Effects of short-term exposure to inhalable particulate matter on DNA methylation of tandem repeats

Liqiong Guo, Hyang Min Byun, Jia Zhong, Valeria Motta, Jitendra Barupal, Yinan Zheng, Chang Dou, Feiruo Zhang, John P. McCracken, Anaité Diaz, Sanchez Guerra Marco, Silvia Colicino, Joel Schwartz, Sheng Wang, Lifang Hou, Andrea A. Baccarelli

Research output: Contribution to journalArticlepeer-review

Abstract

There is compelling evidence that particulate matter (PM) increases lung cancer risk by triggering systemic inflammation, and leukocyte DNA hypomethylation. However, previous investigations focused on repeated element sequences from LINE-1 and Alu families. Tandem repeats, which display a greater propensity to mutate, and are often hypomethylated in cancer patients, have never been investigated in individuals exposed to PM. We measured methylation of three tandem repeats (SATα, NBL2, and D4Z4) by polymerase chain reaction-pyrosequencing on blood samples from truck drivers and office workers (60 per group) in Beijing, China. We used lightweight monitors to measure personal PM2.5 (PM with aerodynamic diameter ≤2.5 μm) and elemental carbon (a tracer of PM from vehicular traffic). Ambient PM10 data were obtained from air quality measuring stations. Overall, an interquartile increase in personal PM2.5 and ambient PM10 levels was associated with a significant covariate-adjusted decrease in SATα methylation (-1.35% 5-methyl cytosine [5mC], P=0.01; and -1.33%5mC; P=0.01, respectively). Effects from personal PM2.5 and ambient PM10 on SATα methylation were stronger in truck drivers (-2.34%5mC, P=0.02; -1.44%5mC, P=0.06) than office workers (-0.95%5mC, P=0.26; -1.25%5mC, P=0.12, respectively). Ambient PM10 was negatively correlated with NBL2 methylation in truck drivers (-1.38%5mC, P=0.03) but not in office workers (1.04%5mC, P=0.13). Our result suggests that PM exposure is associated with hypomethylation of selected tandem repeats. Measuring tandem-repeat hypomethylation in easy-to-obtain blood specimens might identify individuals with biological effects and potential cancer risk from PM exposure.

Original languageEnglish
Pages (from-to)322-335
Number of pages14
JournalEnvironmental and Molecular Mutagenesis
Volume55
Issue number4
DOIs
Publication statusPublished - 2014

Keywords

  • Air pollution
  • Epidemiology
  • Epigenetics

ASJC Scopus subject areas

  • Health, Toxicology and Mutagenesis
  • Epidemiology
  • Genetics(clinical)

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