Yanhua Su1, Benhua Zhao2, Fei Guo1, Zhao Bin3, Yue Yang1, Sheng Liu1, Yaofeng Han1, Jianjun Niu4, Xiayi Ke5, Ning Wang6, Xuesi Geng7, Changnan Jin7, Yichen Dai8, Yuanyuan Lin8. 1. State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Fujian, China. 2. State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Fujian, China. Electronic address: benhuazhao@sina.com. 3. Organ Transplantation Institute of Xiamen University, Fujian, China. 4. Xiamen Center for Disease Control and Prevention, Fujian, China. 5. Institute of Child Health, University College London, London, UK. 6. Department of Hematology, First Affiliated Hospital of Xiamen University, Fujian, China. 7. Xiamen Hospital of Traditional Chinese Medicine, Fujian, China. 8. Digestive System Department of the 174th Hospital of People's Liberation Army, Xiamen, Fujian, China.
Abstract
PURPOSE: Large epidemiologic studies about the relationship between benzo[a]pyrene (B[a]P) and hepatocellular carcinoma (HCC) have been limited. B[a]P diol epoxide (BPDE) is a highly reactive metabolite of B[a]P that binds covalently to form DNA adducts. We evaluated the interaction between B[a]P exposure with other risk factors in HCC, in a case-control study of 345 HCC and 961 healthy controls. METHODS: Concentration of BPDE-DNA adducts in blood was determined by enzyme-linked immunosorbent assay. The interaction between BPDE-DNA adducts and other risk factors on HCC were evaluated by multivariate logistic regression analysis. RESULTS: Mean concentration of BPDE-DNA adducts in blood of cases was significantly higher than that of the controls. The risk of HCC increased with elevated concentration of BPDE-DNA adducts (x(2) = 203.57, Ptrend < .001) and the odds ratio was 7.44 (95% confidence interval, 5.29-10.45) for the first versus fourth quartile of adduct levels. The relative excess risk due to interaction between BPDE-DNA adducts and hepatitis B virus surface antigen and drinking was 34.71 and 54.92, and the attributable proportion due to interaction was 41.53% and 75.59%, respectively. CONCLUSIONS: The high level of BPDE-DNA adducts in blood is associated with HCC and that environmental exposure to B[a]P may increase the risk of HCC, especially among drinkers and populations with hepatitis B virus infection.
PURPOSE: Large epidemiologic studies about the relationship between benzo[a]pyrene (B[a]P) and hepatocellular carcinoma (HCC) have been limited. B[a]Pdiol epoxide (BPDE) is a highly reactive metabolite of B[a]P that binds covalently to form DNA adducts. We evaluated the interaction between B[a]P exposure with other risk factors in HCC, in a case-control study of 345 HCC and 961 healthy controls. METHODS: Concentration of BPDE-DNA adducts in blood was determined by enzyme-linked immunosorbent assay. The interaction between BPDE-DNA adducts and other risk factors on HCC were evaluated by multivariate logistic regression analysis. RESULTS: Mean concentration of BPDE-DNA adducts in blood of cases was significantly higher than that of the controls. The risk of HCC increased with elevated concentration of BPDE-DNA adducts (x(2) = 203.57, Ptrend < .001) and the odds ratio was 7.44 (95% confidence interval, 5.29-10.45) for the first versus fourth quartile of adduct levels. The relative excess risk due to interaction between BPDE-DNA adducts and hepatitis B virus surface antigen and drinking was 34.71 and 54.92, and the attributable proportion due to interaction was 41.53% and 75.59%, respectively. CONCLUSIONS: The high level of BPDE-DNA adducts in blood is associated with HCC and that environmental exposure to B[a]P may increase the risk of HCC, especially among drinkers and populations with hepatitis B virus infection.