Maternal exposure to ambient air pollution and risk of congenital heart defects in offspring: A population-based cohort study in Wuhan, China.

BACKGROUND

Existing evidence on maternal ambient air pollutants exposure during pregnancy and the risk of congenital heart defects (CHDs) and its subtypes in offspring is inconsistent, and few studies have focused on preconception exposure. The critical susceptibility window for air pollutants linked to CHDs remains poorly answered.

OBJECTIVE

We aimed to explore whether maternal exposure to ambient air pollutants before and after conception were associated with the risk of CHDs and its subtypes, and determined the critical susceptibility windows and potential modifiers for air pollutants exposure on CHDs.

METHODS

We conducted a population-based cohort through the Wuhan Maternal and Child Health Management Information System in Wuhan, China, and heart defects data and daily air pollutants concentrations were collected from 2011 to 2017. Individual exposure concentrations of air pollutants were estimated through the inverse distance weighted method. The associations between maternal air pollutants exposure and the risk of CHDs were evaluated using logistic regression models with controlling for covariates.

RESULTS

A total of 510,857 infants participated, with 1055 diagnosed with CHDs. Maternal exposure to PM2.5 in the three months before conception (OR = 1.022, 95 % CI: 1.004-1.039), second and third month of conception (OR = 1.042, 95 % CI: 1.024-1.060; OR = 1.039, 95 % CI: 1.021-1.057, separately) were significantly related to CHDs. The associations of PM2.5 exposure with CHDs were modified by maternal parity and infant sex. For CHD subtypes, we observed the positively relationships between PM2.5 exposure and ventricular septal defect and tetralogy of Fallot. No significant association between exposure to SO2, NO2, CO, and O3 and the risk of CHDs and its subtypes was observed. The second month of conception might be the potential critical susceptibility window of air pollutants with CHDs.

CONCLUSION

Our findings have revealed that maternal exposure to PM2.5 before and after conception increased the risk of CHDs and its subtypes in offspring, as well as identified the modifications of individual characteristics and potential critical susceptibility windows. These results provide potential evidence for improving air quality and focusing on individual characteristics to prevent CHDs.