Thirty minutes of passive smoking rapidly impaired vascular endothelial function in nonsmokers, decreasing %FMD from 10.9% to 5.0% (p<0.001), which correlated with increased oxidative stress.
Observational (n=30)
Does short-term passive smoking cause endothelial dysfunction and oxidative stress in healthy nonsmokers?
Even 30 minutes of passive smoking rapidly impairs vascular endothelial function and induces oxidative stress in healthy nonsmokers, providing pathophysiological insight into the cardiovascular risks of secondhand smoke.
Absolute Event Rate: 5% vs 10.9%
p-value: p=<0.001
Recent studies have shown that passive smoking impairs vascular endothelial function and induces oxidative stress in humans. However, in most of the previous human data regarding tobacco-induced pathophysiology, vascular endothelial dysfunction and oxidative stress have been separately assessed. This study was designed to determine the association between the acute effect of passive smoking on vascular endothelial function and in-vivo oxidative stress status. We studied 30 healthy male Japanese volunteers (32 +/- 7 years) including 15 habitual smokers and 15 nonsmokers. After baseline echocardiographic, hemodynamic recording, and blood sampling, subjects were exposed to passive smoking for 30 min. Endothelium-dependent vasodilation was measured by using % flow-mediated vasodilation (%FMD) of the brachial artery and plasma levels of 8-isoprostane was measured by enzyme immunoassay before and after the passive smoking exposure. Baseline %FMD was lower (4.3% +/- 1.2% vs. 10.9% +/- 3.1%, p < 0.001) and baseline plasma 8-isoprostane level was higher (41.5 +/- 5.8 pg/mL vs. 26.9 +/- 5.4 pg/mL, p < 0.001) in smokers than those in nonsmokers. The %FMD and 8-isoprostane level did not change after passive smoking in smokers. In nonsmokers, however, the %FMD decreased (to 5.0% +/- 1.9%, p < 0.001) and the 8-isoprostane level increased (to 37.8 +/- 9.6 pg/mL, p < 0.001) significantly after 30 min passive smoking exposure, equivalently to the levels of smokers. Sixty corrected samples before and after passive smoking exposure in all patients showed a significant negative correlation between the % FMD and the plasma 8-isoprostane levels (n = 60, r = -0.69, p < 0.001). Even 30 min of passive smoking rapidly impairs vascular endothelial function, which is associated with oxidative stress. Our data provide the pathophysiological insight for the recent epidemiological evidence about the increased risk of coronary heart disease among nonsmokers exposed to passive smoking.
Kato et al. (Mon,) conducted a observational in Healthy volunteers (n=30). Passive smoking exposure vs. Baseline (before exposure) was evaluated on % flow-mediated vasodilation (%FMD) in nonsmokers (p=<0.001). Thirty minutes of passive smoking rapidly impaired vascular endothelial function in nonsmokers, decreasing %FMD from 10.9% to 5.0% (p<0.001), which correlated with increased oxidative stress.