Mycotoxins contamination routes

Table 11.2 Probable routes for mycotoxin contamination of foods and feeds...

Lethality due to ingestion of food contaminated by trichothecenes has been reported in horses (Rodricks and Eppley, 1974), cattle (Hsu et al, 1972), and humans (Joffe, 1974). General clinical signs include emesis, food refusal and weight loss, dermal effects, and immune suppression with secondary infection. Clinical signs are dependent on the specific trichothecene involved, the dose, species, route of exposure, as well as the nature of the exposure. Spontaneous and experimental exposures may give somewhat different results, as can exposure to field contaminated materials, when compared to purified toxin. In the case of field contamination or experimental use of crude extracts, multiple mycotoxins, both known and unknown, may be present at the same time. 

Aspergillus flavus and A. parasiticus produce the mycotoxin aflatoxin Bl. Aflatoxin B1 is a carcinogenic chemical that can cause liver cancer. Both ingestion and inhalation are proven exposure routes. Aflatoxin Bl has been found on contaminated grains, peanuts, and other foodstuffs. A. flavus and A. parasiticus are not commonly considered an indoor contaminant, unless the grains, peanuts, cereal-based animal food, or other foodstuffs are stored in an indoor environment. 

With the exception of mycotoxins examined for military use, the bulk of research with animals has focused on the ingestion route given the potential for contaminated feed and fodder. The World Health Organization has investigated and sought control of mycotoxin exposure to humans. 

The main route of human exposure is ingestion of foods contaminated with mycotoxins. Skin exposure to and inhalation of moldy materials may also be significant sources of exposure in some populations. 

Better known as Fusarium mycotoxin. LD50 (rat) 4 mg/kg. Irritant, produces aleukia in birds. Bread contaminated with this toxin killed 1000s of Russians in the period after WWI. Poisonous by all routes. Produces vomiting and haematemesis. 

Trichothecene Mycotoxins. Only one class of easily produced, membrane-damaging toxins, the trichothecene mycotoxins, is dermally active. Therefore, they must be considered by standards different from those for all other toxins. Trichothecenes can cause skin lesions and systemic illness without being inhaled and absorbed through the respiratory system. Skin exposure and ingestion of contaminated food are the two likely routes of exposure of soldiers oral intoxication is unlikely in modern, well-trained armies. Nanogram quantities per square centimeter of skin cause irritation, and microgram quantities cause necrosis. If the eye is exposed, microgram doses can cause irreversible injury to the cornea. 

In Southeast Asia during the 1970s, symptoms began within minutes after an exploding munition (air-to-surface rocket, aerial bomb, cylinder) caused a yellow, oily, droplet mist to fall on individuals within 100 m of the explosion site. The falling droplet rain was inhaled, swallowed, and collected on skin and clothing contaminated the terrain and food and water supply and caused humans and animals to become acutely ill and to die after a variable period.7 Massive cutaneous contact was prevalent when the sources of exposure were sprays or coarse mists that were used deliberately to contaminate humans and the environment. Although the suspected trichothecene mycotoxin attacks in Southeast Asia would have involved multiple routes of exposure, we can postulate that the skin would have been the major site for deposition of a aerosol spray or coarse mist. 

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