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Even a little secondhand smoke is dangerous.

AS MORE AND MORE NONSMOKERS HAVE COME TO UNderstand the dangers associated with breathing secondhand smoke, the number of communities enacting ordinances requiring smoke-free workplaces and public places has increased rapidly. As of May 2001, hundreds of communities had enacted laws requiring smokefree workplaces, smoke-free restaurants, and smoke-free bars. California requires all workplaces, including restaurants and bars, to be smoke-free. The theme for the World Health Organization’s World No Tobacco Day in 2001 was “clean indoor air” and communities throughout the world are beginning to clear the air of secondhand smoke. Not only do the laws protect nonsmokers from the toxins in secondhand smoke, but they also create an environment that helps smokers cut down or stop smoking. The tobacco industry’s efforts to slow the spread of smokefree environments has included a systematic effort to attempt to undermine the scientific evidence that passive smoking causes disease. One common theme is that the dose of toxins a nonsmoker inhales is tiny compared with the dose the smoker receives, implying that the risks are trivial or nonexistent. Such statements are based on measuring the delivered dose of 1 or more of the 4000 chemicals in secondhand smoke. The problem with such calculations is they can be manipulated by selecting the particular constituent of smoke to be the one that has low absorption or rapid clearance. The real measure of effect should not be the dose of one chemical or another, but rather the biological effect of breathing the secondhand smoke. The article by Otsuka and colleagues in this issue of THE JOURNAL adds substantially to the case that short-term passive smoking adversely affects endothelial function in ways that immediately compromise the cardiovascular system. The investigators demonstrated that, in healthy young volunteers, just 30 minutes of exposure to secondhand smoke compromised the endothelial function in coronary arteries of nonsmokers in a way that made the endothelial response of nonsmokers indistinguishable from that of habitual smokers. The investigators measured blood pressure, heart rate, and coronary flow velocity reserve before and after administering adenosine triphosphate using transthoracic Doppler echocardiography of the left anterior descending coronary artery. This innovative noninvasive approach to measuring coronary endothelial function appears to be ideal in these individuals, who have no evidence of coronary disease. Significantly, these substantial changes in endothelial function were not associated with changes in heart rate or blood pressure. Endothelial dysfunction may be at the heart of the development of atherosclerosis. Normal endothelial cells promote vasodilation and inhibit atherosclerosis and thrombosis, in part because of the release of nitric oxide. Dysfunctional cells, on the other hand, contribute to vasoconstriction, atherogenesis, and thrombosis. Risk factors contribute individually to endothelial dysfunction and appear to be additive. One possible unifying hypothesis for the effects of risk factors is that they increase oxidative stress that mediates these effects. Thus, reduction of risk factors improves endothelial function and reduces clinical coronary events. For example, in patients with hyperlipidemia, lipid lowering improves endothelial function both acutely and chronically. The findings of Otsuka et al are important not only because they illustrate the importance of preventing nonsmokers from any exposure to secondhand smoke, but also because they help to explain the relatively large risk of death and other cardiac events associated with passive smoking compared with active smoking. Passive smoking increases the risk of cardiac death or morbidity about 30% compared with a doubling to quadrupling of risk associated with active smoking. Thus, the effect of passive smoking is as high as one third the effect of active smoking even though the dose of at least some of the constituents is much less than what the smoker inhales.