Prenatal air pollution and early childhood asthma

Abstract

PDS 68: Outdoor air pollution, mortality and morbidity, Exhibition Hall (PDS), Ground floor, August 26, 2019, 10:30 AM - 12:00 PM Background: Prior studies suggest that prenatal air pollution may perturb normal fetal lung development and contribute to risk of child asthma, but few have had opportunity to investigate developmental windows of susceptibility or have been limited in exposure assessment or covariate adjustment. Methods: Our study population included participants in two pregnancy cohorts within the ECHO-PATHWAYS consortium, CANDLE (births in 2007-2011) in Memphis, TN and TIDES (births in 2011-2013) in Seattle, WA; San Francisco, CA; and Minneapolis, MN, who had term births (37+ weeks). Child asthma was defined based on parent-report of ever asthma. Exposure to ambient fine particulate matter (PM2.5) during prenatal phases of fetal lung development was estimated using a spatiotemporal model. We used Poisson regression and adjusted for city, child sex, year and season of birth, maternal race, education, asthma, age at delivery, prior live births, pre-pregnancy body mass index, prenatal smoking, child’s postnatal secondhand smoke exposure, pets in the child’s home, and neighborhood-level socioeconomic status. Results: Children (n=1334) were on average 4.3 years old (standard deviation [SD] 0.5), 49% male, and 11.6% had ever asthma; 46% of mothers were black and 54% had a college/technical school degree. City-specific mean PM2.5 exposures averaged across the prenatal period ranged from 5.2 µg/m3 (SD 0.9) to 10.6 µg/m3 (SD 1.0). A 2 µg/m3 higher PM2.5 exposure during the saccular phase (week 24 to week 36 of pregnancy) was associated with 28% higher risk of asthma (95% confidence interval [CI]: 1.00, 1.64; p=0.055). This effect was larger in boys than in girls, though interaction was not statistically significant. Higher average exposure across all of pregnancy was not associated with asthma (risk ratio 1.06, 95% CI: 0.84, 1.35). Conclusions: Preliminary results suggest that the later phases of prenatal lung development may be particularly sensitive to the developmental toxicity of PM2.5.