title: Short-term passive smoking causes endothelial dysfunction via oxidative stress in nonsmokers.
abstract: 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.
authors.affiliation: Department of Cardiovascular and Renal Medicine, Saga University Faculty of Medicine, 5-1-1 Nabeshima, Saga 849-8501, Japan. katotor@med.saga-u.ac.jp
authors.forename: Toru
authors.initials: T
authors.lastname: Kato
authors.forename: Teruo
authors.initials: T
authors.lastname: Inoue
authors.forename: Toshifumi
authors.initials: T
authors.lastname: Morooka
authors.forename: Nobuo
authors.initials: N
authors.lastname: Yoshimoto
authors.forename: Koichi
authors.initials: K
authors.lastname: Node
mesh_terms: D000328:Adult; D050197:Atherosclerosis / Q000209:etiology; D015415:Biomarkers / Q000097:blood; D001916:Brachial Artery / Q000502:physiology; D002784:Cholesterol / Q000097:blood; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D008297:Male; D005996:Nitroglycerin / Q000494:pharmacology; D018384:Oxidative Stress; D012307:Risk Factors; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*; D014664:Vasodilation / Q000187:drug effects
chemical_list: D015415:Biomarkers; D014028:Tobacco Smoke Pollution; C075750:8-epi-prostaglandin F2alpha; D002784:Cholesterol; D015237:Dinoprost; D005996:Nitroglycerin