January 18, 1996Open Access
View Full PaperPassive Smoking and Impaired Endothelium-Dependent Arterial Dilatation in Healthy Young Adults
Key Result
Passive smoking in healthy young adults was associated with significantly impaired flow-mediated dilatation compared to unexposed controls (3.1% vs 8.2%; P<0.001), similar to active smokers.
Study Design
Type
Observational (n=78)
Structured PICO
Does passive smoking impair endothelium-dependent arterial dilatation in healthy young adults?
P
Population
78 healthy subjects (39 men and 39 women) 15 to 30 years of age (mean 22 +/- 4)
I
Intervention
Passive smoking (exposure to environmental tobacco smoke for at least one hour daily for three or more years) and active smoking
C
Comparator
Control subjects who had never smoked and had no regular exposure to environmental tobacco smoke
O
Outcome
Flow-mediated endothelium-dependent brachial-artery dilatation during reactive hyperemiasurrogate
Passive smoking is associated with a dose-related impairment of endothelium-dependent dilatation in healthy young adults, indicating early arterial damage.
Main Result
Absolute Event Rate: 3.1% vs 8.2%
p-value: p=<0.001
Abstract
BACKGROUND: Passive smoking has been linked to an increased risk of dying from atherosclerotic heart disease. Since endothelial dysfunction is an early feature of atherogenesis and occurs in young adults who actively smoke cigarettes, we hypothesized that passive smoking might also be associated with endothelial damage in healthy young-adult nonsmokers. METHODS: We studied 78 healthy subjects (39 men and 39 women) 15 to 30 years of age (mean +/- SD, 22 +/- 4): 26 control subjects who had never smoked or had regular exposure to environmental tobacco smoke, 26 who had never smoked but had been exposed to environmental tobacco smoke for at least one hour daily for three 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-dependent dilatation), and after sublingual administration of nitroglycerin (an endothelium-independent dilator). RESULTS: Flow-mediated dilatation was observed in all control subjects (8.2 +/- 3.1 percent; range, 2.1 to 16.7) but was significantly impaired in the passive smokers (3.1 +/- 2.7 percent; range, 0 to 9; P < 0.001 for the comparison with the controls) 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 the passive smokers, there was an inverse relation between the intensity of exposure to tobacco smoke and flow-mediated dilatation (r = -0.67, P < 0.001). In contrast, dilatation induced by nitroglycerin was similar in all groups. CONCLUSIONS: Passive smoking is associated with dose-related impairment of endothelium-dependent dilatation in healthy young adults, suggesting early arterial damage.