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Prenatal air pollution exposure is associated with childhood asthma, but mechanisms underlying this association remain unclear. There is some evidence for biological embedding of prenatal air pollution exposure in fetal DNA methylation (DNAm), which may contribute to long-term changes in respiratory health. We used Illumina EPIC DNAm data from cord blood from the CANDLE study to determine whether DNAm links pregnancy-averaged NO2 PM2.5, or PM10 exposure with childhood persistent wheeze, transient wheeze, or diagnosed asthma, and whether maternal diet is associated with reductions in air pollution-associated DNAm changes. Using linear regression with significance thresholds of FDR0.05 and effect size 5%, we found 19, seven, and six unique differentially methylated regions associated with prenatal NO2, PM2.5, or PM10, respectively, of which one, in HLA-DPA, mediated the association between both prenatal NO2 and PM2.5 and transient wheeze at age 4. Across the genome, maternal diet as measured by the Alternative Healthy Eating Index-Pregnancy moderated the effects of all air pollutants on DNAm in cord blood such that better quality diet reduced the impact of air pollution on DNAm. This same direction of moderation was observed with participation in an income supplementation program. Our results provide evidence of the biological embedding of prenatal air pollution and suggest specific pathways that may link air pollution exposure with childhood lung disease. In addition, our work suggests that programs to support high diet quality for low-income families may reduce the biological impact of air pollution on respiratory health in children.
Lee et al. (Fri,) studied this question.