Published Online
on June 4, 2007

A more recent version of this article appeared on June 26, 2007

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Submitted on November 7, 2006
Accepted on April 17, 2007

Tobacco Smoke Exposure Is Associated With Attenuated Endothelial Function in 11-Year-Old Healthy Children

Katariina Kallio MD^*, Eero Jokinen MD, PhD, Olli T. Raitakari MD, PhD, Mauri Hämäläinen PhD, Marja Siltala , Iina Volanen MD, Tuuli Kaitosaari MD, Jorma Viikari MD, PhD, Tapani Rönnemaa MD, PhD, and Olli Simell MD, PhD

From the Research Centre of Applied and Preventive Cardiovascular Medicine (K.K., M.S., I.V., T.K.), and the Departments of Clinical Physiology (O.T.R.), Medicine (J.V., T.R.), and Pediatrics (O.S.), University of Turku, Turku, Finland; Department of Pediatrics (E.J.), University of Helsinki, Helsinki, Finland; and Joint Clinical Biochemistry Laboratory of University of Turku, Turku University Central Hospital and Wallac Oy (M.H.), Turku, Finland.

^* To whom correspondence should be addressed. E-mail: katariina.kallio{at}utu.fi.

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 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.

Key words: smoking, passive • endothelium • pediatrics • atherosclerosis • ultrasonics

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