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The Brookings Institution - Center for Public Policy Education IN COOPERATION WITH N THE INSTITUTE FOR THE STUDY OF SMOKING BEHAVIOR AND POLICY FORUM ON THE POLICY IMPLICATIONS o OF THE 1986 SURGEON GENERAL'S REPORT ON INVOLUNTARY SMOKING ~ MAY 18, 1987 N ~

THE INSTITUTE FOR THE STUDY OF SMOKING BEHAVIOR AND POLICY HARVARD UN!IVERSITY AND THE CENTER FOR PUBLIC POLICY EDUCATION THE BROOKINGS INSTITUTION FORUM ON THE POLICY IMPLICATIONS OF THE 1986 SURGEON GENERAL'S REPORT ON INVOLUNTARY SMOKING May 18, 1987

TABLE OF CONTENTS PREFACE LIST OF PARTICIPANTS . . . . . . . TAB 1 AGENDA .. . . . . . . . . . . . . . TAB 2 READING MATERIAL . . . . . . . . . TAB 3

PREFACE I Is I The purpose of this forum, sponsored jointly by Brookings and Harvard, is to expl!ore the implications of the Surgeon General's finding that involuntary smoking, the inhalation of tobacco smoke by nonsmokers, poses a serious healthirisk. The Report was issued on December 16, 1986, 'following the release of a report by the National Research Council of the National Academy of Sciences that reached similar conclusions. The major findings of the Surgeon General are: • Involuntary smoking is a cause of disease, including lung cancer, in healthy nonsmokers. • The children of parents who smoke, compared with the children of nonsmoking parents, have an increased frequency of respiratory infections and respiratory symptoms, and slightly smaller rates of increase in lung function as the lung matures. • Simple separation of smokers and nonsmokers within the same air space may reduce, but does not eliminate, exposure of non- smokers to environmental tobacco smoke. L I I I d I I I I The Surgeon General's Report comes at a time of increasing activity, in business and government, aimed at restricting or eliminati~ng smoking and the potential for exposure. Many state and local governments have adopted public and workplace smoking ordinances and the federal General Services Administration has issued regulations for builldings under its control. Many businesses have established policies on smoking on the job, and hospitals are beginniing to restrict smokiing for the benefit of their patients and their employees. Nonsmokers are exposed to environmental tobacco smoke at work, at home, and'in public places. Given this ubiquitous exposure and the general decline in smoking in the United States, the Surgeon General's Report raises important questions about the roles of business, labor, government, and medicine in protecting nonsmokers. In this forum, experts will explore what has been done and with what result, what further steps may be necessary, and~what limits if any, should apply to restricting or eliminating smoking, the source of the risk. We hope that these discussions will improve public appreciation of the issues involved.. ~ . o N 0 N . ov ~ _ ~

FORUM ON THE POLICY IMPLICATIONS OF THE 1986 SURGEON GENERAL'S REPORT ON INVOLUNTARY SMOKING' May 18, 1987 LIST OF PARTICIPANTS TENLEY E. ALBRIGHT Doctor 333 Longwood Avenue . Boston, Massachusetts 02115 MATILDA A. BABBITZ Executive Director American Association of Occupational Health Nurses 50 Lenox Pointe Atlanta, Georgia 30324 ANDREA BERMAN Research Assistant Institute for the Study of Smoking Behavior and Policy Harvard University Cambridge, Massachusetts JAMES F. CALLAHAN Special Assistant to the Deputy Director Division of Cancer Prevention and Control The National Cancer Institute Building Three, Room 10A49 9000 Rockville Pike Bethesda, Maryland 20892 PAUL CANO Assistant Director Government Relations American College of Cardiology 9111 Old Georgetown Road Bethesda, Maryland 20814 WILLIAM CHECK Medical-Science Writer Institute for the Study of Smoking Behavior and Policy. Harvard University Cambridge, Massachusetts FRANK M. CODA Executive Director ASHRAE 1791 Tullie Circle, N~.E. Atlanta, Georgia 30329 JEFF COHN Reporter Institute for the Study of Smoking Behavior and Policy Harvard University Cambridge, Massachusetts

 I  CONSTANCE T. CORDOVILLA Senior Program Coordinator Center for Corporate Public Investment American Council of Life Insurance Health Insurance Association of America Washington, D.C. 20004-2599 JOSEPH W. CULLEN Deputy Director Cancer Prevention and Control Division National Cancer Institute Room 10A49, Building 31 9000 Rockville Pike Bethesda, Maryland 20892 BURFORD W'. CULPEPPER Corporate Medical Director E.I. du Pont de Nemours & Company 11400 Nemours Building Wilmington, Delaware 19898 E.C. CURTIS Corporate Medical Director Westinghouse Electric Corporation Gateway Center Pittsburgh, Pennsylvania 15222 JEFF DAY Staff Editor Special Projects Bureau of National Af f airs 1231 25th Street, N.W. Washington, D.C. 20037 PAM DRUMHELLER Special Projects Coordinator Institute for the Study of Smoking Behavior and Policy Harvard University Cambridge, Massachusetts 2 ERVIN DUGGAN Ervin Duggan Associates Suite 300 1919 Pennsylvania Avenue, N.W. Washington, D.C. 20006 FRAN DU MELLE Director Government Relations American Lung Association Suite 402 1101 Vermont Avenue Washington, D.C. 20008 CHARLES P. DUVALL Trustee American Society of Internal Medicine Suite 500 1101 Vermont Avenue, N.W. Washington, D.C. 2.0005 ALAN L. ENGELBERG Director Department of Health American Medical Association 535 North Dearborn Street Chicago, Illinois 60610 ROBERT ENGELMAN Health Correspondent Scripps Howard News Service 1110 Vermont Avenue, N.W. Washington, D.C. 20005 ANN EWING Science Writer 3138 Military Road, N.W'. Washington, D.C. 20015

I IN a k r r w I I I I p I w HAYWARD D. FISK Vice President and Washington Counsel United Telecom Suite 1250 1875 I Street, N.W. Washington, D.C. 20006 LAURA FLINCHBAUGH Research Assistant Institute for the Study of Smoking Behavior and Policy Harvard University Cambridge, Massachusetts RIPLEY FORBES Senior Staff Associate Subcommittee on Health and the Environment U.S. House of Representatives Ro=512 House Annex One Washington, D.C. 20515 SANDI FRANKLIN Program Director IBM Corporation Suite 1200 1801 K Street, N.W. Washington, D.C. 20006 MARY R. GREALY Executive Counsel Federation of American Systems Suite 402 1111 19th Street, N.W. Washington, D.C. 20036 JACK HEFFERNAN Vice President Human Resources GTE Service Corporation One Stamford Forum Stamford, Connecticut 06904 3 BOB HEY Staff Writer The Christian Science Monitor 910 16th Street, N.W. Washington, D.C. 20006 LENORA E. JOHNSON Coordinator Anti-Tobacco Initiative American Public Health Association 1015 15th Street, N.W. Washington, D.C. 20005 RICHARD D. JOHNSON Director Health Programs U.S. Conference of Mayors 1620 Eye Street, N.W. Washington, D.C. 20006 JOHN T. KALBERER Coordinator for Disease Prevention Office of the Director National Institutes of Health Building One, Room 215 Bethesda, Maryland 20852 WILLIAM M. KANE Executive Director American College of Preventive Medicine Suite 403 1015 15th Street, N.W. Washington, D.C. 20005- LANA KATZ N American Federation of p Government Employees N Washington, D.C. a I" Lb k4l W ~

4 TED KLEIN Ted Klein and Company 740 Broadway New York, New York 10003 ROY MARDEN Manager of Industry Affairs Philip Morris, Inc. 120 Park Avenue New York, New York 10017 BILL KRUEGER Washington Correspondent The News & Observer Room 3806 2000 Pennsylvania Avenue Washington, D.C. 20006 ALVIN G. LAZEN Executive Director Commission on Life Sciences National Research Council 2101 Constitution Avenue, N.W. Washington, D.C. 20418 JULIETTE LENOIR Vice President Association of Flight Attendants 1625 Massachusetts Avenue, N.W. Washington, D.C. 20036 JAN LISS Executive Assistant to the Executive Director Consumers' Union 256 Washington Street Mt Vernon, New York 10553 LISA LOPEZ Business & Health 229 Pennsylvania Avenue, N.W. Washington, D.C. 200,03 ALFRED H. LOWREY Research Chemist Code 6030 Naval Research Laboratory Washington, D.C. 20375 ROBERT J. McCUNNEY Corporate Medical Director Cabot Corporation 950 Winter Street Post Office Box 9073 Waltham, Massachusetts 02254 PAUL E. MULLEN Director of Government Relations Joint Commission on Accreditation of Hospitals 875 North Michigan Avenue Chicago, Illinois 60611 NIREN L. NAGDA Vice President GEOMET 20251 Century Boulevard Germantown, Maryland 20874 JUDITH K. OCKENE Director Division of Preventive and Behavioral Medicine Department of Medicine University of Massachusetts Medical School Lake Avenue North Worcester, Massachusetts 01605 ANNE MARIE O'KEEFE Project Officer Advocacy Institute Suite 600 1730 M Street, N.W. Washington, D.C. 20036

5 TERRY F. PECHACER Program Director Community Trials for Smoking Cessation National Cancer Institute Ro=628, Blair Building 9000 Rockville Pike Bethesda, Maryland 20892 THOMAS P. SCHELLING Director Institute for the Study of Smoking Behavior and Policy Harvard University Cambridge, Massachusetts EDWARD L. PETSONK Medical Officer National Institute for Occupational Safety and Health 944 Chestnut Ridge Road Morgantown, West Virginia 26505 JOHN PINNEY Executive Director Institute for the Study of Smoking Behavior and Policy Harvard University Cambridge, Massachusetss JAMES L. REPACE Chief Technical Services Indoor Air Staff Environmental Protection Agency Room ANR 443 Washington, D.C. 20460 WILLIAM ROTHBARD Vice President Board of Directors Americans for Nonsmokers' Rights Washington, D.C. JULIE ROVNER Reporter Congressional Quarterly 1414 22nd Street, N.W. Washington, D.C. 20037 DONALD R. SHOPLAND Executive Editor Surgeon General's Report Office on Smoking and Health Department of Health and Human Services Park Building, Room 110 5600 Fishers Lane Rockville, Maryland 20857 GLORIAN SORENSEN Assistant Professor of Medicine Division of Preventive and Behavioral Medicine University of Massachusetts Medical Center 55 Lake Avenue North Worcester, Massachusetts 01605 CHARLES C. THARP Vice President General Investment Funds Suite 710 5454 Wisconsin Avehue, N.W. Chevy Chase, Maryland 20815 ANN TONJES Manager Government Affairs Association of Flight Attendants 1625 Massachusetts Avenue, N.W. Washington, D.C. 20036

6 WAYNE URY ANDREA M. HODSON Health Fellow Conference Coordinator Senate Committee on Labor Center for Public Policy and Human Resources Education 527 Hart Senate Office Building Washington, D.C. 20510 KENNETH E. WARNER Professor and Chair Department of Public Health Policy and Administration School of Public Health University of Michigan Ann Arbor, Michigan 48109 JAMES A. WHITE Vice President CIGNA Corporation One Logan Square, 27th Floor Philadelphia, Pennsylvania 19103 LORING WOOD Director Medical NYNEX 400 Westchester Avenue White Plains, New York 10604 LESTER E.YORK, JR. Manager Corporate Health Promotion Digital Equipment Corporation 150 Coulter Drive Concord, Massachusetts 01742 BROORINGS STAFF PETER MALOF Senior Staff Member N .~ Center for Public Policy ~ Education ~ ~ ~ ~ ~ W

FORUM ON THE POLICY IMPLICATIONS OF THE 1986 SURGEON GENERAL'S REPORT ON INVOLUNTARY SMOKING May 18, 1987 AGENDA 8:30 a.m. Registration and Coffee/Tea Main Lounge Brookings 9:00 a.m. WELCOMING REMARKS Aud~i tor i um Bruce K. MacLaury President The Brookings Institution 9:10 a.m. INTRODUCTION Auditorium, Thomas C. Schelling Professor of Political Economy and Director, Institute for the Study of Smoking Behavior and Policy Harvard University 9':3&a.m~. THE ROLE AND RESPONSE OF ORGANIZED LABOR Aud'itorium Moderator A. Lee Fritschler Director Center for Public Policy Education The Brookings Institution Discussion Panel John Dunlop Lamont University Professor Emeritus Harvard University Former U.S. Secretary of Labor Kenneth T. Blaylock President American Federation of Government Employees Michael A. Forscey General Counsel - Tobacco Industry Labor Management Committee

MONDAY, MAY 18, 1987 10~:55 a.m. Main Lounge 11:05 a.m. Aud i tor i um (continued) I Coffee/Tea Break THE ROLE AND RESPONSE OF MANAGEMENT Moderator Louis W. Cabot Chairman~ Board of Trustees The Brookings Institution Discussion Panel Gerald W. Blakeley, Jr. Chairman Inncorp Management Corporation Charles R. Nesson Professor of Law Harvard University Frank Bean Vice President Federal Express Corporation 12:3&p.m. Buffet Lunch Room 105, Main Lounge 1:30 p.m. THE ROLE AND RESPONSE OF GOVERNMENT Auditorium Moderator John Pinney Executive Director Institute for the Study of Smoking Behavior and Policy Harvard University Discussion Panel The Honorable Charles Rose (D) U.S. Representative Seventh District, North Carolina Chairman, Tobacco and Peanut Subcommittee Committee on Agriculture The Honorable J. Jarrett Clinton, M.D. Deputy Assistant Secretary of Defense for Health Affairs Department of Defense

MONDAY, MAY 18, 1987 (continued) Terence Golden Administrator General Services Administration Norman B. Rice Chairman Member of Seattle City Council 1 2:55 p.m. Coffee/Tea Break Main Lounge 3:05 p.m. THE ROLE AND RESPONSE OF THE HEALTH CARE SYSTEM Auditorium Moderator Henry Aaron Senior Fellow Economic Studies Program The Brookings Institution DiscussiomPanel William C. Montgomery, M.D. President American Academy of Pediatrics Mary Jane England, M.D. President American Medical Women's Association 4:30 p.m. SUMMARY Auditorium Thomas Schelling and Panel Moderators 5:00 p.m, Adjourn for Reception in the Main Lounge

I I 21 I I N I N I THE HEALTH CONSEQiTENCES OF INVOLUNTARY SMOIiING I a report of the Surgeon General 1986 PREPUBLICATION EDITION This copy is issued as a prepublication edilion containing no subject index. A tinal edition wilhh index will be available approximately eight weeks from dale of release. : ;#i U.S. GEPARTMENT OE HEALTH AND HUMAN SERVICES PubNt Heelth Senke i Cenlers /a Oisease Caw+lrol Cenlei /or Mba111i Prorerolion.nd Edueatlon •_ v rot:r...- e.....~i......w Il..in. - - - _ --.. - a•.(46 Rock.lUe, Marylarid 2057

-1, 1 M r 12 -. __M -M -.W M FOREWORD The data reviewed in 17 previous U.S. Public Ilealth Service reports on the health consequences of smoking have conclusively established cigarette smokinQ ns the largest single preventable cause of premature death and disability in the United States. The question whether tobacco smoke is harmful to smokers was answered more than 20 years ago. As a result, many scientists began to question whether the low levels of exposure to environmental tobacco smoke (El'S) received by nonsmokers could also be harmful. The current Iteport, The Ilealth Consequences of Involuntary Smoking, examines the evidence that even the lower exposure to smoke received by the nonsmoker carries with it a health risk. Use of the term "involuntary smoking" denotes that for many nonsmokers, exposure to ETS is the result of an unavoidable consequence of being in proximity to smokers. It is the first Report in the health consequences of smokh+g scries to establish a health risk due to tobacco smoke exposure fvr individuals other than the smoker, and represents the work of nwre than 60 distinguished physicians and scientists, both in this country and abroad. After careful examination of the available evidence, the following overall conclusions can lxr reached: 1. Involuntary smoking is a cause of disease, including lung cancer, in healthy nonsinokers.. 2. The children of parents who smoke, compared with the children of nonsmoking pnrents, have an increased frequency of respiratory inlections, increased respiratory symptoms, and slightly smaller rates of increase in lung function as the lung matu res: 3. Simple separation of snwkers and nonsmokers within the same air space may reduce, but does not eliminate, exposure of nonsmokers to envirommental tobacco smoke. Exposure to environmental tobacco smoke occurs at home, at the worksite, in public, and in othcr places where smoking is perrniited.

I r I U I I . -M 0 .U The quality of the indoor environment nnust be a concern of all who control and occupy that environment. Protection ol individuals from exposure to environmental tobacco smoke is therefore a responsibili- ty shared by all: • As parents and adults we must protect the health of our children by not exposing them to environmental tobacco smoke. %, • As employers and employees we must ensure that the act of smoking does not expose the nonsmoker to tobacco smoke. . For smokers, it is their responsibility to assure that their behavior does not jeopardize the health of others. • For nonsmokers, it is their responsibility to provide a support- ive environment for smokers who are attempting to stop. Actions taken by individuals, employers, and employee organiza- tions reflect the growing concern for protecting nonsmokers. The number of laws and regulations enacted at the national, State, and local level governing smoking in public has increased substantially over the past 10 years, and surveys conducted by numerous organizations show strong public support for these actions among both smokers and nonsmokers. As a Nation, we have made substantial progress in addressing the enormous toll inflicted by active smoking. lalorts to improve and protect individual health must not only be cuntinued but strength- ened: On the basis of the evidence presented in this Report, it is clear that actions to protect nonsmokers from Cl'S exposure not only are warranted but are essential to protect public health. _ Robert E. Wiiidom, M.D. Assist:mt Secret.ary for llealth

r a W 1'REFACE This, the 1986 Report of Uie Surgeon General, is the U.S. Public Health Service's 18th in the health consequences of smoking series and the 5th issued during my tenure as Surgeon General. Previous Reports have documented the tremendous health burden to society front smoking, particularly cigarette smoking. The evi- dence establishing cigarette smoking as the single largest preventa- ble cause of premature death and disability in the United States is overwhelrninR-totaling more than 50,000 studies from dozens of cultures. Smoking is now known to be causally related a a variety of cancers in addition to lung cancer; it is a cause of cardiovascular disease, particularly coronary heart disease, and is the major cause of chronic obstructive lung disease. It is estimated that smoking is responsible for well over 300,000 deaths annually in the United States, representing approximately 15 percent of all mortality. Thirty years ago, however, the scientific evidence linking smoking with early death and disubilit:v was more limited. By 1964. the year the Advisory Committee to the Surgeon General issued the first rehos-t un smoking and health, a substantial body of evidence had accumulated upon which a judgment could be made that smoking wrts a cause of disease in active smokers. Subsequent reports over the last 20 years have expanded our understanding and knowledge about smoking behavior, the toxicity and carcinogenicity of tobacco smoke, and the specific disease risks resulting from exposure to this ngent. This Report is the first issued since 1964 that identifies a chronic disease risk resulting from exposure to tobacco smoke for individuals other than smokers. lt is now clear that disease risk due to the inhalation of tobacco smoke is not limited to the individual who is smoking, but can extend to those who inhale tobacco smoke emitted into the air. This Report represents a detailed review of the health effects resulting from nonsmoker exposure to environmental tobacco smoke (ETS). E`I5 is the combination of smoke emitted from a burning tobacco product between puffs (sidestream smoke) and the smoke exhaled by Ute smoker. The 1986 Report, The Health Consequences of Involuntary Smoking, is a critical review of all the available scientific evidence pertaining to the health effects of ETS exposure on nonsmokers.'!`he term "involuntary smoking" is used to

 _r  _ar . _W M 0 I I I 1 -I I I I N note that such exposures often occur as an unavoidable consequence of being in close proximity to smokers. Lung Cancer and Environmental Tobacco Smoke The appropriate framework for an examination of Elie lung cancer risk from involuntary smoking is lhat of a low-dose exposure to a known human carcinogen. Over 30 years of research have conclu- sively established cigarette smoke as a carcinogen. This Report presents evidence thal the clrenrical comtrvsition of sidestream smoke is qualitatively similar to the mainstream smoke inhaled by the active smoker, and that both mainstream and sidestrearn smoke act as carcinogens in bioassay systems. Uata related to environmen- tal levels of tobacco smoke constituents and from measures of nicotine absorption in nonsmokers suggest that nonsmokers are exposed to levels of environmental tobacco smoke that would be expected to generate a Iuirg cancer risk; epidemiological studies of populations exposed to CI'S have documented an increased risk for lung cancer in those nonsmokers with increased exposure. It is rare to have such detailed exposure data or hunian epidemio- logic studies on disease occurrence when atterupling to evaluate the risk of low-dose exposure to an agent with established toxicity at higher levels of exposure. The relative abunilance of data reviewed in this Report, their cohesiveness, and their biologic plausibility allow a judgment that irivoluntary smoking can cause lung cancer in nonsmokers. Although the number of lung cnncers due to involun- tary smoking is smaller tlran that due to active smoking, it still represents a number sufficiently large to geuerate substantial public health concern. It is certain that a substantial proportion of Elie lung cancers that occur in nonsmokers are due to Cl'S exposure; however„ more complete data on Elie dose and vnriability of smoke exposure in Elie nonsmoking l1 S. population will be needed before a quantitalive estimate of the number of such cancers can be made. Children and Infants This Report also documents a relationship between parental smoking and the respiratory health of infants and children (under 2 years of age). Infants of parents who smoke have an increased risk of hospitalization for bronchitis and pneurnonia when compared with infants of nonsmoking parents. There is a relationship between parental smoking and an increased frequency of respiratory synrp- toms in children. A slower rate of growth in lung function has been observed in children of smoking p:rrents. In many studies, if both \

0 N N N N N parents smoke, a stronger relationship exists tisan if only one parent smokes. What future respiratory burden these findinga may represent for these children later in life is not known. As a former pediatric surgeon, I strongly urge parents to refrain from smoking in the presence of children as a tneans of prolecting not only their children's current health status but also Urcir own. Diseases Other Than Lung Cancer Several studies have provided data on the relationship between CI'S and cancers other tlian lung cancer and on ETS exposure and cardiovascular disease. I lowever, further research in these areas will be required to determine whether an nssociation exists between CI'S exposure and an increased risk of developing these diseases. Policies Restricting Smoking In Public Places The growth in our understnnding of the disense risk associated with involuntary smoking has been accompanied by a change in tlre social acceptability of smoking and by a growing body of legislation,, regulation, and voluntary action that addresses where smoking may occur in public. Forty States and the District of Columbia now have some form of legislation controiling or restricting smoking in various public settings. Some Strites limit snroking to only a few designated areas; however, States are increasingly developing and implement- ing comprehensive legislation that restricts smoking in many public settings, including the worki)lace. Nine States have restrictions that cover smoking not only by public employees but also by employees in the private sector. No systematic evaluation of the effects these measures may have on smoking behavior has been conducted; but there is little doubt that strong public sentiment exists for implementing such restric- tions. A number of national surveys conducted by voluntary health organWations, government ai;encies, nnd even the tobacco industry have documented that an overwhelming majority of both smokers and nonsmokers support restricting smoking in public. Public Health Policy and Involuntary Smoking The 1986 SSurgeon General's fteport on the llealth Consequences of Involuntary Smoking clearly documents that nonsmokers are placed at increased risk for developing disease as the result of exposure to environmental tobacco smoke. Critics often express thit more research is required, that certain studies are f]awed, or that we should delay action until more conclusive proof is produced: As both a physician and a public health \

official, it is my judgment that the time for delay is past; measures to protect the public health are required now. The scientific case against involuntary smoking as a health risk is more than sufficient to justify appropriate remedial action, and the goal of any remedial action must be to protect the •nonsmoker from environmental tobacco smoke. The data contained in this Report on the rapid diffusion of tobacco smoke throughout an enclosed environment suggest that separation or smokers and nonsmokers in the same room or in different rooms that share the same ventilation system may reduce ETS exposure but will not eliminate exposure. The responsibility to protect the safety of the indoor environment is shared by all who occupy or control that environment. Changes in smoking policies regarding the workplace and other environments necessitated by the data presented in this Report should not be designed to punish the smoker. Successful implementa- tion of protection for the nonsmoker requires the support and cooperation of smokers, nonsmokers, management, and employees and should be developed through a cooperative effort of all groupss affected. ln addition, changes are often more effective when support and assistance is provided for the smoker who wants to quit. Cigarette smoking is an addictive behavior, and the individual smoker must decide whether or not to continue that behavior; however, it is evident from the data presented in this volume that the choice to smoke cannot interfere with the nonsmokers' right to breathe air free of tobacco smoke. The right of smokers to smoke ends where their behavior affects the health and well-being of others; furthermore, it is the smokers' responsibility to ensure that they do not expose nonsmokers to the potential harmful effects of tobacco smoke. C. Everett Koop, M.D. Surgeon Ceneral

1 TABLE OT CONTENTS Foreword .............................................................. vii Preface .......................................,.......................... ix Acknowledgments.................................................. . xiii Qlntroduction , Ov erview, and Summary and Conclusions ........................................................ 1 2. Health Effects of Environmental Tobacco Smoke Ex- posure ............................................................. 17 3. Environmental Tobacco Smoke Chemistry and Expo- sures of Nonsmokers ........................................ 119 4. Ueposition and Absorption of Tobacco Smoke Constit- uents ....:........................................................ 175 5. Toxicity, Acute Irritant Effects, and Corcinogenicity of Environmental Tobacco Smoke ....................... 223 6. Policies Restricting Smoking in Public Places and the Workplace ....................................................... 259

1 I I I ~ f CHAPTER i a I INTRODUCTION, OVERVIEW, I AND SUMMARY AND CONCLUSIONS

I I CONTENTS lntroduction Development and Organization of the 1986 Report p Overview Environmental Tobacco Smoke Constitutents Extent of Exposure Lung Cancer . Respiratory Disease Cardiovascular Disease Irritation Determinants of Exposure Policies Restricting Smoking Summary and Conclusions of the 1986 Report Ileallh Effects of Environmental Tobacco Smoke. Exposure Environmental Tobacco Smoke Chemistry and Exposures of Nonsmokers Deposition and Absorption of Tobacco Smoke Constit- uents Toxicity, Acute Irritaiit L•'ffects, and Carcinogenicity of Environmental! Tobacco Smoke Policies Restricting Smoking in Public Places and the Workplace

Introduction Development and Organization of the 1986 Iteport The 1986 Report was developed by the Office on Smoking and llealth of the U.S. DeparUnent of /lealth and Human Services as part of the Uepartment's reshonsibility, under Public Law 91-222, to report new and current information on smoking and health to Lite United States Congress. The scientific content of this Report reflects the contributions of more than 60 scientists representing a variety of disciplines. individual manuscripts were written by experts known for their understanding of and work in specific content areas. These maiiu- scripts were refined through a series of meetings attended by the authors, OfGce on SAioking llealth staff and consultants, and the Surgeon General. Upon receipt of Lite final manuscripts frorm Lite authors, the Office and its consultants edited and consolidated the individual manu- scripts into appropriate chapters. These draft chapters were subjec- ted to an extensive outside peer review (see Acknowledgments for individuals and their afliliations) whereby each was reviewed by up to seven experts. Their comments were integrated and Lite entire volume was assembled. This revised edition of Lite Report was resubjected to review by l7 distinguished scientists outside the Federal Government, both in this country and abroad. Parallel to this review, the entire Report was also submitted to various institutes and agencies within the U.S. Public Health Service for review and comment. The 1986 Report cotrt:aiiis a Foreword by the Assistant Secretary for Health, a Preface by the Surgeon General of the U.S. Public IlealtlrService, and the followiiig chapters: Chapter 1. Introduclion, Overview, and Summary and Conclu- sions Chapter 2. l lealth Effects of Environmental Tobacco Smoke Exposure Chapter 3. Environinental Tobacco Smoke Chemistry and Expo- suresof Nonsmokers Chapter 4. Deposition and Absorption of Tobacco Smoke Constit- - uents Chapter 5. Toxicity, Acute Irrit:ant Effects, and Carcinogenicity of Environmental Tobacco Smoke Chapter 6. Policies Restricting Smoking in Public Places and the Workplace Overview Inhalation of tobacco smoke during active cigarette smoking remains the largest single preventable cause of death and disability

I I ; t I f r I /or the U.S. }rulrulutiun. Tlre health currsertuences of cigarette smoking and of the use of other tobacco products have been extensively documented in the 17 previous Reports in the health consequences of smoking series issued by the 'J.S. Public ilealtli Service. Cigarette smoking is a major cause or cancer; it is most strongly associated with cancers of the lung and respiratory tract, but also causes cancers at other sites, including the pancreas and urinary bladder. It is the single greatest cause of chronic obstructive lung diseases. It causes cardiovascular diseases, including coronary heart disease, aortic aneurysm, and alherosclerotic peripheral vascular disease. Maternal cigarette smoking endangers felal and neon-Mal health; it contributes lo perinatal mortality, low birth weight, and complications during pregnancy. More than 300,UUU prenrature dealhs occur in the United States each year that are directly attribut:able to tobacco use, particularly cigarette smoking. This Report examines in detail the scienlif ic evidence on involun- tary smoking as a potential cause of disease in nonsmokers. Nonsnrokers' exposure to environmental tobacco smoke is termed involuntary snroking in this Report because the exposure generally occurs as an unavoidable consequence of being in proximity to smokers, particularly in enclosed indoor envirorrments. The term "passive smokitig"'is also used throughout the scientific literature to describe this exposure. The magnitude of the disease risks for active smokers secondary to their "high dose" exposure to tobacco smoke suggests that the "Io.ver dose" exposure to tobacco smoke received by involuntary smokers may also have risks. Allhoul;h the risks of involuntary smoking are smaller than lhe risks of active smokiirg, the number of indi'viduals injured by involuntary smoking is larf;c both in absolute lerms ancl in comparison with the number injured by some other agents in the general environment thut are regulated to curtail their potential to cause human illness. This Report reviews the evidence on the characteristics of main- stream tobacco smoke and of environmmrtal tobacco smoke, on the levels of exposure to environmental tobacco smoke that occur, and on the health effects of involuntary exposure to tobacco smoke. The composition of lhe tobacco smoke inhaled by active smokers and by involuntary smokers is examined fur similarities and differences, and the concentrations of tobacco smoke components that can be measured in a variety of settings are explored, us is smoke deposition and absorption in the respiratory tract. The studies that describe the risks of environmental tobacco smoke exposure for humans are carefully reviewed for their findings and their validity. The evidence on the health effects of involuntary smoking is reviewed for biologic plausibility, and compared with extrapolations of the risks of active

snrukint; to the luwer duse ol exlxrsure tu tub:rctv smoke IuunJ itr nonsmokers. This review leads to three major conclusions: 1. Involuntary smoking is a cause of disease, including lung cancer, In hcalthy nonsmokers. 2. The children of parents who smoke compared with the children of nonsmoking parents have an increased frequency of respiratory infections, increased respira- tory symptoms, and slightly smaller rates of increase in lung function as the lung matures. 3. The simple separntion of smokers and nonsmukers " within the same air space mny reduce, but clves not elimirrate, the exposure of nonsmokers to envirowimen- tal tobacco smoke. The subsequent chapters of this volume describe in detail the evidence Lhat supports these conclusions; the evidence is briefly summarized here. Envirorunental Tobacco Smoke Constituents lmportant considerations in exarnining the risks of involunt.ar,y smoking are the corrrtwsitivn of environmental tobacco smoke (L I'S) and its toxicity and curcincrgenicity relative to the tobacco smoke inhaled by active smokers. Mainstream cigarette smoke is the smoke drawn through the tobacco into the smoker's mouth. Sidestream smoke is the smoke emitted by the burning tobacco between pulfs. Environmental tob.lcco smoke results from the combination of sidestream smoke und the /raction of exlialed mainstream smnke nott retained by the srnuker. irt contrast with mainstream smoke, ETS is diluted into a lar6er volume of air, and it ages prior to inhalation. The cornparison of the chemical composition of the smoke inhaled by active smokers with that inlraled by involuntary smokers suggests that the toxic and carcinogenic effects are qualitatively similar, a similarity that is not too suriwisinK because both mainstream smoke and environmental tobacco smoke result from the combustion of tobacco. Individual mainstream smoke constituents, with appropri- ate testing, have usually been tound in sidestream smoke as well. Ilowever; differences between sidestream smoke and mainstrenm smoke hnve been well documented. The ternperature.of combustion during sidestream smoke formatibn is lower than during main- stream smoke formation. As a result, Rreateramounts of many of the organic constituents of smoke, including some carcinogens, are generated when tobacco burns and forms sidestrearn smoke than when mainstream smoke is produced. For example, in contrast with mainstream smoke, sidestream smoke contains greater amounts of arnmonia, benzene, carbon monoxide, nicotine, and the carcinogens

2-napthylamine, 4-aminobiphenyl, N-nitrosamine, benzja} anthracene, and benzo-pyrene per milligram of tobacco burned. Although only limited bioassay data comparing mainstream smoke and sidestream smoke are available, one study has suggested that sidestream smoke may be more carcinogenic. Extent of Exposure Although sidestream smoke and mainstream smoke differ some- what qualitatively, the differing quantitative doses of smoke compo- nents inhaled by the active smoker and by the involuntary smoker are of greater importance in considering the risks of the two exposures. A number of different markers for tobacco smoke exposure and absorption have been identified for both active and involuntary smoking. No single marker quantifies, with precision, the exposure to each of the smoke constituents over the wide range of environmental settings in which involuntary smoking occurs. However, in environments without other significant sources of dust, respirable suspended particulate levels (RSP) can be used as a marker of smoke exposure. Levels of nicotine and its metabolite cotinine in body fluids provide a sensitive and specific indication of recent whole smoke exposure under most conditions. Widely varying levels of environmental tobacco smoke can be measured in the home and other environments using markers. The time•activity patterns of nonsmokers, which indicate the time spent in environments containing ETS, also vary widely. Thus, the extent of exposure to ETS is probably highly variable among individuals at a given point in time, and little is known about the variation in exposure of the same individual at different points in time. Lung Cancer - The American Cancer Society estimates that there will': be more than 135,000 deaths from lung cancer in the United States in 1986, and 85 percent of these lung cancer deaths are directly attributable to active cigarette smoking. Therefore, even if the number of lung cancer deaths caused by involuntary smoking were much smaller than the number of lung cancer deaths caused by active smoking„the number of lung cancer deaths attributable to involuntary exposure would still represent a problem of sufficient magnitude to warrant substantial public health concern. Exposure to environmental tobacco smoke has been examined in numerous recent epidemiological studies as a risk factor for lung cancer in nonsmokers. These studies have compared the risks for subjects exposed to ETS at home or at work with the risks for people not reported to be exposed in these environments. Because exposure to ETS is an almost universal experience in the more developed countries, these studies involve compnricon of more exposed nnci less

exposed people, rather than comparison of exposed and unexposed people. Thus, the studies are inherently conservative in assessing the consequences of exposure to E75. Interpretation of these studies must consider the extent to which populations with different ETS exposures have been identified, the gradient in ETS exposure from the lower exposure to the higher exposure groups, and the magni- tude of the increased lung cancer risk that results from the gradient in ETS exposure. To date, questionnaires have been used to classify ETS exposure. Quantification of exposure by questionnaire, particularly lifetime exposure, is difficult and has not been•validated. However, spousal and parental smoking status identify individuals with different levels of exposure to ETS. Therefore, investigation has focused on the children and nonsmoking spouses of smokers, groups for whom greater ETS exposure would be expected and for whom increased nicotine absorption has been documented relative to the children and nonsmoking spouses of nonsmokers. Of the epidemiologic studies reviewed in this Report that have examined the question of involuntary smoking's association with lung cancer, most (11 of 13) have shown a positive association with exposure, and in 6 the association reached statistical significance. Given the difficulty in identifying groups with differing ETS exposure, the low-dose range of exposure examined, and the small' numbers of subjects in some series, it is not surprising that some studies have found no association and that in others the association did not reach a conventional level of statistical significance. The question is not whether cigarette smoke can cause lung cancer; that question has been answered unequivocally by examining the evi- dence for active smoking. The question is, rather, can tobacco smoke at a lower dose and through a different mode of exposure cause lung cancer in nonsmokers? The answer must be sought in the coherence and trends of the epidemiologic evidence available on this low-dose exposure to a known human carcinogen. in general, those studies with larger population sizes, more carefully validated diagnosis of lung cancer, and more careful assessment of ETS exposure status have shown statistically significant associations. A number of these studies have demonstrated a dose-response relationship between the level of ET5 exposure and lung cancer risk. By using data on nicotine absorption by the nonsmoker, the nonsmoker's risk of developing lung cancer observed in human epidemiologic studies can be compared with the level of risk expected from an extrapolation of the dose-response data for the active smoker. This extrapolation yields estimates of an expected lung cancer risk that approximate the observed lung cancer risk in epidemiologic studies of involuntary smoking.

Cigarette smoke is well established as a human carcinogen. The chemical composition of EI'S is qualitatively similar to mainstream smoke and aidestream smoke and also acts as a carcinogen in bioassay systems. For many nonsmokers, the quantitative exposure to ETS is large enough to expect an increased risk of lung cancer to occur, and epidemiologic studies have demonstrated an increased lung cancer risk with involuntary smoking. In examining a low-dose exposure to a known carcinogen, it is rare to have such an abundance of evidence on which to make a judgment, and given this abundance of evidence, a clear judgment can now be made: exposure to ETS is a cause of lung cancer. The data presented in this Report establish that a substantial number of the lung cancer deaths that occur among nonsmokers can be attributed to involuntary smoking. However, better data on the extent and variability of ETS exposure are needed to estimate the number of deaths with confidence. Respiratory Disease Acute and chronic respiratory diseases have also been linked to involuntary exposure to tobacco smoke; the,evidence is strongest in infants. During the first 2 years of life, infants of parents who smoke are more likely than infants of nonsmoking parents to be hospital- ized for bronchitis and pneumonia. Children whose parents smoke also develop respiratory symptoms more frequently, and they show small, but measurable, differences on tests of lung function when compared with children of nonsmoking parents. Respiratory infections in young children represent a direct health burden for the children and their parents; moreover„ these infec- tions, and the reductions in pulmonary function found in the school- age children of smokers, may increase susceptibility to develop lung diseased as an adult. Several studies have reported small decrements in the average level of lung function in nonsmoking adults exposed to ETS. These differences may represent a response of the lung to chronic exposure to the irritants in ETS, but it seems unlikely that ETS exposure, by itself, is responsible for a substantial number of cases of clinically significant chronic obstructive lung disease. The small magnitude of the changes associated with ETS exposure suggests that only individuals with unusual susceptibility would be at risk of develop- ing clinically evident disease from ETS exposure alone. However, ETS exlrnure may be a factor that contributes to the development of clinical disease in individuals with other causes of lung injury. Cardiovascular Disease A few studies have examined the relationship between involun- tary smoking and cardiovascular disease, but no firm conclusion on

the relationship can be made owing to the limited number of deaths in the studies. Irritation Perhaps the most common effect of tobacco smoke exposure is tissue irritation. The eyes appear to be especially sensitive to irritation by ETS, but the nose, throat, and airway may also be affected by smoke exposure. Irritation has been demonstrated to occur at levels that are similar to those found in real-life situations. The level of irritation increases with an increasing concentration of smoke and duration of exposure. In addition, participants in surveys report irritation and annoyance due•to smoke in the environment under real-life situations. Determinants of Exposure Exposure to ETS has been documented to be common in the United States, but additional data on the extent and determinants of exposure are needed to identify individuals within the population who have the highest exposure and are at greatest risk. Studies with biological markers and measurements of ETS components in indoor air confirm that measurable exposure to ETS is widespread. How- ever, within exposed populations, levels of cotinine excretion and presumably ETS exposure vary greatly. In a room or other indoor area, the size of the space, the number of smokers, the amount of ventilation, and other factors determine the concentration of tobacco smoke in the air. The technology for the cost-effective filtration of tobacco smoke from the air is not currently available, and because of their small size, the smoke particles remain suspended in tl.ie air for long periods of time; thus, the onlyy way to remove smoke from indoor air is to increase the exchange of indoor air with clean outdoor air. The number of air changes per hour required to maintain acceptable indoor air quality is much higher when smoking is allowed than when smoking is prohibited. Environmental tobacco smoke originates at the lighted tip of the cigarette, and exposure to ETS is greatest in close proximity to the smoker. However, the smoke rapidly disseminates throughout any airspace contiguous with the space in which the smoking is taking place. Dissemination of smoke is not uniform, and substantial gradients in ETS levels have been demonstrated in different parts of the same airspace. The time course of tobacco smoke dissemination is rapid enough to ensure the spread of smoke throughout an airspace within an 8-hour workday. In the home, the presence of even one smoker can significantly increase levels of respirable suspended particulates. These data lead to the conclusion that the simple separation of smokers and nonsmokers within the same airspace will reduce, but

not eliminate, exposure to !;l'S, particularly in those settinge where exposure is prolonged, such as the working environment. The exposure of an individual nonsmoker to ETS is also deter- mined by that person's time-activity pattern; that is, the amount of time spent in various locations. For adults, the duration of time spent in smoke-contaminated environments at work or at home is the principal determinant of ETS exposure, along with the levels of smoke in those environments. For infants and very young children, the smoking habit of the primary caretaker, as well as that person's time-activity pattern, is likely to play a major role in determining ETS exposure. Policies Restricting Smoking Policies regulating cigarette smoking with the objective of reduc- ing explosion or Gre risk, or of safeguarding the quality of manufac- tured products, have been in force in a number of States since the late 1800s. More recently, and with steadily increasing frequency, policies regulating smoking on the basis of the health risk or the irritation of involuntary smoking have been promulgated. State and local governments have enacted laws and regulations restricting smoking in public places. These policies have been implemented with few problems and at little cost to the respective governments. The public awareness of these policies that results from the media coverage surrounding their implementation proba- bly facilitates their self-enforcement. Public awareness may best be fostered by encouraging the establishment of these changes at the local level. Policies limiting smoking in the worksite have also become increasingly widespread and more restrictive. However, changes in worksiUe policies have evolved largely through voluntary rather than governmental action. In a steadily increasing number of worksites, smoking has been prohibited completely or litnited too relatively few areas within the worksite. The creation of a smoke- free workplace has proceeded successfully when the policy has been jointly developed by employees, employee organizations, and man- agement; instituted in phases; and accompanied by support and assistance for the smokers to quit smoking. This trend to protect nonsmokers from ETS exposure may have an added public health benefit-helping those smokers who are at- tempting to quit to be more successful and not encouraging smoking by people entering the workforce. Summary and Conclusions of the 1986 Report The three major conclusions of this report are the following:

1. Involuntary smuking is a cause of disease, including lung cancer, in healthy nonsmokers. 2. The children of parents who smoke compared with the ' children of nonsmoking parents have an increased frequency of respiratory infections, increased respira- tory symptoms, and slightly smaller rates of increase in lung function aa the lung matures. 3. The simple separation of smokers and nonsmokers within the same air space may reduce, but does not eliminate, the exposure of nonsmokers to environmen• tal tobacco smoke. Individual chapter summaries and conclusions follow. Health Effects of Environmental Tobacco Smoke Exposure 1. Involuntary smoking can cause lung cancer in nonsmokers. 2. Although a substantial number of the lung cancers that occur in nonsmokers can be attributed to involuntary smoking, more data on the dose and distribution of ETS exposure in the population are needed in order to accurately estimate the magnitude of risk in the U.S. population. 3. The children of parents who smoke have an increased frequen- cy of hospitalization for bronchitis and pneumonia during the first year of life when compared with the children of nonsmok- ers. 4. The children of parents who smoke have an increased frequen- cy of a variety of acute respiratory illnesses and infections, including chest illnesses before 2 years of age and physician- diagnosed bronchitis, tracheitis, and laryngitis, when com- pared with the children of nonsmokers. 5. Chronic cough and phlegm are more frequent in children whose parents smoke compared with children of nonsmokers. The implications of chronic respiratory symptoms for respira- tory health as an adult are unknown and deserve further study. 6. The children of parents who smoke have small differences in tests of pulmonary function when compared with the children of nonsmokers. Although this decrement is insufficient to cause symptoms, the possibility that it may increase suscepti- bility to chronic obstructive pulmonary disease with exposure to other agents in adult life, e.g., active smoking or occupation- al exposures, needs investigation. 7. }{ealthy adults exposed to environmental tobacco smoke may have small changes on pulmonary function testing, but are unlikely to experience clinically significant deficits in pulmo-

nary function as a result of exposure to environmental tobacco smoke alone. 8. A number of studies report that chronic middle ear effusions are more common in young children whose parents smoke than in children of nonsmoking parents. 9. Validated questionnaires are needed for the assessment of recent and remote exposure to environmental tobacco smoke in the home, workplace, and other environments. 10. The associations between cancers, other than cancer of the lung, and involuntary smoking require further investigation before a determination can be made about the relationship of involuntary smoking to these cancers. 11. Further studies on the relationship between involuntary smoking and cardiovascular disease are needed in order to determine whether involuntary smoking increases the risk of cardiovascular disease. Environmental Tobacco Smoke Chemistry and Exposures of Nonsmokers - 1. Undiluted sidestream smoke is characterized by significantly higher concentrations of many of the toxic and carcinogenic compounds found in mainstream smoke, including ammonia, volatile amines, volatile nitrosamines, certain nicotine decom- position products,,and aromatic amines. 2. Environmental tobacco smoke can be a substantial contributor to the level of indoor air pollution concentrations of respirable particles, benzene, acrolein, N-nitrosamine, pyrene, and carbon monoxide. ETS is the only source of nicotine and some N- nitrosamine compounds in the general environment. 3. Measured exposures to respirable suspended particulates are higher for nonsmokers who report exposure to environmental tobacco smoke. Exposures to E'I'S occur widely in the non- smoking population. 4. The small particle size of environmental tobacco smoke places it in the diffusion-controlled regime of movement in air for deposition and removal mechanisms. Because these submicron particles will follow air streams, convective currents will dominate and the distribution of ETS will occur rapidly through the volume of a room. As a result, the simple separation of smokers and nonsmokers within the same airspace may reduce, but will not eliminate, exposure to ETS. 5. It has been demonstrated that ETS has resulted in elevated respirable suspended particulate levels in enclosed places.

Deposition and Absorption of Tobacco Smoke Constituents 1. Absorption of tobacco-specific smoke constituents (i.e., nicotine) from environmental tobacco smoke exposures has been docu- mented in a number of samples of the general population of developed countries, suggesting that measurable exposure to environmental tobacco smoke is common. 2. Mean levels of nicotine and cotinine in body fluids increase with self-reported ETS exposure. 3. Because of the stability of cotinine levels measured at different times during exposure and the availability of noninvasive sampling techniques, cotinine appears to be the short-term marker of choice in epidemiological studies. 4. Both mathematical modeling techniques and experimental data suggest that 10 to 20 percent of the particulate fraction of sidestream smoke would be deposited in the airway. 5. The development of specific chemical assays for human expo- sure to the components of cigarette tar is an important research goal. Toxicity, Acute Irritant Effects, and Carcinogenicity of Environmental Tobacco Smoke 1. The main effects of the irritants present in ETS occur in the conjunctiva of the eyes and the mucous membranes of the nose,, throat, and lower respiratory tract. These irritant effects are a frequent cause of complaints about poor air quality due too environmental tobacco smoke. 2. Active cigarette smoking is associated with prominent changes in the number, type, and function of respiratory epithelial and inflammatory cells; the potential for environmental tobacco smoke exposure to produce similar changes should be investi- gated. 3. Animal models have demonstrated the carcinogencity of ciga- rette smoke, and the limited data that exist suggest that more carcinogenic activity per milligram of cigarette smoke concen- trate may be contained in sidestream smoke than in main- stream cigarette smoke. Policies Restricting Smoking in Puulic Places and the. Workplace 1. Beginning in the 1970s, an increasing number of public and private sector institutions have adopted policies to prot'ect individuals from environmental tobacco smoke exposure by restricting the circumstances in which smoking is permitted. 2. Smoking in public places has been regulated primarily byy government actions, which have occurred at Federal, Stale,.

and local levels. All but nine States have enacted laws regulating smoking in at least one public place. Since the mid- 1970s, there has been an increase in the rate of enactment and in the comprehensiveness of State legislation. Local govern- ments have enacted smoking ordinances at an increasing rate since 1980; more than 80 cities and counties have smoking laws in effect. 3. Smoking at the workplace is regulated by a combination of government action and private initiative. Legislation in 12 States regulates smoking by government employees, and 9 States and more than 70 communities regulate smoking in the private sector workplace. Approximately 35 percent of busi- nesses have adopted smoking policies. The increase in work- place smoking policies has been a trend of the 1980s. 4. Smoking policies may have multiple effects. In addition to reducing' environmental tobacco smoke exposure, they may alter smoking behavior and public attitudes about tobacco use. Over time, this may contribute to a reduction in smoking in the United States. To the present, there has been relatively little systematic evaluation of policies restricting smoking in public places or at the workplace. 5. On the basis of case reports and a small number of systematic studies, it appears that workplace smoking policies improve air quality, are met with good compliance, and are well accepted by both smokers and nonsmokers. Policies appear to be followed by a decrease in smokers' cigarette consumption at work and an increase in enrollment in company-sponsored smoking cessation programs. 6. Laws restricting smoking in public places have been imple- mented with few problems and at little cost to State and local government. Their impact on smoking behavior and attitudes has not yet been evaluated. 7. Public opinion polls document strong and growing support for restricting or banning smoking in a wide range of public places. Changes in attitudes about smoking in public appear to have preceded legislation, but the interrelationship of smoking attitudes, behavior, and legislation are complex.