Key result
Passive smoking was associated with an attenuated peak flow-mediated dilation response in 11-year-old children (9.10% in noncotinine vs 7.73% in top-decile cotinine group; P=0.03 for trend).
Why the study?
Does exposure to environmental tobacco smoke impair endothelial function in 11-year-old healthy children?
RCT (n=402)
randomized
Does exposure to environmental tobacco smoke impair endothelial function in 11-year-old healthy children?
Absolute Event Rate: 7.73% vs 9.1%
p-value: p=0.03 for trend
Exposure to environmental tobacco smoke impairs endothelial function in a dose-dependent manner in healthy 11-year-old children, highlighting the early vascular harm of passive smoking.
May warrant counseling to reduce children's passive smoke exposure; extends adult data but remains hypothesis-generating.
BACKGROUND: Passive smoking is associated with early arterial damage in adults, but its effect on endothelial function in children is unknown. METHODS AND RESULTS: Serum cotinine concentration was measured annually in children between 8 and 11 years of age who had participated since infancy in a randomized, prospective atherosclerosis prevention trial (Special Turku Coronary Risk Factor Intervention Project for children [STRIP]). At age 11, endothelium-dependent flow-mediated vasodilatory responses of the brachial artery were examined with high-resolution ultrasound in 402 children. These children were divided into 3 groups according to serum cotinine concentrations: the noncotinine group (nondetectable cotinine, n=229), the low cotinine group (cotinine between 0.2 and 1.6 ng/mL, n=134), and the top decile cotinine group (cotinine > or = 1.7 ng/mL, n=39). Longitudinal cotinine data in children aged 8 to 11 years and ultrasound studies were available in 327 children. At age 11, the increase in cotinine concentration was associated with attenuated peak flow-mediated dilation response (mean+/-SD: the noncotinine group 9.10+/-3.88%, the low-cotinine group 8.57+/-3.78%, and the top-decile cotinine group 7.73+/-3.85%; P=0.03 for trend). Similarly, total dilation response (the area under the dilation response versus time curve between 40 and 180 seconds after hyperemia) was affected by the cotinine level (P=0.02 for trend). These trends were not explained by traditional atherosclerosis risk factors. Arterial measures and passive smoking showed even stronger associations when longitudinal cotinine data were used (peak flow-mediated dilation, P=0.01 for trend; total dilation response, P=0.008 for trend). CONCLUSIONS: Exposure to environmental tobacco smoke confirmed by serum cotinine concentrations impairs endothelial function in a dose-dependent manner in 11-year-old children.
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Kallio et al. (2007) conducted an RCT in Healthy children (n=402). Passive smoking (serum cotinine concentration) vs. Noncotinine group (nondetectable cotinine) was evaluated on peak flow-mediated dilation response (p=0.03 for trend). Passive smoking was associated with an attenuated peak flow-mediated dilation response in 11-year-old children (9.10% in noncotinine vs 7.73% in top-decile cotinine group; P=0.03 for trend).
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