| The basic formula of VM, and related analogues (e.g., VX, VE, VG) were first synthesized in the early 1950s. Being structurally similar to VX, VM should have a high toxicological profile, and based on this assumption, we will use the estimates for VX: 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 VM may take many minutes to even hours, while inhalation exposure to aerosolized concentrations could produce casualties much more quickly (seconds to minutes).
Like other nerve agents, the toxic principle of VM 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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