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Fact Sheet on Secondhand Smoke (cont.)

James. Repace, MSc., Physicist Ichiro Kawachi, PhD, Associate Professor Stanton Glantz, PhD., Professor 9/1/99

Secondhand Smoke and Cardiovascular Disease

Law et al. (1997) review the evidence from 19 published studies of passive smoking and heart disease; they report that the average excess risk of ischemic heart disease from passive smoking epidemiological studies is 23% (95% CI:14% to 33%), and conclude that platelet aggregation provides a plausible explanation for the mechanism and magnitude of the effect.

Kawachi, et al. (1997) in a prospective study of coronary heart disease (CHD) in 32,000 female U.S. nurses aged 31 to 61 yr., for nonsmoking women exposed only at work, observed a dose-response gradient for passive smoking and CHD. Adjusted relative risks of CHD were 1.00 [for no exposure], 1.58 (95% CI, 0.93-2.68) [occasional exposure], and 1.91 (95% CI, 1.11-3.28) [regular exposure]. Thus, regular exposure to SHS at work caused a 91% increase in CHD, shown in Figure 3 below.

Figure 3. Risk ratio for CHD for nonsmoking nurses exposed only at work.

1. No safe threshold has been established for cigarette smoking and risk of cardiovascular disease. Even smoking as few as 1-4 cigarettes per day is associated with a doubling in risk of coronary heart disease (CHD) ( Kawachi et al., 1994).
2. Many cardiotoxic compounds are more concentrated in sidestream smoke than in mainstream smoke. For example, carbon monoxide (which is known to aggravate angina symptoms) is 8-11 times more concentrated in sidestream smoke than mainstream smoke.(U.S. EPA, 1992)
3. At least seventeen epidemiological studies have been published on the relationship of passive smoking and risk of CHD. A meta-analysis of 19 studies (including three unpublished reports) found a summary relative risk of CHD from exposure to spousal ETS of 1.30 (95% CI: 1.22 to 1.38, P < 0.001). (Law et al, 1997)
4. A meta-analysis of eight epidemiological studies of workplace ETS exposure and CHD found a summary relative risk of 1.18 (95% CI: 1.04 to 1.34).( Glantz and Parmley, 1991; 1995; Wells, 1998)
5. Several plausible mechanisms exist by which ETS exposure can increase the risk of CHD (Kawachi, 1998), including carboxyhemoglobinemia, increased platelet aggregability, increased fibrinogen levels, reduction in HDL-cholesterol, and direct toxic effects of compounds such as 1,3 butadiene (a vapor phase constituent of ETS which has been shown to accelerate atherosclerosis in animal models (Penn and Snyder, 1996).
6. ETS exposure has also been linked to progression of atherosclerosis as measured by B-mode ultrasound of the carotid wall (Howard et al., 1994; Diez-Roux et al., 1995; Howard et al., 1998), as well as to early arterial damage as assessed by endothelium-dependent brachial artery dilatation (Celermajer et al., 1996).
7. The death toll attributable to passive smoking from CHD is estimated to be 10 to 20 times as large as deaths from lung cancer (Wells, 1988, 1994; Glantz and Parmley, 1991; 1994; Steenland, 1992)

Tunstall-Pedoe et al. (1995), in a Scottish cross-sectional study of passive smoking and heart disease in 786 men and 1492 women, found that increasing quantitative measures of serum cotinine in ng/ml correlated to physician-diagnosed heart disease risk, with an odds ratio of 2.7 (95% CI, 1.3-5.6) for the highest vs. the lowest exposure quartile, adjusted for age, housing tenure, total cholesterol, and blood pressure. This is illustrated below in Figure 4.

Figure 4. Dose-response for heart disease and SHS

Figure 4. Risk of physician-diagnosed coronary heart disease in nonsmokers as a function of the level of the nicotine metabolite, cotinine in blood serum, in units of nanograms per milliliter (ng/ml). This is further powerful evidence that SHS exposures are not "low" as the tobacco industry asserts.

Figure 4A below shows the strong dose-response between tobacco smoke exposure and risk of acute stroke in New Zealand (Bonita, et al., 1999).

• Major finding: 82% increased risk of stroke associated with passive smoking in both men and women
• Study confirms risk of stroke in men and women active smokers
• Study shows ex-smokers have risks intermediate between active and passive smokers
• Study demonstrates risk of stroke with active smoking is even higher when reference group excludes ETS exposed nonsmokers
• 521 Cases, 1851 Controls ; Population-Based New Zealand Study. All results statistically significant, Strong dose-response observed

The most recent comprehensive report on secondhand smoke (referred in the report as environmental tobacco smoke or ETS) in the U.S. is that issued by the California Environmental Protection Agency in 1997. The California EPA report concluded that SHS was a cause of cancer, heart disease, and respiratory disease. The major conclusions of the CalEPA Report (Tables ES.1 and ES.2) are reproduced in Figures 5 - 7 below.

Figure 5.

The most recent report on SHS from the UK, the SCOTH Report (1998), also concluded that passive smoking is a cause of lung cancer and childhood respiratory disease, and that passive smoking is a cause of ischaemic heart disease and cot death (SIDS), middle ear disease and asthmatic attacks in children. The SCOTH report concludes that restrictions on smoking in public places and work places are necessary to protect non smokers (SCOTH, 1998).

Figure 6.

In addition to the above, Wells (1998) recently reported that there are now four studies each, which suggest an increased breast cancer risk from both passive smoking (combined OR for never-smokers: 1.71 (95% CI 1.30-2.25), and active smoking (combined OR 2.17 (95% CI 1.63-2.88), respectively.

Figure 7.

Table 1, adapted from the California EPA Report (CalEPA, 1997) gives the State’s estimates of passive smoking-induced disease morbidity and mortality for the U.S.A., and per 10 million population, assuming that the nonsmoking population is similar in exposure and age to the U.S.A., for purposes of estimation in other countries.