Secondhand Smoke Causes Endothelial Dysfunction in Children

Secondhand Smoke Causes Endothelial Dysfunction in Children


from Heartwire — a professional news service of WebMD


June 6, 2007 — Children as young as 11 develop endothelial dysfunction in response to secondhand smoke, in a dose-dependent fashion, even when exposure is minimal, a new study suggests. The study adds to other evidence demonstrating the harmful effects of passive smoking in teenagers and adults. Dr Katariina Kallio (University of Turku, Turku, Finland) and colleagues report the results of their study in a Rapid Access issue of Circulation, June 4, 2007.

"Because endothelial dysfunction related to passive smoking may be only partially reversible after cessation of the exposure, the present data strongly emphasize the importance of implementing smoke-free environments for children at home and in public places," the authors write.

Study Highlites:


Families of 5-month-old infants were invited to participate in this prospective study from Finland. Subjects were randomized to receive education regarding cardiovascular risk factors in childhood or no intervention (control).

Serum cotinine levels were evaluated annually beginning at the age of 8 years, and flow-mediated vasodilatory responses were measured with ultrasonography of the brachial artery at the age of 11 years.

The main study outcome was the relationship between serum cotinine levels and endothelial function. To interpret this relationship, children were stratified into the following levels of cotinine: none, low (0.2 - 1.6 ng/mL), and top decile (1.7 ng/mL or greater). The main study result was adjusted for other cardiovascular risk factors, including serum lipid and high-sensitivity C-reactive protein levels.


402 (73% of the study cohort) children had ultrasound and cotinine data available for analysis. 57% of the children had undetectable levels of cotinine, whereas 33% and 10% of subjects fit into the low- and top-decile cotinine groups, respectively.

No child reported active smoking. 16% of mothers and 25% of fathers smoked.


There was no significant trend across cotinine groups in terms of body mass index, blood pressure, lipid levels, or C-reactive protein values.

Peak endothelium-dependent dilation fell as cotinine levels increased (9.10% in the no-cotinine group vs 8.57% and 7.73% in the low- and top-decile cotinine groups, respectively). This difference was significant after multivariate analysis. Serum cotinine level was also inversely associated with total dilation response.

Cotinine levels had no effect on brachial diameter at baseline, increase in blood flow after cuff release, or endothelium-independent dilation after administration of sublingual nitrate.

When the authors limited their analysis to only children with 4 cotinine values measured between the ages of 8 and 11 years, the relationship between higher cotinine concentrations and impaired endothelial function was even stronger.

Higher levels of low-density lipoprotein cholesterol also impaired flow-mediated dilation, but C-reactive protein levels did not significantly affect this outcome.

Pearls for Practice:

Both active and passive smoking can reduce levels of intra-arterial nitric oxide and impair endothelial function and as little as 30 minutes of passive smoke exposure can induce changes in coronary flow velocity reserve.

The current study demonstrates that exposure to environmental tobacco smoke impairs endothelium-dependent dilation in children.