Vinyl Chloride Monomer Exposure Research Articles

Improvement of protective facilities in vinyl chloride units on liver injury status of occupational exposed group

To comprehensively evaluate the effectiveness of improvement of protective facilities in a vinyl chloride monomer(VCM) on promotion toward health status of occupational exposed group and safety production at poly-vinyl chloride(PVC) by comparing the liver function indicators and inspection result before and after the improvement, and to analyze the possible influential factors. The information collection concerning facilities improvement in 2013 and 2016, identification toward critical controlling points, data or detection result from occupational on-site survey and physical examination were originated in July 2020, and 227 VCM exposed workers and 179 others without chemical reagents exposure history from production factory with calcium carbide process in Tianjin City were selected as objects. The effectiveness toward improvement of protective facilities in critical controlling points that occupational exposed workers usually involve in were evaluated through comparison toward VCM concentration result, thiodiglycolic acid(TDGA) content in urine, indicators on liver function and biochemistry and liver ultrasound. At the mean time, both binary Logistic regression analysis was used to screen the possible factors that contributed to abnormal symptoms and single dependent variable general linear regression model was used to find out the mutual interaction among influential factors. Prior to improvement on protective facilities, the C_(TWA)of VCM exposed by all 8 positions in G had exceeded 1 to 2 folds of occupational exposure limit(OEL=10 mg/m~3) and the position of synthetic operator and field sampling man were ones exposed to 1, 2-DCE with the range from 50% to 1 OEL, others hazard factors were found to meet relative OELs. Next, the content of TDGA in urine of exposed group was found to correlate strongly to the average concentration of VCM(r=0.79, P<0.05), and result of TDGA content, alanine aminotransferase(ALT), γ-glutamyl transpeptidase(GGT) and abnormal rate toward liver ultrasound test in exposed group were much higher than ones in control group with significant differences(P<0.05 or P<0.001). By contrast, after the improvement, the exposure level toward all identified hazard factors were declined to meet OEL levels with significant differences in TDGA content, and result of ALT, GGT and abnormal rates toward symptoms in liver ultrasound test such as liver calcification with thickened liver echo, peripheral fibrosis of the liver, multiple hepatic cysts were markedly lower than ones before improvement and still were higher than ones in control group(P<0.05 or P<0.001). Further, parameters of gender, length of employment, weekly contact time, VCM exposed level, TDGA content were all important contributing factors to abnormal symptoms in liver ultrasound test before and after improvement on protective facilities(P<0.05 or P<0.001), in which a significant interaction effect between gender and length of employment(F=4.028, P=0.044), weekly contact time and TDGA content(F=2.183, P=0.046) in urine were found in contribution analysis to abnormal symptoms in liver ultrasound test(P<0.05). The improvement measure carried out in VCM facilities by this PVC production factories with calcium carbide process effectively reduced the ambient concentration of hazard factors mainly led by VCM, but workers might still be at risk of liver injury even under VCM exposure at relative lower level, which may referred to factors of long weekly contact time, long length of employment and high fat diet.

Occupational exposure to vinyl chloride and liver diseases.

Portal hypertension, liver fibrosis, and angiosarcoma of the liver (ASL) have been reported among workers exposed to vinyl chloride monomer (VCM) since the 1970s. In 2007, the International Agency for Research on Cancer established the association of VCM with hepatocellular carcinoma (HCC), though only on the basis of the few cases available. Thereafter, recent reports from the United States cohort and a European sub-cohort of vinyl chloride workers provided compelling evidence of a strong association between cumulative VCM exposure and HCC risk. Further areas of research include the risk of liver cancer at lower levels of exposure and different patterns of risk of ASL and HCC with the time since exposure. The evidence of interaction between VCM exposure and other known liver carcinogens such as alcohol and chronic viral infection provides clues for the health surveillance of exposed workers. Notably, also the risk of VCM-associated chronic liver disease is modulated by alcohol consumption, viral infection, and genetic polymorphism. A counter-intuitive finding from cohort studies of exposed workers is the lower mortality from liver cirrhosis with respect to the general population; this can be attributed to the healthy worker effect and to the selection of liver cancer as the cause of death in the presence of concomitant chronic liver disease. Studies designed to overcome these intricacies confirmed an association between cumulative VCM exposure and the risk of liver cirrhosis.

Relative telomere length and gene expression of shelterin complex proteins among vinyl chloride monomer-exposed workers in China.

Vinyl chloride monomer (VCM) is a confirmed carcinogen. The effects of VCM on telomeres and the gene expression of telomere complex proteins, shelterin, have not been well studied but could be of potential relevance to the carcinogenic mechanism of VCM and the health surveillance of VCM-exposed workers. A group of 241 VCM-exposed workers and 101 internal controls from the same plant in Shandong, China were recruited and quantitative polymerase chain reaction was preformed to measure relative telomere length (RTL) and gene expression of shelterin proteins. VCM cumulative exposure dose (CED) was estimated for the exposed workers. The differences in RTL and gene expression between groups were compared by Wald test fitted with robust regression. Shorter RTL was observed in VCM-exposed workers than in the controls (P < 0.001) and was related to CED of VCM. Shortened RTL was also significantly related to increasing age (P = 0.012) and high blood pressure (P = 0.056). Levels of gene expression of shelterin components in exposed workers were all lower than in controls except increased TIN2 expression, and the gene expression differences in TIN2 and POT1 among exposed and control groups were significant (P = 0.014 for TIN2 and P < 0.001 for POT1, respectively). VCM exposure is found associated with altered telomere length and gene expression of shelterin components. This provides new insights into the potential carcinogenic mechanisms of VCM and could be helpful for the health surveillance for VCM-exposed workers. Environ. Mol. Mutagen. 60:361-367, 2019. © 2018 Wiley Periodicals, Inc.

Mortality from liver angiosarcoma, hepatocellular carcinoma, and cirrhosis among vinyl chloride workers.

Occupational exposure to vinyl chloride monomer (VCM) has been established as a cause of hepatocellular carcinoma (HCC) and liver angiosarcoma (ASL). However, some controversy remains due to conflicting results on liver cirrhosis, and to evidence on HCC based on few confirmed cases. The aim of the study is to clarify the association between VCM exposure and mortality from liver diseases. In a cohort of 1658 workers involved in VCM production and polymerization, Poisson regression was adopted to estimate rate ratios (RR) across categories of VCM exposure for mortality due to ASL (n = 9), HCC (n = 31) confirmed by histological/clinical records, and the combination of deaths from liver cirrhosis and from liver cancer with clinical/histological evidence of cirrhosis (n = 63). Cumulative VCM exposure was associated with study outcomes; RRs in the highest compared to the lowest exposure category were: ASL 91.1 (95%Confidence Interval 16.8-497), HCC 5.52 (2.03-15.0), liver cirrhosis 2.60 (1.19-5.67). The risk of death from liver cirrhosis, as well as from HCC in the largest available series of confirmed cases, increased with VCM exposure.

Feasibility of using urinary TDGA as a biomarker for VCM exposures

Thiodiglycolic acid (TDGA) is a major metabolite of vinyl chloride monomer (VCM), and it has been suggested as an exposure biomarker for VCM. The validity of this biomarker when the level of VCM is less than 5 ppm, however, is questionable. The objective of this article is to evaluate the feasibility of using urinary TDGA as a biomarker of VCM exposure in a community health risk assessment setting where the concentration of VCM in air is typically very low (likely below 1 ppm). To achieve this objective, we examine the fraction of urinary TDGA associated with different levels of VCM exposures of three studies from different countries, using estimations of the TDGA metabolite predicted by a PBPK model. It is demonstrated that differences in background TDGA have considerable effect on the adequacy of TDGA as a biomarker of VCM. We conclude that, in a community health assessment setting, TDGA should not be used as an exposure biomarker for VCM without having a proper control group, and a PBPK model can be used first to determine whether or not the amount of TDGA in urine is of concern.

A Luminescent 3d-4f-4d MOF Nanoprobe as a Diagnosis Platform for Human Occupational Exposure to Vinyl Chloride Carcinogen.

A luminescent nanoprobe based on a lanthanide-transition heterometallic metal-organic framework (MOF) is first designed for specific detection of urinary thiodiglycolic acid (TDGA) which is the biomarker of carcinogenic vinyl chloride monomer (VCM) and represents the internal dose of human exposure to VCM. The nanoprobe demonstrates high selectivity to TDGA with about 27.5-fold luminescence enhancement. It also displays excellent sensitivity with a detection limit as low as 89 ng·mL-1 and fast response to TDGA within 4 min, while refraining from the interference of other coexisting species in urine. Such good sensing performance enables the nanoprobe to practically monitor TDGA levels in human urine. Moreover, a portable urine dipstick based on the sensor is developed to conveniently evaluate individuals' intoxication degree of VCM. This fast, sensitive, and selective nanoprobe has promising potential to be a useful tool for point-of-care diagnosis of disease associated with VCM exposure.

Analysis of microRNA expression and micronuclei frequency in workers exposed to vinyl chloride monomer in China.

To identify differently expressed miRNAs associated with vinyl chloride monomer (VCM) and micronuclei (MN) frequency. In discovery stage, we used microarray to detect miRNAs expression in peripheral blood lymphocytes between six low and six high VCM-exposed workers grouped by medium cumulative exposure dose. Then we validated four miRNAs using real-time quantitative reverse transcription PCR (qRT-PCR) and detected the micronuclei frequencies using cytokinesis-block micronucleus assay in 94 VCM-exposed workers and 53 healthy control subjects. We found eight miRNAs significantly downregulated and seven miRNAs upregulated (|Fold Change| >2; p < 0.05) in the high-exposure group through microarray. We validate that miR-222-3p, miR-146a-5p and miR-151a-5p were downregulated, while miR-22-3p was upregulated in VCM-exposed group (all p < 0.01). Furthermore, we found that expression of miR-22-3p was upregulated in the high micronuclei (MN) frequency subjects. In conclusion, our study suggested that these four miRNAs could be biomarkers of VCM exposure, and moreover miR-22-3p was correlated with MN frequency.

The serumproteomics research of vinyl chloride workers

To screen out serum differential proteins between vinyl chloride monomer (VCM)-exposed workers and healthy controls by proteomics and analyze the functions of differential proteins, and to provide a basis for elucidating the pathogenesis of diseases caused by VCM exposure and searching for the protein biomarkers. Fasting venous blood was collected from 125 VCM-exposed workers and 40 healthy controls according to accumulated exposure doses. Proteins were precipitated by acetone precipitation. These proteins were identified by 2D-nano LC-ESI-TOF/MS and quantified by isobaric tags for relative and absolute quantitation. The functions of differential proteins were analyzed by gene ontology. A total of 596 proteins were identified, including 194 quantified proteins. There were 21 differential proteins according to the screening criteria (19 upregulated proteins and 2 downregulated proteins), including complement, apolipoprotein, and glycoprotein. The functions of these differential proteins were binding, enzyme regulator activity, catalytic activity, and transporter activity, and they were involved in the biological processes including immune system process and response to stimulus. The complement, apolipoprotein, and glycoprotein identified in the proteomics may be related to liver injury caused by VCM exposure, and they could be used as candidate protein biomarkers of diseases caused by VCM exposure.

The long-term effects of occupational exposure to vinyl chloride monomer on microcirculation: a cross-sectional study 15 years after retirement

ObjectivesTo assess residual long-term microcirculation abnormalities by capillaroscopy, 15 years after retiring from occupational exposure to vinyl chloride monomer (VCM).DesignCross-sectional study.SettingAllier, one of the major areas of polyvinyl chloride production...

A Comprehensive Analysis of Plausible Genotoxic Covariates Among Workers of a Polyvinyl Chloride Plant Exposed to Vinyl Chloride Monomer

The aim of this study was to assess the frequency of chromosomal aberrations-including chromatid type aberrations (CTAs), chromosomal type aberrations, micronucleus (MN) comet assay, and XRCC1 399 Arg/Gln polymorphism-in peripheral blood lymphocytes of workers occupationally exposed to vinyl chloride monomer (VCM). A total of 52 workers and an equal number of controls were recruited into the study to explore the potential cytogenetic risk of occupational exposure to VCM. Questionnaires were administered to obtain details of habitual cigarette-smoking, alcohol-consumption pattern, and occupation, etc. The exposed subjects and controls were classified into two groups based on age (group I <40 years; group II ≥40 years), and exposed subjects were further classified based on exposure duration (>8 and ≥8 years). CTA, MN, and comet assay frequency were significantly greater in polyvinyl chloride (PVC) factory workers (p < 0.05) with long-duration work. CTA, MN, and comet assay values were found to be increased with age in exposed subjects as well as in controls, with exposed subjects showing a statistically greater degree. An extensively greater MN frequency was observed in smokers exposed to VCM than in the control group (P < 0.05). The mean tail length of exposed subjects was greater compared with controls. The study on XRCC1 399 Arg/gln polymorphism in PVC factory workers showed less significant difference in allele frequency compared with controls. In conclusion, this results of work provides evidence for an apparent genotoxic effect associated with VCM exposure. Our results reinforce the greater sensitivity of cytogenetic assays for biomonitoring of occupationally exposed populations. Statistics indicate that workers exposed to VCM are at carcinogenic risk and should be monitored for long-term adverse effects from their exposure.

Estimation of a Safe Level for Occupational Exposure to Vinyl Chloride Using a Benchmark Dose Method in Central China

The aim of this study was to estimate a benchmark dose (BMD) for chromosome damage induced by vinyl chloride monomer (VCM) in VCM-exposed workers in central China and validate the published results in Shanghai. VCM-exposed workers who had been exposed to VCM for at least one year (n=463) and matched subjects not exposed to VCM or other toxins (n=273) were asked to participate in this study. Micronucleus (MN) frequency based on the cytokinesis-block micronucleus assay (CBMN) was used as a biomarker for chromosome damage induced by VCM exposure. The MN frequency in the VCM-exposed workers was significantly higher than that in the control group, and multivariate Poisson regression suggested that gender, smoking status and VCM exposure were the significant factors influencing the risk of increased MN frequency. When subjects were further stratified according to gender and smoking status, the results showed that female VCM-exposed workers were more susceptible than the males to the risk of increased MN frequency. The MN frequency of smokers was significantly higher than that of nonsmokers in the control group. Our study also suggested that there was a strong dose-response relationship between VCM CED and the increased risk of MN frequency in the total group, males and females. The BMDL(10) was found to be 630.6, 670.2 and 273.7 mg-year for all VCM-exposed workers, males and females, respectively. These results invite further scrutiny of the current VCM occupational exposure limits and warrant further study of the risk of VCM genotoxicity and carcinogenicity.

Time to pregnancy study in male workers exposed to vinyl chloride monomer in the polyvinyl chloride industry

ObjectivesAlthough there were several published works on abnormal liver functions, liver cirrhosis or cancer, and genetic damages of the Taiwan polyvinyl chloride (PVC) cohort, the potential effect of vinyl chloride...

Mortality from liver cancer and leukaemia among polyvinyl chloride workers in Taiwan: an updated study

ObjectivesTo investigate types of cancer caused by occupational exposure to vinyl chloride monomer (VCM) and the temporal mortality trends of these cancers in workers from polyvinyl chloride (PVC) manufacturing factories...

Genetic Polymorphisms in Metabolizing Enzymes and Susceptibility of Chromosomal Damage Induced by Vinyl Chloride Monomer in a Chinese Worker Population

To evaluate whether polymorphisms in metabolizing enzymes contributed to susceptibility of chromosomal damage induced by vinyl chloride monomer (VCM). Cytokinesis block micronucleus test was performed on 185 VCM-exposed workers and 41 control subjects to detect chromosomal damage in peripheral lymphocytes. The polymerase chain reaction and restriction fragment length polymorphism technique was applied to detect polymorphisms of GSTT1, GSTM1, GSTP1G/A, CYP2E1G/C, and CYP2D6G/C. Poisson regression analysis was performed. Sex, age, VCM exposure, GSTP1, and CYP2E1 genotype can influence chromosomal damage. There was a 1.51-fold increased micronucleus frequency for GSTP1GG genotypes individuals compared with those GSTP1AA/GA genotype individuals (P < 0.05), the effect of polymorphism in CYP2E1 gene was more pronounced for allele C compared with allele G (P < 0.05). Polymorphisms of GSTP1G/A and CYP2E1G/C, which are potential susceptibility biomarkers of chromosomal damage in VCM-exposed worker.

Genetic susceptibility of DNA damage induced by vinyl chloride monomer exposure

To explore the association between DNA damage induced by vinyl chloride monomer (VCM) and polymorphisms of DNA repair genes and xenobiotic metabolism genes of VCM. Comet assay was employed to detect DNA damage. Based on the status of DNA damage, the VCM exposure workers were divided into two groups: DNA damage group (75) and control group (75). Case-control design was used to investigate the association between the genetic polymorphisms and DNA damage induced by VCM. Genotypes of XRCC1 (Arg194Trp, Arg280His and Arg399Gln), XPD (Ile199Met, Asp312Asn and Lys751Gln) and CYP2E1 were identified by the PCR-RFLP. PCR assay was used to detect positive and null genotype of GSTT1 and GSTM1. Univariate analysis showed that the CYP2E1 c1c2/c2c2 and XPD751 Lys/Gln and Gln/Gln genotypes were significantly associated with the increased levels of DNA damage, XRCCI 339 Arg/Gln and Gln/Gln genotypes were significantly associated with the decreased levels of DNA damage (P < 0.01, P < 0.05, respectively). Logistic regression analysis showed that there was significant association between the genotypes of XRCC1 194, XRCC1 399, XPD 751, CYP2E1 and DNA damages. A prominent risk decreasing of DNA damage was observed for those individuals possessing XRCC1 399Arg/Gln + Gln/Gln genotypes (OR: 0.35, 95%CI: 0.12 approximately 1.01, respectively); The results also showed that there were significant associations between CYP2E1 c1c2/c2c2 and DNA damage both in high and low VCM-exposed groups (OR: 2.57, 95%CI: 1.01 approximately 6.59 and OR: 2.57, 95%CI: 0.99 approximately 6.87). Cumulative exposure dose and genotypes of XRCC1 194, XRCC1 399, XPD 751 and CYP2E1 may modulate the DNA damage induced by VCM exposure.

Effect of the CYP2E1 genotype on vinyl chloride monomer-induced liver fibrosis among polyvinyl chloride workers

Although a relationship between vinyl chloride monomer (VCM) and liver cirrhosis has been reported, the underlying mechanisms are not clear. Cytochrome P450 2E1 (CYP2E1), aldehyde dehydrogenase 2 (ALDH2) and glutathione S-transferase theta 1 (GSTT1) enzymes are involved in activation and detoxification of VCM, and thus may be important determinants of interindividual susceptibility to VCM-induced liver damage, including liver cirrhosis. The objective of this study was to evaluate if metabolizing genetic polymorphisms could modify individual susceptibility to liver fibrosis of the VCM exposure. CYP2E1, ALDH2, and GSTT1 polymorphisms were determined by the PCR-RFLP method among 320 workers who were employed in five polyvinyl chloride manufacturing plants. Cumulative VCM exposure levels for study subjects were calculated using a job exposure matrix model. Thirteen workers were diagnosed as having liver fibrosis by using ultrasonography. We observed a dose–response trend between VCM exposure and liver fibrosis. Regarding the results on genetic polymorphisms, CYP2E1 c2c2 genotype showed a significant increase in the risk of liver fibrosis as compared to those with CYP2E1 c1c1 or c1c2 genotypes. No differences were observed between GSTT1 and ALDH2 genotypes and liver fibrosis. In summary, our result suggests that genetic polymorphism in CYP2E1 may be responsible for individual differences in susceptibility to liver fibrosis with regard to chronic VCM exposure. Thus, polymorphism analysis of metabolizing enzymes might be useful in the risk assessment of liver damage in workers with VCM exposure.

Glutathione S-transferase M1 and GST T1 genetic polymorphisms and Raynaud’s phenomenon in French vinyl chloride monomer-exposed workers

Occupational vinyl chloride monomer (VCM) exposure can induce Raynaud's phenomenon (RP). However, not all VCM workers developed RP, which suggests an underlying genetic susceptibility. Genetic polymorphisms of glutathione S-transferases (GSTs), involved in VCM metabolism, have been shown to influence certain VCM-related health effects. We have conducted a case-control study of 58 subjects with RP along with 247 subjects without RP, from a population of 305 French workers exposed or formerly exposed to VCM, to assess any association between GST M1 and GST T1 gene polymorphisms, either separately or in combination, and the presence of RP. None of the GST M1 or GST T1 genotypes were significantly associated with the presence of RP among studied VCM workers. A combination of positive genotypes for both GST M1 and GST T1 was significantly associated with RP presence, compared to the other combinations of genotypes (OR=2.1, 95% CI=1.1-3.8). OR adjusted for age, smoking status, alcohol consumption and history of treated hypertension did not reach significance (OR=2.0, 95% CI=0.9-5.2). None of the GST M1 and GST T1 genotypes seem to contribute separately to the presence of RP, suggesting that they are not, when taken alone, a major determinant of interindividual variability for VCM-induced PR. However, the combination of both positive GST M1 and GST T1 genotypes appears to contribute slightly to susceptibility to RP in VCM-exposed subjects. Nevertheless, our study-the first to examine the role of a genetic component in the occurrence of RP secondary to occupational exposure to a chemical-corroborates the previous considerations that interaction between the genetic constitution and environmental factors is of importance in determining the health-adverse effects of VCM exposure.

Liver function assessment in workers exposed to vinyl chloride

To investigate liver function in vinyl chloride workers and assess its relation with current/past occupational exposure to vinyl chloride monomer (VCM). A medical examination including the execution of liver function tests (LFTs) and liver ultrasonography was executed in a group of 757 workers with a long-standing service in the production of VCM/polyvinylchloride (PVC). Cumulative and maximum VCM exposures were calculated. History of viral hepatitis and alcohol intake were carefully investigated. Regression analysis explored the association between abnormal LFTs and a group of possible determinants (VCM cumulative and maximum exposure, BMI, age, history of viral hepatitis, alcohol and triglyceride levels). Also, synergistic effect between VCM and a history of hepatitis was analysed, as well as the possible association between VCM exposure and aspartate aminotransferase/alanine amino transferase (AST/ALT) ratio >1. Distribution of abnormal LFTs was also assessed in relation to the results provided by liver ultrasonography. The most frequently abnormal serum parameters were, in decreasing order: total cholesterol (27.3%), triglycerides (12.2%), total bilirubin (9.1%), gamma glutamil transpeptidase (GGT; 9.0%) and ALT (8.2%). The AST/ALT ratio >1 was present in 28.1% of workers. Abnormal LFTs were not found to be associated with current or past VCM exposure. High ALT resulted positively associated with BMI, AST with alcohol intake, GGT with alcohol intake and triglycerides. No synergistic effect on LFTs of exposure to VCM and a history of hepatitis was observed. The AST/ALT ratio >1 was not found to be associated with VCM exposure. The prevalence of abnormal LFTs was higher in case of liver steatosis (ALT) or periportal fibrosis (GGT), but not in case of pure hepatomegaly, as documented by ultrasonography. Liver function assessment only including LFTs is not able to detect VCM-induced liver damage, but reveals alterations due to non-occupational factors, such as dietary and/or metabolic disfunctions. The LFTs are however of importance to detect conditions that could recommend avoidance of exposure to VCM and are useful for medical counselling and health promotion purposes.

Polymorphisms of DNA repair gene XPD and DNA damage of workers exposed to vinylchloride monomer

Vinyl chloride monomer (VCM) is a human carcinogen. However, the exact mechanism of carcinogenesis remains unclear. 2-Chloroethylene oxide (CEO) and 2-chloroacetaldehyde (CAA), the metabolic intermediates of VCM, induce DNA damage which is mainly repaired by the nucleotide excision repair (NER) pathway. The XPD gene product and the related XPB protein are DNA helicases that are involved in transcription and NER. Polymorphisms of XPD have been implicated in chemical exposure-related health effects. In order to explore the mechanism of VCM-related health effects, a special matched case-control design (exposed workers with DNA damage and without damage) was used to investigate the association between the gene polymorphisms of XPD and DNA damage in 106 male and 44 female workers occupationally exposed to VCM. Exposure and anthropometrics information was collected through in-person interview. Such information was then used to calculate cumulative exposure doses of the workers. DNA damage in peripheral lymphocytes was measured by the single cell gel electrophoresis (SCGE) assay that identified DNA strand breaks. Genomic DNA from lymphocytes was used in genotyping assays. Genotypes of XPD Ile199Met, XPD Asp312Asn, and XPD Lys751Gln were identified by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) procedure. The results indicate that the genotypes of XPD 751Lys/Gln and Gln/Gln were significantly associated with the expression of DNA damages (OR 2.21, P < 0.05 , 95% CI 1.01–5.13). An interesting observation is the reduction of DNA damage for workers with high VCM exposure and possessing the XPD Asp/Asn and Asn/Asn genotypes (OR 0.33, 95% CI 0.11–0.95). Polymorphisms of XPD may therefore be a major reason of genetic susceptibility in VCM-induced DNA damage and health consequences.

Epidemiologic evidence for the carcinogenicity of vinyl chloride monomer

Epidemiologic evidence for the carcinogenicity of vinyl chloride monomer