June 5, 2007Circulation132 citationsOpen Access
View Full PaperTobacco Smoke Exposure Is Associated With Attenuated Endothelial Function in 11-Year-Old Healthy Children
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).
Study Design
Type
RCT (n=402)
Randomization
randomized
Structured PICO
Does exposure to environmental tobacco smoke impair endothelial function in 11-year-old healthy children?
P
Population
402 healthy 11-year-old children from a randomized atherosclerosis prevention trial were assessed for the impact of passive smoking on endothelial function.
E
Exposure
Exposure to environmental tobacco smoke (passive smoking) assessed by serum cotinine concentrations (low cotinine 0.2-1.6 ng/mL, n=134; top decile >=1.7 ng/mL, n=39)
C
Comparator
Noncotinine group (nondetectable cotinine, n=229)
O
Outcome
Endothelium-dependent flow-mediated vasodilatory responses of the brachial artery (peak flow-mediated dilation response and total dilation response)surrogate
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.
Main Result
Absolute Event Rate: 7.73% vs 9.1%
p-value: p=0.03 for trend
Abstract
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.