Effect of passive smoking on endothelial function in: healthy adults

Active smoking predisposes to atherosclerotic vascular disease but recent evidence that inhalation of environmental tobacco smoke (passive smoking) may also have deleterious cardiovascular effects, has enormous public health implications. Endothelial dysfunction is an important early feature of atherogenic process, which may occur due to passive smoking.

To assess the effect of passive smoking on endothelial function (measured by flow-mediated dilatation, a marker of endothelium-dependent arterial dilatation) and compare it with non-smokers.

Case control study.

Out-Patient Department of Medicine, Government Medical College, Nagpur.

Seventy-five young, healthy, male adults between 15-30 years age were studied. There were three groups: (a) Non smokers (n = 25) (b) Passive smokers (n= 25) and (c) Active smokers (n = 25). Subjects with diabetes mellitus, hypertension and ischemic heart disease were excluded. Lipid profile was measured in all. Endothelial function was tested non-invasively by using high frequency linear vascular probe on brachial artery. Resting brachial artery lumen, flow at rest and after hyperemia, flow-mediated dilatation and nitroglycerine-induced dilatation were measured.

The mean brachial artery lumen dilatation and flow at rest were similar in all the three groups. Flow-mediated dilatation (FMD%, a marker of endothelium-dependent dilatation and endothelial function) was significantly higher in non-smokers than passive smokers (8.9 +/- 4.8 Vs 5 +/- 2.3, p < 0.01) and also as compared with active smokers (8.9 +/- 4.8 Vs 6.6 +/- 2.2, p < 0.05). Nitroglycerine-induced dilatation, (a marker of endothelium-independent dilatation ) was similar in all the three groups. Serum lipids (mean cholesterol, LDL, and mean LDL/HDL ratio) were statistically significantly higher in passive and active smokers as compared with non-smokers (p < 0.05).

Like active smoking, passive smoking was also associated with impaired endothelial function, (a key early event in atherogenesis) and altered lipid profile, in healthy young adults.