coronaryevent? If yes, what is known or suspected about how this risk may vary based upon absence or presence (and extent) of preexisting coronary artery disease?

  1. What is the strength of the evidence for a causal relationship between indoor smoking bans and decreased risk of acute myocardial infarction?

  2. What is a reasonable latency period between a decrease in secondhand smoke exposure and a decrease in risk of an acute myocardial infarction for an individual? What is a reasonable latency period between a decrease in population secondhand smoke exposure and a measurable decrease in acute myocardial infarction rates for a population?

  3. What are the strengths and weaknesses of published population-based studies on the risk of acute myocardial infarction following the institution of comprehensive indoor smoking bans? In light of published studies’ strengths and weaknesses, how much confidence is warranted in reported effect size estimates?

  4. What factors would be expected to influence the effect size? For example, population age distribution, baseline level of secondhand smoke protection among nonsmokers, and level of secondhand smoke protection provided by the smoke-free law.

  5. What are the most critical research gaps that should be addressed to improve our understanding of the impact of indoor air policies on acute coronary events? What studies should be performed to address these gaps?

and PM concentrations in regulated venues such as workplaces, bars, and restaurants decreased by more than 80% in most studies; serum, salivary, or urinary cotinine concentrations decreased by 50% or more in most studies, probably reflecting continuing exposures in unregulated venues (for example, in homes and cars).


The pathophysiology of the induction of cardiovascular disease by cigarette-smoking and secondhand-smoke exposure is complex and undoubtedly involves multiple agents. Many chemicals in secondhand smoke have been shown to exert cardiovascular toxicity (see Table 3-1), and both acute and chronic effects of these chemicals have been identified. Experimental studies in humans, animals, and cell cultures have demonstrated effects of secondhand smoke, its components (such as PM, acrolein, polycyclic

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