title: Effects of short-term exposure to inhalable particulate matter on DNA methylation of tandem repeats.
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.
authors.affiliation: Laboratory of Environmental Epigenetics, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts; Key Laboratory of Pollution Processes and Environmental Criteria (Ministry of Education), College of Environmental Sciences and Engineering, Nankai University, Tianjin, China.
authors.forename: Liqiong
authors.initials: L
authors.lastname: Guo
authors.forename: Hyang-Min
authors.initials: HM
authors.lastname: Byun
authors.forename: Jia
authors.initials: J
authors.lastname: Zhong
authors.forename: Valeria
authors.initials: V
authors.lastname: Motta
authors.forename: Jitendra
authors.initials: J
authors.lastname: Barupal
authors.forename: Yinan
authors.initials: Y
authors.lastname: Zheng
authors.forename: Chang
authors.initials: C
authors.lastname: Dou
authors.forename: Feiruo
authors.initials: F
authors.lastname: Zhang
authors.forename: John P
authors.initials: JP
authors.lastname: McCracken
authors.forename: Anaité
authors.initials: A
authors.lastname: Diaz
authors.forename: Sanchez-Guerra
authors.initials: SG
authors.lastname: Marco
authors.forename: Silvia
authors.initials: S
authors.lastname: Colicino
authors.forename: Joel
authors.initials: J
authors.lastname: Schwartz
authors.forename: Sheng
authors.initials: S
authors.lastname: Wang
authors.forename: Lifang
authors.initials: L
authors.lastname: Hou
authors.forename: Andrea A
authors.initials: AA
authors.lastname: Baccarelli
mesh_terms: D000328:Adult; D000393:Air Pollutants / Q000633:toxicity*; D015415:Biomarkers / Q000032:analysis*; D019175:DNA Methylation / Q000187:drug effects* / Q000235:genetics; D004784:Environmental Monitoring; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D019570:Inhalation Exposure / Q000032:analysis*; D008297:Male; D016273:Occupational Exposure / Q000032:analysis*; D052638:Particulate Matter / Q000633:toxicity*; D016133:Polymerase Chain Reaction; D020080:Tandem Repeat Sequences / Q000235:genetics*; D013997:Time Factors
chemical_list: D000393:Air Pollutants; D015415:Biomarkers; D018836:Inflammation Mediators; D052638:Particulate Matter
keywords: air pollution; epidemiology; epigenetics