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Traffic Fumes Plus Genes Boosts Kids' Asthma Risk
Date:8/22/2007

Study finds some children are more vulnerable

WEDNESDAY, Aug. 22 (HealthDay News) -- Traffic pollution raises asthma risk in children who are already genetically susceptible to the disease, according to a new study of more than 3,000 asthmatic children.

According to a team at the University of Southern California Keck School of Medicine, Los Angeles, prior research had spotted variations in genes that control enzymes responsible for clearing harmful chemicals breathed into the body. These gene variants have also been linked to the development of asthma and other respiratory diseases.

In this new study, researchers analyzed the children's microsomal epoxide hydrolase (EPHX1) levels and genetic variations in gluathione S-transferase P1 (GSTP1) -- enzymes that help rid the body of toxins, including polyaromatic hydrocarbons from vehicle exhaust.

Overall, children with very active EPHX1 were 1.5 times more likely to have asthma as children with low EPHX1 activity, and those who had high EPHX1 activity and a variation in the GSTP1 gene were four times more likely to have asthma.

The researchers also found that exposure to traffic pollution was a major factor in triggering genetic susceptibility to asthma.

Children with very active EPHX1 who lived within 75 meters of a main road were more than three times as likely to have asthma as those with low EPHX1 levels. But children with one or two variations in the GSTP1 gene who lived close to a major road were up to nine times more likely to have asthma than children who lived farther away from a major road.

Children with high EPHX1 activity who have genetic variants of GSTP1 have an increased risk of developing asthma, the researchers said, and the risk is even greater among those who are exposed to traffic pollution.

The study is published in the journal Thorax.

More information

The American Lung Association has more about childhood asthma.



-- Robert Preidt



SOURCE: BMJ Specialist Journals, news release, Aug. 21, 2007


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