Aflatoxins exposure

Lasky, T. and Magder, L., Hepatocellular carcinomap53 G>T transversions at codon 249 the fingerprint of aflatoxin exposure Env. Health Perspect., 105, 392,1997. 

Qian, G.S., R.K. Ross, M.C. Yu, J.M. Yuan, Y.T. Gao, B.E. Henderson, G.N. Wogan, and J.D. Groopman. 1994. A follow-up study of urinary markers of aflatoxin exposure and liver cancer risk in Shanghai, People s Republic of China. Cancer Epidemiol. Biomarkers Prev. 3 3-10. 

P. Scholl J. D. Groopman, Epidemiology of Human Aflatoxin Exposures and its Relationship to Liver Cancer. In Molecular Approaches to Food Safety Issues Involving Toxic Microorganisms, M. Eklund, J. L. Richard, K. Mise, Eds. Alaken, Inc. Fort Collins, CO, 1995 pp 169-182. 

Peers F, Bosch X, Kaldor J, Linsell A, Pluijiman M Aflatoxin exposure, hepatitis B virus infection and liver cancer in Swaziland. Int J Cancer 1987 39 545-553. 

Wild CP, Shresma SM, Anwar WA, Montesano R Field studies of aflatoxin exposure, metabolism and induction of genetic alterations in relation to HBV infection and hepatocellular carcinoma in The Gambia and Thailand. Toxicol Lett 1992 64/65 455 61. 

A specific mutation in the genetic material has been detected in people exposed to aflatoxin. An important factor in determining susceptibility may be individual variation in the metabolism of aflatoxin. A significant risk factor in liver cancer is infection by the virus that causes hepatitis B, and it appears that a combination of aflatoxin exposure and the viral infection makes individuals especially susceptible. 

C. P. Wild et al, Molecular dosimetry of aflatoxin exposure contribution to understanding multifactorial etiopathogenesis of primary hepatocellular carcinoma with particular reference to hepatitis B virus . Environmental Health Perspectives, 99 (1993), 115-22. 

Ozturk M, et al. p53 mutation in hepatocellular carcinoma after aflatoxin exposure. Lancet 1991 338 1356-59. 

In the meantime keep in mind that, although considerable progress has been made in reducing aflatoxin exposures, these mold products are still in some foods, and you have probably ingested a few nanograms (billionths of a gram ) recently. You d surely like to know how much your health is threatened by these unusual compounds. 

In most cases it is impossible to calculate the risk (R) from an exposure level as an exact number (e.g., R = l(b5). It may, however, be possible to agree on an exposure level that is so low that R < l(b5. When performing risk extrapolations we bias intentionally in the worst-case direction to be sure that we do not unintentionally bias in the other (unwanted) direction. Figure 10.1 shows difficulties with extrapolation. We may find a good correlation between aflatoxins in the dose interval 1 to 100 ppb and response as frequency of tumors in mice between 0.05 and 1. However, we would like to know the doses that give a response of 10 5. Is it possible to obtain this information from such data Furthermore, we are not at all interested in mice. If we decide upon a safe aflatoxin exposure for mice, we must further extrapolate to humans. 

Hsieh, D.P. and Atkinson, D.N. (1995) Recent aflatoxin exposure and mutation at codon 249 of the human p53 gene lack of association. Pood Addit. Contam., 12, 421-424. 

In contrast, this mutational pattern is not found in hepatocellular carcinoma samples from moderate or low aflatoxin exposure countries or regions. Therefore, this hot-spot mutation is believed to be a molecular fingerprint linking the initial event of aflatoxin Bl-DNA adduct formation with the ultimate development and progress of human hepatocellular carcinomas. 

Hayes R.B., Van Nieuwenhuize J.P., Raatgever J.W. and Ten Kate F.J.W. (1984) Aflatoxin exposures in the industrial setting An epidemiological study of mortality. Food Chem. Toxicol., 22, 39-43. 

As a public health hazard, the major routes for aflatoxin exposure are inhalation, pulmonary mycotoxicosis, especially of grain dusts, and ingestion as a result of eating food made with contaminated grains. The aflatoxin problem was first... 

All urine samples were then analyzed by HPLC and AFMl, AFPl and the major AFB-DNA adducts quantified (Figure 2). When the aflatoxin DNA adduct excretion levels in urine were correlated to aflatoxin B1 dietary intake amount in ug per day, a dose dependent excretion is seen. Because the afla-toxin-DNA adduct has a relatively short half life in DNA (2) this dose dependent excretion pattern reflects exposures during the previous few days. The correlation coefficient for this association of adduct excretion and AFBl intake is 0.6 with a P value of less than 0.00001. Taken together, it appears that the quantifying of aflatoxin DNA adducts in urine is a valid compartment to sample for aflatoxin exposure, but more data must be collected for developing a risk model for people. 

Gamer, R. C. Monitoring aflatoxin exposure at a macromolecular level in man with immunological methods. Bioact Mol., 10(Mycotoxins Phycotoxins 88), 29-35. 

Groopman, J. D. Cain, L. G. Kensler, T. W. Aflatoxin exposure in human populations Measurements and relationship to cancer. CRC Crit. Rev. Toxicol., 19 113-45. 1988. 

Wang, J.-S. and Tang, L., Epidemiology of aflatoxin exposure and human liver cancer, J. Toxicol. Toxin... 

Other foods contributing to total dietary aflatoxin exposure... 

A specific mutation in the p53 tumour suppressor gene has been detected in 10-70% of HCCs from areas of high AFBi exposure and is absent from HCCs from areas with negligible AFBi exposure [28-30]. Support for the implication that the mutation, a G- T transversion at the third base of codon 249, is caused by exposure to aflatoxin has come from in vitro studies. Aflatoxin exposure in bacteria almost exclusively causes G—transversions [31] and the aflatoxin-epoxide has been shown to bind to codon 249 of p53 in vitro [32]. Moreover, human... 

Milk and urine. Aflatoxin Ml can be delected in milk or urine for several days after aflatoxin exposure stops. 

Humans have a surprisingly high tolerance for aflatoxin exposure and rarely develop acute aflatoxicosis. Cases are often sub-clinical or mild in nature. Long-term effects of chronic exposure may include cirrhosis and hepatocellular carcinoma. 

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