Smoke-Free Air: An Important Strategy to Reduce Heart Attacks

Abstract

In September 2011, the United Nations held a high level meeting (heads of state) that concluded that the global burden of noncommunicable diseases posed a threat to development and that identified reducing tobacco use (together with unhealthy diet, physical inactivity, and harmful use of alcohol) as key to reducing the growing global burden of heart and other noncommunicable diseases.[1] While it is widely accepted that tobacco is responsible for a significant disease burden and that reducing tobacco use will reduce these diseases,[2] it is less well-appreciated that reducing exposure to secondhand tobacco smoke produces large and rapid reductions in heart disease-related events, including hospitalization for acute myocardial infarction (AMI).[3] Secondhand smoke (SHS) is a combination of the sidestream smoke from the lit end of a burning cigarette and smoke exhaled by smokers. It is a complex mixture particles and gases, many of which are cardiac toxicants or irritants. SHS is rich in very fine respiratory suspended particulates (RSP) that promote atherosclerosis and trigger heart attacks,[4] so it is not surprising that in 2005 the California Environmental Protection Agency[5] and in 2006 the U.S. Surgeon General concluded that SHS causes coronary heart disease (CHD) morbidity and mortality,[6] with exposure being associated with a 25–30% increased risk. This finding is consistent with the fact that involuntary smokers experience oxidative stress, systemic inflammation, abnormal platelet activation and thrombosis, vascular endothelial dysfunction, and a lowered HDL/LDL ratio and hyperlipidemia, all of which contribute to atherosclerosis, as well as autonomic abnormalities of the heart and vasculature that may trigger a cardiac event.[7, 8] While secondhand smoke is richer in many toxins than mainstream smoke (which is inhaled by smokers),[9] it is more diluted, so involuntary smokers are exposed to substantially smaller doses of these toxins than active smokers. As a result, the 25–30% increase in risk of a cardiac event in involuntary smokers may seem large (compared to the risk of active smoking of 39% for 1 cigarette/day and 78% for 20 cigarettes/day[10]). The explanation for these findings is that the response of the cardiovascular system to the toxins in tobacco smoke is highly nonlinear, with large incremental effects at low doses that tend to saturate at higher levels of exposure.[4, 7, 8, 11]