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Increased Risk of Hepatocellular Carcinoma and Liver Cirrhosis in Vinyl Chloride Workers: Synergistic Effect of Occupational Exposure with Alcohol Intake

机译：氯乙烯工人肝细胞癌和肝硬化的风险增加：职业性摄入与饮酒的协同作用

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Hepatocellular carcinoma (HCC) and liver cirrhosis (LC) are not well-established vinyl chloride monomer (VCM)–induced diseases. Our aim was to appraise the role of VCM, alcohol intake, and viral hepatitis infection, and their interactions, in the etiology of HCC and LC. Thirteen cases of HCC and 40 cases of LC were separately compared with 139 referents without chronic liver diseases or cancer in a case–referent study nested in a cohort of 1,658 VCM workers. The odds ratios (ORs) and the 95% confidence intervals (CIs) were estimated by common methods and by fitting models of logistic regression. We used Rothman’s synergy index (S) to evaluate interactions. By holding the confounding factors constant at logistic regression analysis, each extra increase of 1,000 ppm × years of VCM cumulative exposure was found to increase the risk of HCC by 71% (OR = 1.71; 95% CI, 1.28–2.44) and the risk of LC by 37% (OR = 1.37; 95% CI, 1.13–1.69). The joint effect of VCM exposure above 2,500 ppm × years and alcohol intake above 60 g/day resulted in ORs of 409 (95% CI, 19.6–8,553) for HCC and 752 (95% CI, 55.3–10,248) for LC; both S indexes suggested a synergistic effect. The joint effect of VCM exposure above 2,500 ppm × years and viral hepatitis infection was 210 (95% CI, 7.13–6,203) for HCC and 80.5 (95% CI, 3.67–1,763) for LC; both S indexes suggested an additive effect. In conclusion, according to our findings, VCM exposure appears to be an independent risk factor for HCC and LC interacting synergistically with alcohol consumption and additively with viral hepatitis infection.
机译：肝细胞癌（HCC）和肝硬化（LC）并不是公认的氯乙烯单体（VCM）诱发的疾病。我们的目的是评估在HCC和LC的病因中VCM，酒精摄入和病毒性肝炎感染的作用及其相互作用。在一项涉及1658名VCM工人的队列研究中，将13例HCC和40例LC与分别为139例没有慢性肝病或癌症的参考对象进行比较。优势比（OR）和95％置信区间（CI）通过常用方法和逻辑回归拟合模型进行估算。我们使用了罗斯曼的协同指数（S）来评估互动。通过在Logistic回归分析中将混杂因素保持不变，发现每增加1000 ppm×年的VCM累积暴露量，HCC风险将增​​加71％（OR = 1.71； 95％CI，1.28–2.44）和风险LC降低了37％（OR = 1.37； 95％CI，1.13-1.69）。 VCM暴露超过2500 ppm×年和酒精摄入超过60克/天的共同作用导致HCC的OR为409（95％CI，19.6-8,553），LC的OR为752（95％CI，55.3-10,248）。这两个S指标都表明有协同作用。肝癌的VCM暴露超过2500 ppm×年以上和病毒性肝炎感染的联合效应对于肝癌为210（95％CI，7.13–6,203），对于LC为80.5（95％CI，3.67–1763）。两种S指数均表明存在加和效应。总之，根据我们的发现，VCM暴露似乎是HCC和LC与饮酒协同作用以及病毒性肝炎感染相加相互作用的独立危险因素。

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