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  • ENVPOL-D-20-02687 MS

    Rights statement: This is the author’s version of a work that was accepted for publication in Environmental Pollution. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Environmental Pollution, 275, 2021 DOI: 10.1016/j.envpol.2021.116601

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Short-term personal PM2.5 exposure and change in DNA methylation of imprinted genes: Panel study of healthy young adults in Guangzhou city, China

Research output: Contribution to Journal/MagazineJournal articlepeer-review

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  • Y. Liang
  • L. Hu
  • J. Li
  • F. Liu
  • K.C. Jones
  • D. Li
  • J. Liu
  • D. Chen
  • J. You
  • Z. Yu
  • G. Zhang
  • G. Dong
  • H. Ma
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Article number116601
<mark>Journal publication date</mark>15/04/2021
<mark>Journal</mark>Environmental Pollution
Volume275
Number of pages10
Publication StatusPublished
Early online date28/01/21
<mark>Original language</mark>English

Abstract

DNA methylation (DNAm) plays a significant role in deleterious health effects inflicted by fine particulate matter (PM2.5) on the human body. Recent studies have reported that DNAm of imprinted control regions (ICRs) in imprinted genes may be a sensitive biomarker of environmental exposure. Less is known about specific biomarkers of imprinted genes after PM2.5 exposure. The relationship between PM2.5 and its chemical constituents and DNAm of ICRs in imprinted genes after short-term exposure was investigated to determine specific human biomarkers of its adverse health effects. A panel study was carried out in healthy young people in Guangzhou, China. Mixed-effects models were used to evaluate the influence of PM2.5 and its constituent exposure on DNAm while controlling for potential confounders. There was no significant correlation between DNAm and personal PM2.5 exposure mass. DNAm changes in eight ICRs (L3MBTL1, NNAT, PEG10, GNAS Ex1A, MCTS2, SNURF/SNRPN, IGF2R, and RB1) and a non-imprinted gene (CYP1B1) were significantly associated with PM2.5 constituents. Compared to non-imprinted genes, imprinted gene methylation was more susceptible to interference with PM2.5 constituent exposure. Among those genes, L3MBTL1 was the most sensitive to personal PM2.5 constituent exposure. Moreover, transition metals derived from traffic sources (Cd, Fe, Mn, and Ni) significantly influenced DNAm of the imprinted genes, suggesting the importance of more targeted measures to reduce toxic constituents. Bioinformatics analysis indicated that imprinted genes (RB1) may be correlated with pathways and diseases (non-small cell lung cancer, glioma, and bladder cancer). The present study suggests that screening the imprinted gene for DNAm can be used as a sensitive biomarker of PM2.5 exposure. The results will provide data for prevention of PM2.5 exposure and a novel perspective on potential mechanisms on an epigenetic level. © 2021 Elsevier Ltd Screening imprinted gene for DNAm can be used as a sensitive biomarker of PM2.5 exposure. © 2021 Elsevier Ltd

Bibliographic note

This is the author’s version of a work that was accepted for publication in Environmental Pollution. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Environmental Pollution, 275, 2021 DOI: 10.1016/j.envpol.2021.116601