The aflatoxins are produced by a small number of species of Aspergillus which currently includes A. flavus, A. parasiticus, A. nomius and a species originally isolated from Ivory Coast soil, A. ochraceoroseus (Bartoli and Maggi, 1978; Klich et al., 2000). A strain of A. tamarii has also been shown to produce afla-toxin (Klich et al., 2000), but this may be a brown spored form of A. flavus and is certainly very closely related. It should be emphasised that not all strains within a species are toxigenic. On a worldwide basis the majority of strains of A. parasiticus are aflatoxigenic but only about 35% of strains of A. flavus produce aflatoxins. Indeed some strains of A. flavus have been used to produce koji and the more widely used species A. oryzae is probably a domesticated form of this species (Cruikshank and Pitt, 1990). At the level of acute toxicity the aflatoxins cause liver damage and, in animals such as cattle, the farmer will initially see reduced feed consumption, depressed milk production, weight loss and eventually death due to severe liver damage. They were discovered following an outbreak of acute toxicosis affecting turkey poults and game birds in which large numbers of birds died.
The aflatoxins are a family of compounds the most toxic of which is aflatoxin B1 (Fig. 18.1). In humans it is both acutely toxic and probably carcinogenic. It was responsible for a major outbreak of toxicosis in India, initial reports of which found that 397 people were ill of whom 106 died, following consumption of afla-
toxin contaminated maize (Krishnamachari et al., 1975). This outbreak affected people and dogs in several villages and the most overt symptom was jaundice preceded by vomiting and anorexia.
A fascinating aspect of the toxicology of aflatoxin B1 is the variation in response among different species and even between the sexes within a species. Indeed, for some animal species, such as the rat, it is among the most carcinogenic compounds known and yet in others, such as the guinea pig, it may not be carcinogenic. Although it is difficult to disentangle the interactions of aflatoxin with other carcinogenic agents, such as hepatitis B virus, it is clearly prudent to assume that aflatoxin B1 is a human carcinogen and a review of the risk assessment leading to this assumption is presented by Castegnaro and McGregor (1998). The reason for the diversity of response to aflatoxin B1 is because it has to be metabolised first and the balance of metabolism varies from one species to another. This aspect of the toxicology is reviewed by Moss (1998).
The moulds producing aflatoxins are ubiquitous in their ocurrence but they are only normally active and competitive in the warmer parts of the world, the optimum temperature for growth being 35-37°C, and the optimum temperature for aflatoxin production 30 °C. The commodities most usually contaminated are maize and groundnuts but a wide range of other plant products may also contain aflatoxin B1. These include Brazil nuts, almonds, figs and spices for human consumption as well as cottonseed meal and copra meal for animal feeds. Levels can range from a few mgkg-1 to several mgkg-1 (Pittet, 1998). The moulds producing aflatoxins grow particularly well on appropriate substrates when these are stored at high moisture content and elevated temperatures. Under these conditions levels of contamination can be high enough to cause acute toxicity as occurred in India in 1974 when it was estimated that as much as 2-6mg of afla-toxin could be consumed daily over a period of several weeks (Krishnamachari et al., 1975).
However, these same species can infect crops such as maize and groundnuts in the field, before harvest, by establishing an endophytic relationship with the plant. When such an infected plant is stressed by, for example, a period of drought, aflatoxin may be produced which will then be present in the crop at harvest even though it may look perfectly sound. Under these conditions only relatively low concentrations are formed but they may be higher than the maximum tolerated levels set by individual countries. Incidents of field contamination of crops by aflatoxin B1 have been well documented for the southern states of the USA (Hagler, 1990). In 1980, for example, 65.7% of samples of maize from the harvest in North Carolina contained more than 20 |mgkg-1 of aflatoxin with an estimated cost to producers and handlers of $30816000 (Nichols, 1983). These losses arose because 20 |mgkg-1 is the maximum tolerated level in commodities for human consumption in the USA. Attempts to harmonise national legislation at the international level have so far failed and maximum permitted levels for aflatoxin B1 in foods may be as low as 2 |mgkg-1 (European Union) or as high as 30 |mgkg-1 (India).
Although aflatoxin M1, which is secreted in milk after consumption and metabolism of aflatoxin B1, is less toxic than its precursor, most countries set much more stringent levels (0.05 |mgkg-1 in the EU) because milk may be consumed by very young children who may be at high risk because of an intrinsically higher sensitivity and light body weight.
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