Tobacco Documents Online

FALK, Hans II,.,, Ph.D:, - Associate Director for Program,, National Institute of Environ- mental Health Sciences, Research Triangle Park, N:C. FERRIS, Benjamin G.,,Jr., M.D: - Professor of EnvironmentaliHealth andlSafety,,School of Public,Health, Harvard Uhiversity, Boston„Mass. GOLDSMITH,, John R., M'.D: - Medical Epidemiologist, Epidemiological Studies Labora- tory, California State Department of H'ealth, Berkeley, Calif. GORI„Gio B'.,,Ph.D. - Deputy Director, Division of'Cancer Cause and Prevention„National Cancer Institute,,National lhstitutes of Healtfi, Bethesda,,Md. HARKE„ H:: P:, Ph.D., - Forschunginstitutl der Cigarettenindustrie, e.V:,, Hamburg, Germany. HIGGINS,, Ian T. T., M.D. - Professor of Epidemiology, School of Public Health„Uhiversity ofl Michigan, Ann ~ Arbor, Mich:. HOFFMANN,, Dietrich, Ph.D:, - Member,, and Chief, Division of Environmental Careino- genesis, Naylor Dana Institute for Disease Prevention, American Health Foundation; Valhalla, N.Y. KELLER; Andrew Z., D:M.Di - Chiet, Research, in Geographic Epidemiology Medical Research,Service; Veterans Administration,Central Office„Washingtons D'.C. KRUM1-IOLZ, Richard A., M.'.D:, - Medical Director, Ihstitute of Respiratory Diseases, Kettering Medical Center„Kettering; Ohio. LENFANT, Claude J. M., M'.D: - Associate Diuector for Lung,Progams; National Heart and Lung Institute„National Institutes of Health, Bethesda, Md. MacMAHON, Brian, MID. - Professor; Department of Epidemiology, School of Public Health, Harvard University„Boston, Mass. M'cIvIILLAN, Gardher, C., M'.D; - Associate Director for Etiology of Arteriosclerosis and Hypertension;, National Heart and I6ung; Institute, National Institutes of Health,. Bethesda,, Md. NETTESHEIM, Paul', MID. - Group Leader, Respiratory Carcinogenesis Group, Biology Divisiony, Oak Ridge NationaL Laboratory, Oak Ridge,, Tenn. PAFFENBARGER, Ralph S.,, Jr., M.D. - Epidemiolbgist„ Resource for Cancer Epidemi- ology„California State Department of Health, Berkeley, Califl PETTY, Thomas L.,, M.D. - Professor of Medicine and Head, Division of Pulmonary Diseases„University of'Colorado Medical Center„Denver;,Colo., RALL, David! P., M:D'. - Director, Nationall Institute of EnvironmentaU Health, Sciences, National 1'nstitutes of Health; Research Triangle Park„ N.C. RAUSCHER,, Frank J.,, M.D. - Director, National Cancer Institute, National Institutes of Health, Bethesda, Md., RENZETTI~ Attilio D:, Jt., M.D. - Professor of Medicine and Head, Pulmonary Disease Division; Univ'ersityofUtah~Medical'Center; Salt Lake City„Utah. RINGLER„Robert L., Ph.D. - Acting Director; National Heart and Lung Institute„Nationai Institutes of Health, Bethesda, Md. SAFFIOTTI, Umberto, M.D. - Associate Director for Carcinogenesis, National Cancer Institute; National Institutes of Health, Bethesda„Md.. ~i~ o

SCHMELTZ, IYwin, Ph.D. - Associate Member and Head, Section of Bio-organic Chemistry, Division of Environmental Carcinogenesis, Naylor Dana Institute for Disease Prevention, American Health Foundation„Valhalla; N.Y. SCHUMtYN,, Leonard M,.,, M.D! - Professor and Director,, Division of Epidemiology, School, of Public Health, University of'Minnesota, Minneapoli's„Minn. SHIMKIN, Michael B., M.D:,- Professor of Community Medicine and Oncology;,School of ' ' Medicine, University of California„ La Jolla, Calif. WYNDER., Ernst L., M.D: - President and Medical Director,, Arnerican, Health Foundationa, Valhalla, N.Y. Special assistance for the Cardiovascular Chapter was provided by: JENNINGS, Michael, M.D. - Epidemic Intelligence: Service Officer„CDC, located at Ohio Department of Health, Columbus„Ohio;,and. MtYNNING, Kathleen, M., R.N. - Department of'Staff Development, Boston City Hospital, Bostons Mass: The following staff inembers: of'the Center for Disease Cbntrali also contributed to the preparation of'this report: Bureau of Training,- JUlia M. Fuller, Winthrop N. Davey, M.D., and Seth N. Leiblers Ed.D.; National Clearinghouse for Smoking,and Health, - Nancy M. Johnston and Sanda Lager. Is, ca~ nal cer xi

I NTRODUCTION Overview - The Heal th Consequences of Snnoking_

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OVERVIEVV~~ - HEALTH C@NSEQUENCES~ OF~S~h1OKIlN~G~ i The statement, "Warning: The Surgeon General Has Determined That CigQrette Srnoking, Is Dangerous to Your Healtlr,," has beenn required by Uaw on cigarette packaging since 1970 as a part of the Public Health Cigarette Smoking Actt of 1969. This Act was ai response by the U.S. Congress to the scientific information on the health consequences of cigarette smoking summarized in reports then available (the Surgeon General's Reporti of 1964 and the subsequent 1967', 1968, and 1969 PHS Health Consequences of Smoking). This Act was passed because a series of irnportianfi questions concerning; cigarette smoking and health had been answered. Thefollovvin~g dl'scussiion summarizes, the basicquestions~, tlhemethodology used to, determine the answers, and the answers themselves. The initial question to be answered concerning the health consequences, of smoking was "Arethereanyharmfuthealth, effects of smoking cigarettes ?" The answer to this question was provided in~ two ways. First, it was demonstrated that some diseases occurred more frequently in smokers than in nonsmokers. Second,, a causal relationship was established between, srnoking; and' these diseases. C'orrcernabout the possible health effects, ofsmoking, started wheni scientists, began looking for an, explanation to account forthe: rapidlyincreasing, death rat~efrom, lung cancer. Thsearlyretrospec- tiive studies showed a link between lung cancer and smoking. The first prospective studies, however,, found' that only one-eighth of the excess overall mortality found among srnokers could be accounted for by lung cancer; the rest was largely due to coronary heart disease, chronic respiratory disease, and other forms of cancer. They also, found that the effect on overall' mortality was largely confined to: cigarette, smokers rather than the users of other forms of tobacco. However„ demonstrating an association by statistical probability, is not enough to establish the causal nature of a relationship: Determining that the association between smoking and exeessdeatlhs rates is cause and effect was a judgment made after a number of criteria had been met, no one of which by itself is sufficient to make this ji.udgcnenti. Th~esecrit~'eriaas listed in the Surgeon Ge~neral"s 3

Advisory Committee Report (1,964) were the consistency, strength, specificity,temporal relationship, and coherence, of the association, Im, addition,, convincing, theories about the mechanisms whereby smoking, contributes to the various diseases responsible for the excess mortality among cigarette smokerswere developed from the evidence on the biochemical, cytologic,, pathologic, and pathophysiologiceffects of cigarette smoking, thereby providing the necessary support for the decision that the relationship was causal. The most important specific health consequence of cigarette smoking in terms of the number of people affected is the development of' premature coronary heart disease (CHD). Both prospective andl retrospective studies: clearly established that cigarette smokers have a greater risk of death due to CHD and have a higherr prevalence of CH'D' than nonsmokers. Long-term followup of healthy populations has confirmed that a cigarette smoker is more likely to have a myocardial infarction and to die from, CHD than a nonsmoker. Cigarette smoking has been shown, to be one of the major independent CHD1 risk factors and to act in combination with other major al'terabl& CHD1 risk factors (high blood pressure andd elevated serurn, cholesterol). Autopsy studies have shown that persons who smoked cigarettes have more severe coronary athero- sclerosis than persons who did no~t'smoke. Physiologic studiesandl animal experiments have indicated several mechanisms whereby these effects can, take place. inhale. As a result lungs of pipe and cigar smokers receive much less Fewer pipe and cigar smokers than cigarette smokers report that they pharynx, larynx,, and esophagus when compared, to nonsmokers.. el'evated, risks, for the developrnent of cancer of the oral cavity, tlhan in nonsmokers. Pipe~~ and cigar s~mokers, were~ found~ to have~ bladder was al'so found' to be significantly higher in cigarette smokers larynx, pharynx, orali cavity, esophagus, pancreas, and urinary above~ thatl for~ nonsmokers~.~ The: risk of~ devel~o~ping; cancer~~ o~f~ the: cancer than smokers of nonfilter cigarettes,, but the: risk remains well cigarettes have been shown to have a lower risk of developing lung who have smoked for a, greater number of years. Smokers of filter smokers who report inhaling, who started smoking; at an early age, or the number of cigarettes smoked per day and' is greater iri cigarettee for nonsmokers. The risk of developing lung cancer increases withh cancer was found to be 10 times greater for cigarette: smokers than as the major risk factor irt lung cancer. The risk of developing lung A second major health consequence of smoking, is the devei'op- ment of cancer in smokers. Cigarette smoking was firmly established! 4

exposure to~ smoke than the lungs of cigarette smokers. This is probably the primary reason for the lower incidence of cancer of the lung,for pipe and cigar smokers compared to cigarette smokers. 1 i Women, have had far lower rates of lung cancer than, men. This has been attribut!edl to the fact that fewer women than men smoke and the fact that women smokers generally select filter and low tar andl nicotine cigarettes.H'owever, the percentage of women smokers in the United Stateslia6increa~sed steadilyini the: last 30 years, and: since 1955 the death rates from lung,cancer in women have increasedd proportionatelymorerapid1y than the rates for m:en, reflectlingthisincreased proportion of women smokers. The tar from cigarette smoke has been found~ to induce malignant changes in the skin and respiratory tract of experimentall animals, and a number of specific chemical compounds contained in cigarette smoke were established as potent carcinogens or co-carcino- gens. Malignant changes including carcinoma in situ were found in, the larynx and in the sputum exfoliative cytology of experimentall animals exposed to cigarette smoke. Nonmalignant respiratory disease: is a third area of smoking- ind'uced morbidity and mortality. Ciigare~tt!esrn:okershavee been shown to have more frequent minor respiratory infections, miss moree days from work due to respiratory illness, and report symptoms of cough and sputum production more frequently than nonsmokers. Retrospective and'' prospective s'tudies with llong-term followup havee fonnd' that cigarette smoking is the primary factor in~ the develop- ment of chronic bronchitis and emphysema in the United States. Cigarette smokers have also been found to be more likely to havee abnormalities of pulmonary function and have higher death rates from~ respiratory diseases than nonsmokers. Data from autopsy studies have shown that cigarette smokers were more likely to have the macroscopic changes of emphysema, and that these changes aree closely related to the number of cigarettes smokedl per day. Mucous cell hyperplasia has been foundl more often ini cigarette smokers, Cigarettesrnoke alsoilnhibitsthe ciliary motion responsiblefore cleansing the respiratory tract. An additional area of healthi concern has been the, effect of cigarette smoking during pregnancy. Mothers who: smoke cigarettes during the lastl two trimesters of their pregnancy have been found to have babies with a lower average birth weight than nonsmoking mothers. lni addition cigarette smoking mothers hadl a higher risk of having a stillborn child,, and their infants hadl higher late fetal and

neonatali death rates. There are some datai to show that these risks due to cigarette smoking; are even greater in women who have a high risk pregnancy for other reasons. These effects may occur because carbon monoxide passes freely across the placenta and is readily bound by fetal hemoglobin,, thereby decreasing, the oxygen carrying, capacity of fetal blood.. )}iaving, established that cigarette smoking is a significant causal' factor in a number of seriou.s disease processes, two additionall questions became important. They are "Can the health consequences to the individnal' be avertedl by stopping, smoking or by changing, the cigaret'te, "' and "What are the overall public health consequences of cessation and of the changes made in cigarettes?" The first question is the simpler of the two to answer. In the individual, cessation of cigarette smoking,results inia rapid declane of the carbon monoxide level in the blood over the first 12 hours.. Symptoms of cough, sputum production; and shortness of breath usually improve over the next few weeks. A woman who stops smoking by the fourth month of her pregnancy has no increased risk of stillbirth or perinatal death in her infant related to smoking. Ti he deterioration in pulmonary function tests that occurs in some smokers becomes less rapid than that of continuing, smokers. The death rates from ischerri2c heart disease, chronic bronchitlis;, and emphysema also become less than those of the continuing, smoker. The risk of developing cancer of the lung„ larynx, and oral cavity declines relative to the continuing smoker in the first few years after cessation and 10 to 15 years after stopping smoking approximates that of nonsmokers. A smoker who switches to filter cigarettes and has smoked them for 1'0 years or lbnger has a lower risk of developing, lung cancer than a smoker who continues to smoke nonfilter cigarettes. The risk to a filter cigarette smoker, however,, stlill' remains well above that of a nonsmoker. The public health benef-its of cessation are more difficult to determine than, the: effects of cessation on the~ individual. Just as cause-specific death, rates have reflected the effect of cigarette smoking on certain diseases, they should also reflecti any substantial benefits to be gained by cessation or reduction, in cigarette smoking. Several factors combined to produce a redhiction ini per capita dbsage of tobacco exposure in the United States for the years 1966-1970. First, per capita consumptioni of cigarettes declined fromi 41,287cigarettes per person ini 1966 to 3,985 in 1970. Second, during this period' there was a slow but significant decrease in the average tar and nicotine content of cigarettes as welll as a decrease in the amount of 6

tobacco contained in the average cigarette. The decline in per capitai consumption during those years occurred im the face of a substantiall increase in the proportion of young; women becoming, smokers as compared t& women of previous generationsand so reflected predominantly a decrease in cigarette consumption by men. Since 1970, although the per capita consumption of cigarettes has increased, the average levels of tar and nicotine have continnedl to decline, making it more difficult tlo predict what has happened to per capita dosage.. Examination of cause-specific death rates for the period of this declining per capita consumption reveals that' there was a downturn in the male death rate frorni ischemic hearti disease beginning in 1966 which reversed the: upward trend!thatlhad occurred over the previous two decades. This deciine in, the: death rate from ischernic heartt disease has not occurred in women. The male death, rate from chronic~ bronchitis has also been, declining since 19$7, and the male deathi rate for emphysema has declined since 1968 when, it was first recorded as a separate category. Female death rates for these two diseases have not shown these trends. Despite the impressive coincidences of the decline in death rates among males occurring at the same, time that there was ai deciine in per capita cigaretlte consumption, it is.impossibie tlo be certain of the: exact cause of the decline in t!he death rates. These diseases aree influenced by a variety of fact'~orsini ad!dition to cigarette smoking f such as blood pressure and air pollution. Some of these factors have e I also been subject tlo major control efforts which may have contributed to the decline in the death rates. In addition, there have been therapeutic advances in thetreatmentl of theseproblem~s which may also have helped lower the death rates. to as A decline in male death rates from lung cancer should also kte follow the decline in per capita consumption. This rate would not be ial influenced as much by changes ini other etiologic factors or changes im g, therapy because cigarette smoking, causes frorn 85 to 90 percent of ge all lung cancer and' there have been no major improvrnents in survival 7'0. due to changes ini therapy. With lung cancer, however, two !8:'] additional considerations must! be kept in mind. A decline: in death ~his, rates from lung cancer would be expected to lag severaU years behind ~ndl a decline in per eapit'~a~ consumption. Iln addition, the decline in of consumpt!ionand switch m low tar and nicotine cigarettlesoccurred I 1 7

predominantly in the younger age groups where deathi rates from lung cancer are low. For these reasons, it is necessary to look at lung cancer death rates by age group rather than total lung cancer death rates. The lung cancer rates by age groups for 1'9'71 suggest a decline in the lung, cancer rates for the younger males (under 45), but the confidence limits on _these trends at present remain wide enough that it, is impossible to say whether this is a real decline or merely a leveling off. The national health statistics broken down by 5-year age groups are currently available only through 1971. The dat'a, by age group from a few more years will be: necessary to determine whether the changes in smoking behavior which have taken place have reversed the trend of the preceding; 4'0 years of continually increasing, lung, cancerrates, in, men., In 1971, , the last year for which detailed' mortality statistics are available, the, accumulated exposure to cigarettes reached its peak among men born between 19'15 and 1i919; a group then in their early 50's. Cumulative exposure has continued to decline withi each, successive. 5-year birth cohort borni since, then. The trends of the: last few years offer some hope thatl the peak of the"lung cancerepiderni'c,'"as, someh~ave termed this phenomernon, may have been reached with this group and that future years willi showai slow but consistent d'ecl~ine..