| Autor: |
Yang CF; Department of Pediatrics, Taipei Veterans General Hospital, Taipei 112, Taiwan.; Institute of Environmental and Occupational Health Sciences, National Yang-Ming University, Taipei 112, Taiwan., Karmaus WJJ; Division of Epidemiology, Biostatistics, and Environmental Health, School of Public Health, University of Memphis, Memphis, TN 38152, USA., Yang CC; Institute of Environmental and Occupational Health Sciences, National Yang-Ming University, Taipei 112, Taiwan., Chen ML; Institute of Environmental and Occupational Health Sciences, National Yang-Ming University, Taipei 112, Taiwan., Wang IJ; Department of Pediatrics, Taipei Hospital, Ministry of Health and Welfare, Taipei 242, Taiwan.; School of Medicine, National Yang-Ming University, Taipei 112, Taiwan.; College of Public Health, China Medical University, Taichung 400-439, Taiwan.; National Institute of Environmental Health Sciences, National Health Research Institutes, Miaoli 35053,Taiwan. |
| Abstrakt: |
Epidemiological studies have reported the relationship between bisphenol A (BPA) exposure and increased prevalence of asthma, but the mechanisms remain unclear. Here, we investigated whether BPA exposure and DNA methylation related to asthma in children. We collected urinary and blood samples from 228 children (Childhood Environment and Allergic Diseases Study cohort) aged 3 years. Thirty-three candidate genes potentially interacting with BPA exposure were selected from a toxicogenomics database. DNA methylation was measured in 22 blood samples with top-high and bottom-low exposures of BPA. Candidate genes with differential methylation levels were validated by qPCR and promoter associated CpG islands have been investigated. Correlations between the methylation percentage and BPA exposure and asthma were analyzed. According to our findings, MAPK1 showed differential methylation and was further investigated in 228 children. Adjusting for confounders, urinary BPA glucuronide (BPAG) level inversely correlated with MAPK1 promoter methylation (β = -0.539, p = 0.010). For the logistic regression analysis, MAPK1 methylation status was dichotomized into higher methylated and lower methylated groups with cut off continuous variable of median of promoter methylation percentage (50%) while performing the analysis. MAPK1 methylation was lower in children with asthma than in children without asthma (mean ± SD; 69.82 ± 5.88% vs. 79.82 ± 5.56%) ( p = 0.001). Mediation analysis suggested that MAPK1 methylation acts as a mediation variable between BPA exposure and asthma. The mechanism of BPA exposure on childhood asthma might, therefore, be through the alteration of MAPK1 methylation. The mechanism of BPA exposure on childhood asthma might, therefore, be through the alteration of MAPK1 methylation. |
