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, 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. 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.
RCT Entities:
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, 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. 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.
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