aflatoxin-m1 and Hepatitis-B

Topics: Adolescent; Adult; Aflatoxin B1; Aflatoxin M1; Aflatoxins; Aged; Animals; Carrier State; Child; Child, Preschool; China; Chromatography, High Pressure Liquid; DNA, Viral; Hepatitis B; Hepatitis B virus; Humans; Infant; Infant, Newborn; Liver Neoplasms; Middle Aged; Prospective Studies

Our study was designed to assess the fecal and urinary excretion of 3 aflatoxin B1 (AFB1) metabolites, aflatoxins M1 (AFM1) and Q1 (AFQ1) and aflatoxin B1-N7-guanine (AFB-N7-guanine) that are produced by the predominant forms of cytochrome P450 enzymes responsible for the biotransformation of AFB1. Fecal and urinary AFM1, AFQ1 and urinary AFB-N7-guanine were assessed in 83 young Chinese males selected from a larger population (n = 300) based on detectable urinary AFM1. The concentration of fecal AFQ1 (median 137 ng/g fresh weight, IQR 9.1 to 450) was approximately 60 times higher than that of AFM1 (2.3 ng/g, IQR 0.0 to 7.3). In urine, the median AFQ1 was 10.4 ng/ml (IQR 3.4 to 23.3), and the median AFM1 and AFB-N7-guanine 0.04 ng/ml (IQR 0.01 to 0.33) and 0.38 ng/ml (IQR 0.0 to 2.15), respectively. A subgroup (n = 14) with hepatitis B virus (HBV) infection had significantly higher fecal concentrations of AFQ1 (p = 0.043) and AFM1 (p = 0.001) than those who were hepatitis B-virus antigen (HBsAg) negative, and the respective differences in urinary AFQ1 and AFM1 concentrations approached statistical significance (p = 0.054, p = 0.138). Our study demonstrates that AFQ1 is excreted in urine and feces at higher levels than AFM1, and feces are an important route of excretion of these AFB1 metabolites. AFQ1 should be further assessed for its predictive value as a marker for exposure and risk of dietary aflatoxins.

Topics: Aflatoxin B1; Aflatoxin M1; Aflatoxins; China; Feces; Guanine; Hepatitis B; Humans; Male

A case-control study of primary liver cancer (PLC) was conducted in 1989 at Fusui County, Guangxi Province. There were 99 PLC cases and 99 age-sex-residence matched controls. There were no difference of age, sex, race, cultural, level, marital status and annual income distribution (P > 0.05). The mean dietary AFB1 intakes of cases and controls were 117.72 + 105.68 mg/d, the mean outputs of AFM1 were 22.56 and 21.62 ng per morning urine respectively. The mean sera aflatoxin-albumin adducts in both groups were 24.96 and 18.72 pg per mg albumin respectively. These indicators were of no statistical significance. Conditional Logistic regression showed that HBV infection (OR = 5.33), drinking pond-ditch water (OR = 3.70), family history of PLC (OR = 2.88), and total alcohol intakes (OR = 1.002) were statistically significant as risk factors (P > 0.05) rather than aflatoxins. This may be due to the fact that the samples selected in hyperendemic area both took high quantities of aflatoxin.

Topics: Aflatoxin B1; Aflatoxin M1; Case-Control Studies; China; Female; Food Contamination; Hepatitis B; Humans; Liver Neoplasms; Logistic Models; Male; Oryza; Plant Oils; Risk Factors