Dataset Information

Blood-Based SOX2-Promoter Methylation in Relation to Exercise and PM2.5 Exposure among Taiwanese Adults.

ABSTRACT: Increased ventilation during exercise in polluted areas could trigger airway inflammation. We evaluated blood DNA methylation of the SOX2-promoter region in relation to exercise and PM2.5 in Taiwanese adults. Data of 948 participants aged 30-70 years were retrieved from the Taiwan Biobank Database (2008-2015) and the Air Quality Monitoring Database (2006-2011). PM2.5 was positively associated with SOX2-promoter methylation (? = 0.000216; p < 0.0001). The interaction between PM2.5 and exercise on SOX2-promoter methylation was significant (p = 0.0146). After stratification by exercise habits, PM2.5 was positively associated with SOX2 methylation in only individuals who did regular exercise (? = 0.0003490; p < 0.0001). After stratification by exercise habits and residential areas, SOX2-promoter methylation levels in those who lived in the southern area were higher for both the regular exercise (? = 0.00272; p = 0.0172) and no regular exercise groups (? = 0.002610 and p = 0.0162). SOX2-promoter methylation levels in those who lived in the northern area and did regular exercise were lower; ? = -0.00314 (p = 0.0036). In conclusion, PM2.5 was positively associated with SOX2-promoter methylation in participants who did regular exercise. Living in the southern area was positively associated with SOX2-promoter methylation regardless of exercise habits.

SUBMITTER: Su CL

PROVIDER: S-EPMC7072405 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature

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Blood-Based SOX2-Promoter Methylation in Relation to Exercise and PM2.5 Exposure among Taiwanese Adults.

Su Chun-Lang CL Tantoh Disline Manli DM Chou Ying-Hsiang YH Wang Lee L Ho Chien-Chang CC Chen Pei-Hsin PH Lee Kuan-Jung KJ Nfor Oswald Ndi ON Hsu Shu-Yi SY Liang Wen-Miin WM Liaw Yung-Po YP

Cancers 20200221 2

Increased ventilation during exercise in polluted areas could trigger airway inflammation. We evaluated blood DNA methylation of the SOX2-promoter region in relation to exercise and PM2.5 in Taiwanese adults. Data of 948 participants aged 30-70 years were retrieved from the Taiwan Biobank Database (2008-2015) and the Air Quality Monitoring Database (2006-2011). PM2.5 was positively associated with SOX2-promoter methylation (β = 0.000216; p < 0.0001). The interaction between ...[more]

PMID: 32098209

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Project description:BackgroundPolycyclic aromatic hydrocarbon (PAH)-rich substances like cigarette smoke and PM2.5 induce aryl hydrocarbon receptor (AHR)-mediated aryl hydrocarbon receptor repressor (AHRR) methylation. AHRR cg05575921 and coagulation factor II (thrombin) receptor-like 3 (F2RL3) cg03636183 methylation patterns are well-established biomarkers for smoking. Even though AHRR cg05575921 methylation has recently been associated with PM2.5, the interaction between smoking and PM2.5 on AHRR methylation is yet to be fully explored. We evaluated AHRR and F2RL3 CpG sites to identify potential significant markers in relation to PM2.5 and smoking in Taiwanese adults.MethodsDNA methylation and smoking data of 948 participants aged 30-70 years were obtained from the Taiwan Biobank Database (2008-2015), while PM2.5 data were obtained from the Air Quality Monitoring Database (2006-2011).ResultsSmoking and PM2.5 were independently associated with hypomethylation (lower levels) of AHRR cg05575921, AHRR cg23576855, F2RL3 cg03636183, and F2LR3 cg21911711 after multiple-comparison correction (Bonferroni P < 0.00028409). Cg05575921 was the most hypomethylated AHRR CpG site, while cg03636183 was the most hypomethylated F2RL3 CpG site. Overall, cg05575921 was the most hypomethylated CpG site: β = - 0.03909, P < 0.0001; - 0.17536, P < 0.0001 for former and current smoking, respectively (P-trendsmoking < 0.0001) and - 0.00141, P < 0.0001 for PM2.5. After adjusting for F2RL3 cg03636183, smoking and PM2.5 remained significantly associated with cg05575921 hypomethylation: β - 0.02221, P < 0.0001; - 0.11578, P < 0.0001 for former and current smoking, respectively (P-trendsmoking < 0.0001) and - 0.0070, P = 0.0120 for PM2.5. After stratification by sex, smoking and PM2.5 remained associated (P < 0.05) with cg05575921 hypomethylation in both men (β = - 0.04274, - 0.17700, and - 0.00163 for former smoking, current smoking, and PM2.5, respectively) and women (β = - 0.01937, - 0.17255, and - 0.00105 for former smoking, current smoking, and PM2.5, respectively). After stratification by residential area, former and current smoking remained associated (P < 0.05) with cg05575921 hypomethylation: β = - 0.03918 and - 0.17536, respectively (P-trendsmoking < 0.0001). Living in the central and southern areas was also associated (P < 0.05) with cg05575921 hypomethylation: β = - 0.01356 and - 0.01970, respectively (P-trendarea < 0.0001).ConclusionSmoking and PM2.5 were independently associated with hypomethylation of cg05575921, cg23576855, cg03636183, and cg21911711. The most hypomethylated CpG site was cg05575921 and its association with smoking and PM2.5 was dose-dependent.

Project description:BACKGROUND:Long-term exposure to particulate matter (PM) air pollution may increase blood pressure and the risk of hypertension. However, epidemiological evidence is scarce and inconsistent. OBJECTIVES:We investigated the associations between long-term exposure to PM with an aerodynamic diameter <2.5?m (PM2.5), blood pressure, and incident hypertension in a large Taiwanese cohort. METHODS:We studied 361,560 adults ?18y old from a large cohort who participated in a standard medical examination program during 2001 to 2014. Among this group, 125,913 nonhypertensive participants were followed up. A satellite-based spatiotemporal model was used to estimate the 2-y average PM2.5 concentrations at each participant's address. Multivariable linear regression was used in the cross-sectional data analysis with the 361,560 participants to investigate the associations between PM2.5 and systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse pressure (PP), and Cox proportional hazard regression was used in the cohort data analysis with the 125,913 participants to investigate the associations between PM2.5 and incident hypertension. RESULTS:Each 10-?g/m3 increment in the 2-y average PM2.5 concentration was associated with increases of 0.45?mmHg [95% confidence interval (CI): 0.40, 0.50], 0.07?mmHg (95% CI: 0.04, 0.11), and 0.38?mmHg (95% CI: 0.33, 0.42) in SBP, DBP, and PP, respectively, after adjusting for a wide range of covariates and possible confounders. Each 10-?g/m3 increment in the 2-y average PM2.5 concentration was associated with an increase of 3% in the risk of developing hypertension [hazard?ratio=1.03 (95% CI: 1.01, 1.05)]. Stratified and sensitivity analyses yielded similar results. CONCLUSIONS:Long-term exposure to PM2.5 air pollution is associated with higher blood pressure and an increased risk of hypertension. These findings reinforce the importance of air pollution mitigation strategies to reduce the risk of cardiovascular disease. https://doi.org/10.1289/EHP2466.

Project description:Cytochrome P450 (CYP450) can mediate fine particulate matter (PM2.5) exposure leading to lung injury. Nuclear factor E2-related factor 2 (Nrf2) can regulate CYP450 expression; however, the mechanism by which Nrf2−/− (KO) regulates CYP450 expression via methylation of its promoter after PM2.5 exposure remains unclear. Here, Nrf2−/− (KO) mice and wild-type (WT) were placed in a PM2.5 exposure chamber (PM) or a filtered air chamber (FA) for 12 weeks using the real-ambient exposure system. The CYP2E1 expression trends were opposite between the WT and KO mice following PM2.5 exposure. After exposure to PM2.5,CYP2E1 mRNA and protein levels were increased in WT mice but decreased in KO mice, and CYP1A1 expression was increased after exposure to PM2.5 in both WT and KO mice. CYP2S1 expression decreased after exposure to PM2.5 in both the WT and KO groups. We studied the effect of PM2.5 exposure on CYP450 promoter methylation and global methylation levels in WT and KO mice. In WT and KO mice in the PM2.5 exposure chamber, among the methylation sites examined in the CYP2E1 promoter, the CpG2 methylation level showed an opposite trend with CYP2E1 mRNA expression. The same relationship was evident between CpG3 unit methylation in the CYP1A1 promoter and CYP1A1 mRNA expression, and between CpG1 unit methylation in the CYP2S1 promoter and CYP2S1 mRNA expression. This data suggests that methylation of these CpG units regulates the expression of the corresponding gene. After exposure to PM2.5, the expression of the DNA methylation markers ten-eleven translocation 3 (TET3) and 5-hydroxymethylcytosine (5hmC) was decreased in the WT group but significantly increased in the KO group. In summary, the changes in CYP2E1, CYP1A1, and CYP2S1 expression in the PM2.5 exposure chamber of WT and Nrf2−/− mice might be related to the specific methylation patterns in their promoter CpG units. After exposure to PM2.5, Nrf2 might regulate CYP2E1 expression by affecting CpG2 unit methylation and induce DNA demethylation via TET3 expression. Our study revealed the underlying mechanism for Nrf2 to regulate epigenetics after lung exposure to PM2.5.

Dataset Information

Blood-Based SOX2-Promoter Methylation in Relation to Exercise and PM2.5 Exposure among Taiwanese Adults.

Publications

Blood-Based SOX2-Promoter Methylation in Relation to Exercise and PM<sub>2.5</sub> Exposure among Taiwanese Adults.

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