Passive smoking and early arterial damage.

Active cigarette smoking has long been known to predispose to atherosclerotic vascular disease, but recently passive smoking has been identified as an important risk factor for cardiovascular morbidity and mortality, accounting for up to 20 000 deaths per year in non-smokers in the United States alone' 1 '. Cigarette smoking has deleterious effects on haemodynamics, myocardial perfusion and response to anti-anginal drugs in patients with coronary artery disease and we have previously reported evidence of damage to the vascular endothelium, a key early event in the atherogenic process, in the systemic arteries of young smokers before clinical evidence of arterial disease' 21. In a recent study, we have now been able to demonstrate that endothelial dysfunction may also occur in teenagers and young adults as the result of environmental tobacco smoke exposure' 3 '. Furthermore, the endothelial dysfunction that results is dose-related and may be equivalent to the degree of vascular abnormality in age-matched active smokers. Seventy-eight healthy men and women (age 15-30 years) were studied using a non-invasive high resolution ultrasound technique to compare brachial artery vascular responses to increased flow (an endothelium-dependent dilator stimulus) and to nitroglycerin (an endothelium-independent dilator). Twenty-six of the subjects had never smoked nor had had regular exposure to environmental tobacco smoke, 26 were non-smokers but had had environmental tobacco smoke exposure for at least 1 h per day for 3 or more years and 26 were active cigarette smokers. The three groups were matched for other important baseline characteristics, including blood pressure, lipid profiles and vessel size. Flow mediated dilatation was markedly impaired in the passive smokers to an equivalent degree to that seen in young active smokers. When the average intensity of exposure to environmental tobacco smoke was assessed by questionnaire, there was a significant inverse relationship between the environmental tobacco smoke intensity and endothelial-dependent arterial function. In contrast, arterial responses to nitroglycerin, whose action is independent of endothelial function, were normal in all three groups. Clearly, no quantitative comparison between the deleterious effects of active and passive smoking is possible from this study, but the findings suggest that the toxic substance or substances responsible for vascular injury at this early stage appear to be present in both environmental and inhaled cigarette smoke. Environmental tobacco smoke consists of approximately 85% sidestream smoke (from the burning ends of cigarettes) and 15% exhaled mainstream smoke. It is noteworthy that many toxic components such as …