Feeds contaminated with AFs were shown to result in the accumulation of the metabolites in the animal tissues including liver, adipose tissues, and animal products such as milk, meat, and eggs ^{13, 14, 15}. Those metabolites may cause potential health risks in the people because they can be carried over into the animal products. After AFs were recognized in the 1960s, the Food Drug Administration (FDA) of the USA set an action level of 30 ppb of AFs in raw or finished products ¹⁶. In 1969, the FDA revised the action level for AFs to 20 ppb for food and feed ingredients ¹⁶. The FDA set an action level of 0.5 ppb of AFM₁ in milk ¹⁶. It was reported that only about 1-3% of the AFB₁ might be converted into AFM₁ of the milk ¹⁷.

Previously, feeding diet supplemented with AF was reported to result in the highest level of AF in the gizzard, kidney, and liver tissues ¹³. Feeding a diet including 2500 ppb AFB₁ for 28 days was shown to cause 4.13 ppb AFB₁ deposition in the laying hens’ liver ¹⁸. It was shown that the levels of AFB₁ in the liver and kidney of chickens were significantly higher than the levels in the eggs and breast meat ¹⁹. Residues of AFB₁ were detected in the eggs of hens fed supplemental 500µg per kg feed, at levels that ranged from 0.05 to 0.16 µg/kg ²⁰. Laying chicken fed diets contaminated with AFB₁ (3300 mg/kg) for 28 days was shown to produce eggs contaminated with AFB₁¹³. Also, no aflatoxin residues were recovered from whole eggs after feeding laying chickens with aflatoxin-free diet (i.e. control diet) ¹³. AFM₁, a metabolite of AFB₁, was reported to present in the eggs of laying hens fed AFB₁ contaminated feed ²¹. Also, it was shown that AFM₁ and AFM₂ might be recovered in the poultry litter ²². A study was conducted in laying hens to evaluate the effect of AFB₁ on the egg quality in laying hens fed diet supplemented with mannan-oligosaccharides (MOS) and showed that neither AFB₁ nor AFM₁ residues were found in the eggs of groups ¹⁸. The same study also demonstrated that hepatic levels of AFB₁ were significantly lower in the group fed MOS-supplemented diet compared to the group fed MOS-excluded diet ¹⁸. It was suggested that MOS could have an ability to adsorb and degrade AFB₁, reducing gastrointestinal absorption of AFB₁ and its levels in tissues of laying hens. In another study, synthetic zeolite was shown to have efficacy to counteract some of the toxic effects of AFs in broiler chicks ²³.

Compared to the chickens, dairy cows are less sensitive to AFs due to biodegradation by rumen microorganisms ²⁴. In the liver, AFB₁ and AFB₂ are metabolized into AFM₁ and AFM₂, less toxic metabolites, using cytochrome P-450 associated enzymes ^{15, 17, 25}. AFM₁ in the contaminated feedstuffs may be transferred into milk as AFM₁ in the range of 0.3-6.3% ²⁶.

AFM₁ is very commonly detected in milk and dairy products ^{27, 28} and concentration in the milk was shown to increase linearly depending on the level of the AFB₁ in the feed ²⁹. AFB₁ levels of 20% and 13.6% of the yogurt and ayran samples were found to be exceeded the maximum tolerable limit of the Turkish Food Codex ³⁰. Therefore, nursing animals may be affected as a result of having milk contaminated with the toxin. Those metabolites of the AFs were reported not to be destroyed during pasteurization and thermal processing ³¹. A recent study showed that 36.4% of colostrum samples were found to be contaminated with an above maximum allowable level of AFB₁³². Studies showed that milk including a significant level of AFM₁ may have potential risks especially for infants and children ³³. AFM₁ concentration in the milk was reported to decline to an undetectable level after 72 hours when the intake of AFB₁ is stopped ³⁴. Lactating cows fed a ration including 20 ppb or more AFB₁ was reported to produce milk that exceeds the tolerance level of the toxin in the milk.

Special attention should be paid in food for infants and young children, where more restrictive levels have been regulated. Thus, limits as low as 0.1 µg kg^-1 of AFB₁ are set for baby foods and processed cereal-based foods for infants and young children and 0.025 µg kg^-1 for AFM₁ and 0.5 µg kg^-1 for OTA ³⁵. International legislation on AFM₁ in milk and dairy products for human consumption is shown in Table 1.

Aflatoxins are the hepatotoxic compounds causing health risks in the people consuming them more than the allowable amounts in the foods. As in the animals, these compounds or their metabolites may easily accumulate in the liver, kidney, and adipose tissues. It was reported that AFB₁, the most hepatocarcinogenic compound, caused cancer mainly in the liver and other organs of animals and humans ³⁷. After maternal exposure of AFs during pregnancy, AFB₁, AFB₁-metabolites, and AFB₁-albumen adducts were detected in cord blood of babies ³⁸. In a study conducted in Gambian children, it was reported that there was a relationship between impaired growth, particularly stunting and exposure to AFs ^{39, 40}. The research suggested that ethnicity, dietary practice and socio-economic status of the individuals might influence AF-exposure significantly ⁴¹.

Attempts have been made to develop methods to remove AFs from contaminated feeds or foods by physical, chemical, and biological methods ⁴². It was reported that implementing advanced agricultural technologies, good agricultural, and storage practices could mitigate the mycotoxin contaminations in the products ⁴³. Microwave heating, treatments with ozone, or ammonia were reported to be some of the methods used for detoxification of AFs in the foods ^{44, 45, 46}. Previously, it was shown that ozone treatment could significantly reduce the level of AFs in the red pepper ⁴⁷. Recently, it was shown that AFB₁ could be removed by ozone treatment ⁴⁸. However, the application of ozone treatment for the degradation AFs was reported to have limitations in food products because of the cost factor ⁴⁹.