학술논문
Prenatal exposure to particulate matter and placental gene expression.
Document Type
Academic Journal
Author
Enquobahrie DA; Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, United States; Department of Health Systems and Population Health, School of Public Health, University of Washington, Seattle, WA, United States. Electronic address: danenq@uw.edu.; MacDonald J; Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA, United States.; Hussey M; Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, United States.; Bammler TK; Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA, United States.; Loftus CT; Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA, United States.; Paquette AG; Department of Pediatrics, School of Medicine, University of Washington, Seattle, WA, United States; Seattle Children's Research Institute, Seattle, WA, United States.; Byington N; Seattle Children's Research Institute, Seattle, WA, United States.; Marsit CJ; Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, United States.; Szpiro A; Department of Biostatistics, School of Public Health, University of Washington, Seattle, WA, United States.; Kaufman JD; Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, United States; Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA, United States.; LeWinn KZ; Department of Psychiatry and Behavioral Sciences, School of Medicine, University of California, San Francisco, San Francisco, CA, United States.; Bush NR; Department of Psychiatry and Behavioral Sciences, School of Medicine, University of California, San Francisco, San Francisco, CA, United States; Department of Pediatrics, School of Medicine, University of California, San Francisco, San Francisco, CA, United States.; Tylavsky F; Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, TN, United States.; Karr CJ; Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, United States; Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA, United States; Department of Pediatrics, School of Medicine, University of Washington, Seattle, WA, United States.; Sathyanarayana S; Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA, United States; Department of Pediatrics, School of Medicine, University of Washington, Seattle, WA, United States; Seattle Children's Research Institute, Seattle, WA, United States.
Source
Publisher: Elsevier Science Country of Publication: Netherlands NLM ID: 7807270 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-6750 (Electronic) Linking ISSN: 01604120 NLM ISO Abbreviation: Environ Int Subsets: MEDLINE
Subject
Language
English
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 (PM 2.5 ) 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 PM 2.5 -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/m 3 for CANDLE and 6.0-6.3 μg/m 3 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 PM 2.5 in the first trimester, second trimester, and first month, respectively. While we did not find any statistically significant association, overall, between PM 2.5 and gene expression in GAPPS, we found offspring sex and first month PM 2.5 interaction for DDHD1 expression (positive association among males and inverse association among females). We did not observe PM 2.5 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.
(Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)
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. PM
Results: Mean PM
Conclusion: In CANDLE, but not GAPPS, we found that prenatal PM
(Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)