**3. Health effects of aflatoxins on human and animals (Aflatoxicosis)**

Aflatoxicosis is a condition caused by aflatoxins in both humans and animals. It occurs in two general forms (1) the acute primary aflatoxicosisis produced when moderate to high levels of aflatoxins are consumed. Specific acute episodes of disease may include hemor‐ rhage, acute liver damage, edema, alteration in digestion, absorption and/or metabolism of nutrients, and possibly death [5, 6, 12, 69, 70]. Acute dietary exposure to AFB1 has been im‐ plicated in epidemics of acute hepatic injury [13, 72]. Evidence of acute aflatoxicosis in hu‐ mans has been reported worldwide especially in the third world countries like Taiwan, Uganda, India, Kenya and many others [7]. (2) The chronic primary aflatoxicosis results from ingestion of low to moderate levels of aflatoxins (USAID, 2012). The effects are usually subclinical and difficult to recognize. Some of the common symptoms are impaired food conversion and slower rates of growth with or without the production of an overt aflatoxin syndrome [9]. The chronic forms of aflatoxicosis include (1) teratogenic effects associated with congenital malformations (2) mutagenic effects where aflatoxins cause changes (muta‐ tions) in the genetic code, altering DNA and these changes can be chromosomal breaks, re‐ arrangement of chromosome pieces, gain or loss of entire chromosomes, or changes within a gene (3) the carcinogenic effect in which the carcinogenic mechanisms have been identified such as the genotoxic effect where the electrophilic carcinogens alter genes through interac‐ tion with DNA and thus becoming a potential for DNA damage and the genotoxic carcino‐ gens that are sometimes effective after a single exposure, can act in a cumulative manner, or act with other genotoxic carcinogens which affect the same organs [50, 60]. Chronic effects of aflatoxin has been reported to impair the normal body immune function by either by reduc‐ ing phagocytic activity or reduce T cell number and function as observed immunological suppression in animal model. Aflatoxins have also been reported to interfere with nutrition in a dose response relationship between exposure to aflatoxin and rate of growth in infants and children [4, 9, 20, 50, 60]. Aflatoxins also causes nutrient modification like vitamin A or D in animal models and thus making them unavailable for the normal body physiology and hence leads to nutritional deficiencies [7, 20].

age, decreased milk production, reduced reproductively and suppressed immunity in animals consuming low dietary concentrations. The aflatoxicosis syndrome in animals may also be characterized by vomiting, abdominal pain, pulmonary oedema, convulsions, coma, and death with cerebral edema and fatty involvement of the liver, kidneys, and heart. In dairy and beef cattle, the signs of acute toxicosis include anorexia, depression, dramatic drop in milk pro‐ duction, weight loss, lethargy, gastrointestinal dysfunctions such as ascitis, icterus, tenesmus, abdominal pain, bloody diarrhoea, decreased feed intake and efficiency; weight loss, jaundice, abortion, hepatoencephalopathy, blindness, walking in circles, ear twitching, frothy mouth, photosensitization, bleeding and death [4, 6, 22, 79]. In poultry, beside inappetance, weight loss, decreased egg production, leg and bone problems, poor pigmentation, fatty liver, kidney dysfunction, bruising and death, suppression to natural immunity and susceptibility to para‐

Review of the Biological and Health Effects of Aflatoxins on Body Organs and Body Systems

http://dx.doi.org/10.5772/51201

249

**Figure 4.** Aflatoxin disease pathways in humans (Adopted from Wu, 2010; USAID, 2012; WHO, 2011; Wu and Tritsch‐

**4. Biological effect of aflatoxins on the body organs and body systems**

**4.1. Role of aflatoxins in hepatic injury and other body organs and tissues**

Aflatoxins have been reported to affect the various body organs like the liver, kidneys, lungs, brain, testes and many endocrine and exocrine organs, the heart, skeletal muscles and

Aflatoxins have been reported to cause liver cirrhosis as well as liver cancers [4, 6, 7, 26, 80]. Hepatic injury can be acute or chronic form caused by a variety of toxic agents like aflatox‐

sitic, bacterial and viral infections can occur [6, 22], (Figure 4).

er, 2011) [7, 26, 80]

the different body systems.

The contamination of foods and feeds with aflatoxin can cause serious consequences in hu‐ man and animal health. It is estimated that more than 5 billion people in developing coun‐ tries worldwide are at risk of chronic aflatoxin exposure due to consumption of aflatoxincontaminated foods and of these more than 4 billion people develop aflatoxin related liver cancer especially the hepatocellular carcinoma [64, 69, 73, 74]. Aflatoxin exposure is mainly a problem in poor and developing countries with poor regulatory authorities in food process‐ ing and storage as well as with high levels of malnutrition. Aflatoxins have also been linked with kwashiorkor and marasmus in most of the sub-Saharan countries in children [20]. Many people in these countries experience chronic aflatoxicosis associated with long-term exposure to low to moderate levels of aflatoxin in the food supply chain. AFB1, AFB2 and AFM have been detected in liver, gall bladder, spleen, heart, muscle and kidney [75]. Afla‐ toxin B1 exposure results in both steatosis and accumulation of fat and necrosis or cell death of liver cells. The amount of aflatoxins consumed contributes to the mutagenic, carcinogenic, teratogenic, and immunosuppressive health effects in the body. The adverse effect of afla‐ toxins in humans ranges from acute hepatic toxicity to chronic disease such as liver cancer, haemorrhages, oedema, and even immediate death. Prolonged consumption of aflatoxins has also been reported to cause impaired immune function and malnutrition and stunted growth in children and a number of disabilities and death [7, 76, 77]. Human studies have reported that aflatoxins cause an increase in circulating alpha tumor necrosing factor, sug‐ gesting that these mycotoxins are also immunotoxic in humans. Due to the aflatoxin body immunosuppressant, it has been associated with HIV and tuberculosis [66, 67](Figure 2). Aflatoxins also pose a threat to developing fetuses and they are transferred from mother to infant in breast milk. Aflatoxins have been reported to be associated with a Reye-like Syn‐ drome in Thailand, New Zealand, Czechoslovakia, the United States, Malaysia, Venezuela, and Europe [4, 50, 78].

All species of animals are susceptible to aflatoxicosis and the susceptibility of individual ani‐ mals to aflatoxicosis varies considerably depending on dose, duration of exposure, species, age, sex and nutrition. AFB1, AFB2 and AFM have been detected in liver, gall bladder, spleen, heart, muscle and kidney of growing swine when protein and protein-free portions of the diet were separately fed [75]. Chronic exposure of aflatoxins to animals causes immunosuppres‐ sion and also interferes with protein metabolism and multiple micronutrients that are critical to health due to adduct formation. These adduct are responsible for mutations, cancer, immu‐ nosuppression, lung injury and birth defects [46]. In animals, the aflatoxins cause liver dam‐ age, decreased milk production, reduced reproductively and suppressed immunity in animals consuming low dietary concentrations. The aflatoxicosis syndrome in animals may also be characterized by vomiting, abdominal pain, pulmonary oedema, convulsions, coma, and death with cerebral edema and fatty involvement of the liver, kidneys, and heart. In dairy and beef cattle, the signs of acute toxicosis include anorexia, depression, dramatic drop in milk pro‐ duction, weight loss, lethargy, gastrointestinal dysfunctions such as ascitis, icterus, tenesmus, abdominal pain, bloody diarrhoea, decreased feed intake and efficiency; weight loss, jaundice, abortion, hepatoencephalopathy, blindness, walking in circles, ear twitching, frothy mouth, photosensitization, bleeding and death [4, 6, 22, 79]. In poultry, beside inappetance, weight loss, decreased egg production, leg and bone problems, poor pigmentation, fatty liver, kidney dysfunction, bruising and death, suppression to natural immunity and susceptibility to para‐ sitic, bacterial and viral infections can occur [6, 22], (Figure 4).

gens that are sometimes effective after a single exposure, can act in a cumulative manner, or act with other genotoxic carcinogens which affect the same organs [50, 60]. Chronic effects of aflatoxin has been reported to impair the normal body immune function by either by reduc‐ ing phagocytic activity or reduce T cell number and function as observed immunological suppression in animal model. Aflatoxins have also been reported to interfere with nutrition in a dose response relationship between exposure to aflatoxin and rate of growth in infants and children [4, 9, 20, 50, 60]. Aflatoxins also causes nutrient modification like vitamin A or D in animal models and thus making them unavailable for the normal body physiology and

The contamination of foods and feeds with aflatoxin can cause serious consequences in hu‐ man and animal health. It is estimated that more than 5 billion people in developing coun‐ tries worldwide are at risk of chronic aflatoxin exposure due to consumption of aflatoxincontaminated foods and of these more than 4 billion people develop aflatoxin related liver cancer especially the hepatocellular carcinoma [64, 69, 73, 74]. Aflatoxin exposure is mainly a problem in poor and developing countries with poor regulatory authorities in food process‐ ing and storage as well as with high levels of malnutrition. Aflatoxins have also been linked with kwashiorkor and marasmus in most of the sub-Saharan countries in children [20]. Many people in these countries experience chronic aflatoxicosis associated with long-term exposure to low to moderate levels of aflatoxin in the food supply chain. AFB1, AFB2 and AFM have been detected in liver, gall bladder, spleen, heart, muscle and kidney [75]. Afla‐ toxin B1 exposure results in both steatosis and accumulation of fat and necrosis or cell death of liver cells. The amount of aflatoxins consumed contributes to the mutagenic, carcinogenic, teratogenic, and immunosuppressive health effects in the body. The adverse effect of afla‐ toxins in humans ranges from acute hepatic toxicity to chronic disease such as liver cancer, haemorrhages, oedema, and even immediate death. Prolonged consumption of aflatoxins has also been reported to cause impaired immune function and malnutrition and stunted growth in children and a number of disabilities and death [7, 76, 77]. Human studies have reported that aflatoxins cause an increase in circulating alpha tumor necrosing factor, sug‐ gesting that these mycotoxins are also immunotoxic in humans. Due to the aflatoxin body immunosuppressant, it has been associated with HIV and tuberculosis [66, 67](Figure 2). Aflatoxins also pose a threat to developing fetuses and they are transferred from mother to infant in breast milk. Aflatoxins have been reported to be associated with a Reye-like Syn‐ drome in Thailand, New Zealand, Czechoslovakia, the United States, Malaysia, Venezuela,

All species of animals are susceptible to aflatoxicosis and the susceptibility of individual ani‐ mals to aflatoxicosis varies considerably depending on dose, duration of exposure, species, age, sex and nutrition. AFB1, AFB2 and AFM have been detected in liver, gall bladder, spleen, heart, muscle and kidney of growing swine when protein and protein-free portions of the diet were separately fed [75]. Chronic exposure of aflatoxins to animals causes immunosuppres‐ sion and also interferes with protein metabolism and multiple micronutrients that are critical to health due to adduct formation. These adduct are responsible for mutations, cancer, immu‐ nosuppression, lung injury and birth defects [46]. In animals, the aflatoxins cause liver dam‐

hence leads to nutritional deficiencies [7, 20].

248 Aflatoxins - Recent Advances and Future Prospects

and Europe [4, 50, 78].

**Figure 4.** Aflatoxin disease pathways in humans (Adopted from Wu, 2010; USAID, 2012; WHO, 2011; Wu and Tritsch‐ er, 2011) [7, 26, 80]
