Abstract

BACKGROUND AND AIM: There is increasing evidence indicating that air pollution exposure is associated with neuronal damage. Since pregnancy is a critical window of vulnerability, air pollution exposure during this period could have adverse effects on neurodevelopment. This study aims 1) to analyze associations of prenatal exposure to indoor air pollution (particulate matter with diameters ≤10μm, PM10) and tobacco smoke on neurodevelopment and 2) to determine if these associations are mediated by deviations of epigenetic gestational age from chronological gestational age (ΔGA). METHODS: Data of 734 children from the South African Drakenstein Child Health Study were analyzed. Antenatal PM10 exposure was measured using devices placed in the families’ homes. Maternal smoking during pregnancy was determined by maternal urine cotinine measures. Bayley Scales of Infant Development were used to measure cognition, language, motor, and adaptive behavior development at two years of age. Overall composite scores were calculated as the average of the four sub-scores. Linear regression models adjusted for maternal age, gestational age, sex of child, ancestry, birth weight/length, and socioeconomic status were used to explore associations. A mediation analysis was conducted to analyze if the associations were mediated by ΔGA using DNA methylation measurements from cord blood. RESULTS:An increase of one interquartile range in PM10 (54.40μg/m3) was significantly associated with lower cognition sub-scores (β-estimate [95%-confidence interval]: -0.01 [-0.22, 0.00]). Maternal smoking was significantly associated with lower overall composite scores (-1.84 [-3.52, -0.16]) and lower adaptive behavior sub-scores (-3.39 [-5.63, -1.14]). Other scores were not associated with PM10 or smoking. Associations were not significantly mediated by ΔGA (e.g., for PM10 and cognition, proportion mediated [95%-confidence interval]: 1% [-18, -20%]). CONCLUSIONS:We found an association of prenatal exposure to indoor air pollution (PM10) and tobacco smoke on neurodevelopment at 2 years of age. Further research is needed to understand underlying biological mediators. KEYWORDS: Air pollution, Particulate matter, Neurodevelopmental outcomes, Environmental epidemiology, Epigenomics

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