Abstract
To evaluate the role of aflatoxin B1 (AFB1) exposure on risk of hepatocellular carcinoma (HCC), a case-control study nested within a community-based cohort was conducted. Baseline blood and urine samples were used to determine the level of AFB1-albumin adducts and urinary AFB1 metabolites. Conditional logistic regression analysis was used to calculate odds ratios (OR) and 95% confidence intervals (95% CI) to assess the effect of AFB1 exposure on risk of HCC. The adjusted ORs (95% CIs) were 1.54 (1.01-2.36) and 1.76 (1.18-2.58), respectively, for those with AFB1-albumin adducts and urinary AFB1 metabolite levels above the mean compared with those with levels below the mean. When compared with subjects in the lowest quartile of urinary AFB1 metabolites, there was an increase in risk of HCC, with adjusted ORs (95% CIs) of 0.57 (0.14-2.43), 1.43 (0.32-6.42), and 4.91 (1.18-20.48; Ptrend=0.02), respectively, among noncarriers of hepatitis B virus (HBV) infection. The adjusted OR (95% CI) was 7.49 (5.13-10.93) for carriers of hepatitis B surface antigen compared with noncarriers, regardless of AFB1 status. The ORs (95% CI) were 10.38 (5.73-18.82) and 15.13 (7.83-29.25) for carriers of hepatitis B surface antigens with levels of AFB1-albumin adducts and urinary AFB1 metabolites above the mean, respectively. The combined effect of aflatoxin exposure and HBV infection did not differ by duration of follow-up. Consistent with our previous study with fewer subjects, these data show that AFB1 exposure is a risk factor for HCC risk. However, in this larger study, the effect of combined AFB1 exposure and HBV infection is more consistent with an additive than a multiplicative model.
Highlights
To evaluate the role of aflatoxin B1 (AFB1) exposure on risk of hepatocellular carcinoma (HCC), a case-control study nested within a community-based cohort was conducted
We have developed antibody-based methods for measurement of AFB1 exposure, including AFB1-albumin and urinary AFB1 metabolites, and we have shown that dietary exposure to AFB1 increased HCC risk among the Taiwanese population using a case-control study nested within a community-based Cancer Screening Program cohort [10, 11]
A Pearson partial correlation coefficient was used to determine the correlation between AFB1albumin adducts and urinary AFB1 metabolites adjusted by age and gender
Summary
To evaluate the role of aflatoxin B1 (AFB1) exposure on risk of hepatocellular carcinoma (HCC), a case-control study nested within a community-based cohort was conducted. The adjusted ORs (95% CIs) were 1.54 (1.01-2.36) and 1.76 (1.18-2.58), respectively, for those with AFB1-albumin adducts and urinary AFB1 metabolite levels above the mean compared with those with levels below the mean. When compared with subjects in the lowest quartile of urinary AFB1 metabolites, there was an increase in risk of HCC, with adjusted ORs (95% CIs) of 0.57 (0.14-2.43), 1.43 (0.32-6.42), and 4.91 The ORs (95% CI) were 10.38 (5.7318.82) and 15.13 (7.83-29.25) for carriers of hepatitis B surface antigens with levels of AFB1-albumin adducts and urinary AFB1 metabolites above the mean, respectively. Consistent with our previous study with fewer subjects, these data show that AFB1 exposure is a risk factor for HCC risk In this larger study, the effect of combined AFB1 exposure and HBV infection is more consistent with an additive than a multiplicative model. The reactive epoxides are detoxified by glutathione S-transferase – mediated conjugation [7]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
