Aflatoxins are highly toxic mycotoxins, which are secondary metabolites produced by certain molds, primarily species of the fungus Aspergillus, most notably A. flavus and A. parasiticus. Aflatoxin B1 (AFB1) is the most common form and is recognized as one of the most potent carcinogens found in nature. The presence of these toxins in the food supply poses a significant worldwide challenge to public health. Exposure is particularly concerning in developing countries, where climate conditions and inadequate food storage often lead to higher contamination levels.
Environmental Origins and Contamination Routes
The fungi responsible for aflatoxin production are widely distributed, growing in soil and various food crops. Contamination occurs in commodities such as maize, peanuts, cottonseed, and tree nuts. Crops are susceptible to infection both in the field and after harvest.
Fungal growth and toxin production are promoted by specific environmental conditions. High temperatures combined with high humidity create an ideal environment for the mold to thrive. Drought stress during crop development also makes plants more vulnerable to pre-harvest infection by Aspergillus species.
The contamination process follows two main routes: pre-harvest infection and post-harvest contamination. Pre-harvest infection occurs when the mold enters the crop through damaged tissue caused by insects or adverse weather. Post-harvest contamination occurs when harvested crops are not dried quickly or are stored under high moisture and warm temperatures. Inadequate storage facilities lacking proper ventilation or pest protection greatly increase the risk of toxin accumulation.
Biological Mechanism of Toxicity
The primary route of human exposure is through the ingestion of contaminated foods. Aflatoxin B1 is considered relatively inert until it undergoes bioactivation, a metabolic process carried out by Cytochrome P450 (CYP450) enzymes in the liver.
The CYP450 enzymes convert AFB1 into a highly reactive intermediate called AFB1-exo-8,9-epoxide. This epoxide is an electrophilic molecule. The formation of this unstable epoxide is the direct step that makes the toxin genotoxic.
The reactive epoxide intermediate then covalently binds to cellular macromolecules, primarily DNA. It preferentially attaches to the N7 position of guanine bases, forming an AFB1-N7-guanine adduct. The formation of these adducts interferes with DNA replication and repair, leading to mutations. This damage often results in a specific mutation where guanine is replaced by thymine, a signature event in the initiation of liver cancer.
Acute and Chronic Health Consequences
Exposure to aflatoxins leads to adverse health outcomes categorized by dose and duration. Acute exposure involves ingesting a high concentration over a short period, resulting in acute aflatoxicosis. This condition causes acute liver damage, manifesting as jaundice, vomiting, abdominal pain, and lethargy. In high-dose outbreaks, acute aflatoxicosis can rapidly progress to fulminant liver failure and internal hemorrhage, often leading to death.
Chronic exposure involves the long-term ingestion of low doses, leading primarily to Hepatocellular Carcinoma (HCC), a form of liver cancer. Aflatoxins are classified as a Group 1 human carcinogen, and their effect is dramatically amplified by co-infection with the Hepatitis B virus (HBV). HBV can increase the risk of HCC up to 60 times. Chronic exposure also causes immunosuppression and has been linked to developmental issues in children, including growth retardation and stunting.