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Published on: February 12, 2015
Tobacco smoke exposure is associated with attenuated endothelial function in 11-year-old healthy children
Katariina Kallio1, Eero Jokinen, Olli T Raitakari
1Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Kiinamyllynkatu 10, FIN-20520 Turku, Finland. katariina.kallio@utu.fi
Insights
Passive smoking, measured by serum cotinine, harms endothelial function in children. This study shows a dose-dependent impairment of blood vessel dilation in 11-year-olds exposed to environmental tobacco smoke.
Area of Science:
- Pediatric cardiology
- Environmental health
- Vascular biology
Background:
- Passive smoking is linked to arterial damage in adults.
- Its impact on children's endothelial function remains unclear.
Purpose of the Study:
- To investigate the effect of passive smoking on endothelial function in children.
- To determine if cotinine levels correlate with vascular health in pediatric subjects.
Main Methods:
- Longitudinal study of children (8-11 years) in a prospective atherosclerosis prevention trial.
- Serum cotinine levels measured annually.
- Endothelium-dependent flow-mediated dilation of the brachial artery assessed via ultrasound at age 11.
Main Results:
- Increased serum cotinine concentration was associated with reduced flow-mediated dilation in 11-year-old children.
- A dose-dependent relationship was observed between cotinine levels and impaired endothelial function.
- These associations persisted even after accounting for traditional risk factors.
Conclusions:
- Environmental tobacco smoke exposure, verified by cotinine levels, negatively impacts endothelial function in children.
- The findings indicate a dose-dependent impairment of vascular health in children exposed to passive smoke.
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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