Thursday, March 4, 2010

Even Low-Level Smoke Exposure Increases Atherosclerosis and Lipid Changes in Adolescents

From Heartwire
Sue Hughes

March 4, 2010 (Turku, Finland) — Healthy adolescents frequently exposed to tobacco smoke have arterial changes associated with preclinical atherosclerosis and increased apolipoprotein B (apoB) levels, a new study has shown [1].

The study, published online March 2, 2010 in Circulation: Cardiovascular Quality and Outcomes, was conducted by a group led by Dr Katariina Kallio (University of Turku, Finland).

"Our findings suggest that children should not face exposure to tobacco smoke at all," Kallio said in a press statement. "Even a little exposure to tobacco smoke may be harmful for blood vessels. We need to provide children with a smoke-free environment."

In the paper, the authors explain that passive smoking has been associated with increased carotid intima-media thickness (IMT) in adults, but no studies have previously examined the impact of exposure to tobacco smoke on IMT in healthy children or adolescents.
In addition, it is known that exposure to environmental tobacco smoke may lead to alterations in serum lipid profile in adults, but there are no data on the relation of tobacco-smoke exposure and lipoprotein levels in children.

The current study involved 494 healthy 13-year-old children who were recruited as infants into Finland's Special Turku Coronary Risk Factor Intervention Project (STRIP), which began in 1990 and is aimed at lowering children's risks of heart disease by controlling their exposure to known environmental dangers.

Maximum carotid and aortic IMT and brachial-artery flow-mediated dilation were measured using high-resolution ultrasound. Serum lipid, lipoprotein, and apoA-I and B concentrations were also determined.
Long-term exposure levels to secondhand smoke were estimated by measuring blood levels of cotinine, a byproduct of nicotine that indicates how much tobacco smoke was encountered over the past few days.
Most study participants had six annual blood tests for cotinine levels. These results were averaged, and the participants were divided into three levels of tobacco exposure: high (163 participants), intermediate (171), and low (160).

Results showed that maximum IMT in both the carotid and aorta increased as exposure to cigarette smoke increased, and endothelial function as measured by brachial artery flow-mediated dilation was decreased in the highest-exposure group compared with the lowest. In addition, apoB and apoB/apoA-I ratio increased with increases in cotinine level.

The authors comment: "The present study suggests that even modest exposure to tobacco smoke is associated with increased IMT. As thickness of the arterial wall is a marker of early atherosclerosis, our data suggest that exposure to tobacco smoke may play a role in the development of atherosclerosis."

They note that the results also confirm previous findings reported in 11-year-old children showing an association between secondhand-smoke exposure and endothelial dysfunction. They suggest that endothelial dysfunction may be the first phenomenon in subclinical atherosclerosis preceding the thickening of the vascular wall.

Mechanisms by which exposure to tobacco smoke increases IMT are put forward, including direct toxic effects of cigarette-smoke constituents on endothelial permeability and structure, enhanced platelet activity so that they bind to injured areas and promote growth of smooth-muscle cells, and increased lipid peroxidation in combination with accelerated uptake of LDL cholesterol by macrophages.

On the apoB and apoB/apoA-I ratio results, they note that the concentration of apoB provides a direct measure of the number of circulating atherogenic lipoproteins, the apoB/apoA-I ratio represents the balance of proatherogenic and antiatherogenic lipoproteins, and childhood levels of apoB/apoA-I ratio predict carotid IMT and endothelial function in adulthood. They point out that the apoB/apoA-I ratio in adults is a strong predictor of coronary events and that it may be the best single lipoprotein variable related to coronary risk.

They add that in the present study, exposure to tobacco smoke had an independent association with apoB, but this did not confound the association between passive smoking and IMT.
Thus, although exposure to tobacco smoke can promote atherosclerosis in part by the effects on apoB metabolism, this did not fully explain the relation between smoke exposure and IMT shown in this study.

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