LONDON, UK -- August 21, 2007 -- Exhaust fumes heighten the risk of asthma in children who are already genetically susceptible to respiratory disease, indicates research published ahead of print in the journal Thorax.
Variations in the genes that control enzymes responsible for clearing harmful chemicals breathed into the body have been linked to the development of asthma and other respiratory diseases.
The researchers studied microsomal epoxide hydrolase (EPHX1) levels and genetic variations in gluathione S-transferase P1 (GSTP1) in more than 3000 schoolchildren who had been diagnosed with asthma.
Both EPHX1 and GSTP1 are involved in clearing the body of toxins, including polyaromatic hydrocarbons from vehicle emissions.
Children with very active EPHX1 were 1.5 times as likely to have asthma as those with low EPHX1 activity.
Those with high EPHX1 levels, who also carried a variation of the GSTP1 gene were four times as likely to have asthma.
But proximity to road traffic pollution seemed to have a key role in triggering genetic susceptibility.
Children with very active EPHX1 and living within 75 metres of a main road were more than three times as likely to have asthma as those with relatively low EPHX1 levels.
But children with one or two variations in the GSTP1 gene, and who lived close to a major road, were up to nine times as likely to have asthma as those who lived further away
The results were similar, irrespective of whether the asthma was current, had began early, or late (after the age of 3).
The authors conclude that children with high EPHX1 activity, who carry genetic variants of GSTP1 are at greater risk of developing asthma.
But the risk appears to be even greater in those who live close to main roads and are exposed to road traffic pollution, they say.
Click here to view the paper in full: http://press.psprings.co.uk/thx/august/tx80127.pdf
REFERENCE:
Microsomal epoxide hydrolase, glutathione S-transferase P1, traffic and childhood asthma. Online First Thorax 2007; doi: 10.1136/thx.2007.080127.
SOURCE: British Medical Journal
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