Mycotoxins have provided many benefits for society: penicillin-based antibiotics; cyclosporine A (an important immunosuppressant for transplant patients); even cholesterol-lowering drugs (such as lovastatin) are based on mycotoxins. Even outside the realm of biological weapons, however, mycotoxins are the source of significant human suffering. Aflatoxin contamination of food is a major source of illness in the form of a potential etiology of hepatocellular carcinoma. Another mycotoxin still in use today medically, but also with severe potential toxic effects, is ergotamine. A contamination of rye with ergotamines is believed by some to be the cause of behavioral changes that led to the Salem witch trials in 1692.

Trichothecenes compose a group of mycotoxins. These mycotoxins are derived from many different fungi: fusarium, myrothecium, stachybotrys, trichoderma, and cephalosporium. Fusarium is the source of weaponized trichothecene T-2 mycotoxin. Although other mycotoxins may also possess the potential for human toxicity, the focus here is on what is known about T-2 mycotoxin as a biological weapon, due to known experience weaponizing this toxin. Another member of the trichothecene mycotoxin family is vomitoxin, with the physiological effects directly related to the toxin’s name. Between 1997 and 1998, an estimated 1,700 children in the United States became ill with nausea, abdominal cramps, and of course vomiting after suspected vomitoxin contamination of burritos at a level of less than 1 part per billion in the contaminated food (1). Reports of trichothecene-induced illness from contaminated food date back to 1913 Siberia (2). T-2 mycotoxins have relevance to more modern history. Many are familiar with the “yellow rain” attacks in Southeast Asia in the 1970s, but also in Afghanistan in the late 1970s and reportedly in the Iraqi research weapons machine (3, 4). Some believe T-2 mycotoxins were used in Iraqi warheads released in Desert Storm. T-2 mycotoxin has several properties that increase its utility as a biological weapon: It is resistant to UV light degradation, has high heat stability, and although not soluble in water, it is soluble in solvents such as ethanol, methanol, propylene glycol, and dimethyl sulfoxide (DMSO) (5). An unconfirmed report from the Iran-Iraq war suggested that T-2 mycotoxin was mixed with mustard (a blister agent) (6). Similar to ricin, T-2 mycotoxin can represent not only an inhalation hazard but ingestion in foodstuffs.

T-2 mycotoxins are generally nonvolatile stable compounds. Although stable in high heat, 3% to 5% sodium hypochlorite solution will inactivate the toxins, thus making this the decontamination solution for surfaces and equipment (7). The T-2 mycotoxins’ mechanism of action is complex. Several possible sites of cellular damage exist. Most of the focus on T-2 mycotoxin damage is its effects on protein synthesis. T-2 mycotoxin binds to 60S ribosome, affecting peptidyltransferase and peptide bond formation (8), protein elongation, and protein synthesis termination (9). The inhibition of protein syntheses caused by T-2 mycotoxin starts as soon as 5 minutes after exposure in a cell study (10). Trichothecene mycotoxins can cross cell membranes, and their lipophilicity allows for absorption through skin, gastrointestinal, and respiratory systems.

Other research points to the ability of these toxins to cause cellular apoptosis as demonstrated in an animal model with thymus, spleen, liver, and Kupffer cells affected (11). Apoptosis in intestinal crypt cells has been seen (12) with DNA fragmentation potentially initiating apoptotic changes (13). In addition to cellular damage, direct interference with the proper functioning of brain monoamines is possible as demonstrated in the cerebral changes in T-2 mycotoxin–exposed rats (14).

A victim can be exposed to T-2 mycotoxin by several different routes: aerosol, droplets, or dust. Lethality appears to be a factor of route of exposure. The lethal concentration of 50% of an exposed population (LCt50) is given a range of 200 to 5,800 mg min/m³ (15), (16),(17). For skin injury, T-2 mycotoxin is actually more potent than the vesicant mustard with an LD50 of 2 to 12 mg/kg³. These mycotoxins do not appear to bioaccumulate (18). Metabolism involves utilization of glucuronide conjugation, oxidation, hydrolysis, deepoxidation (19), and enterohepatic recirculation (20).