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Hazard Information

Questions And Answer

• Overview

  Aflatoxin B1 (AFB1) is primarily produced by the common fungus Aspergillus flavus and A. parasiticus, which is a closely related species. Among the aflatoxins, Aflatoxin B1 is the most hepatocarcinogenic and hepatotoxic and occurs as a contaminant in a variety of foods. AFB1 is a potent mutagen, toxin, and carcinogen and can be traced in the etiology of hepatocarcinoma. Although AFB1 commonly affects the life, studies have revealed that it is also produced in the colons, kidneys, and lungs of rodents. It is noteworthy that AFB1 is typically nonreactive until it is ingested and converted by the enzymes in the liver to a reactive intermediate known as AFB1 8,9 –oxide. ;

• Exposure to AFB1

  AFB1 is the most toxic and occurs at the highest levels among the different aflatoxins. The main source of exposure to AFB1 is contaminated food including corn, peanuts, fig, soybeans, nuts, and cheese. Typically, AFB1 production is normally increased in hot and humid environments or climates. As such, AFB1 production is common in South America, South East Asia, and Sub-Saharan Africa. Occupational exposure has been proved to occur in individuals working in pig and poultry production. ;

• Pathology

  AFB1 can enter the body of a human being through the skin, especially in hot or humid environmental conditions. The most vulnerable body organ to AFB1 is the liver. Pathological lesions that are linked to AFB1 in animals include weight loss of the liver, hepatic carcinoma, and vacuolation of hepatocytes. Others include necrosis, hepatic cells, fatty infiltration, fibrosis, hemorrhage, bile duct hyperplasia, and regeneration of nodules. ;

• Mechanism of Action of AFB1 in developing Hepatocellular Carcinoma (HCC)

  Food mutagens are classified as non-genotoxic and genotoxic agents depending on their mechanism of action in triggering cancer. AFB1 is a genotoxic hepatocarcinogen agent that leads to genetic alterations with the mode of action beginning at the DNA level. It causes cancer by inducing DNA adducts, thereby leading to genetic alterations in target cells that then lead to breakage of the DNA strand, oxidative damage and DNA base damage that may cause cancer. Notably, DNA adducts are generated by the chemical modification of the bases in amino acids in proteins or DNA by toxic carcinogenic chemicals. Studies have revealed the p53 gene causes about 50% of cancer in human beings and that mutations affecting the gene are varied by their position and nature. For instance, mutations like the transversion in codon 249 that leads to arginine to serine substitution are present in half of HCCs.
  AFB1 target for metabolism is the liver where its mechanism of action is started. After food is ingested, AFB1 is normally metabolized by cytochrome-P450 enzymes that are reactive to hydroxylated to AFQ1 and AFM1, genotoxic intermediates and demethylated to AFP1 to become less harmful as compared to AFB1. Cytochrome-P450 has to biotransform AFB1 before can exact its hepatocarcinogenic effect. It is noteworthy that this process usually results in the production of AFBO, which is a reactive intermediate chemical compound. AFBO, a genotoxic compound, will then bind to the liver cell DNA as a result, leading to the formation of DNA adducts. In case there is no repair before the replication of DNA, the DNA adducts will interact with the guanine base of the DNA, leading to mutational impacts in the p53 tumour suppressor gene, thus resulting in hepatocarcinogenesis. Inhibition of apoptosis and stimulation of liver cell growth may occur due to the expression of mutated R249p53. ;

• Food Regulation

  Dietary exposure to mutagens and carcinogens depends on distinct ingesting patterns that normally change with the availability of food, age, and lifestyle. AFB1 usually contaminates animal and human foods during cultivation, crop growth, harvesting, and storage. It is noteworthy that prevention of hepatocellular carcinogenesis and hepatotoxicity of AFB1 requires durable interventions such as the implementation of comprehensive food programs. The responses should touch on both local farmers and market vendors to minimize or prevent long-term exposure to AFB1, thereby decreasing HCC incidence rates.
  Pre-harvest interventions include cultivating crops that are resistant to aflatoxin biosynthesis and fungal infection as well as spraying of fungicides and insecticides. Application of low-technology interventions in the reduction of AFB1 ¬after harvesting has been suggested such as drying on mats, hand sorting, and avoids the use of plastics. ;

• Health Hazard Information

  Numerous studies have been conducted regarding the toxicity of AFB1, which might be acute or toxic.
  AFB1 poisoning is referred to as aflatoxicosis, which may occur because of consumption of contaminated food. AFB1 can cause chronic reproduction affects when swine consumer high doses. Chronic symptoms on AFB1 toxicity include reduced growth rate and weight, decreased appetite, poorer carcass quality, lower milk production, immunity to the vaccine, and lower disease resistance.
  
  Notable Exposures
  One of the noteworthy exposure to AFB1 ¬is the 1960’s death of over 100, 000 turkeys in England. In Kenya, 12 patients died of acute AFB1 ¬poisoning after consuming contaminated maize in 1981. ;

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