Trichothecene mycotoxins aerosolized

Decontamination of personnel and equipment after a biological warfare attack is a lesser concern than after a chemical warfare attack because most biological warfare agents are not dermally active (the trichothecene mycotoxins are an exception). Still, decontamination remains an effective way to decrease the spread of infection from potential secondary aerosolization. 

Fig. 30-1. Toxicity, in mouse LD50 (see Table 30-2), plotted against the quantity of toxin required to provide a theoretically effective open-air aerosol exposure, under ideal meteorological conditions, to an area of 100 km2. Although the toxicity is based on direct studies with mice, it is believed to be very similar in humans. The mathematical model corrects for human parameters such as respiration. Ricin, saxitoxin, and botulinum, and trichothecene mycotoxins (T-2) kill at the concentrations depicted. Adapted from Spertzel RO, Wannemacher RW, Patrick WC, Linden CD, Franz DR. Technical Ramifications of Inclusion of Toxins in the Chemical Weapons Convention (CWC). Alexandria, Va Defense Nuclear Agency 1992 18. DNA Technical Report 92-116.

Trichothecene mycotoxins can be delivered as dusts, droplets, aerosols, or smoke from aircraft, rockets, missiles, artillery, mines, or portable sprayers. Because of their antipersonnel properties, ease of large-scale production, and apparent proven delivery by various aerial dispersal systems, the trichothecene mycotoxins (especially T-2 toxin) have an excellent potential for weaponization. 

In Southeast Asia, most of the yellow rain attacks were delivered by aircraft or helicopter spray, bombs, and air-to-surface rockets. The attacks were described as a shower of sticky liquid, a yellow cloud of dust or powder, or a mist (like an insect spray).715 The delivery of the trichothecene mycotoxins was similar in many aspects to the spraying of pesticides on agricultural crops. This would result in a very low-efficiency respiratory aerosol (1-5 pm particles)34 but a highly effective droplet aerosol that could cause severe skin and eye irritation. 

Pharmacokinetic studies60,61 have demonstrated T-2 toxin in the plasma of animals that were administered this mycotoxin both intravascularly and by aerosol. As plasma concentrations of the parent trichothecene mycotoxin decrease, the deacylated and hydroxylated metabolites and their glucu-ronide conjugates rapidly appear and disappear from circulation. From these various observations, we can conclude that the pharmacokinetics of the trichothecene mycotoxins are functions of the rate of absorption into the general circulation, metabolism, tissue distribution, and excretion. 

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

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. 

In the absence of a biological detector or a particular characteristic of the aerosol (such as color or odor), diagnosis of an attack with trichothecene would depend on clinical observations of casualties and identification of the toxins in biological or environmental samples. This would involve a combined effort between the medical and chemical units in the field. The early signs and symptoms of an aerosol exposure to trichothecene mycotoxins would depend on particle size and toxin concentration. For a large-particle aerosol (particles > 10 pm, found in mist, fog, and dust similar to that used in Southeast Asia), the signs and symptoms would include rhinorrhea, sore throat, blurred vi-... 

Later signs and symptoms (8-24 h) would probably be similar (except for the degree of skin rash and blisters) for both large-particle and deep-respiratory aerosol exposure to trichothecene mycotoxins. They could include continued nausea and vomiting, diarrhea, burning erythema, skin rash and blisters, confusion, ataxia, chills, fever, hypotension, and bleeding. 

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. 

The communists used aerosolized mycotoxins ( yellow rain ) in Laos (1975-1981), Kampuchea (1979-1981), and Afghanistan (1979-1981), causing over 10,000 deaths. It is almost certain that weaponized mycotoxins are stiU available in some countries. The GDC rates trichothecene mycotoxins as a Gategory B threat. 

Use the following protocol when responding to a biological attack with aerosolized ricin, trichothecene mycotoxin T2, or staphylococcal enterotoxin B. 

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