Objectives 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, NO2, black carbon and PM2.5 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/m3) of birth year PM2.5 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 NO2, while black carbon did not appear to confer increased risk.
Conclusion 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.
- Air pollution
- birth cohort
- bronchial hyper-reactivity
- land use regression
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Funding This study was supported by the Canadian Institutes of Health Research, the British Columbia Lung Association and the British Columbia Children's Hospital.
Competing interests None.
Ethics approval This study was conducted with the approval of the University of British Columbia Clinical Research Ethics Board.
Provenance and peer review Not commissioned; externally peer reviewed.