TAB E – Trichothecene Mycotoxin (T-2)

Overview: The Russian military discovered the potential use of trichothecene mycotoxins as biological toxins shortly after World War II, when civilians ate bread baked from flour contaminated with species of fusarium mold. Some victims developed a protracted lethal illness characterized by initial symptoms of abdominal pain, diarrhea, vomiting, and exhaustion followed within days by fever, chills, muscular pain, and an imbalance of the red and white blood cells accompanied by pus-forming or other disease-causing organisms or their toxins in the blood or tissues.[120] According to UNSCOM, Iraq researched trichothecene mycotoxins, including T-2.[121]

The trichothecene mycotoxins are nonvolatile compounds produced by molds. These substances are relatively insoluble in water but highly soluble in ethanol, methanol, and propylene glycol. The trichothecenes are very stable and resist heat- and ultraviolet light-induced inactivation. Heating to 500o F for 30 minutes will inactivate the toxins, while exposure to sodium hypochlorite destroys toxic activity.

This discussion focuses on the T-2 mycotoxin, a highly toxic agent that causes several illnesses in humans and animals. From the 1970s and 1980s trichothecene mycotoxins surfaced in the press as a biological warfare agent in incidents labeled "yellow rain" attacks in Southeast Asia.[122]

Unlike most biological toxins and microorganisms that do not affect the skin, T-2 toxin is an active dermal irritant and can severely irritate an unprotected person’s skin and eyes. The pain associated with the exposure occurs within seconds to minutes. Larger doses produce incapacitation and death within minutes to hours. A larger amount of T-2 toxin is required for a lethal dose than of the chemical warfare agents VX, soman, or sarin. Comparisons with blister agents such as sulfur mustard show the T-2 toxin is about 400 times more efficient in producing blisters: it takes approximately 50 nanograms of T-2 toxin to produce the same injury to the skin as 20 micrograms (20,000 nanograms) of mustard. The T-2 toxin has a diverse effect depending on the manner and amount of exposure with vomiting and diarrhea noted at exposure doses one-fifth to one-tenth the lethal dose.[123]

The toxicity of T-2 toxin by the inhalational route of exposure … is similar to that observed for mustard or Lewisite. … However, the lethality of T-2 toxin by the dermal [skin] route … is higher than that for liquid Lewisite … or liquid mustards, … Therefore, the trichothecene mycotoxins are considered to be primarily blister agents that, at lower exposure concentrations, can cause severe skin and eye irritation, and at larger doses can produce considerable incapacitation and death within minutes to hours.[124]

Signs and Symptoms: Exposure causes skin pain, itching, redness, blisters, and sloughing (shedding) of dead skin. Effects on the airway include nose and throat pain, nasal discharge, itching and sneezing, cough, shortness of breath, wheezing, and chest pain; the victim spits blood as a result of pulmonary or bronchial hemorrhage. The T-2 toxin also produces effects after ingestion or eye contact. Severe poisoning results in prostration, weakness, jerky movement, collapse, shock, and death.[125]

Prophylaxis and Treatment: The only protection against T-2 toxin effects is the individual protective mask and chemical protective overgarment. No chemotherapy, vaccine, or specific antidote is available.[126]


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