Prenatal Exposure to Traffic-Related Air Pollution and the DNA Methylation in Cord Blood Cells: MOCEH Study

Particulate matter with a diameter of <= 10 mu m (PM10) and nitrogen dioxide (NO2) affect the DNA methylation in the fetus, but epigenetic studies regarding prenatal exposure to air pollution in Asia are lacking. Therefore, this study aimed to assess whether there is any association between the ambient concentrations of PM10 and NO2 and CpG methylation in the cord blood DNA by using a Korean birth cohort. The concentrations of the air pollutants were incorporated into the final LUR model by using the maternal address data. The methylation level was determined using HumanMethylationEPIC BeadChip and a linear regression analysis model. A multipollutant model including both PM10 and NO2 and models with single pollutants were used for each trimester exposure. The number of differentially methylated positions was the largest for midpregnancy exposure in both the single pollutant models and the multipollutant regression analysis. Additionally, gene-set analysis regarding midpregnancy exposure revealed four gene ontology terms (cellular response to staurosporine, positive regulation of cytoskeleton organization, neurotransmitter transport, and execution phase of apoptosis). In conclusion, these findings show an association between prenatal PM10 and NO2 exposure and DNA methylation in several CpG sites in cord blood cells, especially for midpregnancy exposure.

Automated summary

This study using a Korean birth cohort found that prenatal exposure to PM10 and NO2 can affect DNA methylation in the fetus, especially during midpregnancy.