The committee was tasked with responding to eight specific questions. The questions and the committee’s responses are presented below.
What is the current scientific consensus on the relationship between exposure to secondhand smoke and cardiovascular disease? What is the pathophysiology? What is the strength of the relationship?
On the basis of the available studies of chronic exposure to secondhand smoke and cardiovascular disease, the committee concludes that there is scientific consensus that there is a causal relationship between secondhand-smoke exposure and cardiovascular disease. The results of a number of meta-analyses of the epidemiologic studies showed increases of 25–30% in the risk of cardiovascular disease caused by various exposures. The studies include some that use serum cotinine concentration as a biomarker of exposure and show a dose–response relationship. The pathophysiologic data are consistent with that relationship, as are the data from studies of air pollution and PM. The data in support of the relationship are consistent, but the committee could not calculate a point estimate of the magnitude of the effect (that is, the effect size) given the variable strength of the relationship, differences among studies, poor assessment of secondhand-smoke exposure, and variation in concomitant underlying risk factors.
Is there sufficient evidence to support the plausibility of a causal relation between secondhand smoke exposure and acute coronary events such as acute myocardial infarction and unstable angina? If yes, what is the pathophysiology? And what is the strength of the relationship?
The evidence reviewed by the committee is consistent with a causal relationship between secondhand-smoke exposure and acute coronary events, such as acute MI. It is unknown whether acute exposure, chronic exposure, or a combination of the two underlies the occurrence of acute coronary events, inasmuch as the duration or pattern of exposure in individuals is not known. The evidence includes the results of two key studies that have information on individual smoking status and that showed decreases in risks of acute coronary events in nonsmokers after implementation of a smoking ban. Those studies are supported by information from other smoking-ban studies (although these do not have information on individual smoking status, other exposure-assessment studies have demonstrated that secondhand-smoke exposure decreases after implementation of a smoking ban) and by the large body of literature on PM, especially PM2.5, a