Key result
Acute exposure to passive smoking for 30 minutes reduced flow-mediated dilatation from 18.6% to 12.4%.
Why the study?
Does acute exposure to passive smoking impair endothelial function in healthy nonsmokers?
Observational (n=61)
Does acute exposure to passive smoking impair endothelial function in healthy nonsmokers?
Even brief (30-minute) exposure to low concentrations of passive smoke significantly impairs endothelial function in healthy nonsmokers.
Answers are grounded in this paper and cite their sources.
Acute passive smoking exposure may impair endothelial function; extends mechanistic evidence but should not yet change practice.
Impairment of endothelial functions has been shown to occur after acute and chronic exposure to passive smoking (PS), as assessed by flow-mediated dilatation (FMD) of the brachial artery. A total of 61 participants, 30 male and 31 female, mean ages 26 (18-36) were enrolled in the study. All were clinically well and nonsmokers. All participants stayed for 30 minutes in the smoking room. Carbon monoxide (CO) level was 7.42 ± 0.98 ppm (4.71-10.50). Mean carboxyhemoglobin (COHb) levels of participants were significantly elevated after PS. Mean FMD was 18.6% ± 9% and decreased to 12.4% ± 7% after PS (P < .001). In the current study, with more number of participants at lower CO concentrations (7.42 ppm) and with smaller increase in COHb (51%) significant reduction (33%, P < .001) in FMD was observed.
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Gül et al. (2010) conducted an observational in Healthy nonsmokers (n=61). Passive smoking vs. Baseline (before exposure) was evaluated on Flow-mediated dilatation (FMD) of the brachial artery (33% reduction, p=< .001). Acute exposure to passive smoking for 30 minutes reduced flow-mediated dilatation from 18.6% to 12.4%.
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