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1 ! I am Dr. Carl C. Seltzer, Honorary Research Associate at the Feabody Museum, Harvard University and Professor of Nutrition, Tufts University. I was formerly Senior Research Associate at the Harvard University School of Public Health. My work in the smoking and health area is extensive and I have published over thirty-five (35) articles since 1964 on the subject, many dealing with the relationship between smoking and coronary heart disease (CKD). I was a consultant to the Surgeon General's Advisory Committee on Snicking and Health (contributed a section to the 1964 Report) and am presently a Fellow of the Council on Epidemiology of the American Heart Association. My investigative work in the heart disease field includes -participation in studies involving the Framir.gham Heart Study, The American Medical Association, the Veterans Administration and the Kaiser-Permanente Foundation. H.R proposes that the following label statement appear en cigarette packages: "Warning: Cigarette smoking is a major cause of Heart Disease." This proposal is apparently based on the claim, cut forth as a Congressional "finding" in the first part of the bill, that one third of deaths from CHD are "attributable to smoking." These bald statements are not based on consistent, valid, demonstrable scientific evidence, and are without established proof. Apparently, they are based on the views of a succession of Surgeon Generals subsequent to the 1964 Report, on the statements of the American Heart Association, the Framir.gham Heart Study and others. TI

2 Page 2 f The primary basis for these views can best be characterized by statements from the 1981 Surgeon General's Report and by the Frainingham Heart Study. The 1981 Report stated: "The effect of smoking on CHD risk fulfills many epidemiological criteria for a causal association: powerful, independent, dose related, and reversible." Kannel of the - Frarr.ir.ghan Heart Study sta-ed: "Causal inferences are supported by the fact that: the relationship is strong, consistent, demonstrated prospectively, independent cf associated risk factors, and can be explained by the known effects of cigarette smoking en the cardiovascular apparatus. Finally, it has been shown that those who quit smoking have only half the risk of these who continue to sneke. Epidemiologic data have... tended to indicate an independent, transient, noncumulative, reversible, triggering effect of cigarette smoking." (JAMA, 1981) Accordingly, the main evidence advanced for a causal relationship between cigarette smoking and CKD is essentially epidemiologic, tc the effect that the association is (1) strong, (2) consistent, (3) dcse-related, (4) independent of associated risk factors, and (5) reversible by stopping smoking. (6) In addition, the association is said to be explained by known effects of cigarette smoking on the cardiovascular system. Let us examine these claims in turn. Claim 1. Is the relationship strong? The 1964 Surgeon General's Report stated that in the U.S. the mortality ratio of smokers to nonsmokers is 1.7. But, this is not a strong relationship, according to Professor Hutchison of the Harvard School of Public Health. (Bull MY TIQ

3 Page 3 1 Acad Med, 1968)- This independent observer feels that a mortality ratio of two or less is actually indicative of a weak relationship which may possibly be explained by confounding factors. Can the relationship be characterized as "strong" when the 197S Surgeon General's Report, although discussing smoking and health studies throughout the world, limits its conclusion to "men. and women in the United States," and Kannel of the Framingham Study talks about the excess CHD death rates of smokers "in most of Western societies"? (AHJ, 1981) If the relationship between smokers and CKD is "strong," why is it not present in all Western societies or in r.on-western societies? Claim 2. Is the relationship consistent? Since r.c significant statis-ical associations between smoking and CHD have been reported in Finland, the Netherlands, Italy, Greece, Yugoslavia, Japan and Puerto Rico, it is clearly incorrect to claim that the relationship is consistent. The relationship is not even consistent in the Franir.gham Study. It appeared to be consistent in initial analyses, but when standard risk factors and such psychological factors as Type A personality were controlled, it was found that "cigarettes smoked per day" were not predictive of CHD and myocardial infarction incidence in men, or of CHD and angina pectoris incidence in women. (Am Epidemiol, 1980) TI

4 Page 4 \ Can the relationship be characterized as consistent when the 1979 Surgeon General's Report concluded that "the predictive risk factor association of smoking with the incidence cf angina pectoris is not clear"? The Framingham Heart Study also reports that "the relationship to angina pectoris is modest, if it exists at all." (JAMA, 1981) Is the relationship consistent when che relative risk progressively declines with increasing age? Seltzer demonstrated and Kannel noted that the benefits of quitting smoking do not extend beyond the age of 65 as regards heart attacks. (Am J Med Sci, 1973; JAMA, 1981) Furthermore, the 20 year follow-up data of the Framingham study show no excess incidence of CHD in men or women 55 years and over. {Framingham data made available to Seltzer as consultant.) Can the relationship be characterized as consistent when the Framingham Heart Study reports an absence of a relationship cf smoking and CHD in women? Claim 3. Is the relationship dose-related? CHD rates do not consistently shew a rising gradient in relation to an increased amount of cigarette smoking. (JAMA, 1968) In some studies, the gradient is actually reversed. (JAMA, 1968) I found that data from the Framingham Study do not show a consistent rise in CHD risk with increasing amounts of cigarette smoking because of the "heterogenous" character of its "none" category, a deceptive procedure. The "none" category in Framingham TI

5 Page 5 consists of a combination of never smokers, ex-smokers, pipe z-^ cigar smokers. A Framingham Study report confirmed that "there is no distinct dose-response relation [of CHD and death rates] with increasing amounts of cigarette smoking" over an 18-year surveillance period. (Lancet, 1974) There is no significant dose-respcnse relationship between smoking and CHD in studies of Finland, the Netherlands, Greece, Italy, Yugoslavia and Japan. (Circulation, 1970) No claims have been made lately about the alleged association of CHD with duration of cigarette smoking. In the combined Albany and Framingham Heart Studies (NEJM, 1962), no association was found between duration of heavy cigarette smoking and risk of myocardial infarction. In a study of Canadian veterans, no consistent gradient occurred between CHD mortality and years of cigarette smoking. (JAMA, 1968) In Kahn's analysis of Dorn's U.S. veterans data, there was also no significant relationship between duration of cigarette smoking and risk of death from CHD. (JAMA, 1968) Claim 4. Is the relationship independent of associated risk factors? Smoking has been found to be associated with CHD independently of associated risk factors in some studies when only cholesterol and blood pressure were considered. But this generally has net been the case when ocher T

6 Page 6 I risk factors were investigated, such as Type A personality, and other psychological factors (as seen above in the Framingham Study). Claim 5. Does stopping smoking reduce the risk of CKD? This claim is based on studies from some Western countries which report that CHD rates of ex-smokers are lower than those of continuing smokers. The 1974 Lancet article on the Framingham study is the most widely quoted source for claiming that the rate of CKD among chose who stop smoking is reduced to one-half that of continuing smokers. When I was provided with the CHD rates of Framingham "never smokers" (which had been omitted in the article), however, I was able to show that the CHD rates of ex-smokers were far below those of "never" smokers," while the rates of "never smokers" were not far below those of continuing smokers. (Seltzer letter to Lancet, 1977) Additional evidence about the fallacy of the claim that steeping smoking reduces the rate of CHD comes from two other sources. The first is a study challenging the assumption by epidemiologists that ex-smokers and continuing smokers are alike in all pertinent characteristics, except for their smoking habits. If this assumption is false, which I believe it to be, then comparisons of the two groups would be biased as to their eventual CHD rates. Friedman, Seltzer, and others have shown that ex-smokers, when they still smoked, were net a representative sample of the population of continuing smokers. The data showed, in fact, that ex-smokers were at lewer hearx disease risk TI

7 Page 7 (and healthier) before they stopped snicking, than those persons who continued to smoke. (J Chron Pis, 1979) This would appear to account for the fact that ex-smokers have lower CHD rate outcomes zhan continuing smokers, not because they stepped smoking but because they are different kinds of persons to begin with through self-selecticn. In a subsequent article published in the NEJM, Friedman and others tried to negate the results of that paper by applying theoretical correction techniques through multivariate analysis to the lower CHD-related characteristics of the ex-smokers. They claimed that the lower CHD-related characteristics actually made little difference, that ex-smokers still showed lower CHD outcomes than continuing smokers. Although this paper was criticized by Surch and Seltzer (Burch and Seltzer letters to NEJM, 1981), Friedman evaded virtually every criticism in his reply. (Friedman letter to NEJM, 1981) Friedman did not explain how he could accept the value of CHD-related characteristics (risk factors) in one paper and deny their importance in a second paper. Nor did Friedman explain why the mortality data in his later paper showed that never smokers exhibited higher CHD rates than the ex-smokers (the same anomaly as that found in the Framingham Study). Does this mean that it is better to begin smoking and then to quit than never to have smoked at all? The second source of evidence which points tc the fallacy of the claim that stopping smoking reduces the risk of CHD is the first large-scale TI

8 Page 8 "intervention" trial of the effect of smoking cessation in middle-aged London civil servants at high risk cf cardiovascular disease. (J Epidemiol Comm Health, 1978) After nearly eight years cf surveillance, the group subject to intervention for smoking cessation showed no improvement in its rate of mortality ever cha group which was not urged to stop smoking. Thus, the alleged reversibility of the risk to the smoker's life was not demonstrated. This result is consistent with a more recent intervention trial frcm Norway which examined the effects of both smoking and cholesterol reduction. (Lancet, 1981) Although reductions in dietary cholesterol produced a statisticially significant decrease in CHD, reductions in smoking did not. This led the authors to conclude that past studies may have "overestimated the decline in risk of CKD" following reduced cigarette consumption. Claim 6. Kannel of the Pramingham Study claims that: "causal inferences... can be explained by the known effects of cigarette smoking on the cardiovascular apparatus." (JAMA, 1981) There is no satisfactory evidence for this claim, and, in fact, there are contradictions. The cold reality is that the mechanisms by which tobacco smoking allegedly causes CHD have not been established. Much of the evidence to support this statement is contained in Seltzer's article, "Smoking and Coronary Heart Disease: What Are We to Believe," published in the American Heart Journal as an editorial in September, This editorial T

9 Page 9 i discusses those statements of the 1979 Surgeon General's Report which illustrate the absence of firm evidence of mechanisms by which smoking affects CHD, such as: (1) little is known about the mechanisms by which smoking enhances athercgenesis, (2) further research is needed to show the mechanisms of sudden death and its precursor states, (2) the data on the effect of smoking on blood lipids are not very uniform, (4) the association between cholesterol and smoking is minimized, (5) the acute and transient effects of smckinc are to increase heart rate and blood pressure to a minor degree, (6) smcking is not a risk factor for hypertension, (7) the association of smoking with necropsy manifestations of atherosclerosis, shown principally by Strong's group in New Orleans, now has been contradicted by a study by Holme, Strong and others who found that smoking did not show a significant association with coronary artery lesions. (Arteriosclerosis, 1931} More evidence comes from other sources. An editorial in the August 1980 British Medical Journal states that the mechanism by which smoking affects coronary heart disease is unknown. The American Heart Association Heartbook states: "The mechanisms by which cigarette smoking is associated with higher rates of coronary heart disease are not yet fully understood." The 1981 Surgeon General's Report states: "Estimation of the impact of varying cigarettes on coronary heart disease risk is difficult, because the exact etiologic agent(s) have not been identified." Thus, the bill's proposal to label cigarette packages with levels of tar, nicotine, and carbon monoxide is not TI O

10 Page 10 justified on scientific grounds. The Surgeon General admits that it has not been clearly demonstrated that these factors are crime etiologic agents in the causation of increased CKD in smokers. This is also shown by the conclusion of the 1981 Report that despite radical changes in the composition of cigarettes ever the last 10 to -15 years (filter, tar, nicotine), there was no clearly demonstrated effect on cardiovascular disease. This surprising result is clearly consistent with the proposition that amounts of tar, nicotine, and carbon monoxide in cigarette smoke have no demonstrable effects or. CHD rates, and that these components of tobacco smoke are not proven etiologic agents. Since most cardiologists believe that atherosclerosis is the most important factor in coronary heart disease development, they claim that smoking enhances atherosclerosis, despite the lack of definitive evidence. On the other hand, the Framingham Heart Study has disavowed the atherosclerotic argument and claimed that the effect of smoking en the heart is acute (not progressive), and disappears promptly when smoking is stopped. These are contradictory claims and illustrate the lack of definitive knowledge in this field. It is clear from the above that extensive research data do not support the Congressional finding in H.R that a major proportion of the CKC deaths in this country are attributable to smoking. In turn, the bill's proposed TI

11 - Page 11 I warning, "Cigarette smoking is a major cause of Heart Disease," _is net scientifically valid. In every instance, an examination cf the claims made against cigarette smoking and CHD shows that they are either wrcr.g, inconsistent, selective, unsubstantiated, or, in many respects, contrary to the statements of the Surgeon General, the American Heart Association and "he rramir.ghair. Heart Study. G*~i. -$ J'^iZ Signed ^c^--<. /-\-^L <?; ^ / ^ / ^ 2- T