adolescents). sampling frame (national versus State ba.sed), and the extent of infortnation collected on tohac- rn use. Details of the methodology for the various surveys are provided in the Appen- dix to Chapter 4 and in Table I of that chapter. The amount of information provided varies from survey to survey depending on the availability of information. Validity of Self-Reported Survey Data The validity of self-reports of smoking status from surveys may affect the usefulness of these data in reporting historical trends. Respondents' sensitivity to the social stig- ma associated with smoking has been cited as a reason pe:rsoes might tntdeneport their smoking status (Wamer 1978; Kozlowski 1986). Whereas biochemical asses.sment is generally more reliable than self-report in assessing level of nicotine intake (US DHHS 19RR), self-reported data appear valid for estimating prevalence of smoking in the ,' population. For example, studies of patients in several settings (Petitti. Friedman. Kahn ' 199 1; Pojer et al. 19R4), as well as two large community studies (Fortmann et a1.19R4: , Pierce. Dwyer et al. 1987), have shown that measurement of smoking by self-repcxt or by biochemical markers gives approximately the same estimates of prevalence. A more recent study of 1.317 Hispanics. however, showed that self-n:ported cigarette use un- t derestimated biochemically validated use (Coultas et a1.1988). It is possible that the accuracy of self-reported data will vary depending on whether,l the data collection method is face to face or by telephone interview. Although ; biochemical-validationdatadonotexisttoallowthequantificationofsuchadifference. ,' comparisons of smoking prevalence estimates derived from surveys using telephone ; versus in-person interviews have shtfwn that the former are generally I to 3 percentagee points below the latter (CDC 1987a; see below and NCHS 1987). In addition, concerns have been expressed about the validity of data rtported by one pe+son on behalf of , another C'p'oxy response')(NCHS 1985. p. 54). For adults, these concems relate more to measures of the number of cigarettes smoked per day than to the classification of whether a person is a current smoker (US DHEW 1969, p. 794: Rogot and Reid 1975; National Academy of Sciences 1986, pp. 110-112). For adolescents, proxy reporting may also affect prevalence estimates (Millar 1985). Correlation Between Self-Repcxted Survey Data and Sales Data Warner (1978) compated self-n;potted data on cigateKe consumption with USDA consumption data for the years 1964-75. He found that self-t+eported cigarette con- sumption increasingly underestimated the USDA estimates, possibly because of the in- creasing social stigma associated with smoking. Changing social acceptability of smoking would not be expected to affect the USDA estimates. To the extent that a"so- cial acceptability" bias in self-reported data may have inereased in necent years, the dramatic decrease in smoking prevalence observed during the past 25 years could he in part artifactual. Hatziandreu et al. (in ptes.s) analyzed ntore recent data to determine whether the trend relxnted by Warner (1978) has continued. Self-reported consumption data for adults and teenagcrs were obtained from the National Health Interview Survey (NHIS) (Na- ticxtal Center for Health Statistics (NCHS)) atd the National Household Survey on Drug Abuse (National Institute on Drug Abuse (N1DA)). Self-reported cigarette rnnsump- ticxt was estimated based on the smoking ptevalence, the average self-neported number of cigarcttes smoked per day, and the U.S. population size each year. A"consumption ratiii' was calculated by dividing self-reported consumption by USDA estimates oh- % Sb69 ZBSTS ~ 264 263

1970 19 1 2 1.2 o.e o.~ , oa 1986 MI(aIRF S.-Prevalcnce of chewing tobacco and snuff nse am/mt; men, 1970 (NHIC) and 19% (AlIT3) GN ~RCI?(IC 11/1/1\ ~ lnd..~~, Nowwo. 1•Mrce c~ al. 14R0 . CP.S :Irc rrplrtrd. Fincllly, data from a more detailed analysis of ST use from the 1986 n Ul :ti for Ilx•n clccd 17 ycar% and older ( Novotny, Pierce ct al. 19R9) are described. 11u• Imcv:dcncc ,d crnrrrnt ST o.c from 1964-R6 among persons aged 21 years and c/1drr, str:uilicd by pn+Iluct and scx. is shown in Figurr fi. For ixNh prrxlucts, there has been a stcadv overall deY•linc in oxc by hlNh mcn and women. It is possible that this decline i. dne in L:Irt av the ch:mym in tlle Al l'i;ti interview techni/iue fltxn in-perstxl 1,f1 EL69 I85T9 Prevalence (X) 4 2 o--~_, 64 65 68 87 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 88 Year ' - 8nuff, Mtn -'- Chew. Men --4- 8nuff. Women -'G- Chew. Womsn FIGURF, 6.-Smokeless tobacco use amon6 adults 21 years of age and older, United States,1964-116 ! sOIIRCF: AtJTS% 1 Niwomr. Pierte e+ d. 1919. M per). interview (1964 and 1966) to telephone interview (1970, 1975, 1986); telephone stlr- ~ veys generally provide slightly lower smoking prevalence estimates than in-person sur- veys (see above). The prevalence of ST use among women has consistently been vtry low. However, the use of snuff by older black women in the South is much more com- mon than among women in the general population (Rouse 1989, in press). In 1986. the weighted prevalence of snuff use was 2.2 percent for men and 0.5 per- cent for wolnen; and of chewing tobacco use. 3.1 percent for men and 0.1 percent for women among adults aged 21 years and older. For 1986, overall prevalence of ever and current use of ST among males. aged 17 years and older, is shown in Table 29. More than 10 percent of male respondents had ever used ST product.s; chewing tobac- TABLF. 29.-Prevaknce (96) of ewtti+e and csrr ent tne of smokeless tobacco, males aRed 17 years and older, United States.19R6 Producl uced Ever use Currrm uce Any amnkek- a tnhacco Snurt' t]iewrinlt tofacco~ tkwh 'Inclwka dwwe Whn alcn we chrrinlt Mirao. 1lnclwka tMNe who ako wt aMiff. S(MIRCf:: AI1TS 1VM+IN.w.Nnv.l9eeeelsl. 19119.inlrraal. 121

TARLt:, 25.-Ikxne.die markd slrarr of /ilter dRarnftes as a proportion of total cigarettes.nid, United Stalec,19.S0-16 Year MarkH ahne (%) Year Market share (%) 1950 0.6 1969 77 1951 0.7 1970 RO 1952 1 1971 R2 195i 3 1972 94 l9t.t 9 1973 RS 19tS 19 1974 R6 1956 29 1975 R7 1957 ,1R 1976 RR I9SR 45 1977 90 1959 49 1978 90 1960 tI 1979 91 1961 52 19M1 92 .,r 53 19R1 92 196 4 5111 19R2 93 1964 61 19R3 93 1965 64 19R4 93 1966 68 19R5 94 1967 72 19R6 94 196R 74 C(xIR('F.: IT('I1vRR1. testing mcthod) multiplied by the quantity of sales forthose brands. The sales-weighted avcragc yield of tar fell from 35 mg in 1957 to 13 mg in 19R7. For nicotine, the sales- weightcd average fell from 1.3 mg in 1969 to 1.0 mg in 1985. However, the sales- weighted average yield of tar and nicotine leveled off between 19R1 and 1987. As pointed out in Chapter 2, modifications in the makeup of commercial cigarettes have . profoundly influenced these yielda• for example, the steepest declines occurred in the late 195pc after introduction of filter tips. Trends in the percentage of domestic saks of cigaettes yielding lower tar levels are chown in Table 26. The domestic market share of cigarettes yielding 15 mg or less tar increased from 2.0 percent in 1967 to 56.0 percent in 1981. Since 198 I, this pmpor- tion has fallen slightly and has stabilized at S I to 53 percent. About two-thirds of these cigarettes have tar yields between 9 and 15 mg. It should he noted that the parameters used in the FTC machine-testing method (developed in the I(X,(k) do not necessarily reflect currrnt smoking patterns. Forcx- amplc, the i•TC method uses one puff per minute (Pillsbury et a1.1969), whereas human 0L69 I8StS tIl TABLE 26. Domestk market share of dRarettes with reduced tar, percentage ~' of total cigarettes sold, United States,1967-R6 T. Ykld Year 515 mR 512 m` S9 en 56 mR 53 mR 1967 2.0 196R 2.5 1969 3.0 1970 3.6 1971 3.9 1972 6.6 1973 R.9 1974 R.9 1973 13.5 1976 13.9 1977 22.7 I97R 27.5 1979 40.9 10.6 5.8 2 7 1980 44.11 16.9 7.3 3:3 10R1 56.0 24.6 9.6 3.7 11182 52.2 43.5 27.9 8.9 2.9 110113 53.1 44.9 27.9 9.4 3.1 19R4 51.0 43.4 26.3 9.4 2.9 19R3 51.9 43.1 25.3 8.4 2.3 19R6 32.6 443 22.3 9.9 2.6 soURCE: FTC(t9RRY.Knrloadcipepen). studies of smoking patterns show an average interpuff interval of 34 seconds (that is, about two puffs per minute) (US DHHS 1988, Chapter 4, Table 2). According to the 1986 AUTS. 41 percent of smokers smoke cigarettes yielding 15 mg or less tar (Table 27). The proportion of smokers smoking cigarettes yielding more than 15 mg tar is higher among males, hlacks, and persons with less education com- pared with females, whites, and more educated pt:rsons, respectively. This proportion decreases with age; the higher proportion among those 17 to 19 years of age probably reflects the popularity of the higher tar Marlboro brand among adolescents (Hunter et al. 1986: Goldstein et al. 1957: Glantz 1985). Increased consumer demand for lower yield cigarettes during the past two decades is probably attributed to consumer beliefs that lower yield brands are less haiardous. This impression may have resulted in part from cigarette advertising implying that low- yield brands are iess hazardous or are safe (Davis 1987). According to the 1986 AUTS. m(xe 45 percent of current smokers believe that some kinds of cigarettes are probably hazardous than others (see Chapter 4).

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Princetonc New Jersey: Gallup Organization, 19R7c. GALLUP. Attirudes toward smoking in rataurants. Restaurants USA. In: Mills, S. Gallup SunYyJor tht National Rtstonrant A.rsociation. Princeton. New Jersey: Gallup Organisation, May 19R7d. GALLUP. On-the-go Americans prefer smoke-ftee air. American Journal of Public Health 7R(S):563. May 1998s. University of Michigan, 1995. BACHMAN,I.G.,1O11NSTON, LD.. O'MALLEY, P.M. Monitoring the Future. Qwstion- nairt RtsPonses Fnmr the Nation's High School Seniors, 19Vt6. Ann Arbtx, Michigan: University of Michigan. 1997. BECKER. D.M., LEVINE, D.M. Risk perception. knowledge, and lifestyles in siblings of GALLUP. Majexiticsnowsupportbanonpublicamoking,eigaretleads. ThtGallwpPo//. Presc Release• Princeton. New Jersey: Gallup Organization. September 4,19RRb. HARRIS. L Prevention in America: Steps People Take-Or Fail to Take--4or Better ilrohh. Lrntis Harris and Associates, 1983. HARRIS. L The Pre.rntion Index. Louis Hatris and Associates, May 13.1998 ,. people with premature coronary disease. Amcricanlorrnal of Prtvrntivc Medicine 3(1):45- S0, 19R7. HARVEY. L. SHUBAT. S. Public opinion on health care issue.s, 1996. lIn: AMA Surveys o( Physicianand PahlicOPinion.19R6. Chicago: American Medical Assaciation.Octrd+er 19R6. BEN-SIRA, Z. Health promoting function of mass media and teference groups: Motivating or reinforcing of behavior change. Sorial Scienct and Medicine 16(7):R2.S-R34, 19R2. CANADIAN GALLUP POLL, October 1996. HAR VEY, L., SHUBAT, S. Public opinion on health care issues. In: AMA SrnvYr nfPh.•cicioe •and Public Opinion on Health Care Issres,19R7. Chicago: American Medical AccrK rnlion. April 19117. CENTf?RSFORDISEASECONTROL. Surveytoax.asstheptevaMnce,attitudes,knnwkdltey JOHN,STON, L.D.. BACHMAN. J.G. Menitoring the Funvr. Questionnaire Rcspnnsr.. /rom and helicfk about smnkinR behavior among the adult population. Survey questionnaires. Prepared by Wectat, lnc., for the Office on Smoking and Health, Rackvilk, Maryland, August 19Rh. CENTERS FOR DISFASE CONTROL. Pacsive srnoking: Beliefs, attitudes. and exposurec-- llnited States. 1996. Mnrhidityand MnrtaliryW«k1vRcINVt 37( I S):239-241, A1xil 22.19RR. CHILTON RE.SEARCII SERVICE.S. A SrnwynfAAnlrsrtntandAdaltAnintdrs, ValNrs. Br- horinr, Imrntinns and Knmclrvlge Related to Cigarette Smoking: Final RcMn•t. Submitted In the Federal Trade Commision, June 23.1990. rhrNatiori sHiRhSchMrlScniors,1975. AnnArbor.Michigan:UniversityofMichiRan. 1990. IJOHNSTON. L.D., BACHMAN.I.G., O'MALLEY, P.M. MonHorinR the Fumre- Que.ainn- nairt Responses From the Natirni s High School Seniors. 1977. Ann Arbor. Micln.an: University of Michigan 19ROa. JOHNSTON. L.D.. BACHMAN. J.G., O'MALLEY. P.M. Monitoring the Future. Qnestinn- . noire Responses From the Natiorri s High SchrNrl SeniMs, 1979. Ann ArMrr. MichiFan:,' (Jniversity of Michigan I9ROb. 0V69 Z8SZS 255

effects of socioeconomic status (SES) and selected demographic factors on the odds of ever smoking (versus never smoking) and current smoking (versus former smoking). The SFS/demographic factors included in the models were: sex, employment status, occupation, education, marital status, and poverty status. Tlte investigators found that when they simultaneously controlled for the effects of these factors, unemployed per. sons were more likely than employed persons to he ever smokers or current smoken. However, blue-collar and service workers were not found to have significantly in- creased odds of ever or current smoking compared with white-collar workers. Employed persons were more likely to have quit smoking than unemployed persons. Special Populations: Hispanics Information on smoking among Hispanics was colkcted as part of the Hispanic Health and Nutrition Examination Survey (HHANES) between 1992 and 19R4. This was a geographically based sample of Hispanics from three areas of the United States designed to represent three Iarge Hispanic groups (Puerto Ricans in the New York City area; Cuban-Americans in Dade County, Florida; and Mexican-Americans in the South- west). Sample sises were 9,000 Mexican-Americans, 4,000 Puerto Ricans, and 1 5/tt1 Cuban- Americans. According to the HHANES, the age-adjusted smoking rate,s for males aged 20 to 74 years were 43 percent for Mexican-Ameticans, 42 percent for Cuban-Americans, and 40 percent for Puerto Ricans. Among females, the smoking prevalence was 24 percent for Mexican-Americans and Cuban Americans and 30 percent for Puerto Rican Americans (Haynes 1987). 7ltese rates are higher than those obtained from the NHISs for the years 1979 and 1980 (Marcus and Crane 1985; Rogers and Crank 19R8) and 1985 (Marcus and Crane 1987). However, the number of Hispanics in these NHIS samples was small, making prevalence estimates less reliable. Haynes (19R7) suggests that NHIS data may underestimate smoking prevalenoe amottg Hispanics becau.se ques- tions about smoking were not asked in Spanish. 71te firat estimates of smoking be- havior among Hispanics that are both national and statistically reliable will he avail- able from the 1987 NHIS, which oversampled for this population group. Special Populations: Anterican Indians and Alaskan Natives There are no reliable national estintate.s of smoking prevalence among American In- dians. Several surveys have assessed smoking rates among specific Indian tribes or on certain Indian reservations (CDC 19R7b). Smoking prevalence is highest among North- em Plains Indians (42 to 70 percent) and Alaskan Natives (56 penaent), where rates greatly exceed the rate in the general U.S. population. Much lower rates have been reported for Indians from the Southwest (13 to 28 percent). High rates of smokekcs tohacco use have also been reported among some American Indian groups, especially in Indian youth. According to a survey of approximately 5,000 children 5 to 18 years of age in rural Alaska conducted by the Indian Health Service, 28 percent of girls and 34 percent of boys reported using smokeles.s tobacco products (CDC 19R7c). Similar findings were obtained in other surveys of Native Americans (Schinke et al.1987; CDC 19RR; Hall and Dexter 19RR). 0S69 TBSTS Special Population.s: Asian Americans There are no reliable national estimates of smoking prevalence among Asian Americans. A few local surveys provide estimates of smoking prevalence among Asian Americans in specific geographic regions. The State of Hawaii has a population composed of 29 percent Caucasian, 26 percent Japanese, 15 percent Hawaiian, and 15 percent Filipino. The State conducted a Be- havioral Risk Factor Survey (see below) of 1,002 people by telephone in 1984. Smok- ing prevalence estimates were 28 percent for Caucasians, 27 percent forboth Hawaiians and Filipinos, and 23 percent for lapane.se (Hawaii State Department of Health 1984). A similar survey of 1•557 residents of the State was completed in 1986. Prevalence es- timates from this second survey were 29.3 percent for Caucasians, 28.8 percent for Hawaiians, 25.1 percent for Filipinos, and 20.6 percent for Japanese (Chung 1986). Special Populations: Pregnant Womett National data on smoking during pregnancy are acarce, especially Prior to 1980. Since 1980. several national surveys have directed smoking questions to previously pregnant women, but survey methodologies vary widely and it is not possible to study secular changes in behavior. Probably the best source of national data on sntoking among pregnant women has been the National Natality Surveys (NNSs), which were conducted among national samples of married mothers of live infants born in 1967 aed 1980. Data from these sur- veys were used by Kleinman and Kopstein (1987) to document changes in smoking be- havior during pregnancy over that period of time. Among teenagers, smoking rates temained fairly constant over time at about 38 percent among whites and 27 percent among blacks. Among women over age 20, theee were decreases in smoking prevalence that varied markedly by race and by educational attainment of the mother. Smok ing prevalence among white women over age 20 declined from 40 percent in 1967 to 25 percent in 1980; among black women over age 20, it declined from 33 percent to 23 percent. Among white women over age 20, thete was an increase in the proportion quitting smoking during pregnancy (1 I ptxoettt to 16 percent). while among blacks the proportion quitting actually decreased (17 perceM to I 1 percent). Atttong white wotnen with less than 12 years of education, the prevalence of smoking during ptegnancy declined from 48 percent to 43 percent, while for women with 16 or tttore years of education, it declined from 34 percent to 11 percent. Among white smokers with less than 12 years of education, there was relatively little change in the proportion quitting during pregnancy (1 I percent to 9 percent), but antong smokers with 16 years or rtare of education, the proportion mae than doubled (12 percent to 27 percent). Insufficient numbers of black women were sampled to study trends by education among blacks. The followup study to the NNS, the National Maternal and Infant Health Survey, was begun in 1988. Data from that study will provide the best estimates of smoking during pregnancy for the late 1980s. At this time, however, no comparable national data exist to study women after 1980. Studies that have asked about smoking behavior during pregnancy have not asked about behavior during specific years, so it is not possible to I I ,,4 1 275

during the past year (categories 4 and 5). For prolonged abstinence (1 or more years) (categories 2 and 3), the proportions then become greater for the more educated. Among ever smnkers, about two-fifths of both black.s and whites have not tried to quit during the pact year, with 9 percent in the hard-core smokers category. Twenty- one percent of white ever smokers have made a quit attempt during the past year com- pared with 2R percent of blacks. A perscxi's likelihood of being in different categories of the smoking continuum dif- fers considerably with age. About 44 percent of ever smokers between the ages of 25 and 44 years are smokers who have not made an attempt to quit during the past year, compared with 26 percent of those 65 years of age and older. However, there are rough- ly equal proportions of cach age group in the hard-core smokers category. The pmlx,r- tion of ever smokers who made a quit attempt in the last year was highest (42.7 per- cent) in the youngest age group (lR to 24 years old) and is progressively smaller for each older age grrnip (23.1 percent, 17.3 percent, and 14.8 percent, respectively, in those aged 25 to 44 ycars, 45 to 64 years, and 65 years and older). Summary of Trends in Quitting As with trends in smnking status, trends in quitting activity have exhibited a consis- tent pattern since 1965. .Almost half of the population who have ever been smokers have quit. Although the proportion of males who have quit is higher than that of femaks and the proportion of whites who have quit is higher than that of blacks, the rate of in- crea.se in the quit ratio is similar between these categories. The only diverging trend over time is the quitting activity for the les.s educated compared with the nxxe educated. . One-third of those who smoked during the year prior to the 1986 AUTS quit smok- ing for at least I day during that year. Health education and motivational campaigns targeted at these individuals could help maintain them in "contemplation" and "action" stages ( Pmchaska and DiClemente 1983) and move them toward repeated quit attempts (see Part 11). Trends In the Proportion of Steolters Who Are Heavy Sntolters Although all the NHISs have included information cxt the number of cigarettes stnoked per day, respondent rulea on this question changed In 1974. Prior to that date, smoking information was obtained from either the sampkd individual or a proxy adult living in the same household. Foreach survey since the 1974 NHIS, smoking informa- tion has been accepted only fmrrt the sampled individual. Proxy respondents have been shown to he less accurate in reporting daily cigarette consumption than self-respon- dents (US DI IEW 1969, p. 794: Rogot and Reid 1975; National Reseamh Council 1996. pp. 110-112). Proxy responses can be eliminated from analyses of the pre-1974 data toexamineMng-termtn-ndsindailycigaretteconsumpion. However,excludingpmxy responses may make the sample nonrtpresentative (see Chapter 3). Accordingly, in considering trends in thc prnpnrtiat of the smoking population who smoke 25 or mone cigarcues per day, only NI IIS data from 1974-R5 are used heie. i , The proportion of smokers who smoked 25 or more cigarettes per day in each survey is presented in Table 13 and is shown in Figure 1. This proportion ranged from 25.5 to 29.9 percent and did not change significantly from 1974 through 1985 (p=0.4). In ad- dition, this proportion did not change among sex- attd race-specific subgroups of the snxaking population (Figure 2) or in different age groups (NCHS 1988c). Heavy smok- ing has been consistently more common among whites compared with blacks, and among men compared with wometi; the differential by tace has been greater than the differential by sex (Figure 2). TABLF,1 .3r-SeK-rTpmted dprettell stttoked Per day (peroeetaRe dcnrre"t smtthers). United State.e, aged 20 yem and older.1974-85 I Number of d6aenes amoked per day Year 1-14 15-24 225 i 1974 30.8 43.2 26.0 1976 30.1 44.4 23.5 1977 30.3 43.2 26.5 1979 28.1 42.8 29.1 1979 23.2 43.0 29.9 19110 27.6 42.6 29.9 19a1 28.5 44.9 26.6 19R5 31.0 41.9 27.1 SOURCE: NNISa 1914-I15: wpW* ~d d.a. Otnoe M3nwkiftrd tt<ald~. It is theoretically possible that the proportion of the "heaviest" smoker. is increasing even though the proportion of "heavry" smokers (25 oc tttore cigattttes per day) has not changed. However, no major inrnease occurred from 1974-85 in the proportion of smctken amoking 40 or more cigarettes per day (Table 14). The overall proportion smoking 40 or more cigarettes per day was 12.6 petcent In 1974 and 13.2 percent in 1985. Table 14 also dentortstrates tespondents'inclination to ttiport their daily cigarette consumption in round numbers related to the size of a cigarette peck (e.g.. 10 or 20 cigarettes per day) (see Kozlowski 1986). Because the sales-weighted average nicotine yield declined from 1974-83 (see Figure 14 in Chapter 2), one might expect to have observed an increase in average daily cigarette consumption. Compensatory changes in smoking behavior to maintain rela- tively constant nicotine intake have been shown to occur when smokers switch from high-yield to lower yield cigarettes (US DHHS 1988). Although daily cigarette con- sumption did ttot increase from 1974-85. other compensatory changes may have oc- curred (e.g., increased freqtttatcy of puffing or depth of inhalation) as the smoking population moved toward lower yield brands, "I 6569 i85tS 293 2y2

TABLE 3;.-Gmtinued Snuff tne Chewing lobaceo uac Any smokeless tobacco u.e South Carolina 0.7 5.3 6.1 Georgia 1.4 7.3 9.7 FM.ida 1.1 1.9 2.9 East South Central Division 2.7 9.4 11.6 Kentucky 3.2 11.2 13.6 Tenneccee 1.7 9.3 10.3 Alabama 1.7 6.6 8.3 Micxiccil+hi 3.7 11.4 16.5 Wect South Central Division 4.0 5.5 9.1 Arkanaaa 6.0 9.3 14.7 Lrwiaiana 2.5 5.8 R.0 (Mdahrnna 4.8 6.7 11.0 Texaa 4.0 4.6 8.2 West ReRlan 1.4 3.3 4.5 Mountain [)ivision 2.3 5.4 7.3 Montana 3.3 8.3 13.7 Idaho 2.3 6.7 9.7 Wyoming 3.4 13.0 15.9 Colorado 1.2 6.4 73 New Meuico 5.3 5.2 10.2 Atirona 2.0 3.8 5.4 Utah 0.9 3.0 3.7 Nevada 1.3 2.R 4.3 Pacific Diviaion 1.0 2.6 t.4 Washington 1.8 6.1- 7.1 Orep,n 2.7 5.4 7.6 CalifMnia 0.7 1.7 2.3 Alanka 2.3 6.3 8.8 Ilawaii 0.2 0.4 0.7 t(x1RCF: (PS Iv11S(M.cwetal..ie0iea..) From 1964.R6, there was an g0-percent decline in prevalence of both cigar and pipe smoking among men (Figure 7). The prevalence of cigar smoking declined from 29.7 to 6.2 percent; the prevalence of pipe smoking declined from 18.7 to 3.8 percent. Reasons cited to explain the drop in cigar saks include the effects of the antismoking campaign (several airlines have ccxnpktely hanned cigar and pipe smoking on all tlighta for many years. hut only one airline has done so forciganette smoking), declining image of cigar smokinR, failure to attract new strn*ers, insufficient frce-sample distribution. medincre advertising and promotional activilies, and declining quality of the product (t.a7ants 1979). TABLE 34.--Cigar/pipe snakinR afsttta ('gr) b7 mIJor sociodemograPhk variables, United States, Hg6 CiRaNbipe tanokinR atanu Sample Cw+ent uar Fatmer mer Never wer Total sbt Tefal 4.3 22.2 73.3 100 13.031. Ses Male 9.7 41.8 49.6 100 6.377 Femak 0.3 4.3 95.2 100 6.654 ARe 17-19 1.3 13.6 $5.0 100 20-24 2.0 16.6 91.4 100 1: 23-41 4.4 22.2 73.3 100 45--64 3.9 26.3 67.6 100 3.616 263 3.9 22.6 73.3 100 1.96'1 ~ Race White 4.4 23.4 72.2 100 11.363 Black 3.7 13.9 814 100 1.* i Ot1Kr 3.3 19.4 77.1 100 372 Rtxiera Midwest 4.8 22.6 72.6 100 3.236 NoAheast 4.6 19.6 75.7 100 2.963 Southeast 3.9 23.2 73.0 100 4,101 West 4.1 22.7 73.2 100 2.32¢ MarlfatahM MattiedkdnbitietR 4.8 25.3 69.9 100 R.364 Widowed 1.8 8.9 t;9.2 100 1.011 Divoteedhepuaw 5.6 20.1 74.3 100 1.446 Never nurticd 2.8 17.7 79.4 100 2.179 Unknown 12.4 27.3 60.1 100 31 EA.eNbw • 511 yar. 4.9 22.8 72.3 100 2.431 12 yeus 3.6 20.0 76.3 100 4,872 11-15 yean 3.9 22.3 73.6 100 3.118 216 yeats 5.3 26.0 68.7 100 2.610 t7i 9L69 IBSTS 327 .

Trends in the Initiation otSnMking Information on smoking patterns during adolescence is important because srnoking initiation usually occurs during this age. Presented below are data concerning three measures of smoking behavior during adolescence: (1) age of smoking initiation: (2) trends in smoking prevalence amnng persons 20 to 24 years of age, used as an indicator of smoking initiation; and (3) smoking prevalence among adolescents. Data on age of initiation provide information on the ages during which initiation usually occurs, but provide no information on the extent of tobacco use within the adolescent population. The prevalence of smoking among those 20 to 24 years of age serves as an indicator of smoking initiation among adoiescents during the several years preceding a particular survey. This mcasure offers the advantagcs that smoking initia- tion is relatively complete by the time one enters this age group, and a survcy sample representative of the total age-specific population can he obtained readily. Ifowever, these data offer no information on the ages during which smoking initiation actually occurred and do not necessarily reflect the most current initiation patterns among adolescents. Data on smoking prevalence among adolescents provide direct and cur- rent information on smoking behavior in the population of concem. However, inter- ixetation of adolescent survey data is complicated by the use of different dcfinitions of regular and experimental smoking in different surveys and by the failure of some sur- veys (c.g., school surveys of high school seniors) to include groups known to smoke at higher rates (e.g.. high school dropouts). Age of Initiation Age of smoking initiation is a critical variable in targeting prevention efforts. Infor- mation on self-reported age of initiation is available from surveys of adolescents and adults. Adolescent surveys offer the advantage of providing current information on age of initiation without concerns of recall bias. However, these surveys cannot provide complete information on age of initiation because the sample.c exclude those who may start smoking at older ages. Adult surveys provide complete information on age of in- itiation, but recall bias may occur because adults arc asked about an event (smoking in- itiation) that typically occurred decades earlier. A major value of an adult survey is that, by using birth cohorts, one can assess whethersmoking initiation has changed over time. In the 1996 High School Senirxs Survey sponsored by NIDA (see below), seniors who had ever smoked were asked the grade in which they had smoked their first cigarette. About one-quarter of seniors smoked their first cigarette by grade 6. one-half by grade R, three-fourths by grade 9, and 94 percent by grade I I(Tahle 15). Males and whites were more likely to smoke their first cigarette at earlier graiks than females and biacks, respectively. The pattern of smoking initiation was similar for those with and without plans for higher education. In aikiition, the 1987 National Adolescent Student Health Survey (NASI{S) (see below) collected information on the grade in which Rth and 10th grade students had smoked their first c igarctte. Data are presented in Table 16 for 1()th graders only. Ap- TARLF15: • ~ sM~ United ~ ~ 1~ e(~), HiBhereducHian plans ' p,ak Total Males pennks Whita Blacks Yes No 25 7 6 25.8 31.1 20.7 26.8 23.3 25.3 . 8 57.3 39.5 55.3 59.0 50.2 56.5 5R.0 3 1 9 72.5 72.7 72.3 74.0 63.8 70.8 75. f 7!1 10 R4.2 83.8 84.7 85.0 78.4 83.0 i. R 11 94.3 93.t1 95.0 95.3 89.9 93.5 95.9 12 100.0 100.0 100.0 100.0 100.0 100.0 100.0 SAmpk site 3.079 1.423 1.526 2.308 302 1.791 972 ta Saci.l Re.erch, lMivenNy of Michi6.e (B.eMnr~.lahmton.O-Malky 19R7/. A i 4 e u i()URCE: hM I proximately one-quarter of smokers reported that they had started smoking by grade 6 7~ g, Males were scxnC- had started 8t~ k o ers 7 and approximately one-half of smo ~ females caugh up d ~ e ~ what more likely than females to start smoking pria gra 9 7 . to by grade 9 due to their higher initiation rates in grades i d it e TABLE i6.-Recall of 1Cade at atnoking initiation by 10tU-~rade student+, Un 9lCf States,1 Males Femdel % Cumul.ti.e % qt, Cumulauve % 11.0 11.0 8.3 RS By Rrade 4 5 22 9 17 28.9 14.0 . Ceades 5 or 6 . 49 6 Oeade.7 a 8 24.1 53.0 26.1 . 6.9 59.9 10.9 59.5 Gade 9 64 1 2.1 62.0 4.6 . C,rade 10 0 100 Not xmoking by BraAe 10 38.1 11q.0 35.9 . SOURCE: N.darl AdnkwerM Sadem tteso S-vey 1957 (US D11ttS.lu Oeti b). Information on age of initiation is available for adults from NHISs conducted in 1979. 11979. 1980. and 1987. The 1987 data were not available for inclusion in the data presented below. The 197R-R0 data are derived from responses to the question. :' ~ how old were you when you first started smoking cigarettes fairly reguiarly. ~ ~data have been used in previously published analyses of age of smoking initation (US DIIHS 1985; Harris 1983; MMcGinnis. Shopland, Brown 19R7) and are again used below. The populations from the three NHISs were combined and grouped by 5-year hirth cohorts. In the total satrple, the average age of initiation among ever stnokcrs (aged 2() to 64 years) was 17.2 for men and 19.1 for women (US DHNS 1985). The proportion of ever smokers (20 years of age and older) within each birth cohort who 1969 Z8STS ~ 296 297

TABLE 33.-Prevaknce (%) dtwrent aiee denuRaed chewi19 tobacco by reRion, divWtm, and State, males aged 16 7ears and older, United State.,1985 TABLE 31.--Si6nificsnt.ocfodnnog raphk caKni.hs dcuvl•reet use of any anokekas toh.cra, nules aRed 17 Tan and older, United States,19Q6 Parameter (bds ratio 91% tonfidenee limits ReRlae Stwthesat 3.0 I.R.4.8 West 1.9 1.1.3.3 Midwrst 1.4 O.A. 2.3 Northeast Race White Referenl 2.4 1.3.4.3 Black F.nqisyareik Unemployed Rekrent 3.s 1.9.7.6 ServiceAabMer 2.9 1.9.4.6 Blue collar 3.0 2.1.4.3 White collar RelaerM SOIIRCF.: Al rt'S 191116 ( Novmny. Piece et tl. I91t9, in per). TABLE 3L-Reported aRt d intti.tbn and median apd initiation d amokek~e tobacc» nce anum ever uters, nlales aged 17 years and older, United Statec,1986 Alte Snp at initiation (peKe..Malte reporting) Pmduct <16 16-Ifl 19-20 221 Median Any smokeless mhacco 37.1 7.9 21.4 33.9 19 Snull' 35.5 R.6 23.0 12.9 19 ChewinR~ahaccob 36.6 6.7 20.3 36.,1 19 hnclwk. rtw+a who dsn..e clrwinR kiA.cco. 'Mchwk" tM..e .dwn d«. we .nutr. teNIRCE: AtrTS 19Rh(MMwwnr.Phreeet.1. 19A9.inpm"). SG69 TgSTS Snuff we Chewipgb6ac'om rse Any mrolceless tohacarnuse UaYtd Sbtes 1.9 3.9 5.5 Ne.theasl ReRioe 1.0 1.4 i 2.3 New England Division 0.4 0.e 1.2 Maine 0.9 1.3 2.3 New Hampshire 1.2 1.5 2.7 Vermont 0.9 4.7 5.5 Masachusens 0.2 0.4 0.5 Rhode Island 0.5 0.6 0.9 Connecticut 0.3 0s 0.9 Mid-Atlantie Division 1.2 1.6 2.7 New York 0.5 1.2 1.6 New krsey 0.1 0.6 0.7 Pemsylvani. 3.0 2.9 5.6 Nmih Cewtrsl ReRiee 2.1 3.4 5.3 I East NoAh Central Division 1.9 2.9 4.4 Ohio 2.2 3.2 5.0 Indiana 2.6 3.2 5.6 Illinois 1.1 23 3.3 Michigan 0.8 2.7 3.4 Wistonsin 2.9 2.9 5.9 I West North Central Division 2.9 4.7 7.5 Minnesota 3.5 2.9 6.1 4 6 lowa 1.8 4.6 . Missouri 3.1 3.6 6.7 7 10 North Dakota 6.1 5.1 . 6 1 9 7 South Dakota 1.9 . . NelMUka 1.4 6.E 8.0 Kamas 3.3 9.6 11.7 Gwth ReRMw 2.7 6.0 R.3 South Atlantic Division 1.9 5.2 6.7 Delaware 0.6 2.4 3.0 Maryland 0.4 2.1 2.4 D'n. trict of Columhia 0.0 0.4 0.4 Virginia 2.3 6.2 7.E Wesl Virginia 11.5 13.5 21.1 North Carolina 1.8 3.6 9.R 124 123

Tnendc in the Proportion of Smokers Quitting (Quit Ratio) (NH1S) Quit raties for the total U.S. adult population and stratified by sex, tace, and educa- tion, as derived from the 1965-57 NHISs, are prcsented in Table 9. Linear regression analyses of the weighted data from those surveys cottducted between 1965 and 1985 arc also provided to as%ess time ttend.s. The 1987 data are not used in the regmssinn analyses hecausc they are preliminary. The linear models for the observed data in the subpopulations defined hy sex, race, and education had R2 values all between 0.7R and 0.95. In 1965, 29.6 percent of ever smokers had quit. By 19g7, this proportion had increased to 44.8 percent. The rate of increase in the quit ratio between 1965 and 1985 is 0.68 percentage points per year. Almost half (4R.7 percent) of male smokers had quit by 1997 ccompared with 40.1 percent of female smokers. The rate of increase in the quit ratio is the same among men and women. Regarding racial diffetence.c, 46.4 percent of whites who had been smokers had quit by 1987 compared with 31.5 percent of blacks. For whites, the rate of change in the quit ratio from 1965-li5 was 0.72 percentage points per year, and the linear model fits the data exceedingly well. For blacks, the rate of change during this period was 0.43 percentage points per year. As with smoking prevalence, the quit ratio for blacks did not change between 1965 and 1974 but did change between 1974 and 1985. Fioro and colleagues (in press) have reported trends from 1974-85; during this period the rate of increase in the quit ratio among blacks (0.75 percentage points per year) was similar to that among whites (0.77). However, this similarity masks a difference between the sexes. The change in the quit ratio among blacks from 1974-85 was mainly seen in males, where the rate increased at 1.04 percentage points per year (compared with 0.67 in white males). Among black female.t, the quit ratio increased at 0.46 pen:entage points per year from 1974-85 (compared with 0.95 in white females). Thus, in recent years, black males have been quitting smoking at a significantly higher rate of change than white males (p=0.01). The difference in the rate of change between black and white females is in the opposite direction but is not statistically significant (p=0.3I ) be- cause of the reduced linearity of the ttettds and smaller sample sizes of ever smokers among females than among ntaks. In 1966. about 40 percent of college gtaduates who had ever been smokers had quit. This proportion was 20 to 40 percent higher than the other educational groups. By 19R7, the quit ratio among college graduates had risen to 61 percent, and the rate of change from 1966-85 (+(1.g5 percentage points per year) was greater than in any other educational category. Quitting has been inereasing in all the other educational categories, with the slowest rate of change (0.41 percentage points per year) among per- sons without a high school diploma. Sn,aking Continuum (AUTS) The process of quitting smoking has been categorized by Prochaska and DiClemente (1983) acccwding to cmokers' intention to quit and the status of their most recent quit attempt. They labeled five stages of the quitting process as follows: precontemplation, ~ ~ 0 w a I ~ V ~ ~ ~ ~~ 5~ x I I It A ~,•t a ~q ~.e r e~ ~ v °; 3 : ~ '~ a 9 S ~ ~o ~o r PO N M O h'O, Nt O A, °~ ~, ~ ~ ~ : ^ S .14 ~ ry ~n ~oii x, ~ N A * ~ 600, ~ `~ Q o d a°d ..~f~1 f~1 o n n ~ a ~ A A ° Vt A S as %o er .4 N N N N~ ~R N tV N N N en ~1 n • -I et ~ ey e; ,•! •n n• lr gat SIS(A A A A A I I :I I .e er ryp, ~Q. N N N ~+ ~~ e o o, ~o 0 g ° O ggo M~p h_-o.9% ~ O O _ 3 e~ e~ e~n rPi rn r f •~F YT ~ a P o M O 9569 18S1S a O a ~ LL + . ~ 297 {

co appears to be used slightty more commonly than snuff. Few men (0.5 percent) use both products. The prevalence of ever use and current use of any ST product by maks, stratified by selected sociodemographic variables, is shown in Table 30. The prevalence of both current and ever use was highest among younger men, whites, men living in the Southeast, less educated men, men below the poverty level, unemployed men, and lower income men. Among males 17 to 19 years of age. 8.2 percent were current ST users. In a multivariate mockl using the sociodemographic variables as predictors of ST use (Table 31). white men were mote than twice as likely to use ST as black men; men employed in blue-collar or service/IaFxrer jobs or who were unemployed were 3 times more likely to use ST than white-collar workers; and men in the Southeast and West were more likely to usc ST than men in other regions. Two-thirds of men who ever used ST began use before age 21; more than one-third began before age 16 (Table 32). The median age of initiation of ST use for both snuff and chewing tobacco is 19 years (Novotny. Pierce et al. 19R9). The State- and region-specific prevalence of current snuff and chewing tobacco use among men aged 16 years and older is shown in Table 33. These data are from the 1985 CPS. As mentioned earlier, 45 percent of interviews in the CPS were with proxy respondents. Proxy responses are known to affect the accuracy of information on smok- ing behavior, especially daily cigarette consumption (see above). The effect of proxy responses on data relating to ST use is unknown. Overall prevalence for males in the 1985 CPS was 1.9 percent for snuff and 3.9 per- cent for chewing tobacco. Use of ST was lowest in the Northeast and highest in the South, with intermediate values reported for the North Central and Westem regions. Among women, the overall prevalence of snuff use was only 0.5 percent, with all regions having prevalence rates of 0.5 percent or less except the South (1.4 percent). Prevalence of chewing tobacco use among women was 0.2 percent overall. In summary, ST use is increasing among adolescent males and is decreasing slight- ly overall among men aged 21 years and older in the United States. It continues to be a rare behavior among women. According to national surveya, sociodemographic cor- relates of use include blue-collar and serviceAaboreremployment, unemployment, and residence in the South. Local surveys have also shown high usage rates among American Indian youth (CDC 1987c,1988: Schinkeet al.1987; Hall and Dexter 1988). Because ST use is more common among young males than among young females, while the prevalence of smoking among high school seniors is higher among females than among males (see above), the prevalence of any tobacco use may he similar amcmg young males and young females. Cigar and Pipe Smoking Tahle.M presents data from the 1986 AUTS forcigar and pipe smoking. Cigar and/or pipe smoking mainly occurs among men, in whom prevalence of use is 8.7 percent. The highest pno{xxt ion of users are between the ages of 45 and 64 years. Usage is slight- ly higher in the most and least educated groups than in the intermediate education categories. TABLE 30.-Prevalence (96) of smohteless tobacro use by sociodemoRraphk catemoriGs, males aged 17 years and older, United States,19R6 Category Ever use Cweent u.w Mtc /l-p 17-19 12.3 E.2 20-29 11.4 5.9 30-39 7.3 4.1 40-I9 9.7 5.0 2S0 11.5 4.8 Raee White 11.1 5.6 B1ack 6.6 3.0 Other 7.7 2.9 ('.eoRraphk area Southead 14.5 7.5 West 9.6 4.5 I Midwest 9.5 4.3 Northesst 5.5 3.0 ComPleted years of xhool 511 14.6 7.3 12 11.1 5.6 13-15 9.1 3.9 I 216 4.8 2.9 Te.ertY level Below 16.1 8.5 Above 9.9 4.9 Entoo7nKnt Unempk+yed 13.0 9.1 Ser.icdlalxxer 12.3 6.4 Blue callar 7.0 3.6 White cnllar 2.3 1.0 N~w.eM~M IneMne (dnltan per 7tar) <In,Ot>n 16.1 9.6 IO.nfM1-29.999 4.7 2.2 230.OfR1 3.0 1.6 ScxtRCF.: AtJrC t"6 (No.aay. rk,ce e1 r. 1911P). bL69 TBSIS i ~'z 121

TARLF, 2R.-ik/mestic market share af ciRarette. (%), by cigarette knRth, percentaRe of total cigarNtes sold, United States,1967-86 Ycar 6a-72 mm 79-RR imn 94-101 mm I If?`121 mm lyla 14 77 9 1969 12 74 13 IrN.o 11 74 16 1970 9 71 Ia 1971 R 72 20 1972 ft 71 21 197} 7 71 22 1474 6 71 23' 197S 6 69 24 1 1976 5 69 24 2 1977 5 67 26 2 I97R 5 65 27 2 1979 4 63 30 2 19R/1 3 63 32 2 19R1 3 62 33 2 19R2 3 61 34 2 19113 3 60 34 2 1984 3 39 36 2 1aR5 3 511 37 2 1996 2 58 37 3 Nf1TF.: Recw.e nf munffinRv lAe hiW ar 0e hudividwl Ie.ceMaRe~ n~ nnl eqn.l Iflfl perceM in awnr inaunrea. 'The 1 I/1 w.121-mm knph wa canbined wiih de 94 a 101 .mm keVA. s(KlRCr•.: FTC OmtRl. Summary and Comment During the past 40 years, filtered cigarettes have virtually replaced nonfiltered cigarettes in the United States. The domestic market sharcs of lower (15 mg or less) tar cigarettes and menthol cigarettes have increased during the past two dccades but ' havc leveled off in recent years. The domestic market share of longer (94-1(11 mm) cigarettes has increased substantially sinee the mid-1960s and still appears to be rising slowly. Continued health concems among smokers are likely to encourage the cigarette in- dustry to continue to design new cigarettes that are perceived ac less ha7ardous. Be- sides filtered. low-yield cigarettes, other"high-tech"cigarettes have been marketed that may appear to smokers to he ks.c has.ardews. These include one brand with a rtcessed filtrr and another with a"navor-control fiiter" that apparently allows the smoker to regulatc the tar yickl of individual cigarettes (Davis 19R7). The R.J. Reynolds Tobac- co Company announced in September 1997 plans to market a new product that heats ratllcr than hurns aohacco. R.J. Reynolds as.crts that the product is a cigarette. and it has commonly been referred to in the press as a "smokeless cigarette." In a press I release, the company's chief executive officer stated that "a majority of the compounds produced by burning tobacco are eliminated or greatly reduced, including most cony- pounds that are often associated with the smoking and health controversy" (R.J. Reynolds 1987). The American Medical Association (1988) and the Coalition on Smoking OR Health (1988) have filed petitions with the U.S. Food and Drug Ad- ministration (FDA) seeking FDA regulation of this new product as a drug or medical device based on implicit health claims, among other reasons. As of November 1,98R, these petitions were under review by the FDA. In October 19118, R.1. Reynolds hdgan test marketing the ixoduct, named Pr+emier, in three cities (Phoenix and Tucson; AZ. and St. Louis. MO). (See Chapter 7.) Other Types of Tobacco Use Smokeless Tobacco Use Smokeless tobacco (ST) use, including snuff and chewing tobacco, became a sdbject of concern in the United States during the 19803 (US DHHS 1986). Cross-sectional national surveys and various regional surveys have identified several demogTaphic categories at high risk for the use of these products, including young white malet, per- sons living in the Southern and North Central United States. American Indians; and Alaskan Natives (Rouse 1989, in press; Boyd et al. 1987; CDC 19R7c, 1988; ScNinke et al. 1986). Trend data on ST use are available primarily through the AUTSs. which included persons aged 21 yeara or older in 1964, 1966, 1970, and 1975 (US DNEW 1969; US DHEW 1973; US DHEW 1976), and persons aged 17 years and older in 1986 (Novotny, Pierce et al.1989, in press). In addition, the 1970 and 1987 NHISc included data on ST use among persons aged 17 years and older and aged 18 years and'older, respectively. The Behavioral Risk Factor Surveillance System of the Centers for nis- ease Control collected State-specific data on ST use among persons aged 19 years and older beginning in 1986 (CDC 1987d). The 1985 CPS of the U.S. Bureau of the Cen- sus included questions about ST use among persons aged 17 years and older (Marcus et a1.19R9. in press). This survey also produced State-specific estimates for prevalence of Ioe of these products. Definitions of ST use and questions asked about ST use in these surveys art listed in the Appendix to this Chapter. Figure 5 compares age-specific data for men from the 1970 NHIS and the 1986 A(fl'S. Between 1970 and 1986, snuff use increased fifteenfold and chewing tobacco use more than fourfold among males aged 17 to 19 years. Smaller increases were ob- served among the middle-aged groups, and a decrease in the use of both products was noted for older men (age 50 and above). The NHIS used household interviews, and the AUTS used telephone interviews as their primary mode of data collection; however, this difkrence in methodology is unlikely to account for the substantial increase in ST rse among teenage males. Data on ST use among persona aged 21 years or older are presented below from the 19G4-R6 AUT:Ss. These surveys were based on in-perscxt interviews in 1964 and 1966 and telephone interviews in 1970, 1975, and 1986. State-specific data from the 1995 1 ZL69 T8STS iIQ

F had started smoking before different ages is presented separately for males and females in Tablc 17 and Figures 3 and 4. Among smokers horn since 19;i5, more than four-fifths started smoking before age 21 and almost half started before age I R. The data reveal few diffenencec across birth cohorts in age of initiation before age 16. However, for more recent birth cohorts, then; has been a tendency for a higher percentage of ever smokers to have initiated smoking heforr age 18 or 21. Thc propcxtion starting hefote age 18 has incn;ased from 3R per- cent of ever smokers hrxn from 1910-14 to approximately half of ever smokers hexn between 1950 and 1954. The proportion starting before age 21 has increased hetween these two birth cohorts frexn 66 to 87 percent (Table 17). Stratifying by sex shows that this tendency for more recent birth cohorts to initiate smoking at a younger age has oc. curred among both sexes but has been more striking among females (Figures 3 and 4). The data from the earliest birth cohorts may he hiated somewhat by differential mor- tality among smokers with different ages of initation. Mortality rates for smoking-re- lated diseases are higher for smokers with younger ages of initiation (US DH1IS 19R2, 19Ri, 19R4). Thus, the age of initiation data may be biased upward among. for ex- ample, the 1910-19 birth cohort, whose members were 61 to 70 years old in the last survey year included in these data (1980). However, the trend noted above toward declining age of initiation, especially among femaks, is still apparent when consider- ing only those born since 1930. As pointed out above, the decline in age of initation among males is only seen in the piopottion of ever smokers starting before age 21. In summary, these data indicate that uptake of smoking is now a phenomenon that occurs almost entirely during the teenage years and that the initiation of smoking is oc- curring at younger ages among more recent birth cohoR.s, expecially among females. Data from the 1986 AUTS on age of initiation of smokekss tobacco use are presented in the section on smokeless tobacco later in this Chapter. Prevalence in 20- to 24-Year Age Group The most complete ascertainment of smoking initiation would involve the collection of longitudinal data on children from the ages of ahout 9 to 21 years. Such complete population-based information for the United States is not available. However, trends in smok ing prevalence in the 20- to 24-year age group (Table 19). as determined by the NHIS, provide an indirect measure of trends in smoking initiation. Using this measure hac the advantage that smoking initiation is relatively complete by age 20. However, there is a lag of several years between actual initiation during adolescence and prevalence in this group. The R2 values for the tegression lines derived from these data are above 0.70 for sex-, race-, and education-specific groups, except for females over- all, among whom initiation rates varied considerably. From 1965-R7, cmoking initiation, as measured by prevalence among those aged 20 to 24 year:c, decreased from 47.8 percent to 29.5 percent, at a rate of decline from 1965- R5 of 0.69 percentage points per year. There are marked gender differences in this measure of initiation. Smoking prevalence among young maks hac fallen from 56.3 percent in 1965 to 31.1 percent in 1987 at a ratc of change (1965-85) of -1.19 percent- agc points per year. In contrast, smoking prevalence among young females has fallen 209 Z969 t8StS oD C ~O N N N r1 v~i ~ OD O. a~0 P P d. ~ g ry a? ~ on o od .~~' ~~ ~„ P, `~ w, o S ~ a ir ~ a h 00 ~ ~ ~ O h, -3 n N N ~ ~ , vf a0 n~ P ,~ pp ~ e~p a3 r P P O. ~. N vl w~ Ci0 ~ ~ P ae ae r, N a, O, P~p bp.~-' N In a~0 ~D O• P a-0 ~ ~ ~. .. „~ .q P o .4 .r~ v+f +1 eep ~'! +1 ap ~ ~J P~ P~~ N 1dt~ eD ~ a0 P r a, N N N, ~ N, 1~ CQ 1t ri - O~ O P4O s0 h ~p ~p p~ N< P~ P g~ N~ r v~i oD a h ~ o'. . P P o, `0 pp r.l N a~ N ~~.ft nry.~o v0'f OM D 9 h +~p N ^e•lO~ N ~ T N r I I a t v tl wf o, st 10-0 F O: a~ ~o I 299

National Adolescent Student Health Survey. 1997 The National Adnteccent Student Health Survey was initiated in 1995 by three na. tional health organ'nations: the American School Health A.ssociation, the Association for the Advancement of Health Education, and the Society for Public Health Educa- titm. Funding for the survey was provided by the following agencies of the Public I kalth Service: the Office of Disease Prevention and Health Promotion (Office of the Assistant Secretary for Health), the Center for Chronic Disease Prevention and Health Promotion (CDC), and Naticxtal Institute on Drug Abuse (Alcohol. Drug Abuse, and Mental I lealth Administration). A two-stage cluster sampling procedure was used to survey 5,R59 Rth graders and 5.560 1()th graders from 112 public and private schools. Twenty-four percent of the original sample of schools did not agree to participate and each was replaced by another rarnlomly celected school from the same geographic area. Parents were informed of the content and purpose of the survey and were provided the opportunity to exclude their child from the survey. Students were informed that participation was voluntary and that all information provided would be strictly confidential. Parental request for exclusion, student absenteeism, and voluntary nonparticipation reduced the survey response rate to 97.5 percent (88.9 percent for Rth grade and R6.0 percent for 10th grade). During October to December 19R7, trained survey administraton collected data from three randomly selected clas.ces of Rth or 10th grade students at each participating school. Each student responded to one of three survey forms. The 30-day prevalence of cigarette smoking and smokekss tobacco use appeared on all survey forms. The item nonresponse on these questions was 0.2 percent of those who were surveyed. National Health Interview Surveys The National Health Interview Survey (NHIS), which is conducted regularly by the National Center for Health Stati.stics, uses a sampling frame developed by the U.S. guteau of the Census and is based on a muitistaged randotn probability sampling design. lnformation is collected in face-to-face household interviews using one adult per household and using proxy reporting for other members of the household. Since 1974, information on smoking has been obtained only by self-repott. This has entailed telephone followup to selected household memhers who were not personally inter- viewed. Basic smoking information has been collected for several years, including 1965. 1966. 1970, 1974, 1976-80, inclusive, 19R3,19R5, and 1987 (data prior to 1974 are based on hoth celf-rcported and proxy reporting: all of the more recent surveys were hased on celf-rcports). Sample sizes for the surveys have ranged from 10,00(1 to 30.000 persons. There has been an overall consistency in the smoking questions asked in the different surveys. Beginning in 19R5, an adequate sample of blacks was ensured by the curvey design (using the technique of oversampling). The NHIS generally has a recpnn.c rate of 96 perccnt (NC1IS 19R7). However, the extra step in converting proxy respcxnsc to %elf-rcport leads to a ekcrease in tiic response rate to approximately 90 per- cent. 8£69 T8STS The data presented in this Chapter were taken from the Health Promotion and Dis- ease Prevention Supplement to the 1985 NHIS and the Cancer Control Supplement to the 1997 NNHIS. National Health and Nutrition Examination Survey and Hispanic Health and Nutri- tion Examination Survey Since 1960, the National Center for Health Statistics has conducted periodic health xurveys that have included physical examinations and laboratory tests. Initially called the National Health Examination Survey (NHES), the name of this survey was changed to the National Health and Nutrition Examination Survey (NHANES) in 1970 when a nutrition component was added. The NHES was conducted in 1959, 1963, and 1966, and the NHANES in 1971, 1976, and 1984. ~, Although the NHANES as a population survey included all of the Nation's Tajor, subpopulations including Hispanics, the sample sizes were insufficient to produco nsli- able estimates of health status, particularly if the three major Hispanic subgroups- Mexican-Americans. Cuban-Arnericans, and Puerto Ricans-were consiored separately. Therefore, the Hispanic Health and Nutrition Examination S#rvey (HHANES) was developed by the National Center for Health Statistics. The HHANES was designed to provide sufficient samples of each Hispanic subgroup. The survey, no{ only produces reliable estimates of health status for each subgroup but also permits cross-cultural comparisons within the broader Hispanic cultural context. , The HHANES was a probability-based survey of three distinct subgroups of a major U.S. minority group rather than of a national sample. The sampling methodology used complex, multistaged, stratified, clustered samples of the defined population. When weighted, the sample data repnesent the targeted population. For HHANES, the tar- geted population consisted of three gtvups of civilian, noninstitutionalized persons, aged 6 mtmtths to 74 years from three areas of the country that had a sufficient number or proportion of Hispanics to render it economically feasible to screen households and to operate an examination center. (1) Mexican-Americans residing in selected areas of Texas, Califomia, Colorado. New Mexico. and Arizona: (2) CubataAmericans resid- ing in Dade County. Florida; and (3) Puetto Ricans residing In the New York City area. Data were collected from 19g2 through 1994 via in-person household interviews and via examination at a local examination center. Information was collected regarding a number of health issues, including the use of tobacco. NIDA High School Seniors Surveya on Drug Use Each year since 1975, the Monitoring the Future project has conducted surveys of representative national sampks of high school seniors in the United States (Johnston, O'Malley, Bachman 19R7). Monitoring the Future is conducted by the University of Michigan Institute for Social Research and receives its core funding from the Nation- al Institute on Drug Abuse. Each year, a multistage sampling procedure is used to identify approximately 135 public and private schools (the number of private schools has varied from 14 to 22) that 141

a 9 N ~ e 7 e ` o 11 3] 6 02 ~ K .1 E 9 ~ .~ ~ jjjjassssa= ? ~ .~ 3 0869 T8SIS ing with minors must be resolved; these have slowed undentanding of how depend- ence develops. CoRttition and Decisionmakhg Knowledge of the health effects of smoking is likely to influence initiation for some teenagers. Teenagers reported that one-third of their earliest refusals of cigarettes'were based on fear of the effects of smoking on health, attractiveness, or athletic perforniance (Friedman, Lichtenstein, Biglan 1985). In early adulthood. British medical students' rating of smoking as a"major" or "not major" health risk was associated with their smoking status as reflected by surveys in 1972 and 1981 (Elkind 1982). Heavy smokers among college women evaluated health outcomes of smoking less negatively than did nonsmokers (Loken 1982). The latter two cross-sectional studies, however. may4 pos- sibly reflect the effect of behavior on cognition rather than the effect of cognit;on on behavior. Cognitive appraisals of the attractiveness or desirability of smoking or of sttiokers ate associated with current smoking or intentions to smoke (Barton et al. 1982; McAlister, Krosnick, Milburn 1984), as are beliefs orattributions of the functional rok of smoking (Murray and Perry 1984). Tenth graders inclined to smoke indicated greater congruity between the value they place on interest in the opposite sex and the ext4nt lo which they ascribe such inten~t to smokers (Barton et al. 1982). Intentions to smoke were also associated with congruity between the personal value of a characteristic and its attributicxt to smokers. Murray and Perry's analyses (1984) of the functional mean- ing of substance use by youth elucidated a variety of attributions correlating with young people's substance use. The report that smoking was useful for relieving boredom was most highly correlated with smoking. Data from Englaed (Charlton 1984) demonstrate that children who smoke compared with non.smoking children at+e more likely to agree that "Smoking keeps your weight down." This attribution was especially prominent among older girls. School health education ptograms fo discourage smoking have traditionally assumed that knowledge of the health consequences of smoking would deter adolescents from smoking (Chapter 6). This assumption has received limited support in the prevention literature (Thompson 1978). Despite school health education programs, children, espe- cially those who smoke, continue to harbor several misconceptions about smoking. Tiiese misconceptions include overestimating the prevalence of both peer and adult smoking, underestimating the negative attitudes of their peers, and minimizing the ad- dictive nature of smoking (Leventhal. Glynn. Fleming 1987). The overestimating of prevalence may represent the combined influence of social context and cognitive fac- tors in determining snw*ing. Contemporary smoking preventiott ptogtams ("psychosocial prevention curricula") emphasize knowledge of short-tettn consequences of smoking likely to he mor+e per- tinent to adole.seents who have limited futun: orientations ((lasgow et al. 19R 1); and knowledge about the variety of social influences (parental, peer, and media) that affect the development of smoking (Flay 1985: Evans et al. 1978; Chapter 6). Decisionmak- 11. 115

TA...,F 19.-.Smnking statns Mof high sehool .enlors, Unked States,1975-87 only frmn 40.5 percent in 1965 to 29.1 percent in 1987 at a rate of change (1965-RS) one-quarter that of young mates (--0.28 pereentage points per year). The slower rate of decline among women is due, in large part, to the increase in initiation rates in less edu. cated young women (Pierce. F'rore et al., in press, b). Smoking initiation patterns among whites and blacks have been similar during the past 20 years. From 1965-87, smoking prevalence among whites aged 20 to 24 yeaR has decreased from 47.5 percerit to 30.5 percent, while for blacks the decline has been from 50.9 percent to 25.6 pcrcent. The rates of change between 1965 and 1985 among whites and blacks were similar (-0.6R and -0.79 percentage points per year, respective- ly). The prevalence of smoking had been higher amextg young blacks than among young whites for most survey years between 1965 and 1993. but whites had a higher prevalence in 1985 and 19R7. Marked differences in smoking initiation rates based on educational level have oc- curred. From 1965-87, the smoking initiation rate as measured by prevalence, ages 20 to 24, fell among males with 12 or fewer years of schooling (high school graduate or less) from 63.6 percent to 43.8 percent (-1.00 percentage point per year from 1965- 85). In contrast, for males with 13 or more years of schooling (some college or mcxe), prevalence has fallen from 42.7 percent to 16.3 percent, at a rate of decline (1965-R5) of 1.51 percentage points per year. A similar difference in initiation rates by education was seen among wcxnen, although the rate of decline between 1965 and 1985 was less among women than among men of equivalent education. In the overall sampk (men and women cexnbined), the rate of decnease in initiation among persons with 13 or more years of education (1.10 pencentage points per year) was three times that among per- sons with 12 or fewer years of education (0.35). Trends In Adokseent StnokMg Several surveys have provided national estimates of smoking prevalence among adolescents. Because these surveys differ in terms of the definitions of smoking, ages of respcxtdents, sample size, method of data collection (household versus school ver- sus telephone interview), years in which the surveys were conducted, and overall results, the findings of the major surveys are presented below. NIDA High School Seniors Surveys on Drug Use,1976-87 Data from the. NIDA-sponsored High School Seniors Surveys have been collected annually since 1975 and are presented in Table 19. These surveys have been carried out by the University of Michigan Institute for Social Research (lohnston, O'Maltcy. Rachman 19R7). This data set is most useful for examining trcnds in smoking. In- dividual prevalence figures probably underestimate actual adolescent smoking prevalence because the survey does not include high school dropouts, who are known to have much highcr smoking rates (Pirie et al. 1998. Yates et al. 19R8). Reported daily smoking of cigatettes has decreased among high school seniors from a peak prevalence of 29 percent in 1976 to 19 percent in 1997. 1lnwevcr, the trend has not been linear. The mhjority of the change occurred between 1979 and 1980. aafter Year Daity smoken Le"dw daily smoken prtvioua mroken, not in taat month Never smokers 1975 27 10 37 26 1976 29 10 36 25 i 1977 29 10 3R 24 1979 2R 9 3a 25 1979 26 9 40 26 1990 21 9 41 29 19RI 20 9 42 29 19R2 21 9 40 ~ 19R3 20 9 41 29 IpR4 IA 11 41 .30 19R5 19 11 39 31 19116 I s 1] 39 32 4, Imt1 19 11 39 33,i 5011RCR.: IWihMe fi. srxid aaench. tJrtl.a.iy erMk14<ae QfacMna, JolruMm. o'Mdky 19110..b. 1991.145, 19117. )drntan and B.chmae a9lUF. )ohiMOa. aakoae. o'Malley 19110kb. 19R2.t9N. t9116. awd.epublished dw' 191171t which prevalence has temained relatively stable. The proportion of high school sen • who have smoked within the last month, although not on a daily basis, has not changed substantially during this period. There is also rather little change in the proportion pf ~ this population who has previously smoked but not in the last 30 days. The proportion of high school seniors who have never smoked increased from 26 percent to 33 percent between 1975 and 1987. Trends in smoking status by sex, ratx. and edttadonal plans are Piese^ted in Table 20. The prevalence of daily amoking decreased in all major subcategories of high school seniors between 1976 and 1987. Daily smoking among males decreased from a peak prevalence of 28 percent in 1976 to 16 percent in 1987; most of this drop oc- curred between 1977 and 1980. Daily amoking among females decreased from a peak prevalence of 30 percent in 1977 to 20 percent in 1987• with the largest decrease oc- curring fran 1979-81. Since 1981, the pteva/enee of daily smoking among high school students has remained fairly corMant for both mates and females. In each year since 1977, the prevalence of dsily smoking has been higher in females than in males (median differtnce--4 percentage points). The prevalence of daily smoking fell substantially among blacks, from 26 percent 1976 to 8 percent in 1987. During the satne period, prevalence declined among from 29 percent to 20 percent. The reasons for the dramatic decline among blacks are unclear. It does not appear to be due to increasing sampling bias over time-survey methods and sample sizes by race have been consistent. A substantial decrease in smok- ing initiation among blacks also oocurred. as measured in the NH1S by prevalence in persons 20 to 24 years of age, between 198? (38.7 percent) and 1985 (28.2 percent) (Table 18). This figure declined further to a preliminary estimate of 25.6 percent in 1987. Students with plans to pursue higher education were much less likely to be daily smokers in 1976 than those without such plans (21 percent versus 37 percent). The ah-

TARLF, W.-Cmttinued Cis.ypipe s<mc+kieR st.ha Ctinenl uaer Fm ofr wser Neve. u.er Tdal x Hea.eliold Iecanc (dnMan per year) <I0,/1n0 3.1 16.3 $0.1 tfttl 1.220 10.(Mno-19,999 4.0 21.2 74.9 ton 2.204 20.01n-29.999 4.3 23.1 72.6 101) 2,RS3 30.tlnfl-,i9,999 5.0 24.2 7t1.R IOQ 1.735 240.(M10 3.5 29.1 66.4 100 2.947 Unknown 3.3 17.1 79.6 100 2.072 pbverty levd' Above 4.7 23.9 71.4 IOn 9.913 fletrnv 3.0 19.6 711.3 1nn I,M6 Unknown 3.3 17.1 79.6 Inn 2,1172 roovenr k.el ia A..ed cwn tlw drfinnioe poa;eae Ay the U.S. Ruew of ae cenw.. SOI IRCF.: Alft'S 1914G (U5 ONIIS. ie peu,.). ao -% 70 " eo-a 30 -~ 20 ~ 10 J 0 1964 1966 0cow"ie PART II. CHANGES IN KNOWLEDGE ABOUT THE DETERMINANTS OF SMOKING BEHAVIOR Introduction: Histotrkal and Conceptual Overview This Section reviews the past 25 years' growth in scientific knowledge of the deter- minants of smoking. Broad conceptual shifts in understanding smoking are first reviewed by comparing current knowledge, as reflected in the 1989 Surgeon Gener'al's Report as well as in more recent investigations, with that reflected in two previous.4ur- gecxl Gcneral's Reports during the past 25 years: the 1st Report, issued in 1964. and the 15th anniversary report, issued in 1979. 19iW Surgeon General's Report i, The first Surgeon General's Report devoted a chapter to the psychosocial aspeqts of, smoking and another to the issue of smoking as drug addiction or drug habituation. These topics continue to receive contemporary attention. A third chapter in the 1964 Report discussed morphological characteristics of smokers as important detelminants of smoking (e.g., physique, somatotype, and weight). With the exception of body weight, there has been a decline in the attention paid to these variables. The relation- ship between body weight and smoking cessation, especially among women,,haA received much recent attention (US DHHS 1988). The 1964 Report's Chapter on Psychosocial Aspects of Smoking related smoking to a variety of demographic factora including socioeconomic status (smoking being more prevalent among "lower or working classes" but kss prevalent among extremely poor, e.g., unemployed groups) and gender (smoking being more prevalent among men). With regard to gender, the Report anticipated contemporary concerns about smoking by women (US DHHS 198(1b), noting that "711e proportion of women smokers has in- creased faster than that of inen smokers in recent years" (US PHS 1964. p. 363). The 1964 Report's chapteron psychosocial aspects also linked smoking to such broad personality factors as extraversion and orality. While some research continues to show rclaticxlships with extraversion (e.g., Eysenck 1980; Mangan and Golding 1984). mcnt contemporary research focuses on nwrc specific psychological, biological, and social variables and their interactions. The 1964 Report noted that smoking might function to reduce tension but reported little research related to this possibility. In contrast, the 1998 Report on nicotine addiction reviews considerable laboratory and field research on the relationship between smoking and stness and concludes that stress increases cigarette consumption among smokers and is related to initiation of smoking among acblescents and relapse among abstaint:rs (e.g., US DHHS 1988). The 1964 Report devoted much attention to the role of nicotine in smoking behavior, an issue that continucs to he of central interest, as reflected in the 1988 Report. Both reports concluded that nicotine is a critical and substantial determinant of smoking. The fncus in 1964, however, centered on whether smnking fit the World Health OrgsHliiation's (WHO) definition of addiction, which emphasized the importance of physical dcpendcnce (WHO 1957). The Report concluded that there was no proof of -M 1970 1975 1996 Year FIGURE 7. Trends In prevalence of using ciRarettes, ciRare, and pipes, adult tnen. United States,19fi4-86 C(/tIRCF.: AIITG IIK UIIIIC Iaqt). ! I LL69 ZBSTS 32R i29

solute difference (in percentage points) between the two grmeps remained constant be. twcen 1976 and 1987. In 1997. the prevalence of daily smokers among those with plans for higher education was less than half the prevalence among those without such plans (14 percent versus 30 percent). The percentage of blacks who smoke on less than a daily basis exceeded the percent. age of whites in 1976 (13 and 10 percent, respectively) but was lower than the percent. age of whites in 1987 (6 and 12 percent, respectively). The percentage who havc pre. viously smoked hut not in the past month has consistently been slightly higher arlnnF blacks than among whites and among those with plans for highereducation than among those without college plans. Besides these findings, then: have been few diffenencec between subgroups and few changes between 1976 and 1987 in the proportion of high schcx~l seniors who are in these categories. As mentioned above, the decrease in the proportion of high school seniors who smake on a dai ly ba%is is reflected hy a complementary increase in the proportion of high schaol seniors wh(s have never smoked. This increase has been more marked among males compared with females and among blacks compared with whites. 19R7 National Adolescent Student Health Survey The 1987 NASHS collected data on prevalence of sntoking within the last -30 days (US DHHS. in fxess,b). Respondents to this survey composed a random sampk of the Nation's students in Rth and 10th grades. Sixty-three percent of the 8th graders were 13 yeara old and 27 percent were 14 years old. Sixty-two percent of the 1(hh graders were 15 years old and 28 percent were 16 years old. For each grade, 68 percent were white, 17 percent were black, and 9 penoent were Hispanic. Prevalence data are presented in Table 2 t. Righty-four penxnt of the eighth graders reported that they had not even puffed on a cigarette in the last :10 days, with little dif- ference between the sexes. Forty-nine percent of all eighth graders reported never having smoked a cigan-tte, with no difference between the sexes. Among IQth graders, the proportion not having puffed on a cigarette in the tast 30 days was slightly bwer. 76 percent among males and 71 percent among females. Thirty-eight percent of males and 36 percent of females in this grade reported that they had never had a cigarette. Ln I-A TAB1.F, 21. 3n-&y preraltyr+ce of smokitag (qf,), (lntkd Shdes,1987, 8th and 1rMh grades Ln tp ath gade toth Erack r Maks Fem.ks Males Femaks m ~ Nnt even a pun 84.9 I{3.0 73.9 71 3 m oN 1-4 ciRare" S-I9cittarenes 7.1 2.7 lt.2 3.4 7.A 4.9 . 10.4 3.1 t-S iacks 2.4 1.5 5.6 7.4 Mare Ihan S p.cks 2.9 1.9 6.0 5.9 i(11IRCF: NMIM.I Mkdeai" Sj*kM tk.hh twvey Iql7 f11S fMtlLt, la preiK h1. Approximately equal proportions (7 to 8 percent) of males and females in the eighth Erade reported smoking a pack or more in the last month. Among 1(Nh graders. this pcq+orlion was tnore than twice as high, with 17 percent of males and 19 percent of ' females reporting that they smoked a pack or more in the last month. US DHEW Teenage Smoking Surveys,19fi8-79 Tktaikd questions on smoking were atked in five national telephone surveys;of akolescents (ages 12 to 18 years) conducted by Chilton Research Services for the U'.S. fkpartment of Health, Education, and Welfare from 1968 through 1979 (US DHE,W 1979h). Adolescents were clacsified by smoking status at follows: ntver smokers, had not taken even a few puffs of a cigamtte; exfxrimerttal smoktrs, had had a few puffs but had not smoked as many as 100 cigarettes; tx-srnoktrs, had smoked at least 1(10 cigarettes but no longer smoked: current occasionaf smokers, smoked less than bne cigarette per week; and current reRularstrtoktrs, smoked at kact one cigarette per ,~eek. ; 1n published results for these surveys, data fornever smokers and experimental smqkers were generally aggregated. Summary data from each of the surveys are presented in Table 22 (males) and TAb1e 23 (females). The proportion of both males and females of each age group who are ctacsified as either never smokers or experimental smokers is substantially higher than the proportion of never smokers reported by other surveys. For example, the 1,974 Teenage Smoking Survey showed that 75 percent of males and 82 percent of females aged 15 to 16 years had never smoked or had only experimented with cigarettes: in con- trast, the 1987 NASHS (above) showed that only 38 pencent of males and 36 percent of females in the 10th grade (15 to 16 years old) had never had a cigarette. Similarfy, the 1979 Teenage Smoking Survey showed that 68 percent of males and 64 percent of females aged 17 to 18 years were never-smokers or experimental smokers; in contrast, the 197911igh School Seniors Survey showed that 27 percent of males and 25 percent of females were never smokers. There are at least two possible explanations for the consistently and surprisingly high prvportion of teenagera in the categories of never smokers and experimental smokers. Pirst,100 cigan:ttes may be too high a cutoff to u4e for classifying teenagers as never smokers or experimenters. Second. telephone interviewing may lead to more under- n.7xming of cigarette smoking behavior than other survey modalities. Underreporting may he nxore important for some smoking categories than others-for instance, oc- cacional smokers might be particularly sensitive about their smoking behavior and might be more likely to underreport the total number of ciganettes they have ever smoked. Current smoking rates can also be compared between the Teenage Smoking Surveys and the High School Seniors Surveys. In the 1979 telephone survey. teenagers were classified on their reported smoking on a weekly banis. Of males aged 17 to 18 years, 19.3 percent were classified as current regular smokers (one or nxtre cigarettes per week) and another 0.3 percent were ctaesified as current occasional smokers (lerts than one cigarette per week). For females aged 17 to 18 years, these figures were 26.2 per- cent and 0.9 per+cent, respectively. In the Itigh School Senicxs Survey. studcnts ate tt17

initiation have occurred and have increased over time between more and less edu- cated people. 9. The ek.me-tic market share of filtered cigarettes increased frcxn 1 percent in 1952 to 94 percent in 1996. The market share of low-tar cigarettes (15 mg or less) in- crcased from 2 percent in 1967 te SG percent in 19R1, after which this proportion fell slightly and then stabilised at 51 to 53 percent. The market share of longer cigarctte- (94 to 121 mm) increased from 9 percent in 1967 to 40 percent in 1986. 10. Betwecn 1964 and 19R6, use of smokeless tobacco (snuff and chewing tobacco) declined among men and women 21 years of age and older. Howevcr, among males aged 17 to 19. snuff use increased fifteenfold and use of chewing tobacco incrcaced more than fourfold from 1970-A6. 11. Diffrrencec in prevalence of cigarette smoking and smokeless tobacco use be- tween young males and young females suggest that the prevalence of any tobac- co use is similar in these two groups. 12. From 19fi4-Rh. the prevalence of pipe and cigar smoking declined by 80 percent among men. Part lf l. Chan/;es in Knowledge About Determinants of Smoking Behavior I. Smoking was viewed asa habit in 1964 and is now understood to be an addiction inf luenced by a wide range of interacting factors, including pharmacologic effects of nicotine: conditioning of those effects to numerous activities, emotions, and settings; socioeconomic factors; personal factors such as coping resources; and social influence factors. 2. Since 1964, there has been a gradual evolution of understanding of the progres- sion of smoking behavior through the broad stages of development, regular ua, and cessation. Each of these stages is differentially affected by multiple and in- teracting determinants. 3. Views of determinants of tmoking are affected by the predominating theoretical and methodological perspectives. In smoking, the tarlier focus on broad, dicpexi- ticxial variahlec (e.g., extraversion) has given way to an emphasis on situation- specific and interactional variables; a focus on a search for a single cause has given way to a focus on multiple and interacting causes. Z669 I85I5 Appendix Questions RelCardinR Snakittg Status and Quitting from the 19li6 AUTS Smoking status (current, former, never) is decided from responses to the following two questions: "Have you ever smoked at least 100 cigarettes in your life? "Do you smoke cigarettes now?" Current smokers were then asked: "Have you ever made a serious attempt to stop smoking cigarenes entirely?" "Thinking of your last serious attempt to quit, how long did you stay off ciga- rettes?" "How long ago did that attempt to quit begin?" Current smokers who reported that they had never made a serious attempt were asked:, "Have you ever thought about quitting?" "Would you try to quit if there was an easy way to do so?" l Questions RegardinR Smokeless Tobacco Use 19R6 AUTS ~ Ever use: "Have you ever used (snuff and chewing tobacco asked separately) on a fair- ly regular basis?" Current use: "Do you use (snuff, chewing tobacco) now?" 1964,1966.1970. and 1975 AUTS Ever use: "Have you ever used snuff at all regularly?" "Have you ever chewed tobacco regularly?" Cutrent use: "Do you now use (snuff, chewing tobacco)?" 1985 NIDA National Household Survey on ihug Abuse Ever and current use: "()n the average, in the past 12 months, how oRen, if ever, have you used chewing tobacco or snuff or other smokeless tobacco?" Responses included "never; "'almost daily;`Iess than daily," and "not in past year." 359

I 1985 age distribution, whereas the previously published figures were adjusted to the 1970 age distribution. For each gmup, observed smoking prevalence for each survey year is reported. Ad- ditionally, to assess time trends from 1965-85, weighted least-squares regression analyses have been applied to these data. The 1987 data were not included in the regres- sicxt analyses hecaate these data are preliminary estimates. These estimates can be used to provide a measure of predictive validity of the model; in general, the preliminary 199 7 estimatcs are cimilar to projections from the model (Pierce. Fiore et al., in press,a). The Rz statistic was used for each trend analysis and is a measure of how well the linear model fit% the ohserved data values. RZ values may range from 0 (no linear trend) to 1.0 (a perfect fit between the observed values and a linear model). The data on overall smoking prrvalence, as well as for each sex and racial gtoup presented in Table 3, demonstrate linear trends with RZ values ranging from 0.74 to 0.9R; thus, the models fit the data very well. Trends for three of the four educational categories are also fitted well by a linear model. Forone category, less than high schexot graduatir,n, no R2 value is reported because the rate of change is very close to zero (making the Rz statistic inappropriate as an index of the amount of variation explained by the model). The change (in percentage points) per year is the slope of the line of best fit calculated by the model. The standard error of the slope allows confidence limits to he placed around the estimate of change per year. Ninety-five-pencent con- fidence limits around the estimate of a slope is approximately equal to the slope plus or minus two times the standard error. Overall smoking prevalence declined from 40.4 per+cent in 1965 to 29.1 percent in 1987. The trend from 1965-85 is fitted almost exactly by a linear model (R2=(1.97). Smoking prevalence in the United States adult population is decreasing at a rate of 0.50 percentage points per year with a standard error of 0.03. Thus, the 95-percent con- fidence interval for the change per year is 0.44 to 0.56. There is no evidence of any sudden deviations from the identified trend such as that seen in the per capita consump- tion data in 1983 (Table 2). The prevalence of smoking among men has decreased steadily from 50.2 percent in 1965 to 31.7 percent in 1987. The rate of decline between 1965 and 1985 was 0.94 per- centage points per year (95-pertent confidence limits, 0.76, 0.92). Female smoking prevalence remained stable at 31 to 32 percent from 1965-77. Subsequently. prevalence began to decline slowly and reached 26.8 percent in 1987. The overall rate of decline from 1965-lt5 was 0.21 percentage points per year (95-percent confidence limits, 0. I5, 0.27). Fiore and coworkers (in press) have examined more recent trends in smoking by gender in greater detail. This analysis showed a rate of decline in prevalence among women of 0.33 percentage points per year between 1974 and IQRS (95-percent confidence limits, 0.21, 0.45) (R2=0.88). Although there has been a difference in smoking prevalence between blacks and whites, it may he explained by socioeconomic status (Novotny, Warner et al. 19lIR). and the rate of change in smoking prevalence in recent years has been similar between the races (Fiore et al., in press). Smoking among whites decreased from 40.0 peteem in 1965 to 28.8 percent in 1997. The rate of decline from 1965-85 was 0.50 percrnt- age points per year (95-percent confidence limits, 0.44, 0.56; R2=0.97). For blacks the R2 value for the simple linear nade) is 0.74, suggesting that the data should be reviewed more carefully. In 1965, 43.0 percent of blacks smoked. This number had changed little by 1977 when 41.8 percent smoked. From 1977-87, there was a considerable drop in smoking prevalence to 34.0 percent. Thus, the data suggest that there may be two trends among blacks. Fiore et al. (in press) fitted a linear model to the data for 1974-85 and reported a rate of change among blacks of -0.67 pereent- age points per year with 95-percent confidence limits of 0.37 and 0.97 (RZ--0.80). ~'his rate of change was not significantly higher than that tunong whites for the sarne period (-0.57 percentage points per year). However, smoking prevalence among black men was decreasing at a faster rate than among white men (1.15 percentage points per year compared with 0.87, p-0.03). There were no significant differences noted in the rates of decrease among women of either race (blacks, 0.26 percentage points per year whites, 0.32). Tntnds in smoking among the various educational groups have differed markedly since 1966 (Pierce, Fiore et al., in pnes, b). College graduates have decreased their smoking level from 33.7 percent in 1966 to 16.3 percent in 1987. '11te rate of decline fmm 1966-85 was 0.76 percentage points per year (95-percent confidence limits, 0.60 to 0.92). Smoking prevalence in respondents who reported having attended sorrti col- lege decreased from 42.5 percent in 1966 to 26.1 percent in 1987 at a slightly lower, rate of change (-0.70 peroentage points per year) than that of college graduates. High'- school graduates who did not attend college reduced their smoking from 41.1 percent in 1966 to 33.1 percent in 1987 at a rate (-0.32 pencentage points per year) less than half that for respondents who had attended college. Smoking prevalence in those mpondents without a high school diplottt.did notchange appreciably from 1966 (36.5 percent) to 1987 (35.7 percent); the rate of decline between 1966 and 1985 was only 0.06 percentage points per year. Thus, there is a twelvefold difference in rate of decline in smoking prevalence between the most and least educated groups in our society. The incrasing gap in smoking prevalence by educational attainment is particularly evident when comparing the difference in smoking prevalence between the most and least edu- cated groups in 1965 with the difference in 1987. In 1966, the prevalence rates were similar (33.7 and 36.5 pereeM, respectively); in 1987, prevalence in the most educated group (16.3 percent) was less than half that in the least educated group (35.7 percent). Adult Use of Tobacco Surveys: 1964-86 In 1964, 1966, 1970, 1975, and 1986, the Office on Smoking and Health (formerly drc National Clearinghouse for Smoking and Health) conducted detailed surveys of a tepresentative sample of the U.S. adult population. The purpose of these surveys has been to study the population's knowledge, attitudes, and practiees regarding the use of tobrcco. The first two surveys primarily used in-person household interviews while the last three used telephone interviewa. Prevalence of cigarette smoking in the United States as measured by the AUTSs has declined from 40.3 percent in 1964 to 26.5 per- cent in 1986 (Table 4). This decrease teptesents an overall decline in smoking of more 11121134 percent during this 22-year period. „I

019COHTI/UAT" MTNTION 0EMOPMENr E1fPERMENTAT1pN nEOUTAn S~rort.l0 wqemunoN OONSOl10ATEO AOO/CTqlr nECaN1EMRAnoN cQMTEMA.A*~oN CESSATqN ACTqN MAMTENNICE NEwSE nELA.SE ».. ~ "ECrCI"q o FIGURE R.--F,volving theoretical enncepts of the nataral history of smoking, 1964-it9 197(k, and 19ROc. In 1964, only two broad stages were noted, while in 19RR, as many as nine can be observed. Stages are not explanations of attitudes or behaviors. For example, precontempla- tion is a description of the attitudes toward smoking and likely responses to antismok- ing messages of the individual uninterested in stopping. It is not an explanation or a cause of that la,;k of interest. Neither the sequence of stages nor the boundaries among them are rigid. For example, a young experimenter may stop smoking without ever making the transition to regular smoking. A smoker in the regular smoking stage is, at the same time, a pmcontemplator or contemplator in the cessation stage. The regular smoking stage ic abandoned when the smoker moves into action and stops smoking. Although the boundaries among stages and their sequence may be blurred, the concept serves as a framework for understanding the determinants of smoking behavior. Dif- ferent determinants are operative to different degrees during each stage. Thc three broad stages of smoking and theirmultipk interacting determinants provide the organvation for the remainder of this Chapter. Within the stage framework, his- torical trends in determinants are discussed primarily within three general domains. The three dnma ins do rn,t constitute a model; they are a useful way to organize the deter- minants of smoking. The first domain is composed of pharmacologic processes and cnnditicxting, the basic faetors that interaM to suppott smnking. The combining of these into one domain reflects present awareness that pharmacologic processes and con- ditioning interact tfT produce addiction (US DI IHS 19RR). The second domain includes cognition and decisionmaking. The stages of smoking reflect appraisals of oneself, of .tvial e.perience., anml iTf infixmatim, such as that presented in campaigns to deter xmoking. The ways in which individuals process such information and make choices about smoking have been the foci of substantial research. The third domain includes personal characteristics (e.g., personality and demographic factors) and social context, which includes the important influences of the social, cultural, and economic environ- ment. Personal characteristics themselves are affected by these environmental influen- ces and mediate their effect rather than independently determine smoking. Table 35 presents some of the determinants, within each of the domains, that haye a strcxtg effect on the indicated stage of smoking. As such, the table provides an outiine of the discussion that follows. DeveMpment of Smokins Pharmacokrytic Processes and Conditioning Historically, little attention was paid to the role of pharmacologic effects of nicptine and conditioning in the initial development of smoking behavior, for example, among teenagers (psychosocial determinants have been assumed to play a dominant role) (Table 35). as for other dependence-producing substances. Once a smoker starts Wo in- hale, however, it is possible that the pharmacologic properties of nicotine contribute to continued smoking (Koziowski:, in press). A few studies have•investig~te~ the potential role of individual-specific psychophysidlogical nesponses to nicotine and the development of smoking (Kozlowski and Harford 1976: Silverstein et al. 1982). Reactions to initial cigarettes and the interpretation of these reactions may predispose individualstocontinuingornoteontinuingsmoking. Hirschman,Leventhal,andGlynn (19R4), for example, found that the initial early physical reaction was predictive of con- tinued smoking. Dizziness was related to a rapid progression to a second cigarette, while coughing and a sore throat were telated to discontinuation. It is not clear how long it takes for the transition from experimental to regular smok- ing, and there is likely to he much variation (e.g., Hirschtnan, Leventhal, Glynn 1984). However, results from several recent studies suggest that teenagers become nbre ad- dicted to smoking than was previously believed. Survey data (Green 1979; lohnson 1986) indicate that teenagers make frequent and often unsuccessful quit attempts. Other studies confirm that teenagers have difficulty stopping and report reasons for the dif- ficulty-social pressure, urges, withdrawal symptom.s-similar to those seen with adults (Biglan and Lichtenstein 1984; Hansen et al. 1985: Weissman et al. 19R7). Be- cause smoking among children and adolescents is generally confined to relatively few situations, the level of nicotine dependence is limited in this group. Nevertheless, the reports of withdrawal symptoms and relapses among teenage smokers attest to the strength of nicotine dependence even among thase still in the early stages of smoking. Moxe work is needed in this atea to facilitate our understanding of the development of smoking addiction. Research on adolescent initiation has not applied the samc bio- behavioral concepts and measurement tools (e.g., plasma nicotine or cotinine levek) as have been applied to adult ctm>tcing. Sensitive human sub.jects issues related to work- 6L69 ~ 6L69 I851S ~»

t physical dependence and that smoking was a habit, as was use of cacaine, am- phetamines. and other drugs. More recent perspectives (e.g.. Pomerleau and Pomer. leau 19R4), culminating in the 1999 Repnrt, have integrated psychosocial and phar- macologic processes into a single model of addiction or dependence. The 19RR Report demonstrated that there have been substantial data amassed since 1964 that confirm that by the criteria defining addiction, nicotine should he categorized as addicting. Although the 1964 Report did conclude that "... then: is no single cause or explana- tion of smoking . . ." (US PHS 1964, p. 376), its discussion of research reflected an ex- pectation that one or a very few key causes of smoking might be found. Along these lines, the Report emphasized the extent to which evidence demonstrated a cause to he sufficient. For example, in discussing evidence that smoking as a sign of masculinity may motivate many men to smoke, it labeled as "troublesome" the fact that ".., some, but not so many others choose this particular means [that is, smokingi of giving evidence of their masculinity" (US PHS 1964, p. 373). Since the 1964 Report, models of causal inference in the behavioral sciences have changed to emphasize multiple causes interacting to bring about complex behavior patterns, and not one cause in itself that is necessary or sufficient. 1979 Surgeon General's Report The 1979 Report gave much attention to pnevention and to the determinants of smok- ing and smoking cessation, devoting 9 of 23 chapters to these topics. Thus, there was recognition of different stages of smoking behavior and of determinants varying as the stages change. Since the 1979 Report, researchers have continued to elaborate on mul- tiple stages in the development and cessation of smoking. The 1979 Report also recognized that multiple factors interact to encourage and sup• port smoking. The chapter "Behavioral Factors in the Establishment. Maintenance and Cessation of Smoking" posited smoking as"... a behavior-a highly complex act... based on various biochemical and physiological protxsses.,"(US DHEW 1979a, pp. 16-25). It included researr:h on drug and nondrug factors and called smoking "the prvtotypical substance-abuse dependency " 11te Chapter "Smoking in Children and Adolescents: Psychosocial Determinants and Prevention Strategies" explicitly viewed the initiation of smoking as determined by an array of factors. Likewi.se, the Chapter "Psychosocial Influences on Cigarette Smoking" linked multiple factors to main- tenance and cessation of smoking, including personality eharacteristics, multiple drug use, coexisting chronic disease, price "elasticity" of consumer demand for cigatettes, and differences among cultures in their attitudes toward smoking as personal gratifica- tion. The importance of identifying multiple, interacting factors had been enunciated by Schwartz and Dubitzky in 1968 in their te.search on smoker profiles and the influence of multiple variables on smoking ces.sation, maintenance of cessation, and relapse (Schwartz and Dubitvky 196R). The 1979 Report's recognition of an array of detetminants was reflected in a recom- mendation for future research: "7ltene are multiple psychosocial influences on cigarette smoking. Multivariate research is needed ..." (US DHEW 1979a. pp. 1 R-25). Multi- ple regression analyses and causal modeling have now become much more common in ;.10 8L69 T85ZS smoking research (e.g., McAlister, Krosnick, Milburn 1984; Mosbach and Leventhal 198R). The 1979 Report also was noteworthy in focusing attention on systematic cessation effort.s, taking both pharmacologic and psychosocial factors into account. The exten- sive treatment of cessation research in a separate chapter was a first for the Surgeon General's Report and set a precedent for reviewing the intervention literature in sub- sequent reports. Carrent Views Current explanations assume that smoking is determined by multiple causes, no one of which is sufficient. The interplay of psychosocial and pharmacologic forces con- tinues to occupy investigators of nicotine addiction as it does investigators of other I rug addictions. While the 1964 Report tended to see such factors as mutually exclusive, the 1988 Report (US DHHS 1988) viewed these various phatmacologic, biocheRitical; and psychosocial processes, such as eonditioning, as interacting in the determination of nicotine addiction. In fact, conditioned drug-taking behavior is now thought to be central to the concept of addiction; physical dependence is neither necessary nor sbffi- cient (US DHHS 1988). The biological power of nicotine may make the learncd be- haviors that form smoking patterns stronger and more resistant to change. At the same time, the plentitude of daily circttmstances, activities, and emotions to which smoking is conditioned ties this behavior to numerous rituals of daily life and contributes to the difficulty of hreaking this addiction (Fisher, Bishop et a1.198Ra; Pomerleau and Pomer- kau 1997; Russell, Peto, Patel 1974; US DHHS 1988). This interplay between be- havior and the pharmacologic effects of nicotine is mirrvred in research on smoking ces.sation, in which nicotine-containingchewing gum and behavioral interventions have been shown to enhance one another (e.g.. Hall et al. 1985; Killen, Maccoby, Taylor 1984; Schneider et al. 1983). In reviewing the evidence for defining smoking as ari ad- diction, the 1988 Report made the itnportant point that the interplay between social, be- havioral, ttnd pharmaeologic ffetots that define tobacco addiction is similar to that seen with other drug addictions. The continuum of smoking behavior can be viewed as oocurring in different stages. The 1964 Report identified two stages (or processes): "Taking Up" and "Discontinua- tion " Current work identifies three major stages-development, maintenance of regular smoking, and cessation. Several investigators have offered descriptions of various smaller stages within smoking development (e.g.. Leventhal and Cleary 19110, Flay et al. 1983). These include, for example, preparation, initiation, experimentation, and transition to regular smoking (Flay et al. 1983). Similarly, the process of cessa- tion has been specified in smaller stage.s (e.g., Marlatt 1985: Prochaska and DiClemente 1983; Rosen and Shipley 1983). Tltese include, for exatttple, prccontcmplation (not yet considering quitting), contetnplation, action, and maintenance or relapse (Pmchas- ka and DiClemente 1983). Evolution of theoretical models of stages in smoking over the past 25 years is depicted in Figure 8, indicating the stages described around three periods of time, the 196(1s,

U.S. DEPARTMENT OF HEALTH. EDUCATION. AND WELFARE. Teenage Smoking: In- termediate and Long-Term Partrrns. U.S. Department of Health. Education, and Welfaro, National Institute of Education,1979b. U.S. PUBLIC HEALTH SERVICE. Smoking and Heahh. Report ofAdvlsoryCommittee to the Surgeon General of the Public Health Service. U.S. Department of Health, Education, and Welfare, Public Health Service, Center for Disease Control. PHS Publication No.1103,1964. VELICER, W.F., DICLEMENTE, C.C., PROCHASKA, J.O., BRANDENBURG, N. Decisional balance measure for assessing and predicting smoking status. Journal of Per- sonality and Social Psychology 48(S):1279-1289, May 1985. WALLSTON,K.A.,WALLSTON,B.S.,DEVELLIS,R. Developmentof the Multidimensional Health Locus of Control: (MHLC) scales. Health Education Monographs 6:160-I70, 1978. WARBURTON, D.M., WESNES, K.. SHERGOLD. K.. JAMES. M. Facilitation of leaming and state dependency with nicotine. Psychopharmacology 89(l):S-S-59, May 1986. WARNER. K.E. Possible increases in the underreporting of cigarette consumption. Journal of the American Statistical Assoeiation 7;(362):314-318, June 1978. WARNER, K.E., MURT, H.A. Impact of the aetismoking campaign on smoking prevalence: A cohort analysis. Journal of Public Health Policy 3(4):374-390, December 1982. WEINKAM,IJ.. STERLING. T.D. Changes in smoking characteristics by type of employment from 1970 to 1979/80. Americanlournal of Industrial Medicine 11:359-361. 1987. WEISSMAN, W., GLASGOW, R., BIGLAN. A., LICHTENSTEIN, E. Development and preliminary evaluation of a cessation program for adolescent smokers. Psychology ojAddic- riveBehaviors I(2):84-91, 1987. WEST. R.J., JARVIS. MJ.. RUSSELL M.A.H., CARRUTHERS. M.E.. FEYERABEND. C. Effect of nicotine replacement on the cigarette withdrawal syndrome. Britishlournal ojAd- diction 79:215-219, 1984. WIKLER, A. Requirements forextinction of relapse-facilitating variables and for rehabilitation in a narcotic-antagonist program. Advances in Biochemistry and PsyehopharmacoloRy 8:399-414. 1973. WIKLER, A.. PESCOR, F.T. Classical conditioning of a morphine abstinence phenotnenon, reinforcement of opioid-drinking behavior and "relapse" in morphine-addicted rats. PsychopharmacoloRia(Berlin)10:2SS-284,1967. WILLIAMSON, D.F.. SERDULA. M.K.. KENDRICK, I.S., BINKIN. NJ. Comparing the prevalences of smoking in pregnant and non-pregnant women. 1985-86. Journal of the American Medical Association, in press. WOHLFORD, P. Initiation of cigarette smoki-tg: Is it related to parental smoking behavior7 Journal of ConsultinR and Clinical Prvchology 34(2):148-131, April 1970. WORLD HEALTH ORGANIZATION. Tobacco or Health. Report by the Director-General. Forty-Firm World Health Assembly, provisional agenda item 22. Geneva: World Health Or- ganisation, March 23, 1988. YATES. G.L.. MACKENZIE, R., P&NBRIDGE, J., KOHEN, E. A risk profile comparison of runaway and non-runaway youth. American Journal ojPuhlic Health 78(37):R20-821, July 1988. ZABIN. L.S. The association between smoking and sexual behavior among teens in US con- traceptive clinics. American Journal ojPuhlic Health 74(3):261-Ni3, March 1984. T00L iBSIS CHAPTER 6 f SMOKING PREVENTION, CESSATION, AND ADVOCACY ACTIVITIES ; i7fi 1 377

TARLF. 27.-PercentaRe otcarrent snakers. aged 17 years and older. who use cigarettes of varying tar yields and who use menthol cigarettm by sex, race, and edneation.1986 Pert'e+Mspe of cunent smoken Tar yield (makipwene) MeMAd 510 >10`IS >1S Td.l eiRarcne -mnkern Total 29.6 11.6 tR.R 1f1n 29.2 set Males 26.8 9.0 65.2 NO 29.9 Fernales }2.7 15.6 51.7 I00 34.0 ARe 17-19 31.7 2.7 65.6 100 29.3 20-24 ;10.4 4.9 64.6 100 24.1 25-44 31.5 R.R 59.7 100 34.4 45-M 26.3 17.1t 53.9 100 23.7 265 26.3 22.6 51.1 I(M1 21.1 R.ee While 31.9 12.3 55.9 100 23.1 Htack 14.5 7.6 711.0 100 75.5 Othe- 26.2 5.3 69.5 100 24.9 F.Areatlea 511 reus 23.3 11.6 64.9 100 27.6 12 yeas 29.4 11.9 59.7 100 29.7 13-15 yean 36.a 9.7 53.5 100 32.0 216 yeas 36.4 13.2 50.4 100 27.1 srn iRCF.: Selr.iepnned dna an ciRarene tnand aae. AUTS IqqS tuS t>tIHS. b p~e+w, a). Swjqde vsn ra euh aralan we ~horn in ToMe N. The 19R 1 Surgeon. General's Report (US DHHS 1981) concluded that although smoking lower yield cigarettes appears to reduce the risk of lung cancer, the benefits are minimal compared with giving up cigarettes entirely. Morcover. there is no dcfini- tive evidence that smoking lower yickl cigarettes is associated with reduced risks of other cancers, cardiovascular disease, and fetal damage. Switching to low-yield hrands may even increase the health rick for smokers who compensate for reduced nicotine in- take by increasing the number of cigarettes smoked per day, the rrequency of puffing, and the depth and duration of inhalaticm (US D1II IS IORB). 7 The leveling off of sales-weighted tar and nicotine yields may be related to one or a combination of the following factors (US DHHS 1988): (1) a persistent brand loyalty of some smokers to moderate- or high-yield brands because of brand image; (2) a diminishing perception that low-yield brands are less hazardous (see Chapter 4); and, (3) a tendency of some smokers to smoke cigarettes of such low tar and nicotine yields that further reductions in those yields may be unacceptable; that is, the "lower bound- ary" of comfortable cigarette use has been reached (Kozlowski 1987; in press). Menthol Cigarettes From 1963-76, the domestic market share of menthol cigarettes increased gradually from 16 percent to 28 percent. Since 1976. this proportion has remained at 28 percent (FTC 1988). According to the 1986 AUTS, 29 percent of current smokers smoke mep- tlxol cigarettes. Seventy-six percent of black smokers smoke menthol cigarettes com- pared with 23 perrellt of whites (Table 27). Similar findings were reported by C"- mings and colleagues (1987). Menthol in cigarettes provides a sensation of cooling. which may promote deeper, prolonged inhalation of cigarette smoke. This may help to explain why blacks (-fFio are much more likely to smoke menthol cigarettes) have higher mortality rates from certain smoking-related diseases (e.g.. lung cancer. heart disease, and cerobrovaccular disease) than whites despite smoking fewer cigarettes per day (Novotny. Warner et i1. 1988). Increased lung cancer mortality rates among blacks may also relate to increased occupational or environmental exposures among blacks that promote the carcinogenic effects of smoking, or to the fact that blacks are more likely to smoke higher tar brands (Table 27), which are associated with higher lung cancer mortality rates (US DHHS 1981). There does not appear to be a positive correlation between the presence of men- thol and higher tar yields in cigarette brands: in the FTC's 19851ist of 207 brands (FTC 1985). 67 perc:nt (51/76) of menthol brands had tar yields of less than 13 mg, com- pared with 56 percent (73/131) of nonmenthol brands. Cigarette Length From 1967-86, the domestic market share of cigatettes 68 to 88 mm in length decreased from 91 percent to 60 petsent. During the same time. the domestic market share of cigarcttes 94 to 101 mm in length increased from 9 to 37 percent (Table 28). Because of the dose-re.cponse relationship between smoking and risk of disease (see Chapter 2), this increase in the average length of cigarettes has potentially important public health implications. However. smokers tend to compensate for changes in cigarette length by changing the nttmberof cigarettes smoked per day, puffing frequen- cy, and other measures of smoking behavior so as to minimize the change in overall nicotine intake (US DHHS 1981t). TL69 i8STS I 117

i I Z00L I8SZ5 CONTENTS Introduction ....................................................... 381 Integrating Educational and Behavioral Interventions With Policy Initiatives ........................................... 381 Part 1. Smoking Prevention Activities ................................... 382 Overview of Major Approaches to Smoking Prevention ................... 382 Prevention Opportunities Associated With Stages in the Acquisition of Smoking ........................................... 383 Prevention Program Approaches .....................................384 Media-Based Prevention Programs .............................. 385 Smoking Prevention Programs in the Context of Multicomponent School Health Education Curricula ........................... 386 Psychosocial Curricula ....................................... !387 Youth Smoking Cessation Programs .................................. f 390 History of Agency and Organizational Prevention Activities .............. 1392 National Voluntary Health Organirations ......................... 392 National Interagency Council on Smoking and Health .............. ~93 Federal Government Prevention Support ........................ L 394 Office on Smoking and Health ............................. 395 I National Cancer Institute .................................. 96 National Heart, Lung, and Blood Institute ...................... 397 I National Institute on Drug Abuse ........................... 397 National Institute for Child Health and Human Development ..... 397 Office of Disease Prevention and Health Promotion ............. 398 I Surgeon General's Reports ................................ 398. State Health Departments .... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 399 Other Organizations and Agencies .............................. 400 Problems in Dissemination of Smoking Prevention Programs .............. 401 Problems in Evaluation of Smoking Prevention Programs ................. 403 Need ForLong-Term Followup ................................ 404 Construct Validity ........................................... 404 ( Failure to Reach Dropouts and Other Youth at ( Higher Risk for Smoking ...................................405 Population Factors Related to Diversification of ( Smoking Prevention Programs ..................................... 406 Pan 11. Smoking Education and Cessation Activities ....................... 407 Changes in Cessation Activities Over Time ............................ 407 National Voluntary Health Organizations .............................. 411 Health Professional Associations ..................................... 416 I Federal Government Cessation Support ............................... 419 I Office on Smoking and Health ................................. 419 National Cancer Institute: Smoking. Tobacco, and Cancer Program . 419 ~ National Heart, Lung, and Blood Institute ........................ 421

contemplation. action, maintenance, and relapse. 771is categorization has proven use- ful in longitudinal research studies (see Part 11 of this Chapter and also Chapter 6): howcver, for cros.s-sectional population studils, this process of quitting can he analymd according to current smoking status and the timing and duration of previous quit at- tempts. Thus, everyone can he classified on a smoking continuum. This continuum is presented in Table 10. It is based on questions from the A(1TS (see Appendix to this Chapter). Ten different categories are presented as percentages of the total population and as percentages of ever smokers. Categories of current smokers can also he described as percentages of all current smokera. These percent- ages are not provided below becau.se of the pos.sihlity of misinterpretation. In particular, the percentage of those attempting to quit during the past year should not he calculated using current smokers as the denominator because this percentage excludes those who succes.cfulfv quit during the past year. Instead. a more appropriate denominator (used below) would be those who were smokers at any time during the past year (including former smokers who quit during the past 12 months). TARLF,10.-Smoking continuum, aduks aRed 17 years and older, Unitcd State.t, 1986 Category I Never t<mokers CateRcxy2 Fvnner.mokent.rhohadquil3 or mae ydrs ago Category 3 Forner .ntctken who had been ahctinent for I w 5 yart Category 4 Fr.mer ana4ers who h.d been ahctinent for 3 to 12 tnpNM CateRcxy S Fixmer amokees .rho had quit within the h.q 3 natNhs CmRory 6 Cunem smokerr w4o tmd qtrit for 7 eir moee day. in the past yew Category 7 Cunent attttkerswho had quit for 1-b days in the jnt year Categtxy A Cunent amolcer% who had quit ptevicwsly hut ntx in the Ias1 year CateReny 9 Curmtt .mnkers urla had never tried In quit hut wfip had thotltdN ahwt it or would quit if Ihete wac an easy way to du w Category to Cunent amokers.droh.enever tried to qui1. had na thvught alxmt it. and would not try to quit even if thrre wac an easy way to tln a+ Peteenlaae of populmion PercemaRe ef ever xmnkers 47.3 14.7 27.9 5.7 1o.s 2.0 3.E 3.2 6.1 3.9 7.4 2.0 3.8 11.6 22.0 5.4 10.2 4.s 9.5 stxmeT: AVnt9FAtusrrnts,inFWe...at. LS69 tBStS The first category on this continuum inchldes those who have never smoked ciga- rettes. In 19R6, 47.3 percent of the U.S. population 17 years of age and older was ih this category. Fotmer smokers who had quit smoking 5 or tftore years previously made up 14.7 percent of the population and 27.9 percent of ever smokers. Those in this category can be considered to be confirmed ex-smokers who are unlikely to relapse. Fnmser smokers who had been abstineM for 1 to 5 years represented 10.8 percent of ever smokers. Former smokers who had been abstinent for less than a year represented 9.9 percent of ever smokers (categories 4 and 5 combined). Current smokers who had quit smoking for 7 or more days during the past year made up 7.4 percent of evcr smokers. Another 3.8 percent of ever smokers had quit during the past year but were tat able to stay off cigarettes for a week or mote. Combining categories 4 through 7, 21.1 percent of ever smokers stopped smoking for at least I day during the year prior in the 1986 survey. This is 34 percent of all those who smoked that year. Of ever smokers, 22.0 percent were current smokers who had previously made la serious quit attempt but not during the past year. Approximately 19 percent of evtr smokers were current smokers who had never tried to quit; 45 percent of these have never thought about quitting and say that they would not quit even if there was an easy way to do so. Of those who had smoked during the past year, 70 pencetlt had made ttt least one quit attempt (categories 4 thlough'8 divided by categories 4 through 10). i' For the sake of convenience, category 10 is referred to below as the "hard-core pnokers" category. However, it should be noted that others might also use this term to i describe smokers who have failed to quit despite repeated attempts. Tahks I 1 and 12 give the distribution for this smoking continuum by gender, educa- tion, race, and age. There ate large differences between the subgroups in the ptopor- tion of ever smokers who are long-term abstainers (category 2). Males are more like- ly to be in this category than females, whites more than b4acks, older people more than younger people, and the most highly educated more than the less well educated. The percentages of ever smokers in the categories reflecting recent quitting activity (4 through 7) and no rccent quitting activity (8 through 10) were slightly higher for women than for men, probably resulting from the higher percxntage of men in the combined categories 2 and 3(abstinrnce for a year of more). Educational differences in the smoking continuum are generally consistent with educational differences in smoking prevalence and quit ratio mentioned above. The pmportion of ever smokers who have not tried to quit during the past year (categories R through 10) is 43.5 percent for the least educated group compared with 29.1 percent for the most educated group. The proportion in the hard-core smokers category is 9.8 percent for the least educated group compared with only 5.7 percent for the most edu- cated group. However, the proportion of those who haw made a quit attempt during the past year (categories 4 through 7) is also higher for the least educated group than for the most educated group (21.8 peocent and 17.2 percent, raspectively); this latter difference may reflect a lower success rate for quitting attempts among the least edu- cated group. The differences between the least and most educated in these categorics (4 through 7) become progressively smaller and then disappear as one moves frc~tn failed quit attempts during the past year (categories 6 and 7) to successful quit attemlits ?xx 11 299

Summary The past 25 years have seen a deepening appreciation of the importance of nicotine in maintaining regular smoking. In contrast to the 1964 Surgeon General's Report, cigarette smoking is now defined as an addiction (US DHHS 1988). Earlier emphasis on the maintenance of blood nicotine levels as a means to avoid withdrawal has been balanced by the awareness that nicotine's varied effects make smoking an efficient coping strategy for affect regulation and perhaps weight regulation. Conditioning models of smoking have become more sophisticated and firmly integrated with the pharmacologic actions of nicotine to explain addiction. While the public is now better informed about the health consequences of smoking, many smokers still minimize their perception of their vulnerability amid extensive marketing of tobacco products. Broad, dispositional traits or motives are now seen to be of limited value in understanding smoking. The role of social settings and social influence in encouraging regular smok- ing is also better understood. Cessation and Relapse A large body of literature on determinants of cessation has evolved, driven by the need to provide empirical and theoretical guidelines for intervention programs. All three sets of determinants--pharmacologic processes and conditioning, cognition and decisionmaking, and personality and social context-play an important role in the ces- sation stage (Table 39). It is with respect to cessation, e.specially, that the concept of stages-treating stopping as a proces.s over time-has evolved (Figure 8) and now guides research and interventions (e.g., Marlatt 1985). The influential and well-articu- lated cessation stage model of Prochaska and DiClemente (1993) defines four stages of cessation. Precontemplation is the stage in which the smoker is neither considering stopping nor actively processing smoking-and-health information. During the con- templation stage, smokers are thinking about stopping and are processing infomtation about the effects of smoking and ways to stop. In the action or cessation stage, the smoker is no longer smoking and has been without cigarettes for less than 6 months. The maintenance phase involves establishment of long-term abstinence, while relapse is the resumption of smoking. When relapse occurs, the smoker recycles to any one of the three previous stages. Specific cognitive and behavioral processes are employed during the different stal¢es of cessation (Prochaska and DiClemente 1983). Detenninant.s of each stage arc also different. Thus, factcxs that affect an initial decision to stop smoking may not predict success in stopping or sustained maintenance after stopping. Working from a related but different stage model-initial decision, initial control, maintenance-Rosen and Shipley (1983) uused health locus of control, desire to stop, and self-esteem to predict self-initiated smoking reduction. Using regression analysis, a difkrent set of predic- tors was demonstrated at each stage, suggesting the, possible need for different inter- vention techniques at each stage of the smoking reduction process. An important implication of a stage model is that interventions may need to address cessatitm's several stages. The precontemplator's tendency to ignore quitting str.negies may need to be met with continued personalized information on smoking and health; the contemplator may need social support to attempt cessation; and the abstainer may need help that emphasizes the development of relapse prevention skills. There are as yet no data available to demonstrate the effect of interventions tailored to specific stages of cessation. Thus, models like the Prochaska and DiClemente stage model is best viewed as a tentative conceptualization, useful for guiding research and interventions. The next section considers changes in our understanding of the determinants of cessa- tion in relation to the stages in the cessation process. PharmacoloRic Processes and Conditioning Pharmacologic processes and conditioning exert a strong influence on the process of quitting. One indicator of the role of addiction is that heavier, more dependent smokert; in intervention programs are less likely to quit than are lighter, less dependent smokers (e.g.. Hall et al. 1934; Ockene et al. 1982), especially when smokers with much variability in baseline smoking are studied, as in the Multiple Risk Factor interventioa Trial (MRFIT) (Hughes et al. 1981). As is noted in the 1988 Surgeon General's Repo, "Withdrawal symptoms, whether'elicited by acute deprivation or by conditioned stimuli, are hypothesized to be the link between dependence and relapse" (p. S23), al- though some analyses (e.g.. Niaura et al. 1988) place greater emphasis on positive eY fects of smoking in motivating relapse. Further evidence of the influence of addiction comes from intervention studies evaluating nicotine-containing gum. Several studies have found that nicotine polacrilex gum is more effective when used with nicotine-de- pendent smokers (as measured by the Fagerstrom (1978) addiction questionnaire) than with less dependent smokers (Hall et al. 1985; Killen et al.19R4; Schneider et al. 1983). Nicotine polacrilex gum most likely is effective because it reduces withdrawal symptoms frequently noticed in the first days and weeks of abstinence (Hughes et al. 1984: West et al. 1984). Recent work focuses on nicotine replacement strategies or other pharmacologic treatment adjuncts reflecting the importance of biological factors in smoking and cessation (Grabowski and Hall 1985; US DHHS 1986h; US DHHS 19RR). Conditioning mediates the role of the pharmacologic effects of nicotine in cessation. As noted in the discussion of regular smoking, numerous conditioned environmental stimuli are likely to evoke urges or cues to smoke. Recent work by Abrams and col- leagues demcxtstrates that former smokers manifest psychophysiological reactivity to smoking cues long after they have quit (Abrams et al., in prcss; Abrams 1986). Con- ditioned reactivity to environmental cues, then, may be more decisive in the later stage of maintenance after withdrawal symptoms have subsided. Research on triggers to relapse reflects current interest in specific, situational vari- ables. Primary triggers include stre.ss, interpersonal conflict, dysphoria, presence of other smokers, and alcohol consumption (Marlatt and Gordon 19R0; Shiffman 1982). Although the data primarily are tetrospective reports from relapsed or tempted subject~' there is convincing consistency on the importance of stress and negative affect in deter- mining maintenance or relapse (Baer and Lichtenstein 19RRa; Marlatt and Gordon 19R0; Ockene et al. 19R2• and Shiffman 1992; US DHIIS 19RR). Whether a lapse he- L869 I85TS 149

to attempt cessation; efficacy cognitions about perceived ability to manage temptations or urges are related primarily to maintenance or relapse. Prospective studies indicate that the presence of acute disease, which is likely to affect cognitions about the pros and cons of snoking, is related to cessation. Consistent with an overall increasing ap- preciation of the importance of nicotine in all stages of smoking, more dependent smokcrs are less likely to succeed in quitting. Interpersonal support helps smokers in the early stages of quitting, but current evidence indicates that a low density of smokers in the social network is decisive for long-term abstinence. Summary of Changes In Knowledge About Determinants of Smoking Behavior There has been a dramatic increase in research on the determinants of smoking over the past 25 years. In 1964, there were few studies; by 1979 the number had expanded to a few hundred studies; now there are probably thousands. This increase in research reflects both specific Federal initiatives to support smoking research and larger trends toward recognizing the important relationship of behavioral factors to disease and the effect of preventive strategies in reducing morbidity and mortality. Several historical trends are predominant in considering all three major stages together-development, regular smoking, and cessation. A strong consensus has evolved on the critical role of nicotine in smoking. The pharmacologic effects of nicotine and the role of conditioning are now understood as integrated processes that combine to produce the addictive nature of cigarntte smoking. Cigarette smoking is now recognized to develop over a series of stages with multiple and different deter- minants at each stage (Figure 8; Table 35). The interaction of determinants (e.g., con- ditioning and the pharmacologic effects of nicotine with social influences) has become more clearly articulated. Recognition of these stages and their multiple interacting causes currently guides the devekopment of intervention and educational programs. Smoking onset is associated with social influences, educational and economic disad- vantage, alcohol and other drug use, and antisocial behavior. There continues to he a gap in our knowledge of how to target the educationally and ecmxxnically disadvantaged. Our increased knowledge of phartnaeoingic and psychosocial detetminants has facilitated the development of interventions-hehavicxal or combined behavioral and pharmacologic-to aid cessation of regular smoking. Continued increases in our un- ikrstanding of the stages of cessation combined with better validated interventicros of various levels of intensity or cost will help to offer smokers nKxe choices to meet their needs. As described in the next two chapters, the knowledge gained about the determinants of smoking has guided intetventions and campaigns to reduce the prevalence of smok- ing in adults from 40 perrent in 1965 to 29 percent in 1987. lt has led to promising prevention and cessation programs, which use existing community channels-media. worksites, schools, physicians' offices, and hospitals-to deliver low-cost but effective intervcntions (Chapter 6). T669 ZBSZS CONCLUSIONS Part I. Changes In Smoking Beha.ior 1. Prevalence of cigarette smoking has declined substantially among men, slightly among women, and hardly at all among those without a high school diploma. From 1965-87, the prevalence of smoking among men 20 years of age and older decreased from 50.2 to 31.7 percent. Among women, the prevalence of smoking decreased from 31.9 to 26.8 percent. Smoking prevalence among whites fell steadily. Arnong blacks, the prevalence of smoking changed very little be- tween 1965 and 1974; subsequently, prevalence declined at a rate similar to that of whites during the same period. Smoking prevalence has consistently been higher among blue-collar workers than among white-collar workers. ~ 2. Annual per capita sales of manufactured cigarettes (18 years of age and o1t]er) decreased frcm 4,345 cigarettes in 1963 to 3,196 in 1987, a 26-percent rcdudtion: Total cigarette sales increased gradually to 640 billion cigarettes in 1991 and~then fell to 574 billion in 1987. 3. In 1965, 29.6 percent of adults•who had ever smoked cigarettes had quit. This proportion (quit ratio) increased to 44.8 percent in 1987. The rate of increil.se in the quit ratio from 1965-85 was similar for men and women. The rate of chang4 in quitting activity in recent years is similar for whites and blacks. From 1965.= 85, the quit ratio increased more rapidly among college graduates than among adults without a high school diploma. 4. Of all adults who smoked at any time during the year 1985-86, 70 percent had made at least one serious attempt toquit during their lifetime and one-third stopped smoking for at least I day during that year. 5. The age of initiation of smoking has declined over time, particularly among females. Among smokers born since 1935, more than four-fifths started smoking before the age of 21. 6. Trends in prevalence of cigarette smoking among those aged 20 to 24 years are an indicator of trends in initiation. By this measure, initiation has declined be- tween 1965 and 1987 from 47.8 to 29.5 percent. Initiation has fallen four times nxxe rapidly among males than arnong females. The rate of decline has heen similar among whites and blacks. Initiation has decreased three times morc rapid- ly among those with 13 or more years of education than among thom with less education. 7. The prevalence of daily ciganette smoking among high school senicxs decreased from 29 percent in 1976 to 21 percent in 1980, after which prevalence leveled off at 18 to 21 percent. Prevalence among females has consistently exceeded that among males since 1977. Prevalence was lower for students with plans to pursue higher education than for those without such plans. The difference in prevalence by educational plans widened throughout this period; in 1987, smok ing ratcs were ; 14 percent and 30 percent in these two groups, respectively. 8. The best sociodemographic predictor of smoking pattcrns appearx to he Icva of educational attainment. Marked differcnces in smoking pn:valence, quittine.:md ~s~

• leads the aversive B state to become sttonger, which in turn may be reduced or avoided by the A-state consequences of further smoking. After regular smoking has been es- tahl ished, the A state serves only to avoid or reduce the aversive B state. That is, regular smoking is pursued to reduce displeasure rather than to bring ahout the pleasure that may have been its initial appeal. It is important to note that there is little evidence on the validity of the Wikler theory or opponent-pntcess theory as applied to smoking. In contrast to mcxfels emphasizing relief of withdrawal, a recent review (Niaura et al. 19RR) proposes an "appetitive" model of responses to cues associated with smoking. Evidence indicates that cues surtounding smoking are more strongly conditioned to its positively perceived effects than to withdrawal symptoms. T'hat is, cues associated with intake of nicotine (e.g.. holding a cigarette or inhaling) come to elicit conditioned respcmces similar to the effects of nicotine (e.g., relaxation, heightened arousal). These effects are strong reinforcers and encourage continued efforts to obtain or ingest the drug. These reinforcing effects may he more critical than the reduction of withdrawal symptoms after periods of abstinence. Critical to understanding the appetitive model is the idea that negative emotions an: not necessarily withdrawal symptoms. However, negative emotions previously al- leviated by nicotine may serve as cues for seeking repetition of smoking's reinforcing effects (Stewart. DeW it, Eikelboom 1984). For exampk, social anxiety may be the oc- casion for smoking, which is then reinforced by nicotine's ability to reduce anxiety. The anxiety, however, is a response to a sttessfut situation, not a symptom of withdrawal fro.n cigarettes. Smoking is reinforced by the anxiety reduction, not by reduction of withdrawal symptoms. The many ways smoking is conditioned to circumstances around it may explain "the thorough interweaving of the smoking habit in the fabric of daity life" (Pomerkau and Pomerleau 19R7, p. 11 Q). The sheer repetition of smoking also strengthens such inter- weaving. It is estimated that the average pack-a-day smoker of 20 years' duration has inhaled cigarette smoke over I million times (Fisher and Rost 1986; Pomerleau and Pcnnerkau 19R4), each inhalation providing an opportuniry for conditioning smoking to numerous circumstances of daily life. Moreover, with years of smoking, the emo- tional states and daily circumstances conditioned to it may continue to increa.se, result- ing in urges to smoke being conditioned to almost every circumstance encountered and complicating the task of maintaining abstinence. CoRnition and fkcisionmaking Cognitive and decisicmmaking processes play a lesser role in the maintenance of regular smoking relative to the other factors discussed here. Smokers have long believed that they derive positive effects from smoking. The "pros" of smoking have been embodied in the instruments used in decisiommaking studies (Mausner and Platt 1971; Velicer et al. 1995) and in the Horn and Waingrow (1966) Rea.stxms-for-Smok- ing Scile. As documented in Chapter 4 of this Report, public knowledge of the health conse- quences of smoking has increased steadily over the past 25 years. Eighty-seven per- cent of currcnt smokers now report that they understand that smoking is harmful to their health (ALA 1985) and two-thirds of high school seniors ropott "great risk" being as- sociated with pack-a-day smoking (Johnston, O'Malky, Bachman 1987). Why, then, do so many persist in regular smoking? One teacott may be that they do not appreciate just how dangerous smoking is. For example, 75 penxnt of current smokers agreed that smoking is a cause of lung cancer (ALA 19g5). while 94 percent of nonsmokers and 90 percent of former smokers agreed to this. For emphysema, the parallel figures were 75 percent of current smokers compared with 91 percent and 90 percent of former smokers and nonsmokers, respectively (ALA 1985). Surveys indicate a general insen; sitivity to the relative level of risk associated with smoking. Health professionals ratt?d nonsmoking as the first priority among things Americans can do to protect their health. The public rated nonsmoking as 10th, behind such worthy but, for most Americans, less critical behaviors a,. consuming adequate vitamins and minerals and drinking water of acceptable quality (Fisher and Rost 1986). As discussed below, the health belief model (Rosenstock 1974) requires that smokers believe they are personally vulnerabje to a threat before th;y will be motivated to attempt change. It has been suggested that persortalized acceptance ("Cigarette smoking is dangerous to my health") always lags ' behind general acceptance ('~Cigan:ne smoking is dangerous to health") (Fishb6in 1977; Lichtenstein and Bernstein 19g0; Shiffman 1987) (See Chapter 4). These con- siderations suggest that many smokers still find it possible to discount the riskinesf of their behavior. Another possible reason for some smokers' insensitivity to smoking risks is that they j have not always been given the full ntessage, or they have been given mixed mecsages, including prosmoking messages (advertising) from the cigarette industry. Factors that impede public awareness and acceptance of the health hazards of smoking include cigarette advertising and promotion and cigarette companies' public relations and lob- bying activities, which are also reviewed in Chapters 6 and 7. Other issues related to persistence of smoking will be covered in the Section on Quit- ting and Relape . I Personal Characteristics and Social Context Personal Characteristics The 1964 Surgeon General's Report linked smoking in aduhhood and adolescence to extraversion, or as it defined it, a tendency "to live faster and more intensely" (US PHS 1964, p. 366), and this relationship has been confirtned in later studies (e.g.. Ash- ton and Stepney 19R2). However, reviews indicate that there is no consistent evidence relating smoking to neumticism or emotional instability (Smith 1970; US DHEW 1979a). More recent studies have continued to find relationships with smoking and he- haviors linked to extraversion: coffee and alcohol consumption (lstvan and Mataraz- zo 19R4); circadian phase diffetences, being an "evening type" as opposed to a "morn- ing type" (Ishihara et al, 19g5); alcohol consumption, driving accidents, divorce, frequent job changes, low levels of vocational success, and impulsivity ( Eysenck 0R0). S869 tBSIS i

smoking) at the time efficacy is assessed. Results using partial correlations suggest that efficacy scores do provide limited information above and beyond that of currcnt smok- ing hehavicx (Baer, Holt. Lichtenstein 19R6). A second approach is to correlate self- efficacy measured postintervention with subseqttent followup status only for those clients who initially quit. Studies using this paradigm have fotnnd significant but modest correlation with 3-month followup (Mcintyre-Kingsolver, Lichtenstein, Mertnelstein t 9R3; Coelho 19R4). Self-efficacy also can he asses.sed during the maintenance phase, in order to predict longer term followup. Two studies have examined these relation- ships and both found significant prospective relationships (DiClemente 19RI; Raer, Holt, Lichtenstein 19R6). While intervention studies have usually found pretreatment efficacy unrelated to oirtcome, one study of unaided quitters found that baseline efficacy correlated with continuous abstinence at 1 year (Gritz, Carr, Marcus, in press). Another intervention study found that participants' attribution of stopping to their own skill and effort, gathered 3 months after stopping, were correlated with abstinence at 6-mtxith followup (Fisher. Levenknon et al. 1982). National survey data reviewed by Shiffman (1996) ssuggest that lack of confidence in the ability to stop deters many smokers from attempting cessation. Outcome Expectations From a stage perspective, outcome expectations (perceived cottsequences of smok- ing or stopping) are more likely to he related to the decision to stop smoking or the in- itiation of quit attempts than to success in the stopping process. The effects of brief ad- vice from a physician offer indirect support for the role of outcome expectations (Russell et al. 1979). Patients receiving brief advice to stop smoking were more like- ly to stop relative to control subjects. T1he physicians'advice probably enhanced the salience of the perceived positive consequences of stopping or the negative consequen- ces of continuing to smoke and thus prompted the decision to attempt to stop. Nega- tive consequences of smoking are potentiated by dramatic illness such as myocardial infarction, which is often the occasion for cessation efforts: however, relapse is often considerable (e.g., Baile et al. 19R2), although less than with nondiseased smokers (Ockene et al. 1987). Cognitions concerning the health risks of smoking and the posi- tive benefits of stopping remain very important from a public health perspective (see Chapter 4) and the health-belief model may be useful for guiding interventions aimed at smokers in the precontemplation or contemplation stages of change. The role of disease in smoking cessation is substantial but not well understood. Cer- tain environmental changes following a serious illnes.s may aid cessation and/or the in- formation and fear arousal provided by serious illness may motivate serious quit at- tempts, but continued maintenance is problematic (Ockene et at. 1985; Perkins 19RR). Approximately one-quarter to one-half of survivors of myocardial infarctions are abstinent from smoking at extended followups (Ockene et al. 19R5; Perkins 1999. Rigotti and Tesar 19R5). While rates of cessation are impnessive in some studies ofcar- dutc and other patients, results of smokinF cessation interventions pnxluce inconsistent intervention effects (Perkins 19RR; US DI IIIS 19R6). Research needs to evaluate the impact of diseases and of dimensions of diseases including chronic and acute events, severity, and symptom mitigation following cessation, all of which vary across diffeient diseases. Information about negative effects on the fetus may trigger cessation among preg- nant women, perhaps by potentiating a ntore general awareness of smoking's dangers. Pregnancy does prompt some cessation or reduction relative to the "natural" popula- tion; however, relapse after delivery is high (US DHHS 19R0b). Prevalence of smok- ing among pregnant women and historical shifts are documented in the first part of this Chapter. Personal Characteristics and Social Context Personal Characteristics Less educated srtokers who do stop tend to have higher rates of relapse and sh6rtet' periods of abstinence than do tttote educated persons. Stopping smoking is more tom- mon among those smokers with greater personal skills or socioeconomic resources (US DHHS 1982). Prospective studies Indicate that education level, ittcome, and skYta in self-management or personal coping are significantly related to success in self-initiated efforts to stop (Blair et al. 19R0; Gritz, Carr, Maoctts, in press; Perri, Richards, Schul., aheiss 1977). In a multivariate logistic regression analysis of 1985 NHIS data, blAcks! were significantly less likely than whites to quit smoking, regardless of SES or demographic factors (Novotny et al. 1988). Currently there are several research' ac- tivities funded by NCl that may eventually provide information to explain these dif- ferences. The sections em the initiation of smoking and regular smoking discussed the roles of several personality variables such as extraversion and neuroticism. While associations between extraversion and smoking have been replicated over the years (Eysenck 19R0), it and other broad persottality variables have not shown strong effects in smoking ces- sation (Lichtenstein 1982). Some evidence indicates that persons high in extraversion and low in neuroticism are more able to stop smoking (US DHEW 1979a). Internal- external Iocus of control has been hypothesized to be related to cessation (intemals more successful) but the evidence is inconclusive (US DHEW 1979a). Research on personal characteristics is now focusingon more situation-specific or interactional variables such as self-efficacy, stress, and social support (Condiotte and Lichtenstein 199 I). Stress has been shown to affect initiation of smoking and smoking rate, as well as relapse following smoking cessation (US DHHS 19R8). It appears to be a factor espe- cially influencing women's cessation (Abrams et al. 1987; Sorensen and Pechacek 19R7), as well as their initiation of smoking (Mitic, McGuire, Neumann 19R5). High levels of anxiety (Schwartz and Dubitzky 1968) and self-rcported tendencies to xmoke to relieve negative affect (Ponterleau. Adkins, and Pertschuk 1978) have been as- sociated with reduced success in stopping. The link of smoking to stress and research demonstrating the role of social support in buffering stress (Cohen and Syme 1495) i 352 6869 T8StS 1 .15a

Regular Smoking PharmarnlnRic Pracesses and Conditioning Pharmacologic processe•s and conditioning play complementary and major roles in maintaining regular smoking. Early theories of snmking tended to view pharmacologic processes and conditioning as separate explanations of regular smoking (e.g., Hunt 1970; Table 39~. They are now viewed as complementary and interacting procesKx (US DHHS 198R). The t 9RR Surgeon General's Report on nicotine addiction affinned the critical role of nicotine and its varied and powerful pharmacologic effects on the central nervous system (CNS) in the development and maintenance of regular smok- ing. This acknowledgment, and its implications for intervention, represents a sig- nificant shift in perspective over the 25 year history of the Surgeon General's Reports. Concurrently, increased knowledge of smoking a•c an addiction has clarified the impor- tant role of conditioning in addiction. Conditioning and related processes link the biological effects of nicotine to the many behaviors that make up smoking and to the many concurrent physical and environmental stimuli that guide it. Nicotine Addiction The 1964 Report distinguished between drug addiction and drug habituation (US PHS 1964; Table 36) and concluded that smoking is habituation. As noted in the 1988 Report, the addiction/habituation distinction was drvpped in 1964 by the WHO short- ly after the release of the 1964 Report (US DHHS 198g). The 1988 Surgeon General's Report on nicotine addiction noted the following three major conclusions: (1) cigamttes and other forrns of tobaeeo are addicting; (2) nicotine is the drug in tobacco that causes addiction: (3) the phartnaeologic and behavioral processes that determine tobacco addiction are similar to those that determine addic- tion to drugs such as heroin and cocaine (US DHHS 1999. p. 9). These conclusions were based on a thorough review of msearch on addictive aspects of smoking extend- ing over nearly a century. The criteria that guided the 1989 Report's concltnion that smoking is an addiction are summarized in Table 36. As documented by extensive research cited in the Report. smoking meets all the criteria. Smoking is continued despite a desire to quit and, in many caces, despite clear harm to the individual. A central criterion concerns psychoac- tive effccts of a drug on the CNS. Rapid absorption of nicotine into the hlocxfstrram and consequent delivery to the CNS is a feature common to all popular forms of tnhac- co use. Recent evidence confirms that nicotine is absorbed by the brain, which con- tains receptors specific for this agent (e.g.. Lcxidon et al. 1985: London. Waller, Wamsley I9R5): has euphoric effects and perhaps sedative or nther anxiolytic effects mediated by neumhoxmcxial processes (e.g., Henningfield, Miya•aato,)asinski 19R5): and reinforces behaviox, even among animals or human subjects blind to whether they receivedcalineplacehoornicotine(Henningfield,Chait,Griffiths 19R3,19R4). Atwith other addictive drugs, prolonged ingestion of nicotine leads to tokrance, a tendency to consume incrcasinp amounts of a drug, presumably to achieve a desired euphoric or ~ g. 0 c N ~ 0.1 e c V ~ V ~ w a a e I 9 I I 7A1 z~n

JOHNSTON, L.D., RACHMAN,I.G.. O'MALL.EY, P.M. Moniterinx the Future. Question. nairr Rrsp.ur.ces Frnm the Nation's High School Seniors. 1981. Ann Arfior, Michigan: University of Michigan, 11082. JOHN,ST'ON,1„D., RACHMAN,I.G., O'MALLEY, P.M. Moninxing the Future. Qutstien- noirr Resnnnsrs From the Natioi s High Schonl Seniors, 190. Ann Arbor, Michigan: University of Michigan, 1984. JOHNSTON. L.D., BACHMAN,I.G., O'MALLEY. P.M. Monltoring the Future. QutsNon. nairr Rr•slrnnses Frnm the Nation's High School Seniers, 19RS. Ann Arbor. Michigan: University of MichiRan, 1986. JOHNSTON, L.D.. O'MALLEY. P.M.. BACHMAN. l.G. National Trends in nruR Use and Related Factnrs Among High School Students and YounR Adults,197.5-1914fS. U.S. Depart. ment of Health and Human Services. Public Health Service. Alcrotal, Drug Abuse, and Men- tal Ilealth Administntion, National Institute on Drug Abuse. DHHS Publication No. (ADM) R7-1535, 19R7. LEVENTHAL„ H..GLYNN, K., FLEMING. R. 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American Jnnrnal of Public /Isalth 78(10):1315-1321, (ktober 1988. OSKAMP, S. Attitudr.c and Opinions. Englewood Cliffs, New Jersey: Pn:ntice-Hall.1977. PF.RLSTADT, H.. HOLMES, R.E. The role of public opinion polling in health legislation. American lnurnal njPuhlir Health 77(5):612-L 14, May 1997. REMINGTON, P.L., FORMAN, M.R., GENTRY. E.M., MARKS. 1.S., HOGEL.IN, G.C.. TROWBRIDGE. F.L. Current smoking trends in the United Slates. Thc 19RI-1983 Be- havnxal Rick Factor Surveys. Jnnrnal of the Amrrican Medical Association 253(20):2973- 2978, May 24-31, 19R5. ROPER. A Snrdv of Pnhlic Attitxdes TnNnrrl CiRarrneSnrrnking and the Tobacco /nduslrlr in 1978. Volume 1. Roper tkl¢aniration, 197R. I SCHINKE, S.P., GIL.CHRiST, L.D. Preventing cigarette smoking with youth. Journaf of Primary Prevention 5(1):48-56, Fall 1984. . SHOPLAND. D.R., BROWN.C. Toward the 1990 objectives for smoking: Measuring the Progresswith 1985NHISdata. PrMicHralthRt/Mrts102(1):68-73,lanuary-Felxuary 1987. SLOV IC, P. 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Center for Health Promotion and Education. Office on Smoking and Health. DHHS Publication No. (CDC) 8R-84(16, 198R. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. Adult Use oJTolroccn. I9R& . U.S. Department of Health and Human Services. Public Health Service. Centers for Discace Contrd, Office on Smoking and Halth, in press. Tb69 T85ZS 2st. 2S7

1985 CPS Current other tobacco use: "Does (name) presently use any other form of tobacco, such as snuff or chew- ing tobacco?" Current smokeless tobacco use: "What other form(s) of tobacco does (name) presently use?" The categories "snuff; * "chewing tobacco." "cigars; 'pipe tobacco." or "other" were coded in response to this followup question. 1996.1997. and 198R BRFS Ever use: "Have you ever used or tried any smokeless tobacco products such as chew- ing tobacco or snuff?" Current use: "Do you currently use any smokeless tobacco products such as chewing tobacco or snuff?" 19R7 NHIS Ever Use: "Have you ever used chewing tobacco, such as Redman. Levi Garrett. or Beechnut?" "Have you ever used snuff, such as Skoal, Skoal Bandits, or Copenhagen?" In addition. those who answered "yes" to the above questions were asked, "Have you used chewing tobacco at least 20 times?" Current use: "Do you use (chewing tobacco, snuff) now?" 1970 NHIS Current use: "Do you use any other form of tobacco?" Respondents could answer yes or no to "snuff," "chewing tobacco," or "other." E669 t85tS References ABRAMS. D.B. Roles of psychosocial stras, smoking cues, and coping In smoking relapse prevention. Health PsycholoRy S(Suppkment):91-92, 1982. ABRAMS. D.B., MONTI, P.M., CAREY, K.B., PINTO, R.P.,IACOBUS, S.I. Reactivity to smoking cues and relapse: Two studies of discriminant validity. Behaviour Research and Therapy, in press. ABRAMS, D.B., MONTI, P.M., PfM, R.P., ELDER,I.P., BROWN, R.A., IACOBUS, S.I. Psychosocial stress and coping in smokers who relapse or quit. Health Psychology 6(4):2R9~ 303. 1987. AMERICAN LUNG ASSOCIATION. Sasvty of At-itwdesTowond S>noNng. Princeton, New Jersey: Gallup Organintion, July 1985. AMERICAN MEDICAL ASSOCIATION. Citizen petition of the American Medical Associa- tion to the Food and Drug Administration. Chicago: American Medical Association, April 25,1988. ! AMERICAN PSYCHIATRIC ASSOCIATiON. Diagnostic and Statistical Manual ofMcntal Disorders. Third Edition (DSM-III). Washington. D.C.: American Psychiatric Associatioh, 1980. ANTONUCCIO. D.O., LICHTENS7EIN, E. Peer modeling influenoes on smoking behavior of heavy and light smokers. Addictive Behaviors 5(4):299-306, 1980. ASHTON. H., STEPNEY. R. Smoking: Psychology and Pharmacology. New York: Methuqe, 1982. BACHMAN. J.G., JOHNSTON, L.D., O'MALLEY, P.M. Monitoring the Future. Question, naire Responses From the NarIoe's High School Seniors, 1986. Ann Arbor, Michigan! University of Michigan,1987. BAER,I.S., HOLT. C.S., LICHTENS1'EIN, E. Selfeff6cacy and smoking reexamined: Con- struct validity and clinical utility. Jorrrnl of Conswltirta and Clinical Psychology 54(6):846- 852, December 1986. BAER,I.S., KAMARCK. T.W., LiCH'iENSTEIN, E., RANSOM, C.R. The prediction of smoking relapse from chatacteristia of prior temptations and slips. Poster presented at the Wilford Hall Health Promotion Conference. San Antonio. Texas, May 1988. , BAER,I.S., LICHTENSTEIN, E. Clusifidtion and prediction of smoking relapse episodes: An exploration of individual differences. Journal of Consulting and Clinical Psychology S6(1):104-110.1988a. BAER,I.S., LICHTENSTEtN, E. Cognitive assessment In smoking cessation. In: Marlatt, G.A., Donovan, D.M. (eds.) Assessment oJAddictivt Behaviors. New York: Guilford Press, 1988b. BA1LE, W.F. JR., BIGELOW, G.E., GO77LIEB, S.H., S177ZER, M.L., SACKTOR. J.D. Rapid resumption of cigarette smoking following myocardial infarction: Inverse relation to Ml severity. Addictive Behaviors 7(4):373-380, 1982. BANDURA, A. Self-efficacy: Toward a unifying theory of behavioral change. Psychological Review 84(2):191-21 S, 1977. BANDURA, A. Self-efficacy mechanism in human agency. American Psychologist 37(2):122- 147, February 19112. BARTON, 1., CHASSIN. L. PRESSON, C.C., SHERMAN, S.J. Social image factors as rnotivators of smoking initiation in early and middle adolescence. Child Development 53(6):1499-1511, December 1982. BEST,I.A. Tailoring smoking withdrawal procedures to personality and motivational differcn- ces. Journal ofConsnltinRandClinical Psychology 43(1):1-8, 1975. . I ifdt ZR1

I Office of Disease Prevention and Health Promotion ................ 423 Department of Defense .............................................423 State Health Departments ........................................... 425 Commercial Ventures in Smoking•Control ............................. 425 Phamucoiogic Cessation Aids ................................. 426 Nonpharrnacologic Cessation Aids .............................. 428 Stop-Smoking Programs ...................................... 429 Worksite and Hospital Wellness Programs ........................ 43() Summary ........................................................ . Part 111. Antismoking Advocacy and Lobbying ........................... 4.14 Nature and Objectives of Advocacy and Lobbying ....................... 434 Objectives ................................................. . Organizational Characteristics ................................. 437 The TobaccoL.obby ...............................................435 Antismoking Advocacy and Lobbying: 1964 to the Present ............... 439 Early Efforts ...............................................439 Nonsmokers'Righu ......................................... 440 Coalition Building and the Growth of Advocacy ................... 441 Conclusions ....................................................... :----- 442 References ........................................................ --444 E00L Z$SZS 390 INTRODUCTION The tobacco control movement in the United States has involved the efforts of many diverse groups. Voluntary health agencies. State and local health departnents, the Federal Government, medical organizations, private industry, and grassroots yrganiza- tiuns have all contributed. This Chapter reviews the nonpolicy activities of these groups in the areas of smoking prevention and cessation, and advocacy over the past 25 years. It will not provide a complete review of the efficacy of different prevention aqd cessa- tion methods; this has been done by others (e.g.. Lichtenstein and Brown 1980; Phchacek 1979; Schwartz 1969, 1987; Schwartz and Rider 1978; Flay 1985a,b; Best et AI. 1988; Biglan and Ary 1985; McCaul and Giasgow 1985; Snow, Gilchrist, and Schinke 1985; US DHEW 1979b; US DHHS 1986a). A selective review of the broader trends in these activities will provide a basis for understanding the current status of the smoking con- trol movement and its possible future directions. A review of advocacy activities in- tended to lead to changes in smoking control policies over the last 25 years will serve as a bridge between this Chapter and Chapter 7, Smoking Control Policies. ~ The snx>Ling prevention and cessation activities discussed in this Chapter were designed a.% direct antismoking messages incorporating advice and instruction on how to remain or become a nonsmoker. Smoking prevention programs include schpol cur- ricula, both those specific to smoking and those integrated within a multicqmponent health education approach; media-based efforts; and an array of other materials, events, and campaigns. Smoking cessation programs include a broad variety of activities r4ng- ing from self-help cessation materials to special smoking groups to the use of ri>edica- tion. The programs occur in various channels in the community including worksites, physician of'fices, hospitals, schools, and media. Integrating Educational and Behaviorai Interveatiow With Poiicy Initiatives The integration of educational and behavioral programs with policy initiatives, in- cluding those that affect the price of cigarettes, the information printed on the packag- ing, the manner in which cigarettes can be advertised, the conditions of their sale, and the circumstances under which they may be smoked, has been one of the most impor- tant recent trends in smoking prevention, as well as in cessation-oriented interventions. Projects such as "Tobacco-Free Atnerica aroject" (Bailey 1997) work on both fronts, advocating nonsmoking policies in schools along with providing more traditional smok- ing prevention materials and programs to reduce the number of new smokers. Ad- vmacy activities and lobbying leading to policy changes were almost nonexistent at the time of the 1964 Surgeon General's Report, but became progressively more evident during the 1970s and expanded significantly during the 1980s. setting the stage for many of the changes in prevention and cessation policies and activities. Even when explicit policy components are lacking in prevention or cessation programs, the content and impact of these programs should be considered in the con- text of the social and policy climate prevailing at the time of their design and implemen- tation (see Best et al.l9gtt; Chassin. Presson, Sherman 1985; Chassin et al. 1987; Perry and Murray 1982). For example, the effects of a prevention or cessation activity might 381 I

I clascified based on their reported smoking during the past ;I(1 days. In the 1979 High School Seniors Survey (Table 22).22 percent of males were classified as daily smokers and another 9 perccnt reported having smoked in the last month hut not on a daily basis. In the same year. 29 percent of females were daily smokers and 9 percent smoked on less than a daily basis. Comparing these two data sets shows that, the telephorte turvey obtained lower es- timatcs for wetklv smoking than the school survey obtained for doily smoking (19 vs. 22 perccnt for males. 26 vs. 28 percent for females). The remaining current smokers (dcfincd as less than one cigarette per week in the telephone survey and less than one per day in the school survey) were also estimated at lower rates in the telephexle sur- vcy (0.3 vs. 9 percent for males. 0.8 vs. 9 percent for femaks). This suggests that the telephone survey underestimated both the number of daily smokers and the number of lecs_than-daily smc)kers. Most of the discrepancy appears to he due to a failure to iden- tify the latter. It is unclear whether this diffen-nce is related to the system of clascifying smokers or the telephone survey methodology. NIDA National Household Surveys on Drug Abuse, 197945 NIDA conducted household surveys on drug abuse in 1979, 19g2, and 19g5. For each of these surveys, data were obtained from a stratified random sample of g,(100 U.S. households; approximately 2,000 in-persort interviews were conducted with re.ryron- dents in the 12- to 17-year-old age group. Questions included whether any cigarcttes were smoked within 30 days as well as within the previous year. These surveys indi- cated that approximately 26 peroent of the teenage population surveyed smoked at least one cigarette at some time during 19R5 (Table 24). In 1985,15.6 percent of this popula- tion had smoked within the previous month. Comparisons between data from the 1979 household survey and data from the more recent surveys are not appropriate, because in 1979 prevalence of use within the past year or past month was reported only for those who had smoked 100 cigarettes in their lifetime: this lifetime cutoff was not used in the later surveys. TARLF 24.--4'rcvaknce (96) orcigarette trse snanR youth 112 to 17 rears of agG 1979.1982. and 19g5. United States Sorvey vrar Any uwe in laat yea U.ed in tact ;10 days lu7y' 13.3 12.1 I4IR2 24.8 14.7 I'Mtt 26.0 15.6 ' nrt 1970 ruimaM.me mw ncceavrily cempnMr w laler eainuMea hecwx Ihe 1979 pu.ey pded queuimm Mly of dw.ve wlw, haA mnkeA NK1 eirwrllm i" iAeir liklimr• GNIR('V NInA N~i.~,a111.~~.rM~1,I Gvveyaan IkrR /1M~.e 1070, 10112. I~/ISt~ ~{t{~s IOllfi. 6969 t8SiS Summary Several national surveys provide infortnation on adolescent smoking. These surveys vary substantially in sampie si?e, methodoiogy, definitions of smok ing, agcs of respon- dent.s, and other factors that may appreciably affect prevalence estimates. The best trend data are available from the annual high school seniors survey. This survey shows that prevalence of daily cigarette consumption declined from 29 perccnt of seniors in 1976 to 21 pereent in 19g0, after which prevalence leveled off at I R to 71 percent. Smoking prevalence among females has consistently exceeded that among males since 1977. The leveling off of smoking prevalence among high cchool .eniors raises concern that the steadily declining initiation rates as determined by prevalence among adults aged 20 to 24 (NHIS) may soon level off as well. Smoking prevalence has been consistently lower for high school seniors with plans to pursue higher education than for those without such plans. ln 1987. smoking raies • were 14 and 30 percent in these two groups, respectively. I Differences in prevalence of smoking and smokeles.s tobacco use (see below),be- tween young males and young females suggest that the prevalence of any tobacco use is similar in these two groups. Whereas the prevalence of smoking is higher among female high school seniors than among males, the prevalence of smokeless tobaccd use is higher among young males than among young females. ChanRes in the Types of Cigarettes Snaked Data on the market share of filter and nonfilter cigarettes, cigarettes of different machine-determined "tar" and nicotine yields, menthol and nonmenthol cigarcttes, and cigarettes of different length have been published by the Federal Trade Commission (FTC) from information supplied to the agency by the major cigarette companies. ~ Filtered Cigarettes Filters are the design characteristic of txxnmerciai cigarettes that most affects their machine-measured yield of harmful constituents (US DHHS 198 1). Filters selectively remove nitrosamines and semivolatikphenols from smoke. Thus, filters affect not only the absolute amounts of these constituents delivered in smoke but also their relative concentrations in cigarette "tat. " Since the early I95(k, the proportion of cigarettes in the United States sold a% filtered cigarettes has increased steadily. In 1950, less than I percent of cigarettes -sold in the United States were filtered. That proportion rose to 19 percent in 1955. 51 percent in I9G0, and 94 percent in 1986 (Table 25). Low-Tar, Low-Nicotine Cigarettes Tn:nds in the sales-weighted average yield of tar and nicotinc for cighrcttcs .oM in the United States are shown in Figure 14 of Chapter 2. Thr sales-wciFhtcd avcragc is hascd on the tar and nicotine yield of specific brands (a.s mcamurcd by the FTC machine- - sl1

I conversations, and higher expectations for the sons. It appears that adolescent smok. ing is more likely in restrictive, punitive, and unempathetic families in which children are uninvolved in decisionmaking. On the other hand, families who provide multiple avenues for identity formation and expression of feelings may obviate the utility of smoking or other problem behaviors as a mode of identity expression (Jessor 19g7). Personal characteristics and attitudes may mediate peer influence on smoking as well as other drug dependencies (US DHHS 19RR). Research indicates greater impact of peer smoking among adolescents scoring low on a measure of obedience to parental authority and high on a measure of rebelliousness (McAlister, Krosnick, Milbum 19R4). The interactions amcxng social infiuences, personality, and smoking were highlighted in a study in which seventh and eighth graders described the informal reference or af- filiation groups they observed among their schoolmates and identified the group with which they felt the closest affiliation (Mosbach and Leventhal 198R). Two of the four groups that emerged. "hot-shots" (78 penxnt female, popular leaders in academic and extracurricular activities) and "dirts" (63 percent male, characterized by problem be- haviors such as drinking, poor academic perforrnance, and cutting claoses), were iden- tified as primary reference groups by only 14.7 percent of respondents but accounted for 55.6 percent of the smokers. In discriminant function analyses, a "macho" dimen- sion was highly associated with rxte high smoking prevalence gnaup, the "dirts." but not with the "hot-shots." In contrast, academic and social leaderahip was associated with the "hot-shots" but not with the "dirts." As were the "dirts," the "jocks" were also 63 percent male and high on the macho dimension but low on use of both hard liquor and cigarettes. Adolescent smoking, then, is closely related to individual identification with groups, but these groups differ markedly in their association with other problem behaviors and psychosocial chsracteristics. Depending on group affiliation, different personality and attitudinal characteristics may be related to smoking. Social class differences in the onset of smoking continue to be observed as noted in Part I of this Chapter. Racial differences in onset and prevalence and historical shifts in these differences are also well demonstrated in the first part of this Chapter. Sussman and colleagues (19R7) in their study of psychasocial predictors of cigarette smoking onset by approximately 1,000white, black, Hispanic, and Asian adolescents in Southem California demcnstrated that different variables predict onset in these different groups. A good predictor for whites but not for other ethnic groups was adult and peer models of smoking behavior, while for blacks, risk-taking preference was a good predictor. These findings possibly reflect unique cultural and social contexts and suggest that tailoring socially relevant treatment components to adolescent subgroups may he beneficial (Sussman et al. 1987). Cigarette Marketing Beyond the family and peer group, an important social context determinant of the nnset of smoking is the marketing of cigarettes. There have been longstanding con- cerns about the impact of cigarette advertising on both children and adults as evidenced by the han on radio and television advertisements, effective in 1971. Yet. "cigatette Z869 I85TS advertisements continue to appear in publications with large teenage readerships" (Davis 1997, p. 730). Marketing campaigns seem designed to appeal to specific personality characteristics of groups of potential buyers. In this respect, they exemplify interactions between per- sonal characteristics and the envitontnent. The Marlboro brand was the leading choice of a group of white adolescent male (48 pereent) and female (38 percent) smokers sur- veyed in Louisiana in 1981 (Hunter et al. 19R6). In a sample of 306 high school;stu- dents in Georgia. Marlboro was the preferred brand of 76 percent of smokers who iden- tified a single preferred brand (Goldstein et al. 1987). Similar findings were reported by Glantz (19R5). These figures contrast with the overall domestic market share of Marlboro, which was 24 percent in 1987 (Ticer 1988). Given the associations of rebel- linusness and behavioral problem with adolescent smoking, as reviewed above, there may be a relationship between the noted disparity of overall brand preference anl the emphasis on the tough independence of the "Marlboro Man." In fact, this pattern may be a reflection of extensive market segmentation, in which specific brands are marketed for specific gender or ethnic groups, often with campaign messages and symbols aimed at those groups (Davis 1987). Teenage girls, relative to boys, are more likely to bel jeve that smoking controls weight (Clarlton 1984) and are good targets for advertisertents that emphasize the desirability of being slender (Gritz 19R6). Some market segmentation appears more subtle, guided by smoker characteristicl not as apparent as race and gender. McCarthy and Gritz (1987) surveyed students in grades 6, 9, and 12 regarding their attitudes about cigamtte advertisements. Among their findings was the closer relationship, for those youth more likely to be smokers, between personality self-ratings and personality ratings assigned to models in cigarette advertisements. Thus, the way adolescents see themselves appears to be related to their attraction to certain advertisements. This congruity among psychological correlates of teenage smoking, marketing themes, and teenage preferences is especially striking when one considers that the tobacco industry denies that campaigns are aimed at teenagers (Davis 19R7). Summary The increased understanding of the multiple and interacting determinants of the development of smoking and of the relation of these determinants to the stages of development of smoking is a reflection of progress over the last 25 years. The detinea- tion of stages-fnom onset to regular use-has been an especially influential develop- ment (Figure 2). The development of the addictive processes in teenagers has recent- ly become better appreciated and understood (Biglan and Lichtenstein 1984; Ilirschman, laventhal, Glynn 1984). While information about the long-term disease consequences of smoking has an important role in adolescent smoking initiation, aware- ness of the short-term health consequences and the influence of peerx and advertising ane now seen as more critical for adolescent decisionmaking. The effects of peers and family are both supported. Cigarette marketing appears to target teenagers despite the cigarette companies' reported policy effortc to restrict such advertising. ?:9 I

DAVIS. R.M. Current tnerds in cigarette advertising and marketing. New En4lmedlournol of Medicine 316(12):725-732. March 19. 19R7: DICI.EMENTE. C.C. Sclf<ft5cacy and smoking cessation maintenance: A preliminary report. CnRnUic,r Therapy and Resrarrh 5(2):175-1 87. June 19R 1. EISER, 1.R. Smoking, addiction and decision-making. International Review of AWird PsychnlnRy 32:11-2R, 19R3. E/SF.R,1.R., SUTTON, S.R. Smoking as a subjectively rational choice. Addictivr Rrhaviars 2:129-114, 1977. EISINGER. R.A. Psychosocial predictors of smoking recidivism. Journal ojHrolth and So- rial Rrharior 12:355-1b2, December 1971. ELKIND,A.K. Changesinthesmokinghehaviour,knowledgeandopinionofinedicalstudenls, 1972-19R 1. S.wial Srirnrr and Mrdicine 16(24):2137-2143, 19R2. ETRINGER, R.D., GRr:GORY, V.R.. LANDO. H.A. Influence of group cohesion on the be- havioral trealment of smoking. Journal of Consullin4 and Clinical Psychology 52(6):1080- I0R6, I9R4. . EVANS. R.1., ROZELLE. R.M.. 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New York: Springer Publishing, 1993. pp. 132-183. ` FORTMANN, S.P., ROGERS, T.. VRANIZAN, K., HASKELL, W.L., SOLOMON; D.S.. FARQUHAR. J.W. Indineet measures of cigarette use: Expired-air carbon monoxide versus placma thiocyanate. PncYMicY Medicine 13(1):127-135, January 1984. FOSS. R. Perwnaliry, social influence and cigarette smoking. Journal of Health and Social Brharior 14(3):279-286, September 1973. FRIEDMAN. G.D.. SIEGELAUB. A.B., DAt.ES. LG.. SELTZER, C.C. Characteristics predictive of coronary heart disease in ex-smokers before they stopped smoking: Comp6ison with persistent smokers and nonsmokers. Journal ojChronic Diseases 32:175-190,1I979r FRIEDMAN. LS., LICH7ENSTEIN, E.. BIGLAN, A. Smoking onset among teens: 'An em- pirical analysis of initial situations. AddirrimBehariors 10:1-13, 19R5. GLANTZ, S.A. Death in the West Curriculum Project. New York Srorelorrnal ojMr±dicine 85(7):470-471, luly 1995. 1 GLASGOW. R.E., MCCAUL. K.D., FREEBORN. V.B., O'NEILL, H.K. Immediate and tong term health consequences information in the prevention of adolescent smoking. Brhac4or Thrralrisr4(5):15-16, 1981. ' GOLDSTEIN. A.O.. FISCHER. P.M., RICHARDS,I.W.1R.. CRE7EN, D. Relationship be- tween high school student smoking and recognition of cigarette advertisements. lournal of Pediatrics I 10(3)-4R8-491, March 1987. GGORDON. N.P., MCALISTER, A.L A prospective text of a social kaming risk factor model of smoking onset and cessation among Junior High School students. Health Psychology. 19RS. GRABOWSKI.J.,HALL,S.M.(eds.) PhormacologicalAdjuncrsinSmnkingCa.rsorion,NIDA Research l.tanograph 53. U.S. Depaxtment of Health and Human Services. Public Health Ser- vice, Alcohol. Drug AlMtse, and Mental Health Administration. National Institue on Drug Abuse. DHHS Publication No. 85-1333,1985. GRAHAM. S., GIBSON. R.W. Cessation of patterned behavior Withdrawal from smoking. Social Science and Medicine 5(4):319-337. August 1971. GREEN. D.E. 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I History of Agency and Organiratfonal Prevention Activities Although the concept of disease prevention did not gain its widest currency and im- pact in anti.moking efforts or in health promotion and medieine as a whole until the late 197()s (US DHEW 1979a), young smokers always have been an important focus of antismoking efforts. Prevention activities were under way during the 19SOs and early 196(1s. even as the data on the health consequenees of smoking were being reviewed by the scientific community (US DHEW 1979b). This Section on the history of preven- tion programs covers the national organizations' initial antismoking efforts and State departments' more current responses to the smoking problem, and the activities of a range of other organizations and agencies. The emphasis is on the major directions of their efforts, as opposed to comprehensive cataloging of all programs and initiatives. National Voluntary Health Organizatiora The three major national voluntary health organizations involved in the antismoking campaign, ACS. AHA, and ALA (previously called the National Tuberculosis Assucia- tion and later the National Tuberculosis and Respiratory Diseases Association), developed their own curricular materials and resources for use in schools, as well as mass-distributed brochures, posters. films, and PSAs. In addition, they have funded smoking prevention research conducted by outside in u~ ll I~althl educatioo and have contributed to the development of compre~~ Ve curricula that include €moking. In the late 1960s. in conjunction with CDC and other agencies, ALA began funding the development of the School Health Curriculum Project and the Primary Grades Health Curriculum Project. now jointly referred to as "Growing Healthy" (see descrip- tion in earlier section). In addition to promoting the adoption of Growing Healthy in schools nationwide, ALA has developed smoking education modules and curriculum materials, and a variety of films and posters. More recently, ALA developed the Biofeedback Smoking Education Proja't (BIOSEP) for students in grades 7 through 12, using student smokers and laboratory equipment, as a firsthand demonstration of the immediate negative physiological cf- fects of smoking (Mitchell 1978: Young. Chtat. Cernada 1982). Two studies have evaluated the effect of BIOSEP on the smoking behavior of adolescents, Mitchell (1978) and Young. Chen. and Cernada (1982). However, the outcomes from these two studies are not consistent and offer only modest support for BIOSEP's effects on smuk' ing behavior. An alternative approach for younger studertts aged 9 to 13 years is ALA's "Srtwkmh Deserves a Smart Answer" (Baiky 1985). This kit uses a social influence apprwc centered on specific responses to direct peer pressure to smoke and includes humonws posters. stickers. a teacher resource guide, student worksheets, and sample rok-plaY' ing situations. both chiklrcn Having issued a policy statement in 1963 to tliscourage smoking among and adults. AHA in 1967 developed sets of materials including a kit with a brochurc for children to help their parents quit, a program that again may have had both ce»ta 600L tgSig tion and prevention impact. Similarly, AIIA's "Like Father, Like Son" campaign tapped both cessation and prevention themes. AHA also has developed educational modules to prevent smoking among youth. Both the "Save a Sweet Heart" program and "Let's Talk About Smoking" are based on social influence approaches, the former involving parodies of cigarette advenisements and the use of a pledging procedure, the latter teaching skills to resist peer presxure to smoke (US DHHS 198(a). Brochures have also been aimed at smoking in the yraucxt of the family (Children and Smoking: Message to Parents (AHA 1987)). In 1964, a National Conference on Cigarette Smoking and Youth was held under the auspices of ACS. Forty-four national organizations with a mission conceming,young people participated. ACS developed numerous antismoking PSAs with prevention messages, including a 1967 television spot focused on the influence of parental smok- ing on children's acquisition of smoking. Other early campaigns used popular cartoim and children's story characters such as "The Thrce Little Pigs" to convey antisrftohing messages. ACS has developed a series of health and smoking prevention programs for irtudents in kindergarten through the intermediate grades. "An Early Start to Good F4ealth," "ACS Health Network ""Healthy Decisions,"and "Health Myself"are among thf most widely disseminated ACS youth health education programs (US DHHS 1986;+): The last of these programs, geared to students in the intermediate grades, emphasizes the role of societal influences on smoking. Referred to earlier in this Section. ACS has a4so developed tcrn cessation programs (ACS 1980, 1986). 1 ' In 1987, ACS, AHA, and ALA began a collaborative campaign for a "Tobacco-Free America." The project involves multiple goals and strategies, including smokb-free schools, mass media and advertising campaigns, a smoke-free class of 2(XX) promotion, and legislative initiatives (Bailey 1987). State-level coalitions of the three voluntary organizations also have developed programs of their own in support of this effort (US DHHS 1986a). The prevention program efforts of the voluntary associations were fairly 4uick responses to the accumulating data on the health risks of smoking. Their materials have used several channels of potential influence on young people's smoking, primarily in- cloding family, media, and the school system. Compared with other prevention ap- proaches, the family and parental influences have been emphasiud-specitically, the iudluence of parental srtwking on the initiation of smoking by childien. Antismoking messages in the context of the family thus could have both prevention and cessation ef- fects; parental nonsmoking was advocated as a powerful preventive influence. Wide distribution of materials was possible. The comprehensive school health education cur- ricula were evaluated while the other programs incorporated only limited evaluation. The extent of actual utilization and impact of the specific distributed materials is not known. National Interagency Council on Smoking and Health lAe National Interagency Council on Smoking and Health, created shortly afte( the fmt Surgeon General's Report, fostercd the early development of a variety of innbva- y3

t tive smoking prevention programs. many of which went on to receive continued major support from other Federal agencies. The "Youth Leadership in Smoking Controls Program; " begun in 1976 with funds from CDC and renewed through 1979, was not in- tended as a study of adolescent smoking education programs per se. Rather, its primary goal was "to identify new approaches for involving youth in smoking control activities" (National Interagency Council on Smoking and Health 1979.p. 12.). Anticipating later prevention programs' orientation to the psychosocial factors affecting youth sntoking, the program required that projects "show sensitivity to the rteeds, lifestyles and feel- ings of the 12-18-year-old adolescent;" and involve youth in the design and delivery of the material (p. 12). Thirteen smoking prevention projects were supptxtcd through these contract funds, none receiving more than 10.000 dollars in any one award. Bx- tent of program evaluation varied greatly. Projects resulting from this program were described in the program's final report (National Interagency Council on Smoking and Health 1979) and in Cookbook for a Smokeless Die(, a humorous manual written for teachers and community members (National Interagency Council on Smoking and Health 1977). (See next section for further discussion of the National Interagency Council.) Federal Government Prevention Support The late 1970s were a key time for Federal Government involvement in and funding of prevention programs. Until that time, federally funded research emphasized biomedical mechanisms of smoking-related disease. as opposed to research on smok- ing behavior and interventions to reduce its prevalence (Bell and Levy 1984). Secretary of Health. Education, and Welfare Joseph A. Califano's 1978 initiative to combat smok- ing led to appropriations for Federal agencies to support biobehavioral research into the factors affecting smoking and for the development of prevention and cessation programs (Bell and Levy 1984). Each of the Federal agencies developed initiatives for such research. Depending on the agency, smoking was the sole behavior targeted or, in other cases. one of a.et of behaviors the agency sought to prevent. For instattce, the National In- stitute on Drug Abuse (NIDA) was concerned with substance use more broadly. NHLI3I with cardiovascular risk factors. The agencies within the Department of Health and Human Services (successor to the Department of Health. Education, and Welfare (DH EW )) with initiatives most directly bearing on the prevention of tobacco use among children and adolescents included NCI, the National Institute for Child Health and Human Developrrtent (NICHD), NIDA, NHLBI, and CDC. In addition, OSH (Bell,and Levy 1984) (OSH is now part of CDC) developed such initiatives. Federal health agen- cy and OSH prevention initiatives included both research support leading to the development of prevention programs and the production of prevention rewarces and programs for direct use by schools and other organizations. In addition, guides of ex- isting resources are periodically produced by Federal agencies. including Snxslinc Programs for Youth (US DHHS 1980a) and Setokescretn: Guidelines f~x flelping Teenagers Become Nonsmokers (American Institutes for Research 1980), contracted by CDC. 0t0L Z8SZ5 Office on Smoking and Health The U.S. Public Health Service first officially became engaged in an appraiwl of the available data on sntuking and health in June 1956 when, under the direction of Sur- geon General Leroy Burney, a scientific study group was established (8unney 1959). In 1957, the Public f lcalth Service adopted the position that "excessive smoking is one of the causative factors in lung cancer" (Burney 1959). In 1964, DHEW became active- ly involved in efforts to discourage snwking. `, The seminal smoking-and-health event in this evolution of Federal involvertxnt was the 1964 release of the Surgeon General's Report on Smoking and Health. At that time, Surgeon General Luther Terry established an office within the Public Health Scrvice Chronic Disease Control Program (US DHHS 1986a) to help collect, organixe, and analyze information on smoking and health. This office later became the National Clearinghouse for Smoking and Health and still later (March 1978), OSII. (Se* Chap- ter 7.) , In the early years of the Clearinghouse, a number of innovative smoking control in- itiatives were supported, some of which are continued today by CDC. Cbnter for Chronic Disease Prevention and Health Promotion (which now includes OSH)j and by the Department of Education (US DHHS 1986a). Initially, the Clearinghouse dFveloped curricula and teaching materials to educate young people about the hazards of tobacco use (US DHHS 1986a). Many of these materials are now being used in schools ac" the country. The Clearinghouse pioneered an effort to place PSAs in high'school newspapers. It was also involved with mass distribution of pamphlets, program materials, and television PSAs. Between 1966 and 1971, the Clearinghouse coriducted the first study of a communitywide smoking control intervention in San Diego Coun- ty, CA (US DHEW 1976). This project involved interventions aimed at schoolchildren, health professionals, and adult smokers. The San Diego project developed curriculum guides for studentc in grades I through 12, as well as newsletters to support the efforts of teachers and other health lrofes- sionals involved in the project. A"Youth-to-Youth" prognun, precur.wr to peer-led programs, wa.s also included. Although evaluation of the project was limited, the data collected suggested that the intervention had been successful. Survey results show sig- nificant reductions between 1966 and 1975 in the percentage of teenage and adult smokers in San Diego compared with national samples (US DHEW 1976). The programs of the San Diego Community Laboratory led to the developnent of other cantprchensive health curriculum projects such as the School Health Curriculum Project. Today, OSH continues its effons for smoking prevention through the developnxnt and distributiort of educational materials. It currently has a program of disseminating print PSAs through high school and college newspapers, as well as televised PSAs aimed at teenagers (US DIIHS 1986a). OSH has been the only Federal office devoted solely to the smoking issue. Now part of CDC, the Of•fice continues to perform the same functions that were established for the Clearinghouse in the 1960s (US DHHS l986a). OSH continues to servC as a repository for information on smoking and health and responds to thousands of p4tblic 395 f

t tunities. Spanning this developmental continuum are approaches to keep children from experimenting with tobacco, efforts to disrupt the evolution from experimentation to regular smoking, and earty interventions aimed at influencing the young smoker to stop before the behavior and nicotine dependence become more firmly entrenched. Stage models of smoking acquisition posit that different influences are at play at various ages; for instance, parents have a greater influence than peers in determining smoking intentions and behavior among young adokscents, while peers are more im- portant for otder adolescents. Social factors are viewed as more influential fur begin- ning smokers. and physiological dependence and coping patterns as more important for the older, more established smokers (Flay et al.1983; Leventhal and Cleary 1980; Chas- sin. Presson. Sherman 1985). (See Chapter S, Part ll.) Prevention programs designed to reduce the number of young adolescents who in- itiate smoking reflect the dominant model for current smoking prevention. However, early antismoking education efforts addtessed smoking by high school and college students (US PHS 1964), age groups encompassing several stages in smoking acquisition. The majority of current prevention programs focus on adolescents in grades 6 through 8, the age groups now at maximal risk for cigarette experimentation (Flay et al.1983• Flay 198Sa; Chapter 5). The shift of interest to smoking prevention programs aimed at younger adolescents is related to four considerations: ( I) the find- ings of greater program impact among youngerchildren (Jason, Mollica. Ferrone 1982; Johnson et al. 1986; Merki et al. 1968), (2) the general ineffectiveness of previous prevention approaches (7lampson 1978).(3) the recognition of secular trends toward earl ier initiation of smoking (Evans et a1.1979; Flay et al. 1983; Chapter S), and (4) the appeal of prevention versus the challenge of adult cessation (Evans et al. 1979). A stage model of smoking acquisition and associated pnevention opportunities sug- gests the potential for prevention programs aimed at even younger children in the preparation stage of smoking aequisition, the period during which early attitudes toward smoking are formed. The stage model also suggests cessation programs among older adolescents at the other end of the prevention continuum. Thus. sotne smoking prevention programs ate directed at very young children in preschool or early elemen- tary grades (ACS described in US DHHS 198(5a; Pt:terson described in NCI 1986a; Pigg et al.1983), and there are cessation programs directed at adolescents (e.g., ACS 1980, 1986; Weisstnann et al. 1987). A call for continued development of programs addressing "pne-onset" issues and youth cessation was included in the National Cancer Institute (NCI) expert advisory p.nel's (Glynn, in press). Youth smoking cessation approaches are described in a luter section in this Chapter. Prereatio. Progr.m Appro.cbes As outlined above. the evolution of prevention programs since the 1960s can be clas- sified into tliroe major approaches: media-based peograms. smoking prevention in the context of multicomponent school health education, and psychosocial curricula. 7Ue three major approaches will be more fully described in this Section. Other resources and activities in the field will be described in a subsequent section. 384 500L 185i5 Media-Based Prevention Programs Media-based prevention approaches have included antismoking messages delivered through newspapers and television and radio broadcasts. Most often these have taken the form of brief announcements, but more extended special programs and curricula have also been developed and distributed. The American Lung Association (ALA). American Heart Association (AHA), American Cancer Society (ACS). and National Heart. Lung, and Blood Institute (NHLBI) sponsorcd one such extended prevention program, first aired in November 1984, a I-hr Public Broadcasting System apecial. "Breathing Easy," aimed at young people (Bailey 1985; US DHHS I986a). Mass-media-based messages and programs were included among the earliest smok- ing prevention efforts of the Federal agencies and voluntary health associations. Flay (1986 and 1987b) has provided comprehensive reviews of these and later media-based smoking control efforts. Early evaluations of mass media in health promotion were not encouraging. leitiding to Flay's (1986) appraisal that mass media programs alone are not effective. Review- ing studies of inedia campaigns that were used either as the sole intervention or i4 con~ junction with other material and programming. Flay concluded that the most efftctive use of mass media in substance abuse prevention lies in furthering the dissemination of other prevention resources, such as school-based programs. Parents, for examplmay become more supportive of the efforts of school-based prevention programs brought to their attention through the mass media (Flay 1986). In reviews of mass media Gam~ paigns specifically focused on smoking. Flay (1987a,b) found some basis for optinlism about their potential impact on adult smoking cessation. He tecomrttended, however, further evaluation of mass media campaigns for the prevention of adolescent smoking; only 3 of the 56 evaluations reviewed included specific reference to smoking by children (Flay 1987b). There have been several controlled studies of mass-media-based prevent ion programs in recent years (Bauman et al., in press; Sussman et al. 1986; Flay et al., in press; Wor- den et al., in press; Ramirez and McAlister, in press). A University of Southern Califor- nia study demonstrated that effects on student smoking correlated with amount of at- tention to the television segments and amount of discussion of the program with others (Sussman et a1.1986; Flay 1987b; Flay and Sobel 1983; Flay, Hansen et a1.1987). The program, which parents were encouraged to watch with their children, also had a ces- sation effect on the adults' smoking (Flay 1986). Mass media interventions can also augment other prevention programs, generating prevention effects that occur more broadly, acting over time in the aggregate to affect the level of public awareness and the social acceptability of smoking. 'tlte potential for this level of public health impact is described by Leventhal and Cteary (1980) and Warner and Murt (1982) in their consideration of factors inhibiting the rise of smoking rates in the late 1960s and 1970s. Even small program effects can have a large public health impact, given the very large audiences of mass media (Flay 1987b), making the actual distribution and broad- casting of these programs critical. Dissemination of media materials has been depend- ent on the good will and interest of publishers and broadcast managers, or on funds for 'S

be moderated by whether it was conducted during the era of television cigarette com- mercials alone (pre-1967). the era of both commercials and antismuking public service announcements (PSAs) mandated by the Government (1967-70) (see Chapter 7), or during the subsequent era of no televised cigarette commercials and the end of the man- dated PSAs (post-I970). Other potentially relevant policy contexts include school regulation of student smoking and the level of public debate and restrictions on smok- ing in other settings at the time of the smoking prevention or cessation program. Both the smoking prevention and cessation programs and the public policy context remain in a continuous process of evolution and interaction. PART L SMOKING PREVENTION ACTIVITIES Overview of Mt* Apptn.chea to Smoking Prevention In the years since the release of the first Surgeon General's Report (US PHS 1964), both the basic design of prevention efforts and their designated targets have changed. Generally, there has been a shift in the target group from high school and college stu- dents (US PHS 1964) to middle school and junior high school students, and a shift away from information-orieMed antismoking education to psychosocial curricula designed not only to address youth's motivations to smoke but also to impart skills for resisting influences to smoke (Botvin, Eng. Williams 1980; Flay 1985a; McAlister. Perry. Mac- coby 1979). The changes in focus and design and the proliferation of prevention programs since the early 1960s has resulted in such a variety of approaches that they are now rarely considered together in reviews of smoking prevention programs. 71rcse differing ap- proaches include (1) media-based prevention programs and resources. (2) smoking prevention as a component of multicomponent school health education curricula, and (3) smoking prevention through the psychosocial approaches of social influence and generic life skills curricula. Other smoking prevention resources and activities such as physician presentatiotu to school assemblies. brochures, community campaigns, and educational resources have been sponsored by voluntary. professional, and community groups. While the prevention approaches overlapconsiderably, both in form and content, this differentiation of program types can serve as a framework for tracing the preventiun initiatives and directions taken by various organizations, as well as for highlighting the evolution of smoking prevention programs over the years. The following outline of the major prevention approaches will be expanded upon in a later section. Media-based messages and campaigns were part of the earliest smoking prevention activities. The National Clearinghouse for Smoking and Health (later rcorganixed as the Office on Smoking and Health (OSH)) and the voluntary health organii•rtions were among the early and continuing sponsors of newspaper and broadcast antisnwking can- paigns. These smoking prevention campaigtt: have continued with varying intensitY over the decades, continuing into the present era of controlled research in the devekip- ment and evaluation of media-based smoking prevention programs (e.g.. Bauman et al., in press; Flay et al., in press; NCI 19g6a; Ramirez and McAlister, in press; Sussman et al. 1986; Worden et al., in press). 7?te integration of smoking prcvention curricula into comprehensive and multicom- Iwnent school health education curricula was one response to the findings of limited impact from early smoking-specific prevention efforts (see Davis 1977). The develop- ment of psychosocial approaches including social-influence and life skills programs in the 1970s was another response to the limited impact of early prevention effottf (Evans 1976; US DHEW 1979b). The integration of smoking prevention into gener*l health education represented an important shift in the vehicle for antismoking messages, and the psychosocial approaches were based on a fundamental revision of the model under- lying prevention strategies for smoking by youth. The psychosocial approaches deviated from traditional antismoking education models by deemphasizing communication of the long-term health risks of smoking. In- stead, these new curricula focused on young people's susceptibility to social ptiessures to smoke-influences inferred from consistent findings relating smoking by ~out(t to smoking by their parents, siblings, and peers (Flay et al. 1983; US DHEW 1979c; US PHS 1964). In their various forms, social influence and life skills curricula have been designed to raise young people's awareness of the influences to smoke; to highlP$ht the more immediate, and especially socially based. negative effects of smnking; and to "in- oculate" youth against the effects of continued pressure and examples of others who smoke. The new approaches were bolstered by the literature on communication thebry and on the psychosocial development of adolescents (US DHEW 1979b). ` This Section covers the course of smoking prevention activities over the past 25.years. 7be first part presents a model of developmental stages of smoking acquisition as a framework for describing trends and options for prevention programs. 71tis is followed by further description of the three major categories of current prevention programs and of cessation programs for youth. The next part describes in more detail the history of prevention activities of the major national voluntary health agencies, Federal support with emphasis on their early responses in the campaign to prevent smoking, and the ac- tivities of State and other organizations and agencies with emphasis on their recent ac- tivities. Considered next are problems in program dissemination and the gaps that fn:- quently exist between the scientific literature and widespread program application in the field. Problems in program evaluation are reviewed in the next section. The review cknes with a consideration of population factors such as changing attitudes toward stnuking and secular trends in smoking prevalence as they relate to program diversifica- tion. Prevention Opportunities Associated With Stages In the Acquisition of Smoking As noted in the preceding chaper, several researchers (e.g., Flay et al. 1983; Leven- thal and Cleary 1980) have proposed models of developmental stages in the acquisi- t" of smoking. These models provide one dimension for describing and evaluating prcvention oppottunitiea and trettds. The stages-for example. "preparation and an- ucipation." "initiation," "experirrtentation; • •.transition (becoming)." and "regular '"l0k'ng" (Flay et al. 19g3)--suggest a continuum of associated prevention oppor- 000L Z85iS 13 382

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other effect. Prolonged use also leads to physical dependence, as indexed by various p.ychological and physical withdrawal symptoms following cessation of smoking. The inclusion of tobacco dependence as a disorder in the Diagnostic and Statistical Manual of Mental Discmters 111, the official diagnostic reference for the American Psychiatric Association (19R()), wax another major marker in the shift of scientific opinion about the addictive nature of cigarette smoking. Central to the 1961 view was the distinction between compulsive use (addiction) and the less compulsive "desire" (habituation). The difference wac noted to rest primarily on the .cairce of the desire or compulsion. The 1964 RReport emphasized "serious per- sonality dcfcctc from underlying psychologic or psychiatric discmlers"(US P1IS I9(,4, p. 351) a% a defining factor in compulsive use and therefore in addiction. Evidence gathered since the carly 19l>nc contradicts the assumptions that underlying pathology drivec the compulsive use seen in addiction. Drugs commonly viewed as addictive, e.g., heroin, may he abandoned with little apparent effort as with many Vietnam veteranc addicted to heroin who gave it up after their return to the United States (Robins, Helzer, Davis 1975: US DHHS 19RR). On the other hand, the extent to which snmk- ing can he highly compulsive is suggested by its continuance in the face of substantial awareness of its harm, as by cardiac patients (Raik et al. 1982; Rurling et al. 1984. Ockene et a1.19R5; US DHHS 19R4). The generality of nieotine's effects argues against its compulsive use resting on individual psychopathology: the basis for nicotine addic- tion rests on the interaction of conditioning procecses and nicotine action in the brain. Mechanisms of Nicotine Action Much research in the 1970s on the behavioral effects of nicotine has been guided by the nicotine regulation (or titration) model put forth over the years by Jarvik (1977), Jarvik, Glick, and Nakamura (1970), Russell (1976), and Schachter, Silverstein and col- leagues (1977). According to this model, smokers regulate their smoking to maintain a certain level of blood nicotine within a range of upper and lower limits (Herman and Kozlowcki 1979; Kozlowski and Herman 19R4). This includes the avoidance of withdrawal symptoms or anticipated withdrawal by maintaining a nicotine level above a lower limit and avoidance of toxicity by maintaining it below an upper limit This formulation has been criticized as failing to explain the self-perceived positive effects or benefits of smoking that may promote use (Pomerleau and Pomerleau 1979; Leventhal and Cleary 19R0). Interestingly, the 1964 Surgeon Gtneral's Report devoted only I 1/2 pages to such effects. In the last few years, several investigators (e.g., Ock- ene et al. 1999. Pornerleau and Ponxrleau 1984) have proposed that smoking, by vir- tue of the varied actions of nicotine, provides several positively perceived effects and is employed by many smokers as a responsive and effective coping strategy. This im- plies that smokers can he reinforced forcontinued smoking without maintaining a min- imum blood nicotine level. The 19RR Report deveted an entire chapter to this topic. An influential and historically important model of perceived positive effects of smok- ing stressed the psychological effects of nicotine and other pharmacologic aspects of smoking (Porncrlcau and Porrxrleau 19RR4). This model holds that nicotine increases thc relca%c of a number of ncuroregulatory hcxtnones, conferring on smoking the ability to act as stimulant or sedative depending on level of ingestiorr, background hormone levels, and the like. Nicotine thus can serve to reduce anxiety or produce euphoria (U~ DHHS 1998) and enhance vigilance for certain cognitive tasks (e.g.. Warburton et al. 1986). The work of Grunberg (1986; US DHHS 1988) also suggests that nicotine may aid smoken in maintaining lower body weight. Although objective judgment indicates that the health effects of smoking are tnotie important than the weight maintenance ef- fects (Abrams et al.1987), the latter seem to he of particular importance to some women (Klesges and Klesges, in press: US DHHS 1988). This growing recognition that smokers may value several effects of cigarettes can be used not so much to justify the behavior but rather to direct intervention strategies (e.g., physical activity) that might help people meet needs previously served by cigarettes. Interventions also are likely to be seen as more credible to smokers if the coping value of cigarettes is recognized (Ockene et al. 1988). Conditioning and Smoking What most distinguishes recent analyses of the conditioning of xmoking from eatlier views (e.g., Hunt 1970) is their emphasis on the conditioning of the biological e#ects of nicotine. The occurrence of stimuli previously associated with the effects of nicotine will tend to evoke responses telated to those effects or cues for further consumptio~ (e.g., Abrams et al., in ptess; Hernmt 1974; Niaura et al. 1988; Rickard-Figueroa' and Zeichner 1985). Such conditioned effects may link smoking to aversive states al- leviated by nicotine. Forexample, investigations described earlier (e.g., Schachter; Sil- verstein et al. 1977) suggested that smoking covatties with stress, which is hypothesized to deplete nicotine. Leventhal and Cleary (1980) suggested that stress as well as other emotions may be alleviated by nicotine and would then come to serve as cues for smok- ing. Pomerleau and Pomerleaa (1984. 1987) identified neurvhumoral effects of nicotine as the paths of its impact and elaborated on the ways such effects might be con- ditioned to circumstances surrounding smoking so as to regulate it in the future. Two influential theories of addiction emphasize the role of relief of withdrawal or anticipated withdrawal in smoking. As suggested by Wikler's classic work with opioids (Wikier 1973; Wikler and Pescor 1967), withdrawal symptoms tnay be conditioned to the circumstances in which they occur. 91tis would set the stage for stimuli associated with prior drug taking to elicit withdrawal symptoms and urges. With smoking, greater withdrawal symptoms have been noted when cessation occurs in natural rather than ar- tificial env':ronments, ptesurnably because those natural environments contain numerous cues associated with prior smoking (Hatsukami, Hughes. Pickens 1985). Within this nadel, return to smoking after brief or extended abstinence is reinforced by the reduction in such conditioned withdrawal symptoms. Opponent-process theory (Solonan and Corbit 1973) suggests that the reduction of aversive withdrawal symptoms may be the result of the interaction of the immediate response to a drug, called the "A" state, and the delayed response, the "B" state The B state is "opposed" to or opposite the A-henee "opponent process "; if the A is pleasurable, the B will be aversive. Initially, the A state is stronger. While initial, pleasurable responses to nicotine may encourage incoeasod smoking, regular smoking Ie t

/ health threats are also seen as bearing txt smoking by youth (Glynn, lxventhal, Hirschtnan 1985). A prevention program based on this model has been developed for students in the early stages of contemplating and experimenting with smoking. This cognitive developtent program significantly deviates from the social influence cur- ricula in its inclusion of both young nonsmokers ard smokers and in its examination of nonsocial influertces on their experience of smoking. However, the age groups targeted are the same, social influences are also part of the curticula, and, more fundamentally, the program shares with the social influence curricula a theory-based approac h to dirtct- ly intervening in the processes and needs thought to underlie the development of snwk- ing among young people. An 18-month followup of program and control students in grades 6 through a; revealed significant differences in attitudes toward smoking and in students' self-rcports of snwking (Glynn, Leventhal. Hirschman 1985). Youth Smoking Cessatioe Programs Youth smoking cessation programs are ptopedy viewed as part of smoking preven- tion efforts to the extent that their ultimate goal is the prevention of the establishment of dependent, regular smoking. The limited research in this area cannot yet suggest the optimal balance of traditional "prevention" and cessation strategies for programs tar- geting young smokers. Some young smokers may exhibit much variability in their smoking; others slaw a pattern of consumption very closely resembling older, addicted smokers. (See Chapter 5.) Recent interest in teenage cessation has been heightened by increasing social disap- proval of smoking and acceptance of its restrictionon the part of adolescents and society more broadly (Johnston, O'Malley, Bachman 1987; US DHHS 1986b), as well as voluntary health association and public health agency commitments to promoting non- smoking environments in the schools (National School Boards Association 1987; US DHHS 1986a). Data on naturally occurring rates of quit attempts and cessation among young smokers support interest in teenage cessation. These rates range from 18 to over SO percent cessation with varying followup periods and suggest considerable flux in the natural history of smoking, as well asopprxtunities for intervention with young smokers after they begin experimenting with cigarettes (Alexander et al. )983; Cha.sin, Pres- son, Sherman 1984; Er.hleret al., in press; Hansen 1983. Hansen et al. 1985; O'Roude. Nolte, Smith 1985; Skinner et al. 1985; US DHHS 1982b). Many of the early antismoking education programs incorpexated cessation functions by virtue of their inclusiot: of older youth. Description of these early teenage smoking cessation programs, including those among the prototypes of antismoking education for youth, is included in the 1979 Surgeon General's Report (US DI IEiW 1979b) and in Seffrin and Bailey (1985). Smoking cessation programs specifically for youth have been developed by researchers (Wei..wnan d al. 1987; St. Pierre, Shute. Jaycox 19g3), voluntary associations (ACS 1980, 1986; Bennett. Austin. J•rnir.ewski 1986). and school personnel (Hulbert 1978). Program effects on cessation rates amnrtg young snxtkers have also been examined in sttdies thatemphasize prevention of initation (13ea et al. 1984; B(Avin, Renick, Baker 1983; Johnson et a1.1986; Perry, Kilkn, Telch et al. 1980b). Ce.wtion programs addressing young fx(rple's use of unokelc.a tobacco habq ' also been dr.igtkd (iluvet 1986; Sw vcrson ct al. 1987). NCI is currently funding re.earch on Ixnh prevention and cessation interventions for smokeless tulwcco u..e, though no uutconK, havr bcut rclxxted as yet (NIH 19M6). ' Tcenagc cessation programs have met with mixed success, in terms of bolh recruit- nxnt and retcntion of pnrgrrm participants, and of program impact. Study of teenage cexwtiun programs has also gctKrally sul lerrd f rum rrry• small numbers of participants (in part, a reflection of difficulty in mcruituKnt) and from a dearth of finrnal outcome evaluations. Subject characteristics, including baseline smoking levels, vary b+teatly faHn study to .tudy, as do length of fbllowup periods and outcome criteria conatkred. Although these limitations to the research are substantial and restrict conclusions that can be made concerning the cfficacy of tcen smoking cessation programs, the cnrer- gcnce of new demands fior and research on such programs warrants the following review in comparatively nwre detail Utan for other fargerand more controlled smoking preven- tion studies. 4 St. Pierre. Shute, and Jaycox (1983) found reductions in self-reponed rates of crin- sumption among 1Uuf dte I I teen smokers who regularly participated in their ptkograln of peer-designed and peer-led "stop smoking" clinics. In evaluating AHA's "Save a Sweet Heart" program's nu-snKtking pledge day component, Bennett, Au.tiq, and Janizewski (1986) ffound that Ihe pledging was related to cessation at a I-year pifsttest in their sample of 194 1(Rh-gr:Nle male snx)kers only, but not in the sample of 31 K 10th- grade female smokers. Uverall, female students, including nonsmokers and smqker,s, were more apt than males to participate in the pledge component of the progrrmt 1, Weissman and colleagues' tcti:n cessation program (1987) used a contingency-baxed .y.tem of munetary rewards lix reduction of expired carbon monoxide levels.+ 'I'he study suggested some prumize anxxtg the males; fiwrof the six male participants main- tankr) abstinence during the 5-nxxnh followup period, with only limited "slips." fluwcver, all of the live 1'emales dropped out of the program before completion. Pcrry. Killen, Telch, and colleagues (1980) ccompared the effects of a four-session program emphasiLing the immedi:rte physiological effects of smoking and the role of social influences with outcomes from a nKxe traditional curriculum emphasizing the lung-term health effects of snwking. Statistically signif icanl differences in self-reports of smoking 5 nxmth+ later were lound within the treatment group of 498 10th-grade students, pre-axd posttezt for daily and nKxnhly smoking; and between treatment and control (399 1(Mh-gradc students) groups IKrsuest ordy for weekly and monthly smok- ing. Significant differences in corresponding measures of expired carbon monoxide Were also found. Taken in .um, there is suHne evidence that ad)le+cent smoking cessation programs are efI IcaclUu\, althlNl f;h the data and analyses are limited and difficult to InterprCt, and results are, therefore, f'ar front cut>Llusive. Further research and continued program development in this area are greatly needed. 390 g00L Z85Z5 _ ' •9f

STF.W ART, l., DEW IT, H., EIKELBOOM, R. The rok of unconditiased and conditioned drug effects in the sclf-administntisxt of opiates and stimulants. Psychology Review 91(2):251- 2FiR, 19R4. STRAITS. B., SECHRF.ST,1.. Further support of some findings about the characteristics of smokers and nrxssmnkers. Journal af Cnn.sulting and Clinical Psychology 27:282. 1963. SUSSMAN. S.. DENT, C.W., FLAY. B.R., HANSEN, W,B„ JOHNSON, C.A. Psychosocial predictors of cigarette smoking onset by white, black. Hispanic and Asian adolescents in southern California. Morbidity and Mortality Weekly Repnrt 3f+(4S, Supplement), Septem- her 4,1997. SUTTON, S. Sncial-f+sychnlogical approaches to understanding addictive behaviours: At- titude-hehaviour and decision-making models. Rriti.sh Journal ojAddictian R2:355-37(i, 1997. SUTTON. S.R.. EISER, J.R. The effect of fear-arousing communications on cigarette smok- ing: An expectancy-value approach. Journal of Behavioral Medicine 7(1):13-33, March 1984. 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Another personality consttvct that received a great deal of attention earlier in the snx.king literature was Rotter's (1966) internal versus external locus-of-control dimen- sion (c.g.. Foss 1973. Rest and Steffy 1975; Rest 1975; Straits and Sechrest 1963). Two general hypotheses characterized work in this area. The first noted that smokers tended to have a more external locus of contr+nl, that is, perceive that things occur because of fate, not because of one's own actions, compared with txxt.cmokers. The second held that -,mukcrs with a greater internal locus of control, that is, a perception that things happen because of one's own actions, would he more successful in quitting. A review of thi- literatorc revealed inconsistent support for both hypotheses (Raer and Lich- tenstein 19RRh). Thc multidimensional health locus of control swk (Wallston, Wallston, DeVellis 1978) was an attempt to anchor the locus of control construct specifically to health be- havior consistent with the trend away from broad, dispositional traits (Mischcl 1973). Most studies using this scale examined the effect of health locus of control on cecca- tion attempts. Three investigations reported small but significant prospective rolation- ships between subscales of the Health Locus of Control Scale and maintenance of abstinence (Kaplan and Cowles 1978; Rosen and Shipley 1983; Shipley 198 1). A popular approach to understanding social or psychological problems has been through typologies. Tomkin's typology of smoking and affect regulation was v