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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Atherosclerosis, Brachial Artery, Child, Cohort Studies, Cotinine, Dose-Response Relationship, Drug, Endothelium, Vascular, Female, Finland, Follow-Up Studies, Hemorheology, Humans, Life Style, Male, Nitric Oxide, Observer Variation, Parents, Prospective Studies, Risk Factors, Surveys and Questionnaires, Tobacco Smoke Pollution, Ultrasonography, Vasodilation.
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Is tobacco smoke exposure associated with attenuated endothelial function in 11-year-old healthy children? Context: Passive smoking is associated with early arterial damage in adults, but its effect on endothelial function in children is unknown. 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).
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Exposure to environmental tobacco smoke confirmed by serum cotinine concentrations impairs endothelial function in a dose-dependent manner in 11-year-old children. Final Decision: yes