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Short Communication |
Departments of Environmental Health Sciences [S-Y. C., R. M. S.], Biostatistics [W-Y. T.] and Epidemiology [H. A.], Mailman School of Public Health of Columbia University, New York, New York 10032; Graduate Institute of Epidemiology, College of Public Health, National Taiwan University, Taipei 10018, Taiwan [C-J. C., S-R. C.]; Department of Public Health, Chang Gung University, Taoyuan, Taiwan [L-L. H.]; and Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan [L-Y. W.]
Chronic hepatitis B virus (HBV) infection and aflatoxin B1 (AFB1) exposure interact synergetically to induce hepatocellular carcinoma. One suggested mechanism for this interaction is the enhanced activation of AFB1 in chronically HBV-infected individuals. Whereas no associations between chronic HBV infection and AFB1-albumin adducts were observed in several studies in adults, hepatitis B surface antigen (HbsAg)-positive children were found to have elevated adducts in Gambia. To assess the association between chronic HBV infection and AFB1-albumin adduct level in Taiwan, 200 junior high school adolescents from 20 townships were assayed for HBsAg and AFB1-albumin adducts. The mean AFB1-albumin adduct level was higher in HBsAg-positive compared with HBsAg-negative subjects. The association between HBsAg status and AFB1-albumin adducts remained after multivariate adjustment. This finding additionally supports the synergetic interaction between HBV and AFB1, but the mechanism remains to be elucidated.
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C.P. Wild and P.C. Turner The toxicology of aflatoxins as a basis for public health decisions Mutagenesis, November 1, 2002; 17(6): 471 - 481. [Abstract] [Full Text] [PDF] |
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