**6. Occurrence of Aflatoxin in Other Foods of Animal Origin**

Meat refers to meat flesh, skeletal muscles, connective tissue or fat and others than meat flesh, including brain, heart, kidney, liver, pancreas, spleen, thymus, tongue and tripe that is used as food, excluding the bone and bone marrow and it contains high biological value protein and important micronutrients that are needed for good health throughout life. Resi‐ dues of aflatoxins and their metabolites could be present in the meat, offal and eggs of ani‐ mals receiving aflatoxin contaminated feeds (Table 5). In addition to the economic losses, aflatoxin in feeds could pose a risk to human health because of ingestion of aflatoxin con‐ taining foods derived from the animals fed the toxin-contaminated diet [118].

Poultry birds fed AF contaminated rations under experimental conditions resulted in the presence of AF residues in their edible tissues like liver and muscles. Residues of AFB1 in liver of broiler and layer birds have been reported to vary from no detection to 3.0 µg kg-1 by feeding 250-3310 µg kg-1 AFB1 for variable periods [118, 119]. The wide variations in the tis‐ sue AF residue concentration suggested that these levels might be influenced by different factors including dietary AF levels, duration of administration, age, type of the birds etc. However, effect of such factors upon concentration of AFB1 residues in poultry meat (liver and muscles) and clearance of AFB1 from the body tissues after withdrawal of dietary AF

Dietary contamination of aflatoxins pose a big risk to human health including acute aflatoxi‐ cosis, Hepatocellular carcinoma, hepatitis B virus infection, growth impairment in different regions of the World particularly Asian and African countries [122]. European community and many other countries have imposed 2 µg kg-1 AFB1 as maximum tolerance level in hu‐ man food products. Birds fed Afs, following ingestion are rapidly metabolized into nontoxic substances in the body. A rapid decrease in AFB1 residues below the tolerance limits from the muscles and liver within 3 and 7 days of withdrawal of dietary AFB1 and that it may not become a significant human health risk. However, in areas with no regulatory limits on AFB1 levels of poultry feed, the secondary exposure to aflatoxins through consumption of chicken liver and meat derived from the poultry fed AF contaminated feed may pose a risk

> **Aflatoxin Concentration (ppb)**

0/25 Totala NDb ELISA [126]

3/25 Totala 0.61-1.19 ELISA [126]

Thailand 96/450 AFB1 Mean 0.0451 HPLC [118]

Chicken LiverThailand 248/450 AFB1 Mean 0.6092 HPLC [118]

Meat Jordan 12/50 Totala 0.15-8.32 HPLC [124] Fresh Fish Egypt 10/30 Totala 22-70.5 Florometric [125] Salted fish Egypt 12/30 Totala 18.5-50 Florometric [125] Smoked Fish Egypt 8/30 Totala 32-96 Florometric [125] Egg Jordan 5/40 Totala 0.01-6.15 HPLC [124]

**Method Reference**

Occurrence of Aflatoxins in Food http://dx.doi.org/10.5772/51031 159

have not been adequately studied [120].

to consumers health [123].

**Country Contaminated/**

**Total examined**

**Food Type**

Chicken Muscle

Processed egg

Unwashed egg

b. ND: Not detected

Saudi Arabia

Saudi Arabia

a. Total: AFB1+ AFB2+ AFG1+ AFG2

**Table 5.** Aflatoxins in other foods of animal origin.

Cytochrome P450 enzymes (CYP) (including CYP1A2, CYP3A4 and CYP2A6) in the liver and other tissues convert AFB1 to epoxides (AFB1-8,9-exo-epoxide, and AFB1-8,9-endo-ep‐ oxide), and to AFM1, AFP1, AFQ1, and its reduced form aflatoxicol. Of the epoxides, the AFB1-8,9-exo-epoxide can form covalent bonds with DNA and serum albumin resulting in AFB1-N7-guanine and lysine adducts, respectively. Like AFB1, AFM1 can also be activated to form AFM1-8,9-epoxide that binds to DNA resulting in AFM1-N7-guanine adducts. These guanine and lysine adducts have been noted to appear in urine. The metabolites AFP1, AFQ1, and aflatoxicol are thought to be inactive and are excreted as such in urine, or in the form of glucuronyl conjugates from bile in feces [119].

When chicken exposed to AFB1 with contaminated rations, AFB1, AFM1, and aflatoxicol have been detected in liver, kidneys, and thigh muscles. Besides these, AFB2a has also been detected in livers of both broilers and layers on a ration contaminated with a mixture of afla‐ toxins [120]. In laying hens the effects of exposure to AF are a dose-dependent decrease in egg production and egg quality with increased susceptibility to salmonellosis, candidiasis, and coccidiosis. AFs and some of their metabolites can be carried over from feed to eggs in ratios ranging from 5,000:1 to 66,200:1 and even to 125,000:1, whereas in other trials no measurable residual AFB1 or its metabolites were found in eggs. These contrasting results may be ascribed to the administration of naturally contaminated feeds containing different AF with different levels of toxicity [8].

Wolzak et al. [121] have reported that tissue residues of aflatoxins were highest in kidney, gizzard, and liver (average concentration 3 µg kg-1 mass) when broilers were exposed for 4 weeks to a mixture of AFB1 and AFB2. After 7 days of removal of the contaminated feed, aflatoxin residues could not be detected in above tissues. Hussain et al. [120] also indicated that the elimination of AFB1 in chicken increased during longer exposure to AFB1. They fed broiler chicks on rations containing 0, 1.6, 3.2, and 6.4 µg AFB1/kg for 7, 14, or 28 day's age. After 2 to 3 days of exposure, AFB1 could be detected in livers of the birds exposed to 1.6 µg AFB1/kg and higher dietary levels of the toxin. After cessation of toxin feeding, AFB1 resi‐ dues decreased in livers and muscles of all the chicks, with lower levels at 10 days post-ces‐ sation in the chicks exposed to higher toxin levels. They concluded that the residues of AFB1 in tissues increase with increase in dietary concentration of the toxin but decrease with in‐ crease in age (or after longer exposure) of broiler chicks. The elimination of AFB1 from tis‐ sues was rapid in older birds than in younger birds [120].

Poultry birds fed AF contaminated rations under experimental conditions resulted in the presence of AF residues in their edible tissues like liver and muscles. Residues of AFB1 in liver of broiler and layer birds have been reported to vary from no detection to 3.0 µg kg-1 by feeding 250-3310 µg kg-1 AFB1 for variable periods [118, 119]. The wide variations in the tis‐ sue AF residue concentration suggested that these levels might be influenced by different factors including dietary AF levels, duration of administration, age, type of the birds etc. However, effect of such factors upon concentration of AFB1 residues in poultry meat (liver and muscles) and clearance of AFB1 from the body tissues after withdrawal of dietary AF have not been adequately studied [120].

Dietary contamination of aflatoxins pose a big risk to human health including acute aflatoxi‐ cosis, Hepatocellular carcinoma, hepatitis B virus infection, growth impairment in different regions of the World particularly Asian and African countries [122]. European community and many other countries have imposed 2 µg kg-1 AFB1 as maximum tolerance level in hu‐ man food products. Birds fed Afs, following ingestion are rapidly metabolized into nontoxic substances in the body. A rapid decrease in AFB1 residues below the tolerance limits from the muscles and liver within 3 and 7 days of withdrawal of dietary AFB1 and that it may not become a significant human health risk. However, in areas with no regulatory limits on AFB1 levels of poultry feed, the secondary exposure to aflatoxins through consumption of chicken liver and meat derived from the poultry fed AF contaminated feed may pose a risk to consumers health [123].


**Table 5.** Aflatoxins in other foods of animal origin.

**6. Occurrence of Aflatoxin in Other Foods of Animal Origin**

taining foods derived from the animals fed the toxin-contaminated diet [118].

in the form of glucuronyl conjugates from bile in feces [119].

sues was rapid in older birds than in younger birds [120].

AF with different levels of toxicity [8].

158 Aflatoxins - Recent Advances and Future Prospects

Meat refers to meat flesh, skeletal muscles, connective tissue or fat and others than meat flesh, including brain, heart, kidney, liver, pancreas, spleen, thymus, tongue and tripe that is used as food, excluding the bone and bone marrow and it contains high biological value protein and important micronutrients that are needed for good health throughout life. Resi‐ dues of aflatoxins and their metabolites could be present in the meat, offal and eggs of ani‐ mals receiving aflatoxin contaminated feeds (Table 5). In addition to the economic losses, aflatoxin in feeds could pose a risk to human health because of ingestion of aflatoxin con‐

Cytochrome P450 enzymes (CYP) (including CYP1A2, CYP3A4 and CYP2A6) in the liver and other tissues convert AFB1 to epoxides (AFB1-8,9-exo-epoxide, and AFB1-8,9-endo-ep‐ oxide), and to AFM1, AFP1, AFQ1, and its reduced form aflatoxicol. Of the epoxides, the AFB1-8,9-exo-epoxide can form covalent bonds with DNA and serum albumin resulting in AFB1-N7-guanine and lysine adducts, respectively. Like AFB1, AFM1 can also be activated to form AFM1-8,9-epoxide that binds to DNA resulting in AFM1-N7-guanine adducts. These guanine and lysine adducts have been noted to appear in urine. The metabolites AFP1, AFQ1, and aflatoxicol are thought to be inactive and are excreted as such in urine, or

When chicken exposed to AFB1 with contaminated rations, AFB1, AFM1, and aflatoxicol have been detected in liver, kidneys, and thigh muscles. Besides these, AFB2a has also been detected in livers of both broilers and layers on a ration contaminated with a mixture of afla‐ toxins [120]. In laying hens the effects of exposure to AF are a dose-dependent decrease in egg production and egg quality with increased susceptibility to salmonellosis, candidiasis, and coccidiosis. AFs and some of their metabolites can be carried over from feed to eggs in ratios ranging from 5,000:1 to 66,200:1 and even to 125,000:1, whereas in other trials no measurable residual AFB1 or its metabolites were found in eggs. These contrasting results may be ascribed to the administration of naturally contaminated feeds containing different

Wolzak et al. [121] have reported that tissue residues of aflatoxins were highest in kidney, gizzard, and liver (average concentration 3 µg kg-1 mass) when broilers were exposed for 4 weeks to a mixture of AFB1 and AFB2. After 7 days of removal of the contaminated feed, aflatoxin residues could not be detected in above tissues. Hussain et al. [120] also indicated that the elimination of AFB1 in chicken increased during longer exposure to AFB1. They fed broiler chicks on rations containing 0, 1.6, 3.2, and 6.4 µg AFB1/kg for 7, 14, or 28 day's age. After 2 to 3 days of exposure, AFB1 could be detected in livers of the birds exposed to 1.6 µg AFB1/kg and higher dietary levels of the toxin. After cessation of toxin feeding, AFB1 resi‐ dues decreased in livers and muscles of all the chicks, with lower levels at 10 days post-ces‐ sation in the chicks exposed to higher toxin levels. They concluded that the residues of AFB1 in tissues increase with increase in dietary concentration of the toxin but decrease with in‐ crease in age (or after longer exposure) of broiler chicks. The elimination of AFB1 from tis‐
