Abstract
Fine particulate matter (PM2.5) potentiates in utero oxidative stress influencing fetal development while antioxidants have potential protective effects. We examined associations among prenatal PM2.5, maternal antioxidant intake, and childhood wheeze in an urban pregnancy cohort (n = 530). Daily PM2.5 exposure over gestation was estimated using a satellite-based spatiotemporally resolved model. Mothers completed the modified Block98 food frequency questionnaire. Average energy-adjusted percentile intake of β-carotene, vitamins (A, C, E), and trace minerals (zinc, magnesium, selenium) constituted an antioxidant index (AI). Maternal-reported child wheeze was ascertained up to 4.1 ± 2.8 years. Bayesian distributed lag interaction models (BDLIMs) were used to examine time-varying associations between prenatal PM2.5 and repeated wheeze (≥2 episodes) and effect modification by AI, race/ethnicity, and child sex. Covariates included maternal age, education, asthma, and temperature. Women were 39% Black and 33% Hispanic, 36% with ≤high school education; 21% of children had repeated wheeze. Higher AI was associated with decreased wheeze in Blacks (OR = 0.37 (0.19–0.73), per IQR increase). BDLIMs identified a sensitive window for PM2.5 effects on wheeze among boys born to Black mothers with low AI (at 33–40 weeks gestation; OR = 1.74 (1.19–2.54), per µg/m3 increase in PM2.5). Relationships among prenatal PM2.5, antioxidant intake, and child wheeze were modified by race/ethnicity and sex.
Highlights
We examined the main effects of maternal antioxidant intake and prenatal PM2.5 exposure on children’s repeated wheeze in separate models
We conducted sensitivity analyses by adjusting for (1) prenatal maternal smoking, secondhand smoke exposure, and averaged postnatal PM2.5 level over the first year of the child’s life (Online Supplement, Figure S7) and (2) study site, birthweight for gestational age z-score, and season of birth (Online Supplement, Figure S8). These models were materially unchanged. In this multiethnic inner-city population, we found that increased prenatal PM2.5 exposure during late pregnancy was associated with early childhood repeated wheeze, in boys born to Black mothers with low antioxidant intake
This study found that increased exposure to prenatal PM2.5 may have sex-specific and time-dependent effects that varied by race/ethnicity and maternal antioxidant intake
Summary
Life wheezing respiratory illnesses account for significant morbidity and health care utilization [1]. Episodic wheezing frequently precedes asthma and is related to reduced lung function with potential lifelong consequences [2]. A key step in identifying children at risk for chronic respiratory disorders is characterizing risk factors and mechanisms that lead to early predisposition. The high prevalence and substantial costs of these disorders have motivated efforts to identify factors that mitigate risk. Wheezing respiratory illnesses and asthma have their roots in utero [3]; identifying modifiable or mitigating factors in critical windows of development can inform prevention strategies
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