There are no known direct antidotes to<unk>  exposure. Therefore, risk management in contaminated areas is primarily defined by the treatment of exposure symptoms as well as prevention of future exposure. Treatment Typical routes of exposure to<unk>  toxins include topical absorption, ingestion, and inhalation. Severity of symptoms depends on the dose and type of exposure, but treatment is primarily focused on supporting bodily systems damaged by the mycotoxin. The first step in most exposure cases is to remove potentially contaminated clothing and to flush the sites of exposure thoroughly with water. This prevents the victim from repeated exposure. Fluids and electrolytes can be given to victims with high levels of gastrointestinal damage to mitigate the effects of reduced tract absorption. Fresh air and assisted respiration can also be administered upon the development of mild respiratory distress. Increasingly severe symptoms can require the application of advanced medical assistance. The onset of leukopenia, or reduction of white blood cell count, can be treated with a plasma or platelet transfusion. Hypotension can be treated with the administration of norepinephrine or dopamine. Development of severe cardiopulmonary distress may require intubation and additional drug treatments to stabilize heart and lung activity. Additionally, there are a variety of chemicals that can indirectly reduce the damaging effects of<unk> s on cells and tissues. Activated charcoal solutions are frequently administered to ingestion cases as an adsorbent. Here, the charcoal acts as a porous substance for the toxin to bind, preventing its absorption through the gastrointestinal track and increasing its removal from the body through bowel excretion. Similar detoxifying adsorbents can also be added to animal feed upon contamination to reduce the bioavailability of the toxin upon consumption. Antioxidants are also useful in mitigating the damaging effects of<unk> s in response to the increase of reactive oxygen species they produce in cells. Generally, a good diet rich in probiotics, vitamins and nutrients, proteins, and lipidis is thought to be effective in reducing the symptoms of<unk>  poisoning. For example, vitamin E was found to counteract the formation of lipid peroxides induced by T-2 toxin in chickens. Similarly, cosupplementation of modified glucomannas and selenium in the diets of chickens also consuming T-2 toxin, reduced the deleterious effects of toxin associated depletion of antioxidants in the liver. Despite not being a direct antidote, these antioxidants may be critical in reducing the severity of<unk>  exposures. Prevention Biological approach to<unk>  decontamination. De-epoxidases are capable of reducing epoxide rings (red) to double bond groups (green) which significantly reduces the toxicity of<unk> s.<unk> s are mycotoxins produced by molds that frequently contaminate stores of grain products. This makes<unk>  contamination a significant public health problem, and many areas have strict limits on permitted<unk>  content. For example, in the European Union, only .025 ppm of T-2 toxin is permissible in bakery products intended for human consumption. The molds that can produce<unk> s grow well in dark, temperate places with high moisture content. Therefore, one of the best ways to prevent<unk>  contamination in food products is to store the resources in the proper conditions to prevent the growth of molds. For example, it is generally advised to only store grains in areas with a moisture content of less than 15%. However, if an area has already been contaminated with<unk>  toxins, there are a variety of possible decontamination strategies to prevent further exposure. Treatment with 1% sodium hypochlorite (NaOCl) in 0.1M sodium hydroxide (NaOH) for 4–5 hours has been shown to inhibit the biological activity of T-2 toxin. Incubation with aqueous ozone at approximately 25 ppm has also been shown to degrade a variety of<unk> s through a mechanism involving oxidation of the 9, 10 carbon double bond. UV exposure has also been shown to be effective under the right conditions. Outside of the strategies for physcial and chemical decontamination, advancing research in molecular genetics has also given rise to the potential of a biological decontamination approach. Many microbes, including bacteria, yeast, and fungi, have evolved enzymatic gene products which facilitate the specific and efficient degradation of<unk>  mycotoxins. Many of these enzymes specifically degrade the 12,13 carbon epoxide ring which is important for the toxicity of<unk> s. For example, the Eubacteria strain BBSH 797 produces de-epoxidase enzymes which reduce the 12,13 carbon epoxide ring to a double bond group. These, along with other microbes expressing<unk>  detoxifying properties, can be used in feed stores to prevent to toxic effect of contaminated feed upon consumption. Furthermore, molecular cloning of the genes responsible for producing these detoxifying enzymes could be useful in producing strains of agricultural products that are resistant to<unk>  poisoning.
Trichothecene
Scyllatoxin
Laudanum
Toxicon
Simmondsin
Coal tar
Mersa
Chloracne