exposure and coronary heart disease and was the precursor to work on the effects of secondhand smoke on acute coronary events. The epidemiologic studies that investigated the relationship are discussed briefly here and then what is known regarding the dose–response relationship and the potential biases and confounding effects that could affect the relationship.

Epidemiologic Evidence

Many prospective cohort studies and case–control studies have examined the association between exposure to secondhand smoke and the risk of coronary heart disease (Butler, 1988; Chen et al., 2004; Ciruzzi et al., 1998; Dobson et al., 1991; Garland et al., 1985; He, 1989; He et al., 1994; Helsing et al., 1988; Hole et al., 1989; Humble et al., 1990; Jackson, 1989; Kawachi et al., 1997; La Vecchia et al., 1993; Layard, 1995; Lee et al., 1986; LeVois and Layard, 1995; McElduff et al., 1998; Muscat and Wynder, 1995; Pitsavos et al., 2002; Rosenlund et al., 2001; Sandler et al., 1989; Steenland et al., 1996; Svendsen et al., 1987; Tunstall-Pedoe et al., 1995; Whincup et al., 2004). They all showed a trend toward increased risk of coronary heart disease associated with secondhand smoke; most but not all of the relative risk (RR) estimates in individual studies were statistically significant. Several published meta-analyses of the epidemiologic studies pooled RR estimates from individual studies and showed a significant 25–30% increase in the risk of coronary heart disease associated with various exposures to secondhand smoke (Barnoya and Glantz, 2005; He et al., 1999; HHS, 2006; Law et al., 1997; Thun et al., 1999; Wells, 1994, 1998). Two recent and comprehensive meta-analyses are particularly worthy of mention (He et al., 1999; HHS, 2006).

He et al. (1999) conducted a meta-analysis of secondhand smoke and the risk of coronary heart disease in nonsmokers. A total of 10 prospective cohort studies and 8 case–control studies were included (Butler, 1988; Ciruzzi et al., 1998; Dobson et al., 1991; Garland et al., 1985; He, 1989; He et al., 1994; Hirayama, 1990; Hole et al., 1989; Humble et al., 1990; Jackson, 1989; Kawachi et al., 1997; La Vecchia et al., 1993; Lee et al., 1986; Muscat and Wynder, 1995; Sandler et al., 1989; Steenland et al., 1996; Svendsen et al., 1987). In all the cohort studies, the outcome was myocardial infarction (MI) or death due to coronary heart disease. Secondhand-smoke exposure at home was measured in all the cohort studies, but only four measured workplace exposure. In four case–control studies, secondhand-smoke exposure was assessed both at home and in the workplace; in the other four, it was assessed only at home. Such incomplete exposure assessment biases results towards the null. Overall, nonsmokers exposed to secondhand smoke had an RR of coronary heart disease of 1.25 (95% confidence interval [CI], 1.17–1.32) compared with nonsmokers not



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