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June 07, 2007

Secondhand smoke causes endothelial dysfunction in kids

by Shelley Wood

Turku, Finland - 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 [1]. The study adds to other evidence demonstrating the harmful effects of passive smoking in teenagers and adults.

Dr Katariina Kallio (University of Turku, Finland) and colleagues report the results of their study online in 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.

To heartwire, Kallio emphasized that while endothelial effects of passive smoking in children might have been expected on the basis of studies in older subjects, the effects were all the more striking because of the low levels of smoke to which children were exposed.

"Parents of these study children smoked less than Finnish adults in general," she told heartwire. "Sixteen per cent of the mothers and 25% of the fathers smoked either daily or occasionally; many of the parents report that they never smoke inside or near their children; and in Finland, smoking is prohibited in public places. Thus, children's exposure to tobacco smoke is not very extensive in general."

Smoke exposure measured directly

Kallio et al's study used data from the ongoing Special Turku Coronary Risk Factor Intervention Project for Children (STRIP), in which concentrations of serum cotinine—a nicotine metabolite and sensitive marker of recent nicotine exposure—were measured annually in kids age eight through 11. As the authors point out, the method permits more precise assessment of cigarette-smoking exposure; other studies have used self-reported hours of secondhand smoke. At age 11, endothelial function was measured using brachial artery endothelium-dependent flow-mediated vasodilation, and values were assessed in relation to cotinine concentrations.

When examined by tertile of cotinine concentration, 11-year-olds with the highest cotinine levels (>1.7 ng/mL) had the greatest attenuation in endothelial dilation, whereas children with undetectable cotinine levels had the least impairment of endothelial function. The trend remained unchanged after researchers controlled for traditional risk factors for atherosclerosis.

Of note, even in the highest-exposure group, cotinine levels were lower than in other studies of British and American children, suggesting that no level of secondhand smoke is safe, Kallio and colleagues emphasize.

"Knowing the tobacco-smoke exposure levels of children in Finland, it was slightly surprising that these differences in endothelial function were found," she told heartwire.

Youth no protection

Commenting on the study for heartwire, Dr Stanton Glantz (University of California, San Francisco) pointed out that endothelial and platelet effects of smoke are believed to be the dominant mechanisms by which smoking damages the cardiovascular system, and the fact that these are occurring even at low exposures, in young people, is important new information.

"This is the first time anybody has shown these endothelial effects in young children, and while I suppose you would have expected this, the possibility always existed that children, as they're developing, might be protected. There's a lot of things about young healthy people that are more robust than older people, so the fact that you're getting this insult to the endothelium in these very young children, and the fact that it's occurring at very low exposure to secondhand smoke, and the fact that there is a dose-response are all very important findings."

Glantz emphasized that the investigators' use of a cut point of >1.7 ng/mL for the highest tertile of exposure was still low, even for a passive smoker.

"Most of the work in this area has been focused on things like asthma and respiratory effects," Glantz observed. "This isn't causing these kids to drop dead of heart attacks, but it is inducing changes that are predictive of developing heart disease later in life and at cotinine levels that are pretty low."

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