Abstract
BACKGROUND: Ambient fine particulate matter (PM(2.5)) exposure adversely impacts child airway health; however, research on prenatal PM(2.5) exposure, and child lung function is limited. We investigated these associations in the ECHO-PATHWAYS Consortium, focusing on the role of exposure timing during different phases of fetal lung development. METHODS: We included 675 children in the CANDLE cohort born between 2007 and 2011 in Memphis, TN, USA. Prenatal exposure to ambient PM(2.5) was estimated using a spatiotemporal model based on maternal residential history and averaged over established prenatal periods of lung development. Forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC) were measured by spirometry at age 8-9 years. We used linear regression and Bayesian Distributed Lag Interaction Models (BDLIM) to estimate associations between exposure and lung function z-scores, adjusting for maternal/child characteristics, prenatal/postnatal tobacco exposure, and birth year/season, and evaluating effect modification by child sex and allergic sensitization. RESULTS: The average ambient concentration of PM(2.5) during pregnancy was 11.1 µg/m(3) (standard deviation:1.0 µg/m(3)). In the adjusted linear regression and BDLIM models, adverse, but not statistically significant, associations were observed between exposure during the pseudoglandular (5-16 weeks of gestation) and saccular (24-36 weeks) phases of lung development and FEV1 and FVC. The strongest association was between a 2 μg/m(3) higher concentration of PM(2.5) during the saccular phase and FEV1 z-score (-0.176, 95% Confidence Interval [CI]: -0.361, 0.010). The FEV1/FVC ratio was not associated with PM(2.5) in any exposure window. No effect modification by child sex or allergic sensitization was observed. CONCLUSIONS: We did not find strong evidence of associations between prenatal ambient PM(2.5) exposure and child lung function in a large, well-characterized study sample. However, there was a suggested adverse association between FEV1 and exposure during late pregnancy. The saccular phase of lung development might be an important window for exposure to PM(2.5).