| Originally developed from research in organophosphate insecticides, the basic structure of VX and related analogues (e.g., VE, VG, VM) were first synthesized in the early 1950s. VX is an odorless, amber-colored oily liquid, with similar viscosity to that of motor oil, and is very persistent. Like other oils, VX is soluble in fat, and skin absorption of the liquid presents a significant hazard. Even more so than the first-generation nerve agents (tabun, sarin, and soman), VX is extremely toxic, with a concentration of 10mg-min/m3 being the inhaled median lethal dose (LD50), while 15mg absorbed on the skin is sufficient to kill most adults. Injury or death from contact with VX may take many minutes to even hours, while inhalation exposure to aerosolized concentrations could produce casualties much more quickly (seconds to minutes). Binary munitions involving the production of VX, such as that produced in the United States during the 1980s, might involve a ready precursor such as QL and mixed with sulfur. The reaction between QL and sulfur proceeds generally as follows:
However, due to the exacting and complex engineering requirements involved in such devices, it is more likely to encounter VX in its unitary form. Like other nerve agents, the toxic principle of VX is its ability to inhibit acetylcholinesterase (AChE), the body’s enzyme required for proper nerve transmission at the molecular level. Increased levels of acetylcholine produce exaggerated levels of bodily secretions and muscular twitching, as well as pronounced effects on the cardiovascular and central nervous systems. While death from respiratory paralysis can occur as a consequence, victims are also prone to asphyxiate due to mucous and salivary excretions from the upper respiratory tree. Without timely medical intervention and follow-up treatment, those who do survive exposure to large doses of nerve agents can suffer permanent neurological damage. |
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