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

BACKGROUND: Combined effect of both prenatal and early postnatal exposure to ambient air pollution on child cognition has rarely been investigated and sensitive periods of sensitivity are unknown. This study explores the temporal relationship between pre- and postnatal exposure to PM10 , PM2.5 , NO2 and child cognitive function.

METHODS: Using validated spatiotemporally resolved exposure models, pre- and postnatal daily PM2.5 , 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: Median exposure from conception until the 60th month of life was 19.3 μg/m3 for PM10 , 12.4 μg/m3 for PM2.5 and 16.9 μg/m3 for NO2 . Increased maternal exposure to both PM10 and PM2.5 between the 5th and the 11th gestational weeks was related to higher General, Verbal and Non-verbal abilities among males. On the contrary, increased maternal exposure to PM10 between the 22nd and 29th gestational weeks was associated with lower General and Non-verbal abilities among males. Similar trends were observed for PM2.5 . No significant sensitive exposure windows were detected for postnatal exposure, NO2 or among females.

DISCUSSION: These results suggest poorer cognitive development among males at 5-6 years following increased maternal exposure to PM10 during mid-pregnancy. Apparent protective associations observed for early prenatal exposure to PM10 and PM2.5 are unlikely to be causal and might be due to live birth selection bias.