coronary event? 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?

  1. the association between secondhand smoke exposure and cardiovascular disease, focusing on coronary heart disease and not stroke (Question 1);

  2. the association between secondhand-smoke exposure and acute coronary events (Questions 2, 3, and 5); and

  3. the association between smoking bans and acute coronary events (Questions 4, 5, 6, 7, and 8).

The committee reviewed the epidemiologic, clinical, and experimental studies relevant to the pathophysiology of secondhand smoke and cardiovascular effects, including coronary heart disease and acute coronary events. The pathophysiologic data not only provide insight into the potential modes of action underlying any effects of secondhand smoke on the cardiovascular system but also provide evidence on a causal relationship between secondhand-smoke exposure and adverse cardiovascular outcomes.

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