Glantz S A, Parmley W W
Department of Medicine, University of California, San Francisco 94143-0124.
Circulation. 1991 Jan;83(1):1-12. doi: 10.1161/01.cir.83.1.1.
The evidence that ETS increases risk of death from heart disease is similar to that which existed in 1986 when the US Surgeon General concluded that ETS caused lung cancer in healthy nonsmokers. There are 10 epidemiological studies, conducted in a variety of locations, that reflect about a 30% increase in risk of death from ischemic heart disease or myocardial infarction among nonsmokers living with smokers. The larger studies also demonstrate a significant dose-response effect, with greater exposure to ETS associated with greater risk of death from heart disease. These epidemiological studies are complemented by a variety of physiological and biochemical data that show that ETS adversely affects platelet function and damages arterial endothelium in a way that increases the risk of heart disease. Moreover, ETS, in realistic exposures, also exerts significant adverse effects on exercise capability of both healthy people and those with heart disease by reducing the body's ability to deliver and utilize oxygen. In animal experiments, ETS also depresses cellular respiration at the level of mitochondria. The polycyclic aromatic hydrocarbons in ETS also accelerate, and may initiate, the development of atherosclerotic plaque. Of note, the cardiovascular effects of ETS appear to be different in nonsmokers and smokers. Nonsmokers appear to be more sensitive to ETS than do smokers, perhaps because some of the affected physiological systems are sensitive to low doses of the compounds in ETS, then saturate, and also perhaps because of physiological adaptions smokers undergo as a result of long-term exposure to the toxins in cigarette smoke. In any event, these findings indicate that, for cardiovascular disease, it is incorrect to compute "cigarette equivalents" for passive exposure to ETS and then to extrapolate the effects of this exposure on nonsmokers from the effects of direct smoking on smokers. These results suggest that heart disease is an important consequence of exposure to ETS. The combination of epidemiological studies with demonstration of physiological changes with exposure to ETS, together with biochemical evidence that elements of ETS have significant adverse effects on the cardiovascular system, leads to the conclusion that ETS causes heart disease. This increase in risk translates into about 10 times as many deaths from ETS-induced heart disease as lung cancer; these deaths contribute greatly to the estimated 53,000 deaths annually from passive smoking. This toll makes passive smoking the third leading preventable cause of death in the United States today, behind active smoking and alcohol.
有证据表明，接触环境烟草烟雾会增加心脏病死亡风险，这与1986年美国卫生局局长得出的环境烟草烟雾会导致健康非吸烟者患肺癌的结论时所存在的证据类似。有10项在不同地点进行的流行病学研究表明，与吸烟者共同生活的非吸烟者死于缺血性心脏病或心肌梗死的风险大约增加30%。规模较大的研究还显示出显著的剂量反应效应，接触环境烟草烟雾越多，死于心脏病的风险就越高。这些流行病学研究得到了各种生理和生化数据的补充，这些数据表明，环境烟草烟雾会对血小板功能产生不利影响，并以增加心脏病风险的方式损害动脉内皮。此外，在实际接触水平下，环境烟草烟雾还会通过降低身体输送和利用氧气的能力，对健康人和心脏病患者的运动能力产生显著不利影响。在动物实验中，环境烟草烟雾还会在线粒体水平上抑制细胞呼吸。环境烟草烟雾中的多环芳烃还会加速并可能引发动脉粥样硬化斑块的形成。值得注意的是，环境烟草烟雾对非吸烟者和吸烟者的心血管影响似乎有所不同。非吸烟者似乎比吸烟者对环境烟草烟雾更敏感，这可能是因为一些受影响的生理系统对环境烟草烟雾中的低剂量化合物敏感，然后达到饱和，也可能是因为吸烟者由于长期接触香烟烟雾中的毒素而发生了生理适应。无论如何，这些发现表明，对于心血管疾病来说，计算被动接触环境烟草烟雾的“香烟当量”，然后根据直接吸烟对吸烟者的影响来推断这种接触对非吸烟者的影响是不正确的。这些结果表明，心脏病是接触环境烟草烟雾的一个重要后果。流行病学研究与接触环境烟草烟雾时生理变化的证明相结合，再加上生化证据表明环境烟草烟雾的成分对心血管系统有显著不利影响，得出的结论是环境烟草烟雾会导致心脏病。这种风险的增加导致环境烟草烟雾诱发的心脏病死亡人数大约是肺癌死亡人数的10倍；这些死亡人数在每年估计因被动吸烟导致的53000例死亡中占了很大比例。这一死亡人数使被动吸烟成为当今美国第三大可预防的死亡原因，仅次于主动吸烟和酗酒。
