| Literature DB >> 31241004 |
Rachael V Phillips1, Linda Rieswijk1, Alan E Hubbard1, Roel Vermeulen2, Jinming Zhang3, Wei Hu3, Laiyu Li4, Bryan A Bassig3, Jason Y Y Wong3, Boris Reiss5, Yongshun Huang4, Cuiju Wen4, Mark Purdue3, Xiaojiang Tang6, Luoping Zhang1, Martyn T Smith1, Nathaniel Rothman3, Qing Lan3.
Abstract
Human exposure to trichloroethylene (TCE) is linked to kidney cancer, autoimmune diseases, and probably non-Hodgkin lymphoma. Additionally, TCE exposed mice and cell cultures show altered DNA methylation. To evaluate associations between TCE exposure and DNA methylation in humans, we conducted an epigenome-wide association study (EWAS) in TCE exposed workers using the HumanMethylation450 BeadChip. Across individual CpG probes, genomic regions, and globally (i.e., the 450K methylome), we investigated differences in mean DNA methylation and differences in variability of DNA methylation between 73 control (< 0.005 ppm TCE), 30 lower exposed (< 10 ppm TCE), and 37 higher exposed ( ≥ 10 ppm TCE) subjects' white blood cells. We found that TCE exposure increased methylation variation globally (Kruskal-Wallis p-value = 3.75e-3) and in 25 CpG sites at a genome-wide significance level (Bonferroni p-value < 0.05). We identified a 609 basepair region in the TRIM68 gene promoter that exhibited hypomethylation with increased exposure to TCE (FWER = 1.20e-2). Also, genes that matched to differentially variable CpGs were enriched in the 'focal adhesion' biological pathway (p-value = 2.80e-2). All in all, human exposure to TCE was associated with epigenetic alterations in genes involved in cell-matrix adhesions and interferon subtype expression, which are important in the development of autoimmune diseases; and in genes related to cancer development. These results suggest that DNA methylation may play a role in the pathogenesis of TCE exposure-related diseases and that TCE exposure may contribute to epigenetic drift.Entities:
Keywords: DNA methylation; TCE; autoimmune disease; epigenetic variability; epigenetics; epigenome-wide association study (EWAS); occupational exposure
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Year: 2019 PMID: 31241004 PMCID: PMC6773405 DOI: 10.1080/15592294.2019.1633866
Source DB: PubMed Journal: Epigenetics ISSN: 1559-2294 Impact factor: 4.528