Associations of prenatal exposure to air pollution with fetal growth trajectories phenotype in a cohort study: Implications for child neurodevelopment

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Abstract

Sensitive periods of prenatal air pollution exposure on fetal growth and its impact on fetal growth trajectories (FGTs) remain unclear. We investigated the associations of prenatal air pollution exposure with fetal size/FGTs, and their mediating roles in childhood neurodevelopment in a cohort. Air pollutant exposures were estimated using inverse distance weighting. Fetal size was measured by ultrasound; FGTs were identified by Time Series k-means clustering. Multiple linear regression, linear mixed-effect models, and multinomial logistic regression analyzed associations of air pollution with first-trimester crown-rump length (CRL), estimated fetal weight (EFW), and FGTs. Mediation analyses tested the mediating roles. First-trimester NO2, SO2, PM10, and PM2.5 exposures were negatively associated with CRL Z-scores (e.g., per Standard Deviation (SD) SO2 increment: -0.11 (95 % Confidence Interval (CI): -0.16, -0.07)). Mid-pregnancy and third-trimester CO, NO2, SO2, PM10, PM2.5 exposures were negatively associated with EFW Z-scores (e.g., per SD PM2.5 increment (15-20 weeks): -0.10 (95 % CI: -0.13, -0.07)). Higher air pollution exposure was linked to increased odds (9 %-32 %) of high-risk FGTs for neurodevelopment. Mediation analyses results show that first-trimester CRL and mid-pregnancy (15-20 weeks) EFW mediated the effects of air pollution on psychomotor development index (PDI). Late-pregnancy (37-41 weeks) EFW mediated the effects on mental development index (MDI). High-risk FGTs mediated the effects of air pollution on PDI but not MDI. Prenatal air pollution exposure impaired fetal growth (potential sensitive periods: 0-20 and 27-41 weeks) and increased odds of suboptimal FGTs, which mediated the association between prenatal air pollution and poorer 2-year-old neurodevelopment.

Abstract as published, via PubMed.