The effects of acute passive smoke exposure on endothelium-dependent brachial artery dilation in healthy individuals

Passive smoking has both short-term and long-term vascular effects. It is not clear whether impairment of endothelial function reflects the acute effects of passive smoke exposure or the chronic effects. The purpose of this study was to assess the hypothesis that short-term exposure to passive smoke impairs endothelium-dependent vasodilation in healthy nonsmokers. Eighteen healthy young never smokers (12 men, 6 women) 21 to 55 years old (mean SD: 34 9 years) underwent ultrasonography measuring baseline brachial-artery diameter and brachial-artery diameter during hyperemia and after sublingual administration of nitroglycerin, twice: in a smoke-free environment, and then in the same environment polluted by 30 to 35 ppm carbon monoxide. Each subject served as his/her control. Carboxyhemoglobin was measured in blood samples of subjects tested. Mean value of carboxyhemoglobin was 0.6 +/- 0.5% in a smoke-free environment and 1.4 +/- 0.5% in a smoking environment (p < 0.02). Mean values of flow-mediated dilation (FMD) were 12.6% +/- 7.8% in a smoke-free environment versus 6.8 +/- 7.8% in a smoking environment (p < 0.01). On the contrary, nitroglycerin-induced vasodilation did not show any statistical difference (21 +/- 9.8% versus 23 +/- 1.4%). Finally, the increase of carboxyhemoglobin was related statistically to the impairment of flow-mediated dilation (r = 0.51; p < 0.002). Passive smoking impaired flow-mediated vasodilation in healthy never smokers in a smoking environment. The impairment was strongly related to carboxyhemoglobin level.