Prenatal and childhood exposure to ambient air pollution and cognitive function in school-age children: Examining sensitive windows and sex-specific associations

Abstract

Background

Combined effect of both prenatal and early postnatal exposure to ambient air pollution on child cognition has rarely been investigated and periods of sensitivity are unknown. This study explores the temporal relationship between pre- and postnatal exposure to PM₁₀, PM_2.5, NO₂ and child cognitive function.

Methods

Using validated spatiotemporally resolved exposure models, pre- and postnatal daily PM_2.5, PM₁₀ (satellite based, 1 km resolution) and NO₂ (chemistry-transport model, 4 km resolution) concentrations at the mother's residence were estimated for 1271 mother-child pairs from the French EDEN and PELAGIE cohorts. Scores representative of children's General, Verbal and Non-Verbal abilities at 5–6 years were constructed based on subscale scores from the WPPSI-III, WISC-IV or NEPSY-II batteries, using confirmatory factor analysis (CFA). Associations of both prenatal (first 35 gestational weeks) and postnatal (60 months after birth) exposure to air pollutants with child cognition were explored using Distributed Lag Non-linear Models adjusted for confounders.

Results

Increased maternal exposure to PM₁₀, PM_2.5 and NO₂, during sensitive windows comprised between the 15^th and the 33^rd gestational weeks, was associated with lower males’ General and Non-verbal abilities. Higher postnatal exposure to PM_2.5 between the 35^th and 52^nd month of life was associated with lower males’ General, Verbal and Non-verbal abilities. Some protective associations were punctually observed for the very first gestational weeks or months of life for both males and females and the different pollutants and cognitive scores.

Discussion

These results suggest poorer cognitive function at 5–6 years among males following increased maternal exposure to PM₁₀, PM_2.5 and NO₂ during mid-pregnancy and child exposure to PM_2.5 around 3-4 years. Apparent protective associations observed are unlikely to be causal and might be due to live birth selection bias, chance finding or residual confounding.