Prenatal Polycyclic Aromatic Hydrocarbon (PAH) Exposure and Early Childhood Asthma in a Diverse US Pregnancy Cohort

Background/AimExposure to polycyclic aromatic hydrocarbons (PAH) may increase risk of pediatric asthma. Effects of prenatal PAH exposure, specifically, are hypothesized but understudied. The ECHO PATHWAYS Consortium investigated these relationships in a large, diverse prospective cohort study.MethodsWe included 919 mother-child dyads from the CANDLE Study, a longitudinal pregnancy cohort set in Shelby County, TN. PAH metabolites were measured in second trimester urine and adjusted for specific gravity. Seven metabolites detected in >80% of women were included in analysis. When children were 4-6 years old, mothers completed the International Study on Allergies and Asthma in Childhood survey. Poisson regression with robust standard errors was used to estimate relative risk of current wheeze, current asthma, and ever asthma associated with each metabolite in separate models, adjusted for maternal age, race, education and other asthma risk factors. Effect modification by child sex and maternal asthma was assessed using interaction models. We did not adjust for multiple comparisons.ResultsParticipants were 66% Black, 44% White; 58% with high school education or less. On average, urinary PAH metabolite concentrations were higher than in other US cohorts. Mean (SD) child age at assessment was 4.3 (0.4) years. Prevalence of reported current wheeze and asthma and ever asthma was 19.4%, 16.1%, and 14.6%, respectively. In multivariable models, we observed no evidence that any metabolite was associated with any outcome. No differences by child sex were observed. Maternal asthma modified associations between 1/9-hydroxyphenanthrene and current asthma (RRmaternal asthma = 0.88; 95%CI: 0.78, 0.99 versus RRwithout maternal asthma = 1.09; 95%CI: 0.97, 1.23 per two-fold increase in exposure; pinteraction=0.012).ConclusionsResults of our analysis, the largest cohort study of prenatal PAH and childhood airway outcomes conducted to date, did not support the hypothesis that prenatal PAHs increases risk of early childhood asthma.