The clinical condition it causes is alimentary toxic aleukia and a host of symptoms related to organs as diverse as the skin, airway, and stomach.

Alimentary toxic aleukia (ATA), a disease which is caused by trichothecenes like T-2 mycotoxin, killed many thousands of USSR citizens in the Orenburg District in the 1940s.

[5] Another alternative theory was developed by Harvard biologist Matthew Meselson, who proposed that the "yellow rain" found in Southeast Asia originated from the excrement of jungle bees.

[6] The first indication for this theory came from finding high levels of pollen in the collected samples, giving the substance its yellow color.

It was also found that jungle bees in this area fly collectively in great numbers, at altitudes too high to be easily seen, producing showers of feces that could have been mistaken for sprays from aircraft.

[8] Despite this conclusive analysis, the United States has not withdrawn its allegations and declares that the issue has not been fully resolved.

US troops suffered from mycotoxicosis-like symptoms after an Iraqi missile detonated in a US military camp in Saudi Arabia during Operation Desert Storm in the Persian Gulf War, in 1991.

It has been shown that Iraq researched trichothecene mycotoxins, among other substances, and thus was capable of its possession and employment in chemical warfare.

The reactivity of epoxides can lead to reactions with endogenous compounds and cellular constituents like DNA bases and proteins.

The toxic compound influences the metabolism of membrane phospholipids, leads to an increase of liver lipid peroxidases and has an inhibiting effect on DNA and RNA synthesis.

In addition it can bind to an integral part of the 60s ribosomal subunit, peptidyltransferase, thereby inhibiting protein synthesis.

Furthermore, the level of Fas, an apoptosis-related cell-surface antigen and p53, a protein regulating the cell cycle, were increased.

T-2 mycotoxin is produced naturally by Fusarium fungi of which the most important species are: F. sporotrichioides, F. langsethiae, F. acuminatum and F. poae.

The production of this compound for research and commercial purposes is generally accomplished by cultivating some strain of T-2 mycotoxin producing fungi on agar plates.

The second to last step is the oxidation of the eighth carbon to make neosolaniol, which then undergoes slight modification to create the T-2 toxin.

This makes it a potential biological weapon, however large amounts of the compound are required for a lethal dose.

In a different study involving pigs, the distribution after four hours of IV injection was seen to be 15–24% in the GI tract and 4.7–5.2% in various other tissues.

In vivo studies showed that the most occurring reactions are ester hydrolysis and hydroxylation of the isovaleryl group.

Acute toxic symptoms include vomiting, diarrhea, skin irritation, itching, rash, blisters, bleeding and dyspnea.

[citation needed] If the individual is exposed to T-2 over a longer period alimentary toxic aleukia (ATA) develops.

In the end the following symptoms might occur: a high fever, petechial haemorrhage, necrosis of muscles and skin, bacterial infections of the necrotic tissue, enlarged lymph nodes.

After exposing zebra fish embryos to a concentration of 20 μmol/L or higher malformation and mortality rates increased.

[21] Exposure of the mycotoxin is typically followed by standardized treatment for toxic compounds in order to reduce the effect of the toxin.

Due to their abilities, research shows possible uses for the mycotoxin as growth promoters, antibiotics, antivirals, as an antileukemic, and as an antimalarial.