Trichothecene mycotoxins dermal exposure

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. 

From these data, we can conclude that the trichothecene mycotoxins very rapidly cross the pulmonary and intestinal mucosa and enter the systemic circulation to induce the toxin-related toxicoses. In contrast, trichothecene mycotoxins are only slowly absorbed through skin, especially when applied as a dust or powder.56 Systemic toxicity and lethality can be produced by dermal exposure to higher concentrations of T-2 toxin, however, especially if the mycotoxin is dissolved in a penetrant such as DMSO.6... 

Acute oral, parenteral, dermal, or aerosol exposures to trichothecene mycotoxins produce gastric... 

Symptomatic measures for the treatment of exposure to trichothecene mycotoxins are modeled after the care of casualties of mustard poisoning.85 Irrigation of the eyes with large volumes of isotonic saline may assist in the mechanical removal of trichothecene mycotoxins, but would have limited useful therapeutic effects. After the skin has been decontaminated, some erythema may appear, accompanied by burning and itching. Most casualties whose skin has been treated with soap and water within 12 hours of exposure will have mild dermal effects these should be relieved by calamine and other lotion or cream, such as 0.25% camphor and methanol. 

Prophylactic induction of enzymes involved in the conjugation of xenobiotics reduced or prevented the acute toxic effects of T-2 toxin in the rat, while inhibition of these enzymes resulted in a higher toxicity for this trichothecene.96 Pretreatment with flavonoids,97 ascorbic acid,98 vitamin E," selenium,100 or chemoprotective compounds such as emetine101 that block trichothecene-cell association all reduce acute toxicity of these mycotoxins. However, none of these chemoprotective treatments have undergone extensive efficacy studies to evaluate their ability to protect against an aerosol or dermal exposure to trichothecene mycotoxins. 

No specific therapy for trichothecene mycotoxin poisoning is currently available. Skin decontamination with soap and water or the hypochlorite- (M258A1) or resin-based (M291) military decontamination kits can effectively remove toxin up to six hours after exposure, although none of them neutralize the toxin. Treatment of respiratory, dermal, and GI effects currently must be symptom based and supportive in nature. Superactive activated charcoal, for example, a common treatment for many orally taken poisons, has been shown to bind 0.48 mg T-2/gm charcoal in mice and improve survival rates significantly. 

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. 

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