Background: Environmental tobacco smoke (ETS) acutely affects vascular function through many pathophysiological mechanisms including nicotine sympathoexcitatory effects and oxidative stress. However, a secondary vascular reflex following smoke sensory stimulation cannot be excluded, since the vascular effects of ETS exposure have never been compared to these of a non-tobacco smoke. We therefore tested the hypothesis that acute ETS exposure, when compared to non-tobacco smoke, is responsible for a specific increase in aortic wave reflection and that this is accompanied by an alteration of endothelium dependent microvascular function.

Materials and methods: We examined the vascular effects of one hour ETS exposure, compared to a non-tobacco smoke and a normal-air exposure, in 11 healthy non-smokers men, using a randomized, single blind cross over study design. Augmentation index (AIx), and wave transit time (Tr) have been used to assess aortic wave reflection, while skin microvascular response to a local heating stimulation has been measured with a laser doppler flowmeter to assess endothelial function.

Results: Air particle densities did not differ during the ETS and non-tobacco smoke sessions. We observed no effect of ETS or non-tobacco smoke on central and peripheral blood pressures. However, AIx increased both during (p=0.01) and after (p<0.01) the ETS session, but remained unchanged in the non tobacco smoke session as compared to normal air. A strong correlation between serum nicotine levels (n=10) after ETS exposure and Aix change (r=0.84, p<0.01) was also noted. Tr decreased both during (p=0.02) and after (p<0.01) ETS, but remained unchanged in the non tobacco smoke session as compared to normal air. ETS exposure reduced the skin blood flow response to heating (p=0.03), which was not seen during the non tobacco smoke and the normal air sessions.

Conclusions: Passive exposure to tobacco smoke increases aortic wave reflection and impairs endothelium dependent microvascular function as compared to passive inhalation of non tobacco smoke. The increase in wave reflection after ETS exposure is strongly related to the rise in serum nicotine levels.