Review of the Toxicology of Aflatoxin

Most laboratory animals, with the exception of the mouse, are readily killed by the aflatoxins. Following the administration of aflatoxin B1 to the rat, the species most extensively studied, the main lesions are seen in the liver, while kidney and adrenals show damage. The other afiatoxins are less toxic to the the rat and duckling. Aflatoxin M1 is similar to B1 in its acute toxicity. The acute toxicities may be modified by the nutritional state of the animal. A marginal choline diet affords protection from the hepatotoxic action B1. The afiatoxins are widely recognized as being carcinogenic for many species. In the rat B1 induces hepatic carcinoma at levels of 15 ppb in the diet. G1 is less carcinogenicfor the rat liver, but also induces renal carcinoma. Aflatoxin M1 has been shown to induce carcinoma in trout liver but feeding trials in rats have been unsuccessful in inducing neoplasia. Neoplasms at sites other than the liver have been induced by the aflatoxins. The 'mycotoxin hypothesis' for the etiology of human hepatic carcinoma has not been conclusively demonstrated although the circumstantial evidence to support the hypothesis is increasing. Some control measures employed to control the hazards of mycotoxins are justified and warrant further investigation. At this Meeting considerable emphasis has been placed on the methodology of assay of aflatoxins in food and feed, and their application to the control of mycotoxins. It would appear to be reasonable at this stage to consider what control measures are justified in making some assessment of the problem of aflatoxins. The hazards presented by mycotoxins may be conveniently divided into two classes. The first is related to the economic loss to producers of agricultural products, which will result from poor growth of livestock and subsequent failure to reach market weight. The second hazard is that to man. This may result from direct ingestion of mycotoxins from the food such as groundnuts and cereals contaminated with fungi and also from secondary contamination from eating meat from animals with residues of mycotoxins or their metabolites in the tissues. The hazards to man may be either those of acute toxicity or those of long-term chronic toxicity and carcinogenicity. In this paper I will confine my comments to aflatoxin and give some evidence which enables us to make an assessment of these hazards. Most species are susceptible to the acute toxic action of aflatoxin when