학술논문

Associations of prenatal exposure to NO 2 and near roadway residence with placental gene expression.
Document Type
Academic Journal
Author
Hussey MR; Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, USA. Electronic address: husseymi@uw.edu.; Enquobahrie DA; Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, USA; Department of Health Systems and Population Health, School of Public Health, University of Washington, Seattle, WA, USA.; Loftus CT; Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA, USA.; MacDonald JW; Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA, USA.; Bammler TK; Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA, USA.; Paquette AG; Department of Pediatrics, School of Medicine, University of Washington, Seattle, WA, USA; Seattle Children's Research Institute, Seattle, WA, USA.; Marsit CJ; Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA.; Szpiro AA; Department of Biostatistics, School of Public Health, University of Washington, Seattle, WA, USA.; Kaufman JD; Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, USA; Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA, USA.; LeWinn KZ; Department of Psychiatry and Behavioral Sciences, School of Medicine, University of California, San Francisco, San Francisco, CA, USA.; Bush NR; Department of Psychiatry and Behavioral Sciences, School of Medicine, University of California, San Francisco, San Francisco, CA, USA; Department of Pediatrics, School of Medicine, University of California, San Francisco, San, Francisco, CA, USA.; Tylavsky F; Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.; Zhao Q; Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.; Karr CJ; Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, USA; Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA, USA; Department of Pediatrics, School of Medicine, University of Washington, Seattle, WA, USA.; Sathyanarayana S; Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, USA; Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, WA, USA; Department of Pediatrics, School of Medicine, University of Washington, Seattle, WA, USA; Seattle Children's Research Institute, Seattle, WA, USA.
Source
Publisher: Elsevier Country of Publication: Netherlands NLM ID: 8006349 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1532-3102 (Electronic) Linking ISSN: 01434004 NLM ISO Abbreviation: Placenta Subsets: MEDLINE
Subject
Language
English
Abstract
Introduction: Traffic-related air pollution (TRAP), a common exposure, potentially impacts pregnancy through altered placental function. We investigated associations between prenatal TRAP exposure and placental gene expression.
Methods: Whole transcriptome sequencing was performed on placental samples from CANDLE (Memphis, TN) (n = 776) and GAPPS (Seattle and Yakima, WA) (n = 205), cohorts of the ECHO-PATHWAYS Consortium. Residential NO 2 exposures were computed via spatiotemporal models for full-pregnancy, each trimester, and the first/last months of pregnancy. Individual cohort-specific, covariate-adjusted linear models were fit for 10,855 genes and respective exposures (NO 2 or roadway proximity [≤150 m]). Infant-sex/exposure interactions on placental gene expression were tested with interaction terms in separate models. Significance was based on false discovery rate (FDR<0.10).
Results: In GAPPS, final-month NO 2 exposure was positively associated with MAP1LC3C expression (FDR p-value = 0.094). Infant-sex interacted with second-trimester NO 2 on STRIP2 expression (FDR interaction p-value = 0.011, inverse and positive associations among male and female infants, respectively) and roadway proximity on CEBPA expression (FDR interaction p-value = 0.045, inverse among females). In CANDLE, infant-sex interacted with first-trimester and full-pregnancy NO 2 on RASSF7 expression (FDR interaction p-values = 0.067 and 0.013, respectively, positive among male infants and inverse among female infants).
Discussion: Overall, pregnancy NO 2 exposure and placental gene expression associations were primarily null, with exception of final month NO 2 exposure and placental MAP1LC3C association. We found several interactions of infant sex and TRAP exposures on placental expression of STRIP2, CEBPA, and RASSF7. These highlighted genes suggest influence of TRAP on placental cell proliferation, autophagy, and growth, though additional replication and functional studies are required for validation.
Competing Interests: Declaration of competing interest All authors have read and approved the submission of the manuscript. The Institutional Review Boards of all participating institutions approved study protocols. Neither the authors nor the institutions with which they are affiliated have any direct or indirect financial interest in the subject matter of our research. All authors report no conflicts of interest.
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