Response to Lead, Smoking, and Peripheral Vascular Function
Tobacco smoke contains thousands of different compounds, including a mixture of metals such as aluminum, arsenic, cadmium, chromium, copper, lead, mercury, nickel, and zinc. In our study, 1-hour exposure to passive smoking exerted some acute deleterious effects on aortic wave reflection and microvascular function.1 We incriminated the neurohumoral effects of nicotine as a main determinant of the cardiovascular reaction after environmental tobacco smoke exposure. However, a potential hazardous effect of other components (such as metals) contained in the tobacco smoke cannot be ruled out by the present study. In addition, we reported recently in vitro that the acute endothelial toxicity of passive smoking cannot be simply ascribed to a nicotine-dependent mechanism.2
We appreciate the letter by Kisters et al,3 and we agree that a nonnicotinic tobacco component, such as metal constituents, may also impair the vascular endothelium. Indeed, metals enhance oxidative stress of cytoskeletal proteins4 and damage endothelial cell gene transcription.5 We also believe that further works are needed to examine the contribution of metal exposure to arteriosclerosis arising from active and passive smoking.
Sources of Funding
This study was supported and funded by the Erasme Foundation, AstraZeneca, Pfizer, Medtronic, Novartis, the David and Alice Van Buuren Fund, the Belgian National Fund for Research, the Lambertine Lacroix Prize, the Foundation Saucez-Van Poucke, and the Foundation for Cardiac Surgery. None of the funding sources intervened in any aspects of the study.
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