Aflatoxin Group: (B1, B2, G1, G2)

Optimal Result: 0 - 0.8 ppb.

Aflatoxins were initially isolated and identified as the causative toxins in Turkey X disease (necrosis of the liver) in 1960 when over 100,000 turkeys died in England (Asao, 1963). They are the most studied mycotoxins with over 5,000 research papers published through 2002. There are four generally recognized Aflatoxins designated B1, B2, G1 and G2 . The metabolites, M1 & M2, are found in milk (Thirumala-Devi et al (2002).

The order of toxicity is B1 greater than G1, greater than G2, greater than B2. (IARC, 1976). However, Aflatoxin B1 is the major mycotoxin produced by most species under culture conditions (Ciegler & Bennet, 1980). Because of this and its toxicity, B1 is the most frequently studied of the four.

Aflatoxins are produced by different species of Aspergillus, particularly flavus, oryzae, fumigatus and parasiticus, as well as members of the genera Penicillium (El-Naghy et al, 1991; Searle 1976; Aflatoxins 2002). Strains of Aspergillus flavus and parasiticus produce mycotoxins under favorable conditions.

Aflatoxins can contaminate corn, cereals, sorghum, peanuts and other oil-seed crops. Thus, food contamination by this group of mycotoxins has been implicated in both animal and human Aflatoxicosis.

Aflatoxins are carcinogenic to humans and animals. Overall summary evaluation of carcinogenic risk to humans is Group 1 (IARC, 1976; Searle, 1976; Dominguez-Malagon & Gaytan-Graham (2001).

Aflatoxin B1 is a potent liver carcinogen in a variety of experimental animals. It causes liver tumors in mice, rats, fish, marmosets, tree shrews and monkeys following administration by various routes. Types of cancers described in research animals include hepatocellular carcinoma (rats), colon and kidney (rats), cholangiocellular cancer (hamsters), lung adenomas (mice), and osteogenic sarcoma, adenocarcinoma of the gall bladder and carcinoma of the pancreas (monkeys) (IARC, 1976).

In humans, Aflatoxin B1 has been linked to hepatocellular carcinoma from three studies reported in the medical literature, as follows:

An increased incidence (10 % excess) of hepatocellular carcinoma was reported in the southeastern portion of the U.S. in areas of high daily intake of Aflatoxin B1. The daily intake of B1 in the southeastern subjects was 13-197 ug/kg body weight as compared to those in northern and western areas with a daily intake of 0.2-0.3 ug/kg body weight (IARC, 1987).

In China, a strong correlation between the intake of peanut, peanut oil and corn and increased mortality rates for liver cancer were reported in five groups of inhabitants from four villages. The mortality rates were 125, 97.40, 41.65, 24.01 and 1.05, respectively. The median intake of aflatoxin B1 for each group was 6.05, 6.36, 2.69, 1.83 and 0 ug/day. The median daily urine concentrations of M1 metabolite were 16.46, 8, 29, 4.78 and 1.21 ng/person. A significant correlation was found between the mortality rates of primary liver cancer and intake of aflatoxin B1. Further, analysis of M1 in the urine can be used as an index for human exposure to aflatoxin B1 in an epidemiological study (Aflatoxins, 2002).

Cancer in 67 men who had inhaled particles contaminated with aflatoxin were reported in an 11-year follow up study. They worked in a mill crushing peanuts and other oil seeds. Two of the men developed fatal liver disease, while eleven developed cancers of various organs. The 13 men had inhaled doses estimated to be between 160 to 395 ug/cubic meter/man/wk. In 55 matched control men, 4 developed cancer and none died from liver disease. The excess cancers in this study was not significant, however the number of subjects was insufficient to exclude a significant positive correlation (Aflatoxins, 2002; IARC,1976).

Finally, it was reported that in hepatocellular carcinoma cases exposed to aflatoxin B1, mutation of p53 gene is fixed at codon 249 third base and takes the form of G to T transversion. It appears from the reported observations that it is a definite marker of mutation, which is induced by aflatoxin B1 mutagen and is applicable for molecular epidemiology survey of sufferers of aflatoxin B1 exposure among hepatocellular carcinoma cases (Deng & Ma, 1998).

What does it mean if your Aflatoxin Group: (B1, B2, G1, G2) result is too high?

Aflatoxins are some of the most carcinogenic substances in the environment. Aflatoxin susceptibility is dependent on multiple different factors such as age, sex, and diet. Aflatoxin can be found in beans, corn, rice, tree nuts, wheat, milk, eggs, and meat. In cases of lung aspergilloma, aflatoxin has been found in human tissue specimens. Aflatoxin can lead to liver damage, cancer, mental impairment, abdominal pain, hemorrhaging, coma, and death. Aflatoxin has been shown to inhibit leucocyte proliferation. Clinical signs of aflatoxicosis are non-pruritic macular rash, headache, gastrointestinal dysfunction (often extreme), lower extremity edema, anemia, and jaundice. Treatment should include fluid support to prevent dehydration. The toxicity of Aflotoxin is increased in the presence of Ochratoxin and Zearalenone. The drug Oltipraz can increase glutathione conjugation of aflatoxin while inhibiting the toxic effect of P450 oxidation, reducing liver toxicity and promoting safer elimination. A diet of carrots, parsnips, celery, and parsley may reduce the carcinogenic effects of aflatoxin. Bentonite clay is reported to reduce the absorption of aflatoxins found in food. Supplementation with chlorophyllin, zinc, and vitamins A, E, and C has been used to treat aflatoxicosis. 


Aflatoxicosis, be it humans or animals, is characterized by liver damage. Based on what information is available with respect to human exposure, encephalopathy can occur and is also observed in domestic animals. In addition, preliminary evidence from human studies demonstrates that aflatoxins cause an increase in circulating alpha tumor necrosing factor, suggesting that these mycotoxins are also immunotoxic in humans. In animals, immunosuppression does occur in a variety of different species.

Aflatoxins are present in the food chain. They have been found in human cord blood and apparently can enter the developing fetus in humans and animals (Hintz, 1990; Denning et al, 1990).

In addition, aflatoxins have been found in human breast milk (El-Nesami HS et al, 1995), cow’s milk and dairy products (Srivastava VP et al 2001; Thirumala-Devi et al, 2002) and infant formula (Aksit et al, 1997). Not only has exposure to aflatoxins been implicated in hepatocellular carcinoma, hepatic failure, encephalopathy and Reye’s syndrome, such exposure may also be important in the health and well-being of the fetus and neonates. Thus, it has been postulated that intra-uterine and neonate exposure from contaminated food products may play an etiology in (1) Kwashiorkor, (2) neonatal susceptibility to infection and jaundice, (3) childhood infections and malignant disease and compromised response to prophylactic immunizations in children (Hendrickse, 1991).

Finally, aflatoxin B1 can cause mutations to both nuclear and mitochondrial DNA. Albumin-aflatoxin adducts apparently are increased in individuals with the genetic polymorphism in association with GSTM1 null, mEH heterozygote and CYP3A5 mutations.

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