J Clin Epidemiol

Vol. 45,

No. 8, pp. 815-819,

1992

0895-4356/92

Printed in Great Britain. All rights reserved

$5.00 + 0.00

Copyright 0 1992 Pergamon Press Ltd

Dissent PASSIVE SMOKING CAUSES HEART LUNG CANCER STANTON

DISEASE

AND

A. GLANTZ* and WILLIAM W. PARMLEY

Division of Cardiology, Department of Medicine, Cardiovascular Research Institute, Institute for Health Policy Studies, University of California, San Francisco, CA 94143, U.S.A. (Received 28 January 1992)

The last 10 years have witnessed a dramatic increase in understanding the effects of environmental tobacco smoke (ETS) on the nonsmoker. This growing literature has resulted in several important scientific consensus documents from the U.S. Surgeon General [l], National Academy of Sciences [2], U.S. Environmental Protection Agency [3], National Institute of Occupational Safety and Health [4], and the International Agency for Research on Cancer (IARC) [5], among others, identifying ETS as a cause of lung cancer, disease in children, and, more recently, heart disease [6,4,7]. The growing awareness that tobacco smoke endangers not only smokers but nonsmokers has led to growing restrictions on where people can smoke as a way to protect non-smokers from the toxins in secondhand smoke [8]. While this trend has benefits for non-smokers who have been able to reduce their exposure to ETS, it has a negative effect on the profits of the tobacco industry because the declining social acceptability of smoking and opportunities to smoke lead some smokers to quit and others to cut down cigarette consumption. For example, Stillman et al. [9] found that 1 year after the Johns Hopkins Medical Institutions became a smokefree workplace one quarter of the smokers had quit and continuing smokers had reduced daily consumption by 20%. These two changes combined to reduce *All correspondence should be addressed to: Stanton A. Glantz, PhD, Professor of Medicine, Division of Cardiology, Box 0124, University of California, San Francisco, CA 94143-0124, U.S.A. [Tel: (415) 476-3893; Fax: (415) 476-04241.

total cigarette sales to Johns Hopkins’ 9000 employees by about 41% or 250,000 packs of cigarettes per year, around $500,000 in sales. Mantel’s [lo] criticisms of our work [6] and that of others must be read against this background. The tobacco industry has clearly identified the issue of the effects of smoking on the nonsmoker as a serious problem since the mid1970s. For example, in 1978 a confidential survey of public attitudes related to smoking conducted for the Tobacco Institute by the Roper organization [ 1l] concluded that: “The original Surgeon General’s report, followed by the first “hazard” warning on cigarette packages, the subsequent “danger” warning on cigarette packages, the removal of cigarette advertising from television and the inclusion of the danger warning in cigarette advertising were all “blows” of sorts for the tobacco industry. They were, however, blows that the cigarette industry could successfully weather because they were all directed against the smoker himself. [and have] not persuaded many smokers to give up smoking. The anti-smoking forces’ latest tack, however,-on the passive smoking issue-is another matter. What the smoker does to himself may be his business, but what the smoker does to the nonsmoker is quite a different matter. . This we see as the most dangerous development to the viability of the tobacco industry that has yet occurred.” [emphasis added]

The tobacco industry has dealt with the growing public awareness and interest in the health effects of involuntary smoking just as it has dealt with the effects of active smokiqg: by attacking the scientific evidence and trying to create an artifical controversy about the validity of scientific evidence that ETS causes disease. That this strategy was well established as early 815

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as 1969 is clear from documents the Federal Trade Commission obtained (under subpoena) from Brown and Williamson Tobacco. In discussing how to deal with the growing evidence that active smoking was dangerous, one document said: “Doubt is our product since it is the best means of competing with the “body of fact” that exists in the mind of the general public. It is also the means of establishing a controversy. If we [Brown and Williamson] are successful at establishing a controversy at the public level, then there is an opportunity to put across the real facts about smoking and health.” [12]

Mantel has played a key role in implementation of such a strategy for over a decade. In January 198 1, Hirayama [ 131published the first large study linking ETS with lung cancer in non-smokers in the British Medical Journal. The Tobacco Institute then retained Mantel to prepare a critique of Hirayama’s work. Rather than publishing his criticisms in the British Medical Journal, where Hirayama would have an opportunity to reply and the scientific community an opportunity to judge the competing arguments, Mantel provided his critique privately to the Tobacco Institute, where it became the basis of a year-long public relations campaign designed to discredit Hirayama and his work. This campaign included full page advertisements in major U.S. magazines and newspapers [14]. Mantel’s detailed criticisms were. not made available to the general scientific community during this campaign. Because of this campaign, the British Medical Journal took what the editors called the “exceptional step” of reopening correspondence on Hirayama’s work in October 1981, and obtained and published Mantel’s letter to the Tobacco Institute, together with Hirayama’s response [15]. The fact that Hirayama responded effectively to what turned out to be a minor technical criticism is attested to by the fact that his work has been widely accepted. More important, his conclusion that ETS causes lung cancer has been replicated over and over again in studies throughout the world [l, 3, 161. Given this history, we were not surprised that Mantel has joined other tobacco industry consultants [17, 18, 19, 20,211 in criticizing our paper [6,22,23] demonstrating that passive smoking causes heart disease and accounts for 53,000 deaths annually, making passive smoking the third leading preventable cause of death. Instead of providing specific examples of errors or omissions in the evidence we cite,

together with specific quantitative evidence that these errors have an important effect on the primary conclusion that ETS causes disease, Mantel vaguely dismisses all the evidence that we present relating to the direct physiological and biochemical effects of exposure to ETS. This evidence is important in establishing the biological plausibility of the epidemiological findings, and establishing causality. Mantel asserts that the power computations we present in our paper are wrong by a huge margin, but does not provide any specific computations for the values he cites or the assumptions behind these computations, so they can be adequately judged. He also states that “Lee [a British statistician who is another regular consultant to the tobacco industry] could not have approved of the statistical powers in [Table 1 of our paper].” We find this assertion puzzling, since Glantz and Lee [24] jointly published a letter in Environment International confirming this agreement. Mantel states that the combination of a nonsmoking wife with a smoking husband may be atypical “in ways which could influence outcomes.” Again, he does not present any quantitative analysis to demonstrate the nature and magnitude of the problem. Such computations, together with a clear statement of the underlying assumptions, would be necessary to convince anyone that this is a real problem. Mantel raises several questions in connection with misclassification errors, but presents no quantitative analysis of this problem to demonstrate the precise quantitative effects of these potential problems. Simply raising the issue does not mean that it is a real problem. Indeed, Wells [25] provided an analysis of the effects of misclassification errors on risk assessment of ETS which showed that the net effect of misclassification errors and background exposure to ETS is to increase the total risks associated with ETS. The procedures Wells used to correct for misclassification and background exposures are well established [2,3,7] for finding the risk of ETS exposure compared to a truly non-exposed reference group. Mantel, of course, discounts Wells’ work, including adjustments for ETS until the passive smoking effect “is clearly established.” To comment on this assertion, Mantel would have had to provide the specific errors in Wells’ calculations and how these errors affect the final result, both in terms of the numbers and the general conclusions regarding the effects of ETS. It would also be useful to

Dissent: Passive smoking, Heart Disease and Lung Cancer

know what information Mantel believes would be necessary to “clearly establish” an effect on ETS. In criticizing Wells’ work, Mantel ignores the detailed defenses that Wells has already published [26,27] in response to letters criticizing his work from other tobacco industry consultants. Mantel refers to Vandenbroucke’s note raising the issue of publication bias [28] as the reason that so many papers have been published linking ETS exposure with lung cancer, but fails to discuss Wells’ response [29] that demonstrates that the unpublished work on male passive smoking risks had higher than the average of the published work, not lower as Mantel implies. This practice of citing criticisms of work demonstrating adverse effects of passive smoking without acknowledging the authors’ defense of their work [30] is a common tactic employed by the tobacco industry. As with all the other criticisms Mantel raises, he does so only in general terms without providing detailed evidence to back up his assertions. Mantel criticizes the work of Kawachi and Pearce [31] without making it clear how these criticisms relate to our paper. While we believe that the Kawachi and Pearce paper is a reasonable contribution, we did not make any use of its quantitative techniques in our paper. Had we, we would have arrived at a higher risk estimate. Mantel criticizes the estimates of Repace and Lowrey [32] of passive smoking and lung cancer as being based upon a cohort study yielding a comparison of the lung cancer mortality rate difference between lifelong non-smoker Seventh Day Adventists (SDAs) with lifelong nonsmoker non-SDAs. According to Mantel, this comparison is flawed because SDAs and nonSDAs differ “in many other ways” other than their exposure to passive smoking. Mantel does not say what these differences are or how they might affect lung cancer risk. Contrary to Mantel’s assertion, Repace and Lowrey did address this issue and concluded that such confounders were unlikely to account for the difference. Repace and Lowrey devote an Appendix to the discussion of possible confounding factors and sources of bias, such as misclassification, differential exposure to industrial carcinogens, radon gas, and diet. They emphasize that the most significant difference between the SDA and nonSDA cohorts is their difference in exposure to ETS. Because SDAs proscribe smoking on religious grounds, few SDAs would be exposed to ETS at home; moreover, 40% of the SDA

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cohort worked for organizations owned or operated by their church, making this cohort far less likely to be exposed to ETS. Repace and Lowrey further observed that the lung cancer rate difference derived from the SDA study was nearly identical to that reported by Hirayama [13] in his cohort study of passive smoking and lung cancer, and further, were able to explain quantitatively the differing results of the American Cancer Society study of passive smoking and lung cancer [33] and those of Hirayama. Finally, Mantel cavalierly dismisses the risk assessment of ETS and lung cancer conducted by Repace and Lowrey [32] as “not demonstrating any kind of effect (of passive smoking), they just made a calculation.” Risk assessment is used by federal and state regulatory agencies in evaluating suspect carcinogenic agents in air, water, and food, including industrial pollutants, radioactive substances, pesticides, and biological contaminants. Repace and Lowrey applied the IARC criteria for judging the potential carcinogenic activity of suspect environmental agents to environmental tobacco smoke, and found that it satisfied those criteria, which include: agreement of independent studies, strength of association, presence of doseresponse relationships, reduction in risk following reduction in exposure, and discussion of confounding factors. Subsequently, IARC itself recognized ETS as a carcinogenic risk to humans [5]. Mantel states that socioeconomic factors relating to heart disease and ETS “would warrant much more attention.” Indeed, there is evidence that being in a lower socioeconomic class is associated with higher mortality among patients already diagnosed with coronary artery disease [34]. Mantel, however, does not present any quantitative evidence that these factors account for the observed increased risk of developing heart disease when exposed to ETS. How large are the resulting errors? What are the assumptions behind his computations? Simply saying that such differences exist does not make them large or important. In fact, there is some evidence that the ETS is a greater risk factor for heart disease for higher socioeconomic classes [351* Mantel lists many potential confounding variables that might explain the observed link between ETS and disease in children. He needs to provide a quantitative analysis of the magnitude of these effects and how they might bias the published studies. Again, clear and careful list-

STANTONA. GLANTZand WILLIAMW. PARMLEY

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ing of the assumptions behind his computations would be important for judging his assertions. Mantel dismisses the primary conclusion of our paper [6] that passive smoking causes heart disease as “opinions and beliefs” that may be “competely fiction.” In making such a strong statement, he needs to review all the evidenceepidemiological, physiological, and biochemical-not just list some hypothetical objections or possible problems in the epidemiology. To discredit our work he needs to show convincingly that the hypothesized confounding variables introduce real errors that are large enough to change the overall conclusions from the epidemiology and provide plausible alternative explanations for the physiological and biochemical changes observed following ETS exposure. Based on past history [30], it is likely that the tobacco industry will be citing Mantel’s paper [lo], together with other criticism the industry has generated [17, 18, 19,211, as evidence of “serious questions” about our work from “eminent biostatisticians” [ 141. We are confident, however, that, as with lung cancer, the scientific community (and the public) will choose to evaluate all the evidence-epidemiological, physiological and biochemical-and concur that passive smoking causes not only lung cancer, but also heart disease. Acknowledgements-This study was supported in part by funds nrovided bv the Cigarette and Tobacco Surtax Fund of the* State of California through the Tobacco-Related Disease Research Program of the University of California (awards lRTl45 and lRT520).

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17. 18. 19. 20.

REFERENCES 1. US Surgeon General. The Health Consequences of Involuntary Smoking: A Report of the Surgeon General. Rockville, MD: U.S. Public Health Service, Dept of Health and Human Services; 1986. 2. National Research Council. Environmental Tobacco Smoke: Measuring Exposure and Assessing Health Effects. Washington, DC: National Academy Press; 1986. 3. U.S. Environmental Protection Agency. Health Effects of Passive Smoking: Assessment of Lung Cancer In Adults and Respiratory Disorders in Children. Washington, DC: U.S. Environmental Protection Agency Publication EPA/600/6-90/006A; May 1990. 4. US Department of Health and Human Services. Environmental Tobacco Smoke in the Workplace: Lung Cancer and Other Health Effects: NIOSH Current Intelligence Bulletin 54; June 1991. 5. World Health Organization, International Agency for Research on Cancer. IARC Monographs on tbe EvaIuatlon of the Carlnogenic Risk of Chemicals to Humans: Vol. 38, Tobacco Smoking. Lyon, France: IRAC, 1986. f6. Glantz SA, Parmley WW. Passive smoking and heart

21. 22.

23.

24. 25.

26. 27. 28. 29.

disease-epidemiology, physiology and biochemistry. Clrculatlon 1991; 83: l-12. Steenland K. Passive smoking and the risk of heart disease. JAMA 1992; 261: 94-99. US Surgeon General. Reducing the Ha&h Conaequences of Smokhtg-25 Yeats ofProgress: A report of the Suraeon General. Rockville. MD U.S. Public Health Service, Dept. of Health and Human Services; 1989. Stillman FA, Becker DM, Swank RT, Hantula D, Moses H, Glantz S, Waranch HR. Ending smoking at the Johns Hopkins medical institutions: An evaluation of smoking prevalence and indoor air pollution. JAMA 1990; 264: 1565-1569. Mantel N. Dubious evidence of heart and cancer deaths due to passive smoking. J ClIn Epidemlol 1992; 45: 809-813. The Roper Organization. A Study of Public Attitudes Toward Cigarette Smoking and the Tobacco Industry in 1978, Vol. I. 1978. Myers ML, Iscoe C, Jennings C, Lenox W, Minsky E, Sacks A. StaIf Report of the Cigarette Advertising Investigation. US Federal Trade Commission; May 1981. Hirayama T. Non-smoking wives of heavy smokers have a higher risk of lung cancer. A study from Japan. Br Med J 1981; 282: 183-185. Glantz S. The tobacco industry’s response to scientific evidence on involuntary smoking. In: Proceedings of the Fifth World Conference on Smoking and Health, Winnipeg, Canada. Canadian Council on Smoking and Health; 1983. Kornegay HR, Kastenbaum MA, Mantel N, Harris JE, DuMouchel WH, Macdonald EJ, Hirayama T. Non-smoking wives of heavy smokers have a higher risk of lung cancer. Br Med J 1981; 283: 914-917. Fontham ETH, Correa P, Wu-Willimas A, Reynolds P, Greenburg RS, Buffler PA, Chen VW, Boyd P, Alterman T, Austin DF, Liff J, Greenburg SD. Lung cancer in nonsmoking women: A multicenter case-control study. Cancer Epld Biomarkers and Prev 1991; 1: 35-43. Simmons WS. Environmental tobacco smoke and cardiovascular disease. Circulation 1991; 84: 956. Decker WJ. Environmental tobacco smoke and cardiovascular disease. Circulation 1991; 84: 956-957. Holcomb LC. Environmental tobacco smoke and cardiovascular disease. Circulation 1991; 84: 957-958. Huber GL, Brockie RE. Passive smoking and heart disease. (Letter). Circulation 1991; 84: 1878. Raebum P. Scientists Charge Tobacco Consultants with Disinformation. Associated Press; 14 October 1991. S. Glantz and W. Parmley. Environmental tobacco smoke and cardiovascular disease. (reply to Letter to Editor). Circulation 1991; 84: 958-959. S. Glantz and W. Parmley. Passive smoking and heart disease. (reply to Letter to Editor). Circulation 1991; 84: 1879. Glantz S, Lee P. Risk assessment of passive smoking (Letter). Environ Int 1991; 17: 382. Wells AJ. An estimate of adult mortality in the United States from passive smoking. Environ Int 1988; 14: 249-265. Wells AJ. An estimate of adult mortality in the United States: A response to criticism (Letter). Environ Int 1990; 16: 187-193. Wells AJ. An estimate of adult mortality in the United States from passive smoking: A response to criticism. Environ Int 1991; 17: 382-385. Vandenbroucke JP. Passive smoking and lung cancer: A publication bias? Br Med J 1988; 296: 391. Wells AJ. Passive smoking and lung cancer: A publication bias? Br Med J 1988; 296: 1128.

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Reinken J. ‘Ibrough the Smokescreen: A Critique of the Literature by the Tobacco Institute of New Zealand. Auckland, New Zealand: NZ Department of Health; 1990. 3 1. Kawachi I, Pearce NE, Jackson RT. Deaths from lung cancer and ischaemic heart disease due to passive smoking in New Zealand. NZ Med J 1989; 102: 337-340. 32. Repace JL, Lowrey AH. A quantitative estimate of nonsmokers’ lung cancer risk from passive smoking. Environ Int 1985; 11: 3-22. 33. Garfinkel L. Time trends in lung cancer mortality among nonsmokers and a note on passive smoking. J Nat1 Cancer Inst 1981; 66: 1061-1066.

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34. Williams RB, Barefoot JC, Califf RM, Haney TL, Saunders WB, Pryor DB, Hlatky MA, Siegler IC, Mark DB. Prognostic importance of social and economic resources among medically treated patients with angiographically documented coronary artery disease. JAMA 1992; 267: 520-524. 35. Humble C, Croft J, Gerber A, Casper M, Hames CG, Tyroler HA. Passive smoking and twenty year cardiovascular disease mortality among nonsmoking wives in Evans County Georgia. Am J Public Health 1990; 80: 59960 1.

Passive smoking causes heart disease and lung cancer.

J Clin Epidemiol Vol. 45, No. 8, pp. 815-819, 1992 0895-4356/92 Printed in Great Britain. All rights reserved $5.00 + 0.00 Copyright 0 1992 Per...
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