Aspergillus flavus and A. parasiticus (Aflatoxins)

Aflatoxin is a problem in many commodities; however, as far as grains are concerned, it is primarily a problem in maize. This is because maize is colonized in the field depending on environmental conditions, whereas other grains are not. Of the other grains, rice is an important dietary source of aflatoxin in circumstances of poor storage in tropical and subtropical areas. The character of the problem varies by region. In the United States, storage systems are very good (71) and the problem is preharvest contamination of maize and peanuts (4,72). In tropical countries, such as Thailand and the Philippines, crop storage is a substantial problem (73). Aflatoxin contamination is managed by the development of systems to detect and segregate contaminated kernels and better storage systems. For corn and peanuts, all manner of efforts have been made to prevent aflatoxin contamination, including plant breeding and biological control to little effect (74).

In the United States, Mexico, and South America, A. flavus and A. parasiticus infect corn, although A. parasiticus is relatively uncommon (72). In the environmental circumstances prevalent in the corn belt of the United States, A. flavus contamination of corn occurs in two basic ways: (1) airborne or insect-transmitted conidia contaminate the silks and grow into the ear when the maize is under high temperature stress, or (more commonly) (2) insect- or bird-damaged kernels become colonized with the fungus and accumulate aflatoxin. In either case, drought-, nutrient-, or temperature-stressed plants are more susceptible to colonization by A. flavus (75). This is also the case for peanuts, which are mainly colonized by A. parasiticus. Aflatoxin contamination can be limited by preventing late season drought by irrigation where this is possible (74).

Insects and arthropods readily become contaminated with A. flavus. Soil-inhabiting mites feed on the germinated sclerotia and hence acquire conidia. Nitidulid beetles feed on moldy ears of maize, perhaps preferentially. Nitidulids are attracted to damaged ears, including those caused by corn ear worms and the European corn borer spreading the fungus into damaged kernels (4,76). In drought years, insects are attracted to peanuts and both wound the plant and bring the fungus.

The ecology of A. flavus in corn in subtropical regions of Asia appears to be different from that already described. In subtropical Asia there is a rapid rise in aflatoxin concentrations immediately postharvest. American studies have shown that, typically, A. /7ai>us-infested kernels are randomly distributed in ears after wound inoculation (77). The kernels that were the sites of initial infection have very high aflatoxin contents. In studies done in Thailand, approximately 19% of kernels from 130 samples of maize collected from farmers fields throughout Thailand contained A. flavus (73).

There are many detailed reviews of the toxicology of aflatoxin, including that of the International Agency for Research on Cancer (IARC) (17). Aflatoxin Bl, the most toxic of the aflatoxins, causes a variety of adverse effects in different animal species, especially chickens. In poultry, these include liver damage, impaired productivity and reproductive efficiency, decreased egg production in hens, inferior eggshell quality, inferior carcass quality, and increased susceptibility to disease (78). Swine are somewhat less sensitive than poultry species, with the LD50 being perhaps half of that of chickens. Aflatoxin is hepatotoxic, and its acute and chronic effects in swine are largely attributable to liver damage (79). In cattle, the primary symptom is reduced weight gain as well as liver and kidney damage. Milk production is reduced (80). Aflatoxin is also immu-notoxic in domestic and laboratory animals with oral exposures in the ppm range. Cell-mediated immunity (lymphocytes, phagocytes, mast cells, and basophils) is more affected than humeral immunity (antibodies and complement) (63). The effects of aflatoxin on laboratory animals has been exhaustively reviewed by IARC (17).

Naturally occurring mixtures of aflatoxins were classified as class 1 human carcinogens, and aflatoxin Bx is also a class 1 human carcinogen. There was inadequate evidence of the human carcinogenicity of aflatoxin M1; the metabolite of aflatoxin Bj found in human and animal milk (17). Many people in developing countries are seropositive for hepatitis B and C, which are also liver carcinogens. Although aflatoxin is a potent chemical carcinogen, its ability to alter response to the hepatocarcinogenic viruses is perhaps of greater importance. The relative rates of liver cancer in hepatitis B-positive populations are an order of magnitude greater (60X) when exposed to aflatoxin. This is because the toxin interferes with the processing of the virus (81,82).

The immunotoxicity of aflatoxin is also being increasingly studied; some think that it would have to be regulated for this toxicity regardless of its carcinogenicity. In one study, serum aflatoxin-lysine adducts were higher in protein energy malnourished (PEM) children compared with control children. Aflatoxin metabolism was affected, with relatively higher serum concentrations in PEM children. A second study compared PEM children with high and low serum aflatoxin concentrations. The serum aflatoxin positive group of PEM children showed a significantly lower hemoglobin level (p = 0.02), longer duration of edema (p = 0.05), an increased number of infections (p = 0.03), and a longer duration of hospital stay (p = 0.008).

This finding was echoed in another study, which suggested that malaria infections in children were increased in children exposed to aflatoxin (18).

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