Abstract
BackgroundThere is evidence that altered DNA methylation is an important epigenetic mechanism in prenatal programming and that developmental periods are sensitive to environmental stressors. We hypothesized that exposure to fine particles (PM2.5) during pregnancy could influence DNA methylation patterns of the placenta.MethodsIn the ENVIRONAGE birth cohort, levels of 5’-methyl-deoxycytidine (5-mdC) and deoxycytidine (dC) were quantified in placental DNA from 240 newborns. Multiple regression models were used to study placental global DNA methylation and in utero exposure to PM2.5 over various time windows during pregnancy.ResultsPM2.5 exposure during pregnancy averaged (25th-75th percentile) 17.4 (15.4-19.3) μg/m3. Placental global DNA methylation was inversely associated with PM2.5 exposures during whole pregnancy and relatively decreased by 2.19% (95% confidence interval [CI]: -3.65, -0.73%, p = 0.004) for each 5 μg/m3 increase in exposure to PM2.5. In a multi-lag model in which all three trimester exposures were fitted as independent variables in the same regression model, only exposure to PM2.5 during trimester 1 was significantly associated with lower global DNA methylation (-2.13% per 5 μg/m3 increase, 95% CI: -3.71, -0.54%, p = 0.009). When we analyzed shorter time windows of exposure within trimester 1, we observed a lower placental DNA methylation at birth during all implantation stages but exposure during the implantation range (6-21d) was strongest associated (-1.08% per 5 μg/m3 increase, 95% CI: -1.80, -0.36%, p = 0.004).ConclusionsWe observed a lower degree of placental global DNA methylation in association with exposure to particulate air pollution in early pregnancy, including the critical stages of implantation. Future studies should elucidate genome-wide and gene-specific methylation patterns in placental tissue that could link particulate exposure during in utero life and early epigenetic modulations.
Highlights
There is evidence that altered DNA methylation is an important epigenetic mechanism in prenatal programming and that developmental periods are sensitive to environmental stressors
The association between placental global DNA methylation and PM2.5 exposure from the post-implantation window onwards weakens compared with the implantation exposure windows (−0.59% per 5 μg/m3 increase, 95% CI: -1.17, -0.005%, p = 0.05) and appeared not significant after additional adjustment for the corresponding Nitrogen dioxide (NO2) and maximum 8-hour average O3 exposure period (−0.58% per 5 μg/m3 increase, 95% CI: -1.34, 0.18%, p = 0.14)
Studying all different weeks of trimester 1, we found in addition to the implantation period (Figure 2), a significant inverse association between PM2.5 residential exposure estimates for only week 7 adjusted for NO2 and maximum 8-hour average O3 and placental global DNA methylation (−1.03% per 5 μg/m3 increase CI: -1.68, -0.38%, p = 0.002)
Summary
There is evidence that altered DNA methylation is an important epigenetic mechanism in prenatal programming and that developmental periods are sensitive to environmental stressors. We hypothesized that exposure to fine particles (PM2.5) during pregnancy could influence DNA methylation patterns of the placenta. The human placenta forms the interface between fetal and maternal circulation and plays a critical role in the regulation of fetal growth and development through controlled nutrient supply. Fetal adaptations and developmental plasticity arising from perturbations in uteroplacental exchange to meet fetal requirements “program” the fetus for an increased risk of developing cardiovascular. Mean ± SD or range and number (%) Maternal.
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