BACKGROUND

Mounting evidence suggests that exposure to ambient air pollution is associated with the development of childhood allergic diseases, but the effect of prenatal exposure to air pollution on the risk of childhood asthma and allergy is unclear.

OBJECTIVES

We evaluated the association between maternal exposure to outdoor air pollution during different trimesters of pregnancy and incidence of asthma, allergic rhinitis, and eczema in 2598 preschool children aged 3-6 years in China.

METHODS

Children's lifetime incidence of allergic diseases was obtained using questionnaire. Individual exposure to outdoor air pollutants during trimesters of pregnancy was estimated by an inverse distance weighted (IDW) method based on the measured concentrations at monitoring stations. We used multiple logistic regression method to estimate the odds ratio (OR) of asthma, allergic rhinitis, and eczema for per interquartile range (IQR) increase in the exposure to air pollutant in each trimester, which was adjusted for the effect of other air pollutants and its effect in other trimesters by a multi-pollutant/trimester model.

RESULTS

Incidence of asthma (6.8%), allergic rhinitis (7.3%), and eczema (28.6%) in children was associated with maternal exposure to traffic-related pollutant NO2 during entire pregnancy with OR (95% confidence interval [CI]) respectively 1.63 (0.99-2.70), 1.69 (1.03-2.77), and 1.37 (1.04-1.80). After adjustment for other pollutants and trimesters, we found the association was significant only in specific trimester: the first trimester for eczema (1.54, 1.14-2.09), the second trimester for asthma (1.72, 1.02-2.97), and the third trimester for allergic rhinitis (1.77, 1.09-2.89). Sensitivity analysis indicated that the trimester sensitive to the development of allergic diseases was stable.

CONCLUSION

Maternal exposure to traffic-related air pollutant NO2 during pregnancy, especially in specific trimesters, is associated with an increased risk of developing asthma, rhinitis, and eczema in children. Our results support the hypothesis that childhood allergic diseases originate in fetal life and are triggered by traffic-related air pollution in sensitive trimesters.