Epigenetic Effect Biomarkers Of Environmental Pollutants Exposure

Environmental pollutants exposure can affect the epigenetic changes in humans. However, it is lack of related research in the study of people investigation tha t whether epigenetic marks can be treated as a biomarker or health risk index of the ev aluation process, especially in environmental pollutants induced specific diseases or ta rget organ damages. This study discusses the association between environmental pollutants exposure and the changes and terminal effects of specific gene methylation, leading to physical injury based on two groups of data, namely data on kidney damages caused by environmental cadmium exposure and that immune injury from waste incineration pollutants. It will provide clues and support for the work on the discovery of specific epigenetic biomarkers and the health risk assessment application.It is used atomic absorption method to detect the blood cadmium (BCd),urine cadmium (UCd) levels in cadmium exposure blood samples. Then using quantitative analysis to test the renal parameters and using the CKD-EPI equation to calculate renal glomerular filtration rate (eGFR). It is used RT-PCR to test CYP1A1 gene expression and used Bio-Plex system to test Th17 related cytokines. The DNA methylations were analyzed by pyrosequencing system.1. Exposure to cadmium (Cd) can affect both DNA methylation and renal function, but there are few examples of the association between epigenetic markers and Cd-induced kidney damage. The heavier Cd-exposed persons exhibited higher levels of NAG and B2M, as well as lower values of eGFR. The results suggest that long-term Cd exposure induced renal dysfunction in a dose-dependent manner.The levels of BCd and UCd correlated positively with the levels of DNA methylation in RASAL1 and in KLOTHO. The more heavily exposed residents exhibited obvious renal dysfunction. Notably, the increased level of DNA methylation in RASAL1 was inversely correlated to the level of eGFR (P< 0.05) even if the Cd concentration in blood and urine were adjusted. The methylation of RASAL1 increased along with the increased abnormal prevalence of eGFR. Our findings suggest that Cd exposure can induce the hypermethylation of RASAL1 and KLOTHO. Hypermethylation of RASAL1 may be an indicator of the progress for chronic kidney disease.2. It is found that Th17 related cytokine levels of plasma in residents of waste incineration pollutants were significantly higher than those inside its perimeter area and control area residents (P< 0.05). The methylation levels of CYP1A1 and IL-6 in Closely exposure group were decreased compared with those in control group. The correlation coefficient of the methylation levels of CYPIA1 and IL-6 were-1.42 and-1.72 respectively (P< 0.05). It is suggested that waste incineration pollution exposure can affect Th17 cytokines changes in blood, and can affect the methylation levels of CYP1A1 and IL-6. CYP1A1 gene methylation were negatively correlated with IL-6 cytokine levels (P< 0.05) and IL-6 gene methylation were also negatively correlated with IL-17A, IL-17 F, IL-6, IL-21, IL-22, TNF-a (P< 0.05), when adjusted confounding factors such as age, sex, smoking, drinking. The results suggested that IL-6 gene methylation levels can predict Th17 cytokines changes. Using the Principal Component Analysis also found that the IL-6 gene methylation have negative effect with Th17 cytokines and it can comprehensively regulate the Thl7 cytokine network. The research results showed that the long-term waste incineration pollutants exposure can affect CYP1A1 and IL-6 gene methylation levels, CYP1A1 and IL-6 gene methylation may be a biomaker in waste incineration pollution caused immune poison effects.All the results suggested that cadmium and waste incineration pollutants exposure can change the effect of peripheral blood specific molecular gene methylation levels. And DNA methylation changes were related with health damage effect caused by environmental pollutants exposure. So specific gene methylations can be specific epigenetic biomarkers in the health risk assessment.