ABSTRACT
Although most of the discussion of the health effects of passive smoking on nonsmokers has concentrated on lung cancer (US Environmental Protection Agency, 1992), heart disease is a much more important end-point (Wells, 1988, 1994, 1998; Glantz and Parmley, 1991, 1995; Office of Environmental Health Hazard Assessment, 1997). Whereas passive smoking-induced lung cancer accounts for about 3000 deaths per year, passive smoking-induced heart disease accounts for up to 62 000 deaths annually (Office of Environmental Health Hazard Assessment, 1997), with about an equal number of non-fatal events (Glantz and Parmley, 1991, 1995; Wells, 1994,1998). Epidemiologic studies of the effects of passive smoking on both fatal and non-fatal end-points associated with heart disease reveal about a 30 percent increase in risk (Law et al., 1997), and the American Heart Association has formally concluded that passive smoking is an important risk factor for heart disease in both adults (Taylor et al., 1992) and children (Gidding et al., 1994). The primary issue related to passive smoking and heart disease has been the size of this effect compared with the effect of active smoking on smokers. Active smoking, which involves a dose of the toxins in second-hand smoke that is at least two orders of magnitude greater than a non-smoker receives, only about doubles the risk of heart disease. Thus, the effect of second-hand smoke seems large for the dose, assuming a linear dose-response relationship. There are, however, a wide variety of clinical and experimental studies which demonstrate that the effects of second-hand smoke on the cardiovascular system occur at low doses in non-smokers, with the effects being about one-third of that observed in active smokers. These effects are manifest through effects on platelets and vascular function, among other end-points. The doseresponse relationship between second-hand smoke exposure and heart disease is probably not linear; it is superlinear.
