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Circulation. 1996;94:596-598

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(Circulation. 1996;94:596-598.)
© 1996 American Heart Association, Inc.

Articles

Passive and Active Smoking

A Problem for Adults

Stanton A. Glantz, PhD; William W. Parmley, MD

the Division of Cardiology, Department of Medicine, University of California, San Francisco.

Correspondence to Stanton A. Glantz, PhD, Professor of Medicine, Box 0124, University of California, San Francisco, CA 94143-0124. E-mail glantz@cardio.ucsf.edu.


Key Words: Editorials • smoking • coronary disease


*    Introduction
up arrowTop
 *Introduction
down arrowReferences
 
Over the last 10 years, 14 epidemiological studies1 2 3 4 5 6 7 8 9 10 11 12 13 14 and experimental studies15 16 17 have consistently shown that passive smoking increases the risk of heart disease death. Combining these studies in a meta-analysis yields an estimate that passive smoking significantly increases the risk of death from heart disease by about 20% (RR, 1.2; 95% CI, 1.1 to 1.4). As with the evidence that passive smoking causes lung cancer,18 19 20 the tobacco industry has vigorously attacked these studies as too small, biased, or failing to control for confounding variables adequately. These arguments have become harder to make over time as the number and quality of epidemiological studies on both lung cancer and heart disease have improved, so the tobacco industry has started to emphasize a new explanation: publication bias.

For example, in the 1994-1995 hearings held by the federal Occupational Safety and Health Administration (OSHA) on a proposed rule making workplaces smoke free,21 several of the tobacco industry's witnesses argued that the reason that there were so many studies in the literature showing an elevation in risk of death associated with passive smoking was that journals simply did not publish "negative" studies because of a bias on the part of editors against the tobacco industry despite the fact that formal studies of the question of publication bias demonstrated that at least in the case of passive smoking, no such bias existed. Faced with this evidence, the tobacco industry took the argument one step further and said that publication bias included people not doing research or analyzing data that might not support the view of the health establishment. In particular, both at the hearing and in print,22 tobacco industry consultants speculated that because of its antismoking bias, the American Cancer Society had failed to analyze its large Current Population Survey (CPS) data set to examine the relationship between passive smoking and heart disease.

Several years ago the tobacco industry's lawyers obtained the American Cancer Society's CPS data set, ostensibly to help in preparation of the defense of a wrongful death suit against a tobacco company. The industry's lawyers subsequently provided this data set to two consultants, LeVois and Layard,22 who conducted an analysis of these data, which concluded that passive smoking did not affect the risk of heart disease. This analysis was presented to OSHA and subsequently published as evidence of publication bias.

These allegations prompted the American Cancer Society to conduct a proper analysis of the CPS data set, which is reported in this issue of Circulation by Steenland et al.23 In a series of careful analyses of the CPS-II data set, Steenland and colleagues demonstrate that passive smoking increases the risk of death from heart disease. While they include some analysis of exposure outside the home, the primary analysis compares heart disease death rates in nonsmokers married to smokers with nonsmokers married to nonsmokers. Consistent with the earlier studies, they find a relative risk (more precisely, a rate ratio) of approximately 1.2 for both men and women. When these data are combined with the earlier epidemiological studies in a meta-analysis,24 the overall estimate for the risk of heart disease death associated with involuntary smoking becomes 1.23 (95% CI, 1.14 to 1.33; letter from A.J. Wells, April 1996).

This work is important for several reasons. First, it further discredits the claim that the reason that there are not more negative studies on passive smoking and heart disease is because antismoking organizations like the American Cancer Society refuse to do the studies.

Second, Steenland et al23 provide an analysis of the largest data set that has been studied to date; their study roughly doubles the total number of deaths related to passive smoking included in published studies. In addition, their study is based on prospectively collected data and contains enough information on other possible risk factors for heart disease to control for possible confounding variables. They also have analyzed the data in several different ways (such as limiting the analysis to cases in which both partners reported spousal smoking) to minimize the chances that the associations they report are an artifact of the analysis.

Third, for the most part Steenland and colleagues'23 analysis shows no effect of being married to a former smoker at baseline, which is consistent with a strong acute component of the effect of passive smoking on heart disease.17 There appears to be both an acute and a chronic risk to smoking. The acute risk may relate to hemodynamic effects (increased heart rate and blood pressure) and increased myocardial oxygen consumption, increased carboxyhemoglobin, and adverse effects on endothelial function, which can cause inappropriate vasoconstriction. All these effects may predispose to plaque rupture. This acute risk is consistent with the fact that the risk of heart disease in active smokers declines rapidly with smoking cessation, dropping by half in 1 year and essentially disappearing in 5 years.25 The fact that they also found increasing risks with exposure duration in their most accurately characterized subcohort, however, also suggests a chronic effect of involuntary smoking. This chronic risk may reflect secondhand smoke–induced atherosclerosis.

The fact that marriage to a former smoker is not associated with an elevation in risk of heart disease may explain LeVois and Layard's22 failure to find an increased risk of heart disease in their analysis because they considered marriage to an ever smoker (not a current smoker) to indicate exposure to secondhand smoke, which strongly biases the results toward the null. Another article by Layard26 that purports to study the relationship between involuntary smoking and heart disease with the use of death certificate data suffers even more strongly from this problem. To the extent that the effects of involuntary smoking on the heart are acute, Steenland and colleagues' results also will be biased toward the null because they only measured smoking status at the beginning of their study and people were followed-up for several years, during which some smokers will stop.

Just as the epidemiological evidence about involuntary smoking has continued to accumulate, so has the supporting experimental evidence. We have shown that passive smoking worsens endothelial function in lipid-fed rabbits, leading to inappropriate vasoconstriction.27 Recently, Celermajer et al28 demonstrated this same adverse effect in healthy young adults: Passive smoking impaired endothelium-dependent arterial dilation in the brachial artery. This effect may be a marker of early vascular damage. Passive smoking accelerates atherosclerosis in rabbits and cockerels.29 Moreover, specific constituents of the secondhand smoke that accelerate atherosclerosis are being identified: 1,3 butadiene, a vapor phase constituent of secondhand smoke, accelerated atherosclerotic plaque development in cockerels at realistic exposures.30

In addition to our rapidly increasing knowledge of the effects of involuntary smoking, knowledge of the effects of active smoking on the heart continue to accumulate. Recent epidemiological studies show a dose-response relationship between exposure to secondhand smoke as well as active smoking in the progression of atherosclerosis in humans.31 Waters et al32 followed-up smoking and nonsmoking patients with angiographically documented coronary artery disease as part of a randomized controlled trial of the cholesterol-lowering drug lovastatin. They found that atherosclerosis progressed more rapidly in smokers than nonsmokers and that lovastatin had a greater effect on the progression of atherosclerosis in smokers both in terms of extent of atherosclerosis and number of lesions. They noted that the rate of progression in placebo-treated smokers was more than double that of placebo-treated nonsmokers. In addition, new lesions developed in more than half of placebo-treated smokers compared with less than one quarter of placebo-treated nonsmokers. Cholesterol lowering also slowed the progression of coronary atherosclerosis and the development of new lesions in smokers. The fact that cholesterol lowering benefitted smokers more than nonsmokers emphasizes the synergistic effect of tobacco smoke exposure in combination with other risk factors for cardiovascular disease.

A major effect of smoking in Waters and colleagues' trial was greatly enhanced new lesion formation; in fact, smoking was the strongest predictor of new lesions in the control group. Although new lesions are rarely severe enough to cause myocardial ischemia, they are clinically relevant because the risk of a coronary event increased with the number of coronary lesions, and the lesion responsible for a coronary event is usually mild until it undergoes plaque rupture. Lesions at highest risk for plaque rupture are not large but have a high lipid content and a thin fibrous cap. The propensity for smokers to develop new lesions is probably one factor that contributes to their higher myocardial infarction rates by providing them with more sites to develop plaque rupture.

Both these studies reinforce the importance of controlling smoking-both involuntary and active-to reduce the burden of heart and vascular diseases. Smoking causes about 480 000 deaths annually (424 000 smokers and 53 000 nonsmokers). In recognition of this fact, OSHA proposed a rule to make all workplaces smoke free.21 Unfortunately, at a time that the public health community has mobilized aggressively to support regulation of tobacco products as nicotine delivery devices by the Food and Drug Administration,33 34 with the goal of preventing children from starting to smoke, it has virtually ignored the proposal by OSHA, with the net result that the tobacco industry has been able to stall OSHA with essentially no opposition. This fact is doubly problematic because the primary end point used by OSHA to justify proposing that workplaces be made smoke free is cardiovascular disease.21 Not only would smoke-free workplaces prevent heart disease caused by involuntary smoking but they also would create an environment that makes it easier for smokers to stop.35

Despite the fact that there are clear and immediate benefits to both nonsmokers and smokers of reductions in tobacco consumption, the national agenda on tobacco control, as embodied in the proposed Food and Drug Administration regulations, is shifting away from achieving a smoke-free society36 and toward simply preventing children from starting.37 While politically appealing, this approach reflects a retreat to ideas that were prevalent in the 1960s. For example, when he released the original Surgeon General's report on smoking in 1964,38 Surgeon General Luther Terry said, "The principal factor of lung cancer in this country is cigarette smoking. If we are going to be successful in this country in our program against smoking of cigarettes, it is going to depend on our success in appealing to the youth of this country." While primary prevention should be part of any comprehensive tobacco control program, the studies by Steenland et al23 and Waters et al32 indicate that the current single-minded focus on children will ultimately mean accepting many unnecessary deaths from heart and vascular diseases among current adult smokers and the people around them.


*    Footnotes
 
The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.


*    References
up arrowTop
 up arrowIntroduction
 *References
 

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