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. 2022 Jul:165:107310.
doi: 10.1016/j.envint.2022.107310. Epub 2022 May 25.

Prenatal exposure to particulate matter and placental gene expression

Daniel A Enquobahrie  1 , James MacDonald  2 , Michael Hussey  3 , Theo K Bammler  2 , Christine T Loftus  2 , Alison G Paquette  4 , Nora Byington  5 , Carmen J Marsit  6 , Adam Szpiro  7 , Joel D Kaufman  8 , Kaja Z LeWinn  9 , Nicole R Bush  10 , Frances Tylavsky  11 , Catherine J Karr  12 , Sheela Sathyanarayana  13
Affiliations

Prenatal exposure to particulate matter and placental gene expression

Daniel A Enquobahrie et al. Environ Int. 2022 Jul.

Abstract

Background: While strong evidence supports adverse maternal and offspring consequences of air pollution, mechanisms that involve the placenta, a key part of the intrauterine environment, are largely unknown. Previous studies of air pollution and placental gene expression were small candidate gene studies that rarely considered prenatal windows of exposure or the potential role of offspring sex. We examined overall and sex-specific associations of prenatal exposure to fine particulate matter (PM2.5) with genome-wide placental gene expression.

Methods: Participants with placenta samples, collected at birth, and childhood health outcomes from CANDLE (Memphis, TN) (n = 776) and GAPPS (Seattle, WA) (n = 205) cohorts of the ECHO-PATHWAYS Consortium were included in this study. PM2.5 exposures during trimesters 1, 2, 3, and the first and last months of pregnancy, were estimated using a spatiotemporal model. Cohort-specific linear adjusted models were fit for each exposure window and expression of >11,000 protein coding genes from paired end RNA sequencing data. Models with interaction terms were used to examine PM2.5-offspring sex interactions. False discovery rate (FDR < 0.10) was used to correct for multiple testing.

Results: Mean PM2.5 estimate was 10.5-10.7 μg/m3 for CANDLE and 6.0-6.3 μg/m3 for GAPPS participants. In CANDLE, expression of 13 (11 upregulated and 2 downregulated), 20 (11 upregulated and 9 downregulated) and 3 (2 upregulated and 1 downregulated) genes was associated with PM2.5 in the first trimester, second trimester, and first month, respectively. While we did not find any statistically significant association, overall, between PM2.5 and gene expression in GAPPS, we found offspring sex and first month PM2.5 interaction for DDHD1 expression (positive association among males and inverse association among females). We did not observe PM2.5 and offspring sex interactions in CANDLE.

Conclusion: In CANDLE, but not GAPPS, we found that prenatal PM2.5 exposure during the first half of pregnancy is associated with placental gene expression.

Keywords: Air pollution; Fine particulate matter; Gene expression; PM(2.5); Placenta; Pregnancy.

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Conflict of interest statement

Declaration of Competing Interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Fig. 1.
Fig. 1.
Offspring Sex and First Month PM2.5 Exposure Interaction on DDHD1 Gene Expression in the GAPPS Study.
See this image and copyright information in PMC

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