Soman in chemical attacks
Soman is a highly toxic chemical agent classified as a nerve agent, first developed in Germany during World War II. It is a colorless liquid with a camphorlike odor and is chemically similar to sarin, though it is considered to be more toxic and persistent in the environment. Due to its potential use in terrorist attacks, law enforcement agencies maintain heightened vigilance regarding soman and similar substances; its manufacture and storage are prohibited under the United Nations Chemical Weapons Convention. When exposed to soman, the enzyme acetylcholinesterase (AChE) is inhibited, leading to a buildup of the neurotransmitter acetylcholine, which can cause severe symptoms including respiratory failure and convulsions. Although the United States opted to develop sarin instead of soman for military use, there are indications that soman may have been used during the Iran-Iraq war in the 1980s, although this remains unconfirmed. Treatment for soman poisoning typically involves the administration of atropine and pralidoxime chloride, but the effectiveness of these treatments is limited by a phenomenon known as "aging," which occurs shortly after exposure. Research continues to improve antidote options and detection methods for soman to enhance public safety.
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Soman in chemical attacks
DEFINITION: Highly toxic colorless liquid that has potential for use as a chemical weapon.
SIGNIFICANCE: Concerns that terrorists could employ chemical agents in attacks have increased law-enforcement agencies’ attention to substances such as soman. The manufacture and storage of soman are banned by the United Nations Chemical Weapons Convention of 1993.
The nerve agent soman was first prepared in 1944 in Germany as part of that nation’s chemical warfare program. Soman, which has a camphorlike odor, is chemically similar to sarin, but more toxic. Nerve agents such as soman act as inhibitors of the enzyme acetylcholinesterase (AChE). The neurotransmitter acetylcholine is released at nerve endings and causes muscle contraction. In the normal course of affairs, the acetylcholine is soon destroyed by a reaction catalyzed by AChE. If this enzyme is disabled in its function by binding to a nerve agent, the continued presence of acetylcholine produces the symptoms of poisoning: pain and watering in the eyes, contracted pupils (meiosis), respiratory failure, runny nose, incontinence, convulsions, coma, and death. A study published in 2024 indicated that exposure to soman may cause long-term health problems.
Although soman is twice as toxic as sarin and more persistent in the environment, the US Army decided in 1948 to develop sarin as a weapon instead of soman. The manufacture of soman would have been more costly, and the lack of a sufficiently effective antidote was felt to be a disadvantage in case of accidental exposures. The Soviet Union did manufacture soman using captured German technology.
According to the US Centers for Disease Control and Prevention, soman may have been used during the Iran-Iraq war in the 1980s, although there was no confirmation of its use. As of the early 2020s, the chemical had not knowingly been used in warfare or terrorism. Soman poisoning leaves detectable traces on, around, or in the bodies of victims, and blood samples can be tested for AChE levels, which are abnormally low in individuals exposed to the agent. The US military employs test kits and instruments that can detect nerve agents and provide warnings. In the laboratory, soman can be detected through the use of gas chromatography-mass spectrometry (GC-MS) or capillary column gas using a chiral medium.
Treatment of nerve agent poisoning involves injection of atropine and administration of pralidoxime chloride (2-PAM chloride). This treatment needs improvement, and research in the area is active. A complicating factor that is particularly prominent with soman is an irreversible reaction known as aging, which renders the soman-AChE complex inactive to pralidoxime within about ten minutes of exposure.
During the Persian Gulf War of 1991, US soldiers were given pyridostigmine bromide (PB) as a prophylactic measure in the mistaken belief that Iraq might attack with soman. Carbamates such as PB bind reversibly with AChE and block the soman so that when exposure to the nerve agent ends, AChE can re-form. Nerve agent scavengers such as exogenous AChE can also provide protection.
Bibliography
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