TY - JOUR
T1 - Urinary aflatoxin biomarkers and risk of hepatocellular carcinoma
AU - Ross, R. K.
AU - Yu, M. C.
AU - Henderson, B. E.
AU - Yuan, J. M.
AU - Qian, G. S.
AU - Tu, J. T.
AU - Gao, Y. T.
AU - Wogan, G. N.
AU - Groopman, J. D.
N1 - Funding Information:
cancer. There is no obvious source of bias to explain our results. Individuals with early symptoms of liver cancer could have changed their diet and somehow increased consumption of aflatoxin-contaminated foods. In a detailed survey of aflatoxin contamination of foodstuffs in Shanghai, we found that aflatoxin is detectable in various foods, but the level of contamination is usually low. Peanuts, peanut-containing foods, and soy sauce are important exceptions. It is unlikely that consumption of these foods would have increased. Adjustment for other known risk factors for liver cancer (HBsAg, alcohol consumption, and smoking)24 did explain our findings. Urinary aflatoxin metabolites and DNA-adducts reflect only recent dietary exposure to aflatoxins. Assays for serum albumin adducts to aflatoxin are now available25 and may assess dietary intake in the longer term. Such assays would therefore be expected to show even stronger associations with liver-cancer risk. As our study continues, we will make such serum measurements, compare them with urinary findings, and use them as independent and combined indicators of liver-cancer risk. We will continue to assess the extent to which aflatoxin markers interact with other risk factors, especially markers of chronic infection with hepatitis B virus, in defming liver-cancer risk. This study was supported by grant CA 43092 Institute, Bethesda, Maryland, USA. J. D. G. is a research career development award K04 CA01517.
PY - 1992/4/18
Y1 - 1992/4/18
N2 - Aflatoxins have long been suspected to be human hepatic carcinogens but no direct study was feasible until assays to measure individual aflatoxin exposure became available. We have used assays for urinary aflatoxin B1, its metabolites AFP1 and AFM1, and DNA-adducts (AFB1-N7-Gua) to assess the relation between aflatoxin exposure and liver cancer, as part of an ongoing prospective study of 18 244 middle-aged men in Shanghai, People's Republic of China. After 35 299 person-years of follow-up, 22 cases of liver cancer had been identified. For each case, 5 or 10 controls were randomly selected from cohort members without liver cancer on the date the disorder was diagnosed in the case and matched to within 1 year for age, within 1 month for sample collection, and for neighbourhood of residence. Subjects with liver cancer were more likely than were controls to have detectable concentrations of any of the aflatoxin metabolites (relative risk 2·4, 95% confidence interval 1 ·0-5·9). The highest relative risk was for aflatoxin P1 (6·2, 1·8-21·5). In an analysis adjusting for the effects of hepatitis B surface antigen seropositivity, level of education, cigarette smoking, and alcohol consumption, the relative risk for the presence of aflatoxin metabolites was 3·8 (1·2-12·2). There was a strong interaction between serological markers of chronic hepatitis B infection and aflatoxin exposure in liver-cancer risk. Reduction of aflatoxin exposure may be a useful intermediate goal in prevention of liver cancer, since the benefits of wide-scale hepatitis B vaccination will not be apparent for many years.
AB - Aflatoxins have long been suspected to be human hepatic carcinogens but no direct study was feasible until assays to measure individual aflatoxin exposure became available. We have used assays for urinary aflatoxin B1, its metabolites AFP1 and AFM1, and DNA-adducts (AFB1-N7-Gua) to assess the relation between aflatoxin exposure and liver cancer, as part of an ongoing prospective study of 18 244 middle-aged men in Shanghai, People's Republic of China. After 35 299 person-years of follow-up, 22 cases of liver cancer had been identified. For each case, 5 or 10 controls were randomly selected from cohort members without liver cancer on the date the disorder was diagnosed in the case and matched to within 1 year for age, within 1 month for sample collection, and for neighbourhood of residence. Subjects with liver cancer were more likely than were controls to have detectable concentrations of any of the aflatoxin metabolites (relative risk 2·4, 95% confidence interval 1 ·0-5·9). The highest relative risk was for aflatoxin P1 (6·2, 1·8-21·5). In an analysis adjusting for the effects of hepatitis B surface antigen seropositivity, level of education, cigarette smoking, and alcohol consumption, the relative risk for the presence of aflatoxin metabolites was 3·8 (1·2-12·2). There was a strong interaction between serological markers of chronic hepatitis B infection and aflatoxin exposure in liver-cancer risk. Reduction of aflatoxin exposure may be a useful intermediate goal in prevention of liver cancer, since the benefits of wide-scale hepatitis B vaccination will not be apparent for many years.
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U2 - 10.1016/0140-6736(92)91528-G
DO - 10.1016/0140-6736(92)91528-G
M3 - Article
C2 - 1348796
AN - SCOPUS:0026566829
SN - 0140-6736
VL - 339
SP - 943
EP - 946
JO - The Lancet
JF - The Lancet
IS - 8799
ER -