DOI: 10.5281/zenodo.8186830
title: Prenatal exposure to environmental air pollution and psychosocial stress jointly contribute to the epigenetic regulation of the serotonin transporter gene in newborns

description: This database includes the raw data linked with the paper “Prenatal exposure to environmental air pollution and psychosocial stress jointly contribute to the epigenetic regulation of the serotonin transporter gene in newborns” accepted for publication on Molecular Psychiatry. This study is part of the longitudinal and multi-centric “Measuring the outcomes of maternal COVID-19-related prenatal exposure (MOM-COPE)” study. Here, we report on the interactive influence of variations in antenatal exposures to maternal pandemic-related stress (PRS) and PM2.5 on SLC6A4 DNAm levels in newborns. Procedures Mother–infant dyads (N=307) were enrolled at delivery during the COVID-19 pandemic. Infants’ methylation status was assessed in 13 CpG sites within the SLC6A4 gene’s region (chr17:28562750–28562958) in buccal cells at birth and women retrospectively report on PRS. PM2.5 exposure throughout the entire gestation and at each gestational trimester was estimated using a spatiotemporal model based on residential address. Among several potentially confounding socio-demographic and health-related factors, infant’s sex was significantly associated with infants’ SLC6A4 DNAm levels, thus hierarchical regression models were adjusted for infant’s sex. Mother–infant dyads (N = 276) were recruited at delivery. Maternal trait anxiety, as a marker of antenatal chronic stress exposure, was assessed soon after delivery using the Stait-Trait Anxiety Inventory (STAI-Y). Infants’ BDNF DNAm at birth was assessed in 11 CpG sites in buccal cells whereas infants’ NE was assessed at 3 (N = 225) and 6 months (N = 189) using the Infant Behavior Questionnaire-Revised (IBQ-R). Analytical plan Principal component analysis (PCA) was used to reduce the number of CpG sites into a smaller set of factors. A four-factor solution, where the targeted CpG sites were aggregated in 4 main factors, showed the best fit to the data (Table 2). Principal Component 1 (PC1; composed of 6 CpG sites) and Principal Component 2 (PC2; composed of 3 CpG sites) accounted, respectively, for 31.6% and 12.8% of the total variance in SLC6A4 DNAm and were used in further analyses. Pearson correlations and independent samples t-tests were employed to explore the potential effect of sociodemographic and health-related variables on infant methylation levels. All variables found to be significantly associated with the outcomes examined were included as covariates in subsequent analyses. Separate hierarchical regression analyses were performed to evaluate the independent and interactive effects of maternal PRS and exposure to air pollution on infant methylation levels. Findings in brief Higher levels of SLC6A4 DNAm at 6 CpG sites were found in newborns born to mothers reporting higher levels of antenatal PRS and greater PM2.5 exposure across gestation, while adjusting for infant’s sex. These effects were especially evident when exposure to elevated PM2.5 occurred during the second trimester of pregnancy.