Aflatoxins are toxic compounds produced by molds that grow on crops like peanuts, corn, and tree nuts. They are among the most potent naturally occurring carcinogens known, classified as a Group 1 carcinogen (the highest category) by the International Agency for Research on Cancer. Even at very low levels, long-term exposure increases the risk of liver cancer, and high-dose exposure can cause acute liver failure and death.
Where Aflatoxins Come From
Two species of mold are primarily responsible: Aspergillus flavus and Aspergillus parasiticus. These fungi thrive in warm, humid environments and colonize crops both in the field and during storage. The molds don’t need extreme conditions to flourish. Optimal growth occurs around 25°C (77°F) with high moisture levels, and physical damage to crops from insects or rough handling makes contamination more likely.
There are four main types of aflatoxin: B1, B2, G1, and G2. Aflatoxin B1 is the most common and the most dangerous. A fifth form, aflatoxin M1, appears in milk and dairy products when cows eat contaminated feed. Their bodies metabolize aflatoxin B1 into M1, which then passes into the milk supply.
Foods Most Likely to Be Contaminated
The FDA identifies peanuts, corn, tree nuts (especially Brazil nuts and pistachios), and certain small grains like rice as the foods most susceptible to aflatoxin contamination. These crops are vulnerable because they grow in climates that favor mold growth and are often stored for long periods in conditions where moisture can accumulate.
Contamination can happen at any stage. Mold may colonize crops while they’re still growing in the field, particularly during droughts or insect infestations that stress or damage the plants. It can also develop after harvest if grain or nuts aren’t dried properly before storage. In tropical and subtropical regions, where temperatures and humidity stay high year-round, the risk is significantly greater.
How Aflatoxins Damage the Body
The liver is the primary target. When you consume aflatoxin B1, your liver enzymes convert it into a highly reactive compound that binds directly to your DNA. This binding creates what scientists call DNA adducts, which are essentially chemical attachments that interfere with normal cell function. If the body doesn’t repair this damage before the cell divides, it can trigger mutations in a critical gene called p53, a tumor suppressor that normally prevents cells from growing out of control. This mutation, specifically at a well-known hotspot on the gene, is a key driver of hepatocellular carcinoma, the most common type of liver cancer.
The risk compounds dramatically for people who also carry hepatitis B. Chronic hepatitis B infection combined with ongoing aflatoxin exposure multiplies liver cancer risk far beyond what either factor causes alone, which is why aflatoxin-related liver cancer is concentrated in parts of sub-Saharan Africa and Southeast Asia where both exposures are common.
Symptoms of Acute Poisoning
Large single exposures to aflatoxin cause a condition called acute aflatoxicosis. Symptoms include nausea, vomiting, abdominal pain, and convulsions. In severe cases, the toxin triggers fulminant liver failure, with symptoms escalating to jaundice (yellowing of the skin and eyes), bleeding, edema, mental confusion, and coma. Roughly 25% of high-dose acute exposures are fatal. Children are especially vulnerable, as acute high-dose poisoning can be deadly at lower thresholds than in adults.
Outbreaks of acute aflatoxicosis have occurred in developing countries where food safety infrastructure is limited. These events typically involve contaminated corn or other staple grains consumed over a period of days to weeks.
Chronic Exposure and Child Development
You don’t need a large dose for aflatoxins to cause harm. Chronic low-level exposure, the kind that comes from eating slightly contaminated food over months or years, suppresses the immune system and appears to stunt growth in children. A cross-sectional study of 480 children aged 9 months to 5 years across Benin and Togo found that children who were stunted or underweight had 30 to 40% higher aflatoxin levels in their blood compared to children growing normally. The correlation between aflatoxin levels and reduced height-for-age and weight-for-age was highly significant statistically.
This is particularly concerning because chronic exposure often begins when infants transition to solid foods, which in many regions means weaning onto porridges made from maize or groundnuts. The timing overlaps with when children are also most vulnerable to infectious diseases like malaria and diarrheal illness, compounding the nutritional damage.
Regulatory Limits in Food
The FDA considers human food adulterated if it contains total aflatoxins above 20 parts per billion (ppb). For milk, the threshold is much lower: 0.5 ppb for aflatoxin M1, reflecting both the sensitivity of the dairy supply chain and the fact that children are major consumers of milk. The European Union sets even stricter limits, with total aflatoxin levels capped at 4 micrograms per kilogram (equivalent to 4 ppb) for most foods, though regulators have considered raising the limit to 10 ppb for certain tree nuts.
These numbers are extremely small. One part per billion is roughly equivalent to one drop of water in an Olympic swimming pool. The tight limits reflect just how potent aflatoxins are as carcinogens: there is no safe level of exposure, only levels considered low enough to pose acceptable risk.
How Aflatoxins Are Detected
Testing for aflatoxins relies on two main approaches. For rapid, large-scale screening, labs use an immunological test called ELISA, which is fast, inexpensive, and can process many samples at once. When confirmation is needed, the gold standard is high-performance liquid chromatography with fluorescence detection (HPLC-FL), which provides precise identification and measurement of specific aflatoxin types. In practice, ELISA catches potential problems quickly, and HPLC-FL confirms them with accuracy.
Preventing Contamination
The most effective defense starts with proper drying. Grain and nuts need to be dried to low moisture levels before storage, as mold growth accelerates when moisture content is high. In temperate climates, ventilating stored grain during cooler nights and through winter temperatures has largely controlled the problem. In tropical regions, where that natural temperature advantage doesn’t exist, other methods are necessary.
One promising approach uses airtight (hermetic) storage containers that deplete oxygen through the natural respiration of any insects or microorganisms sealed inside. Without oxygen, mold can’t grow and aflatoxin production stops, all without chemicals or fumigants. Another strategy, used in parts of Africa through a product called AflaSafe, introduces a harmless strain of Aspergillus mold into the soil around crops. This non-toxic strain outcompetes the aflatoxin-producing molds, dramatically reducing contamination before harvest even begins.
Breeding programs have also developed crop varieties with improved resistance to mold colonization, giving farmers in high-risk regions another tool. At the consumer level, sorting and discarding visibly moldy or damaged nuts and kernels removes a significant portion of contaminated material, since aflatoxin concentrations tend to be highest in visibly damaged pieces.