Passive Smoking and Impaired Endothelium-Dependent Arterial Dilatation in Healthy Young Adults
David S. Celermajer, Ph.D., Mark R. Adams, M.B., B.S., Peter Clarkson, M.B., B.S., Jacqui Robinson, R.N., Robyn McCredie, B.Sc., Ann Donald, and John E. Deanfield, M.B., Ch.B.
Background Passive smoking has been linked to an increased riskof dying from atherosclerotic heart disease. Since endothelialdysfunction is an early feature of atherogenesis and occursin young adults who actively smoke cigarettes, we hypothesizedthat passive smoking might also be associated with endothelialdamage in healthy young-adult nonsmokers.
Methods We studied 78 healthy subjects (39 male and 39 female)15 to 30 years of age (mean ±SD, 22±4): 26 controlsubjects who had never smoked or had regular exposure to environmentaltobacco smoke, 26 who had never smoked but had been exposedto environmental tobacco smoke for at least one hour daily forthree or more years, and 26 active smokers. Using ultrasonography,we measured the brachial-artery diameter under base-line conditions,during reactive hyperemia (with flow increase causing endothelium-dependentdilatation), and after sublingual administration of nitroglycerin(an endothelium-independent dilator).
Results Flow-mediated dilatation was observed in all controlsubjects (8.2±3.1 percent; range, 2.1 to 16.7) but wassignificantly impaired in the passive smokers (3.1±2.7percent; range, 0 to 9; P<0.001 for the comparison with thecontrols) and in the active smokers (4.4±3.1 percent;range, 0 to 10; P<0.001 for the comparison with the controls;P = 0.48 for the comparison with the passive smokers). In thepassive smokers, there was an inverse relation between the intensityof exposure to tobacco smoke and flow-mediated dilatation (r= -0.67, P<0.001). In contrast, dilatation induced by nitroglycerinwas similar in all groups.
Conclusions Passive smoking is associated with dose-relatedimpairment of endothelium-dependent dilatation in healthy youngadults, suggesting early arterial damage.
Source Information
From the Department of Cardiology, Royal Prince Alfred Hospital (D.S.C., M.R.A., J.R., R.M.), and the Heart Research Institute (D.S.C., J.R., R.M.), Sydney, Australia; and the Cardiothoracic Unit, Hospital for Sick Children, London (P.C., A.D., J.E.D.).
Address reprint requests to Dr. Celermajer at the Department of Cardiology, Royal Prince Alfred Hospital, Missenden Rd., Camperdown 2050, Sydney, Australia.
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