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Ananth S Bommakanti, and Farid Waliyar.


Aflatoxins are one of the most potent toxic substances that occur naturally. These are a group of closely related mycotoxins produced by fungi Aspergillus flavus and A. parasiticus. Aflatoxicosis is poisoning that result from ingestion of aflatoxins in contaminated food or feed. Aflatoxin poisoning is reported from all parts of world in almost all domestic and non domestic animals like cattle, horses, rabbits, and other non human primates. Aflatoxicoses is also reported in humans in many parts of the world.

Exposure to Aflatoxin

Diet is the major way through which humans as well as animals are exposed to aflatoxins. Apart from this, exposure to aflatoxin can be through ingestion of contaminated milk containing Aflatoxin M1(metabolite of AFB1).Occupational exposure to aflatoxins in agricultural workers, people working in oil mills, and granaries have been reported (Sorenson et al 1984).

Aflatoxin carcinogenecity

After wide experimentation on many animal species like rats, rainbow trout's, aflatoxin especially aflatoxin B1 is confirmed as a potential carcinogen (IARC 1993). Metabolism plays a major role in deciding the degree of toxicity (Eaton et al 1994). After ingestion, aflatoxin is metabolized by cytochrome p450 group of enzymes in the liver, where it is converted to many metabolic products like aflatoxicol, aflatoxin Q1, aflatoxin P1, and aflatoxin M1, depending on the genetic predisposition of the species. Along with the above another metabolite called aflatoxin 8,9 epoxide is also formed. The amount of this metabolite decides the species susceptibility as this can induce mutations by intercalating in to DNA ,by forming an adduct with guanine moiety in the DNA (Smela. et al 2001). This intercalation of Epoxide causes a Gà T transversion at codon 249 in p53 gene in liver, which may lead to hepatic carcinoma. This was observed in most of the experimental models, and it is presumed that this is the major reason for aflatoxin carcinogenecity (Katherine et al 1997 , Railey et al 97). Moreover species susceptibility to aflatoxin mainly depends on its liver detoxification systems, genetic make up, age and other nutritional factors (Howard et al 1990.)

According to Ames et al, 1990 only dioxins ( TD50 = 6.7 X 10-6 mg/kg/d) significantly exceeds AFB1 (TD50=9.3 x 10-4 mg/kg/d) in its potency. Using TD50 parameter aflatoxin B1 is 1000 times more potent as a carcinogen when compared to benzo pyrene ( Eaton. et al 1997). IARC has classified Aflatoxin as a group one carcinogen ( IARC 7th annual report on Carcinogens, 1987).

Health Aspects

Epidemiological, clinical, and experimental studies reveal that exposure to large doses(>6000mg) of aflatoxin may cause acute toxicity with lethal effect whereas exposure to small doses for prolonged periods is carcinogenic (Groopmann et al 1988 ) The adverse effects of aflatoxins on animal can be categorized into two general forms.

  • Acute Toxicity
  • Chronic Toxicity

Acute Toxicity

Acute toxicity is caused when large doses of aflatoxin are ingested. This is common in livestock. The principal target organ for aflatoxins is the liver. After the invasion of aflatoxins into the liver, lipids infiltrate hepatocytes and leads to necrosis or liver cell death. This is mainly because aflatoxin metabolites react negatively with different cell proteins, which leads to inhibition of carbohydrate and lipid metabolism and protein synthesis. In correlation with the decrease in liver function, there is a derangement of the blood clotting mechanism, icterus (jaundice), and a decrease in essential serum proteins synthesized by the liver. Other general signs of Aflatoxicosis are edema of the lower extremities, abdominal pain, and vomiting. The most sever case of acute poisoning of aflatoxin was reported in north-west India in 1974 where 25% of the exposed population died after ingestion of the molded maize with aflatoxin levels ranging from 6250 to 15600 mg/kg.

Chronic Toxicity

This is due to long term exposure of moderate to low aflatoxin concentration. The symptoms include decrease in growth rate, lowered milk or egg production, and immuno suppression. There is some observed carcinogenecity, mainly related to aflatoxin B1. Liver damage is apparent due to the yellow color that is characteristic of jaundice, and the gall bladder becomes swollen. Immuno-suppression is due to the reactivity of aflatoxins with T-cells, decrease in Vitamin K activities, and a decrease in phagocytic activity in macrophages. These immuno suppressive effects of aflatoxins predispose the animals to many secondary infections due to other fungi, bacteria and viruses. (Robens et al 1992, Mclean 1995)

Aflatoxin and Hepatitis

Many experiments conducted in different areas especially in China and in the African countries, have shown high incidence of hepatitis B virus infection where dietary exposure to aflatoxins was prevalent. Subsequent research proved that both aflatoxins and hepatitis B virus act synergistically in the etiology of liver cancer (Montesano et al 1997, Groopman et al 1996.)

Aflatoxins and Animal Health

No animal species is resistant to the acute toxic effects of aflatoxins.A wide variation in LD50 values has been obtained in animal species tested with single doses of aflatoxins. For most species, the LD50 value ranges from 0.5 to 10-mg/kg body weight. Animal species respond differently in their susceptibility to the chronic and acute toxicity of aflatoxins. Environmental factors, exposure level, and duration of exposure beside age, health, and nutritional status of diet can influence the toxicity ( FAO web library 2000).

Table 1. Acute toxicity of aflatoxin B1 expressed as a single oral dose LD50 (FAO web library)

Species LD50 mg kg -1 bodyweight
Rabbit 0.30
Duckling (11 day old) 0.43
Cat 0.55
Pig 0.60
Rainbow trout 0.80
Dog 0.50 - 1.00
Sheep 1.00 - 2.00
Guinea pig 1.40 - 2.00
Baboon 2.00
Chicken 6.30
Rat (male) 5.50 - 7.20
Rat (female) 17.90
Macaque (female) 7.80
Mouse 9.00
Hamster 10.20

Specific Species Affects (Reed et al, 1987)


Aflatoxicosis in swine is mainly due to the fact that corn is a large part of their diet. Studies show that 0.4 ppm in the diet, from weaning to market weight, will have negative effects on health and growth rate. This is due, in part, to the decrease in feed efficiency of the infected feed. Piglets are more susceptible than adults and it has been shown that feeding sows AFM 1, during lactation, can cause stunted growth in her litter. Large doses of aflatoxins have been shown to produce hepatic necrosis. The effects of aflatoxicosis can be compounded with the addition of stress. This can lead to ataxia and induced hemorrhaging. The hemorrhaging is due to the prolonged blood clotting time caused by lack of Vitamin K utilization. Treatment with Vitamin K, menadione, and even protein supplementation have shown to have some proactive affects for reducing the effects of aflatoxicosis in swine.


Aflatoxicosis has the same toxic effects in poultry as it does in mammals. A dose of 0.25 ppm in turkey pouts and ducklings impairs growth, and a dose of 1.5 ppm in broilers and 4 ppm in Japanese quail has a negative affect on growth. An increase in blood clotting time increases the susceptibility of the carcass to bruising even at doses below that to have an affect on growth. In poultry, aflatoxins impair the availability of bile salts, which decreases Vitamin D3 production. This causes a decrease in the absorption of fat-soluble vitamins. Aflatoxins also decrease the production of Vitamin A in the liver, and it has secondary effects such as decreased blood calcium levels, decreased bone strength, and a decreased tissue and serum tocopherol level. This decrease in tocopherol levels can lead to Vitamin A and E deficiencies.


The effects of aflatoxicosis in ruminants are similar to those of non-ruminants. Calves are more sensitive than yearlings and adults. A dose of 0.2 mg/kg body weight can cause a decrease in weight gains. This can be attributed to poor feed utilization and a dramatic increase in alkaline phosphate activity in the rumen. Chronic aflatoxicosis in adult ruminants can cause anorexia, drying and peeling of the skin on the muzzle, rectal prolapse, and abdominal edema. Aflatoxicosis has also been shown to cause decreased fertility, abortion, and lowered birth weights in sheep. Some evidence on aflatoxicosis shows an effect on rumen microflora. This is characterized by a decrease in cellulolysis, VFA production, and ammonium formation.


These are highly susceptible species to afaltoxins. The LD50 in rabbits was determined as 300mg/kg Aflatoxin contaminated feed cause hemolytic anemia in rabbits fed with a dosage of 15 mg/kg for 30 days. Strong cytotoxic effects are also seen (Verma et al, 1998).

Aflatoxin and Human health

Aflatoxicoses in humans was reported in many countries like India, China, Thailand, and several African countries. In African and Asian countries, where environmental condition favor the aflatoxin contamination, threat to human health from aflatoxins is quiet high. Studies on aflatoxin exposure and incidence of liver cancer by Groopmann and Wild(1994-2001) in places like China and West Africa showed that the situation was alarming. (Aspen cancer conference, 2001).

Studies relating to aflatoxin exposure of humans in India are not being done actively. However, this problem is present and may break loose at any time in near future, as incidence of aflatoxin contamination in foods and feeds is very common.

Aflatoxin and children

Foetal and childhood environment, including the nutritional status of the pregnant mother and the infant, are considered critical for growth and risk of disease in earlier life. Mal-nourishment is one of the common problems in developing countries. Apart from these, they are also exposed to high levels of mycotoxins. Aflatoxins are the major among these. It has been proved that these aflatoxins are immunogenic, teratogenic, and they retard the growth among experimental animals. In the developing countries like India and China, the environmental conditions favor their production. High exposure of these aflatoxins occurs through out these regions. A study in West Africa showed a significant correlation among the aflatoxin exposure and stunted growth in children who are exposed to aflatoxin right for neonatal stages ( Gong et al 2002). Apart from that due to the capacity of aflatoxins to cross the placental barrier, can cause genetic defects at foetal stages itself (Maxwell et al 1998 ).

In view of the importance of mycotoxins in food and feed, ICRISAT has developed major partnerships with several institutions to address this problem. Approaches such as developing resistant varieties, biological control, agronomic practices and Integrated Aflatoxin management are exploited. Such information is available at ICRISAT and in this web site. These technologies will contribute reducing risk on human and animal health.


1. Sorenson WG, Jones W, Simpson J and Davidson JI. 1984. Aflatoxin In Respirable Airborne Peanut Dust, Journal of Toxicology and Environmental Health, Vol.14, pages 525-533.

2. Eaton L Dave and Gallhager EP. 1994. Mechanism of aflatoxin Carcinogenisis, Annu Rev Pharmacol Toxicol. 34:135-72.

3. Marryann E Smela and Sophie S Curier. 2001. Elisabeth A Bailey and John M Essingmann: The chemistry and biology of aflatoxin B1, Carcinogenesis. Vol 22 No.4 535-545.

4. Katherine Mace, Fernando Augilar, Jia Sheng Wang and Andrea MA Pfeifer. 1997. AFB1 induced DNA adduct formation and p53 mutation in CYP450 expressing human liver cell lines. Carcinogensis. Vol. 18 no. 7 pp. 1291 - 1297 .

5. Joan Railey, H George Mandel, Subatra Sinha, David L Judahand and Gordon E Neal. 1997. Invitro activation of human Harvey -ras Proto Onco gene by aflatoxin b1. Carcinogensis. Vol 18 905-910 ).

6. Howard S Ramdell and David L Eaton. 1990. Species susceptibility to Aflatoxin B1 carcinogenesis. Cancer Research. 50 615-620 .

7. Bruce N Ames, Margie Profet and Lois Swirsky Gold. 1990. Nature's chemicals and synthetic Chemicals : Comparative toxicology PNAS 1990 October, Vol.87, pp. 7782-7786.

8. Eaton L Dave. 1997. Aflatoxin toxicology Chapter 9.26 Comprehensive Toxicology, Pergamon publications 1997.

9. Groopmann JD and Thomas W Kensler. 1999. CRC Critical Reviews in Toxicology 1999 Chapter 19 113-124.

10. Encyclopedia Of Food Mycotoxin, M.Weidenborner Springer-Verlag publications 2000.

11. Robens JF and Richard JL. 1992. Aflatoxins in animal and human health. Rev Environ Contam Toxicol 1992, No. 127 :69-94.

12. Mclean M and Dutton MF. 1995. Cellular interactions and metabolism of aflatoxin: an update. Pharmacol Ther 1995 , 65(2):163-92.

13. Montesano R, Hainaut P and Wild CP. 1997. Hepatocellular carcinoma : From gene to public health, Review, Journal of National Cancer Institute 1997, 89,1844-51.

14. Groopman JD and Kensler W. 1996. Temporal patterns of aflatoxin-albumin adducts in hepatitis B surface antigen-positive and antigen-negative residents of Daxin, Qidong County, People's Republic of China. CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION; 5 (4). 1996. 253-261.

15. Reed JD and Kasali OB. 1987. Hazards to live stock of consuming Aflatoxin contaminated meal in Africa ICRISAT proceedings of international workshop on Aflatoxin contamination in ground nuts 6-9 oct 1987.

16. Verma RJ and Mehta DN. 1998. Occurance of hemolytic anemia during aflatoxicosis, Indian Journal of Environment. & Toxicology, 1998, 8(1):5-7.

17. Molecular Epidemiology : Aflatoxin , p53 mutations and liver cancer as a paradigm

18. Maxwell SM , Apeagyei F, de Vries HR , Mwanmut DD and Hendrickse RG. 1998. Aflatoxins in breast milk, neonatal cord blood and sera of pregnant women. J Toxicol Toxin Rev 1989; 8(1-2):19-29.

19. Gong YY, Cardwell K, Hounsa A, Egal S, Turner PC, Hall AJ and Wild CP. 2002. Dietary aflatoxin exposure and impaired growth in young children from Benin and Togo: cross sectional study; BMJ 2002; 325:20-21.

20. IARC : Some naturally occurring substances : Food items and constituents. IARC monographs on Evaluation of carcinogenic risk to humans No. 56 (1993).


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