Traffic-related air pollution and incident asthma in a high-risk birth cohort.
OBJECTIVE
The risk of incident asthma and bronchial hyper-reactivity associated with early life exposure to traffic-related air pollution has not been fully elucidated. We aimed to evaluate the hypothesis that the risk of new onset asthma is positively associated with early exposure to traffic-related air pollution in a well-characterised high-risk birth cohort.


METHODS
Infants at high-risk for asthma were recruited for an intervention study. Birth year exposures to NO, NO(2), black carbon and PM(2.5) were estimated by land use regression. At 7 years of age, asthma was assessed by a paediatric allergist and bronchial hyper-reactivity was measured by methacholine challenge. Associations between exposures and outcomes were analysed by stepwise multiple logistic regression, adjusted for potential confounding variables.


RESULTS
Exposure estimates were available for 184 children; 23 were diagnosed with asthma and 68 with bronchial hyper-reactivity. The IQR (4.1 μg/m(3)) of birth year PM(2.5) was associated with a significantly increased risk of asthma (OR 3.1, 95% CI 1.3 to 7.4) and with a trend to increased risk of bronchial hyper-reactivity. Similar findings were noted in association with NO and NO(2), while black carbon did not appear to confer increased risk.


CONCLUSIONS
Modest elevations in exposure to some traffic-related air pollutants during the year of birth are associated with new onset asthma assessed at age 7. That significant associations were revealed in spite of a limited sample size emphasises the strengths of a high-risk birth cohort model, along with individual air pollution exposure estimates and well-characterised data on covariates and outcomes.
Carlsten
Chris
C
Department of medicine, University of British Columbia, Vancouver, Canada. chris.carlsten@vch.ca
Dybuncio
Anne
A
Becker
Allan
A
Chan-Yeung
Moira
M
Brauer
Michael
M
D000393:Air Pollutants / Q000032:analysis / Q000633:toxicity; D000397:Air Pollution / Q000009:adverse effects* / Q000032:analysis; D001249:Asthma / Q000209:etiology* / Q000235:genetics / Q000517:prevention & control; D016535:Bronchial Hyperreactivity / Q000209:etiology / Q000517:prevention & control; D004781:Environmental Exposure / Q000009:adverse effects / Q000032:analysis; D004784:Environmental Monitoring / Q000379:methods; D004812:Epidemiologic Methods; D062665:Epidemiological Monitoring; D005260:Female; D040362:Geographic Information Systems; D006801:Humans; D007231:Infant, Newborn; D008297:Male; D052638:Particulate Matter / Q000032:analysis / Q000633:toxicity; D001335:Vehicle Emissions / Q000032:analysis / Q000633:toxicity*
D000393:Air Pollutants; D052638:Particulate Matter; D001335:Vehicle Emissions