Epidemiology

British Journal of Cancer (2002) 87, 966–970. doi:10.1038/sj.bjc.6600584 www.bjcancer.com
Published online 21 October 2002

Determinants of formation of aflatoxin-albumin adducts: a seven-township study in Taiwan

C-A Sun1, D-M Wu1, L-Y Wang2, C-J Chen3, S-L You3 and R M Santella4

  1. 1School of Public Health, National Defense Medical Center, School of Public Health, No. 161, Section 6, Min-Chuan East Road, Taipei 114, Taiwan, Republic of China
  2. 2Institute of Aboriginal Health, Tzu Chi University, Hualien County 970, Taiwan, Republic of China
  3. 3Graduate Institute of Epidemiology, College of Public Health, National Taiwan University, Taipei 100, Taiwan, Republic of China
  4. 4Division of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY 10032, USA

Correspondence: C-A Sun, E-mail: sunca@ndmctsgh.edu.tw

Received 27 May 2002; Revised 31 July 2002; Accepted 7 August 2002.

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Abstract

Dietary exposure to aflatoxins is one of the major risk factors for hepatocellular carcinoma. Individual susceptibility to aflatoxin-induced hepatocarcinogenesis may be modulated by both genetic and environmental factors affecting metabolism. A cross-sectional study was performed to evaluate determinants of the formation of aflatoxin covalently bound to albumin (AFB1-albumin adducts). A total of 474 subjects who were free of liver cancer and cirrhosis and were initially selected as controls for previous case–control studies of aflatoxin-induced hepatocarcinogenesis in Taiwan, were employed in this study. Aflatoxin-albumin adducts were determined by competitive enzyme-linked immunosorbent assay, hepatitis B surface antigen and antibodies to hepatitis C virus by enzyme immunoassay, as well as genotypes of glutathione S-transferase M1-1 and T1-1 by polymerase chain reaction. The detection rate of AFB1-albumin adducts was significantly higher in males (42.5%) than in females (21.6%) (multivariate-adjusted odds ratio=2.6, 95% confidence interval=1.4–5.0). The formation of detectable albumin adducts was moderately higher in hepatitis B surface antigen carriers (42.8%) than in non-carriers (36.6%) (multivariate-adjusted odds ratio=1.4, 95% confidence interval=1.0–2.1). In addition, the detection rate of AFB1-albumin adducts tended to increase with the increasing number of null genotypes of glutathione S-transferase M1-1 and glutathione S-transferase T1-1. In conclusion, this cross-sectional study has assessed the relative contributions of environmental exposure and host susceptibility factors in the formation of AFB1-albumin adducts in a well characterised Chinese adult population. This study further emphasises the necessity to reduce aflatoxin exposure in people living in an area endemic for chronic hepatitis B virus infection.

Keywords:

aflatoxin-albumin adducts, glutathione S-transferase M1-1, glutathione S-transferase T1-1, hepatitis B surface antigen