Min Yu1,2, Jianlin Lou2, Hailing Xia2, Min Zhang2, Yixiao Zhang2, Junqiang Chen2, Xing Zhang2, Shibo Ying2, Lijin Zhu2, Lihong Liu3, Guang Jia4. 1. Department of Occupational and Environmental Health Science, School of Public Health, Peking University, 38 Xueyuan Road, Beijing, 100191, People's Republic of China. 2. Department of Occupational Diseases, Zhejiang Academy of Medical Sciences, 182 Tian Mu Shan Road, Zhejiang, 310013, People's Republic of China. 3. Department of Occupational Diseases, Zhejiang Academy of Medical Sciences, 182 Tian Mu Shan Road, Zhejiang, 310013, People's Republic of China. zjwstllh@163.com. 4. Department of Occupational and Environmental Health Science, School of Public Health, Peking University, 38 Xueyuan Road, Beijing, 100191, People's Republic of China. jiaguangjia@bjmu.edu.cn.
Abstract
PURPOSE: To examine the effect of asbestos exposure on global DNA methylation and determine whether lung function and inflammatory and fibrosis biomarkers are correlated with the methylation state. METHODS: A total of 26 healthy subjects without asbestos exposure (Group 1), 47 healthy subjects with exposure (Group 2), and 52 subjects with benign asbestos-related disorders (ARDs) (Group 3) participated in this cross-sectional study. Blood global 5-methylcytosine (5mC) and serum TNF-α, collagen IV, CCL5 and CC16 concentrations were analyzed using enzyme-linked immunosorbent assay-like assays. Spirometric maneuvers were performed to assess lung function. RESULTS: Decreased 5mC levels were observed in Groups 2 and 3 compared to Group 1, irrespective of lung function (p < 0.01). There was no significant change in 5mC between Groups 2 and 3. Overall, 5mC was negatively correlated with CCL5 and collagen IV (p < 0.05), but no significant inverse relationship was found between 5mC and CCL5 or collagen IV in each group. Additionally, both 5mC and CC16 were inversely associated with FEV1/FVC% (p = 0.001, adjusted R 2 = 0.145) for non-smokers, and consistently significant inverse relationships were found between CC16 and FEV1/FVC%, independent of asbestos exposure. CONCLUSIONS: Asbestos exposure causes global DNA hypomethylation. DNA hypomethylation has no influence on serum biomarkers and lung function in asbestos-exposed population with or without pleural and pulmonary parenchymal abnormalities.
PURPOSE: To examine the effect of asbestos exposure on global DNA methylation and determine whether lung function and inflammatory and fibrosis biomarkers are correlated with the methylation state. METHODS: A total of 26 healthy subjects without asbestos exposure (Group 1), 47 healthy subjects with exposure (Group 2), and 52 subjects with benign asbestos-related disorders (ARDs) (Group 3) participated in this cross-sectional study. Blood global 5-methylcytosine (5mC) and serum TNF-α, collagen IV, CCL5 and CC16 concentrations were analyzed using enzyme-linked immunosorbent assay-like assays. Spirometric maneuvers were performed to assess lung function. RESULTS: Decreased 5mC levels were observed in Groups 2 and 3 compared to Group 1, irrespective of lung function (p < 0.01). There was no significant change in 5mC between Groups 2 and 3. Overall, 5mC was negatively correlated with CCL5 and collagen IV (p < 0.05), but no significant inverse relationship was found between 5mC and CCL5 or collagen IV in each group. Additionally, both 5mC and CC16 were inversely associated with FEV1/FVC% (p = 0.001, adjusted R 2 = 0.145) for non-smokers, and consistently significant inverse relationships were found between CC16 and FEV1/FVC%, independent of asbestos exposure. CONCLUSIONS:Asbestos exposure causes global DNA hypomethylation. DNA hypomethylation has no influence on serum biomarkers and lung function in asbestos-exposed population with or without pleural and pulmonary parenchymal abnormalities.
Entities:
Keywords:
Asbestos; CC16; CCL5; Fibrosis; Global DNA methylation; Lung function
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