Aflatoxins are among the most potent naturally occurring toxic substances. They belong to a group of closely related mycotoxins produced by certain molds. Aflatoxicosis refers to the poisoning that occurs after consuming food or feed contaminated with aflatoxins. Cases of aflatoxin poisoning have been reported worldwide in a wide range of domestic and wild animals, including cattle, horses, rabbits, and various primates. Additionally, aflatoxicosis has been documented in human populations across many regions globally.
The primary route of exposure to aflatoxins for both humans and animals is through dietary intake. In addition to contaminated food, aflatoxin exposure can occur through the consumption of milk containing Aflatoxin M1, a metabolite of aflatoxin B1. Occupational exposure is also a concern, particularly among workers in agricultural settings, oil processing mills, and grain storage facilities.
Extensive studies across various animal species have confirmed that aflatoxins, particularly aflatoxin B1, are potent carcinogens. The level of toxicity largely depends on metabolic processing, which occurs primarily in the liver. After ingestion, aflatoxins are metabolized by liver enzymes into several metabolites, including aflatoxicol, aflatoxin Q1, aflatoxin P1, and aflatoxin M1. A critical metabolite, aflatoxin 8,9-epoxide, plays a key role in toxicity and species susceptibility. This metabolite can bind to DNA by forming adducts with guanine bases, causing mutations. One specific mutation involves a transversion at codon 249 of the p53 gene, which is strongly linked to liver cancer development.Read more
The susceptibility of different species to aflatoxin toxicity is influenced by factors such as liver detoxification capacity, genetic background, age, and nutritional status.
In terms of carcinogenic potency, aflatoxin B1 is among the most powerful known carcinogens, significantly exceeding many other chemicals, including benzo[a]pyrene. Based on such evidence, aflatoxins are classified as Group 1 carcinogens by leading health organizations.
Epidemiological, clinical, and experimental evidence indicates that exposure to high doses of aflatoxins (greater than 6000 mg) can result in acute toxicity, which may be fatal. In contrast, prolonged exposure to lower doses is primarily associated with carcinogenic effects. The adverse impacts of aflatoxins on animals can generally be divided into two categories: acute toxicity and chronic toxicity.
Acute toxicity occurs following the ingestion of large doses of aflatoxins and is commonly observed in livestock. The liver is the primary organ affected. Upon exposure, aflatoxins cause lipid infiltration into liver cells (hepatocytes), leading to cell necrosis and liver damage. This results from aflatoxin metabolites interfering with cellular proteins, which disrupts carbohydrate and lipid metabolism as well as protein synthesis. As liver function declines, blood clotting mechanisms become impaired, jaundice develops, and the production of essential serum proteins decreases. Additional symptoms of acute aflatoxicosis include swelling of the lower limbs, abdominal pain, and vomiting. One of the most severe outbreaks of acute poisoning occurred in northwest India in 1974, where 25% of the affected population died after consuming maize contaminated with extremely high levels of aflatoxins.Read more
Chronic toxicity results from long-term exposure to moderate or low levels of aflatoxins. Symptoms include reduced growth rates, decreased milk or egg production, and immune system suppression. Carcinogenic effects, primarily linked to aflatoxin B1, have also been observed. Liver damage is often evident, characterized by jaundice, which gives the skin a yellowish tint, and swelling of the gall bladder. The immunosuppressive effects are caused by aflatoxins’ interaction with immune cells such as T-cells, a reduction in vitamin K activity, and decreased phagocytic function of macrophages. This weakened immune state increases susceptibility to secondary infections from various fungi, bacteria, and viruses.
Studies conducted in various regions, particularly in parts of Asia and Africa, have revealed a high prevalence of hepatitis B virus infection in populations exposed to dietary aflatoxins. Further research has demonstrated that aflatoxins and hepatitis B virus interact synergistically, significantly increasing the risk of developing liver cancer.
No animal species is completely resistant to the acute toxic effects of aflatoxins. The lethal dose (LD50) varies widely among species, generally ranging from 0.5 to 10 mg/kg of body weight. Susceptibility to both acute and chronic aflatoxin toxicity differs between species and is influenced by environmental conditions, the level and duration of exposure, as well as factors such as age, overall health, and nutritional status.
Cases of aflatoxicosis in humans have been reported in several countries, including regions of Asia and Africa. In these areas, environmental conditions often promote aflatoxin contamination, posing a significant risk to public health. Research investigating the link between aflatoxin exposure and liver cancer incidence in affected regions has highlighted an alarming situation.
Although active studies on aflatoxin exposure are limited in some countries, the widespread presence of aflatoxin contamination in food and feed suggests that the risk to human health remains substantial and could escalate in the near future.
The prenatal and early childhood environment, including the nutritional status of both the mother and infant, plays a critical role in growth and disease risk. Malnutrition remains a common challenge in many developing regions, where exposure to high levels of mycotoxins—aflatoxins being the most significant—is widespread. Studies have demonstrated that aflatoxins are immunogenic, teratogenic, and can impair growth in experimental animals. Environmental conditions in developing countries often promote aflatoxin production, leading to high exposure levels.
Research in West Africa has shown a strong correlation between aflatoxin exposure from the neonatal period and stunted growth in children. Additionally, the ability of aflatoxins to cross the placental barrier raises concerns about potential genetic damage during fetal development.
To address this issue, integrated approaches such as breeding resistant crop varieties, biological controls, improved agricultural practices, and comprehensive aflatoxin management strategies have been developed and implemented. These efforts aim to reduce the risk posed by aflatoxins to both human and animal health.
