Vinyl chloride monomer (VCM) is hepatotoxic as well as carcinogenic in humans. There are reports that exposure to VCM seems to induce abnormal liver function, liver fibrosis, cirrhosis, and angiosarcoma of the liver. In vivo, VCM is metabolized by cytochrome P450 2E1 (CYP2E1) to form chloroethylene oxide (CEO) and chloroactetaldehyde (CAA), both electrophilic metabolites, which may either cause cell damage or are further metabolized and detoxified by glutathione S-transferases (GSTs). This study investigated whether or not the genotypes, CYP2E1, glutathione S-transferase θ (GST T1) and μ (GST M1), correlated the abnormal liver function in vinyl chloride exposed workers. We enrolled 251 workers from 5 polyvinyl chloride plants for this study. The workers who were exposed to VCM were classified into two, high and low exposure groups and the degree of exposure was determined based on their job titles and airborne VCM concentration. The enzyme activities of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were used as the parameters of liver function. The genotypes, CYP2E1, GST T1 and GST M1, were determined by performing PCR and RFLP on peripheral white blood cell DNA, Other potential risk factors were also ascertained and the confounding effect was adjusted accordingly. Stratified analyses were used to explore the correlation between the alteration of liver function and the genotypes, CYP2E1, GST T1 and GST M1, among the workers exposed to different levels of VCM.

氯乙烯 ； 麩胺基硫轉移酶 ； 細胞色素P450 2E1 ； 肝功能

vinyl, chloride, glutathione s-transferases, CYP 2E1, liver function