Soman.

Soman was first synthesized in 1944 by the German chemist Richard Kuhn. It was the third of a family of related organophosphate or organophosphorus (OP) compounds that were developed for use as chemical warfare agents during World War II (tabun (GA) and sarin (GB) were developed several years earlier). Unlike tabun and sarin, soman was not produced in large quantities or loaded into munitions during World War II due to its late discovery and difficulties associated with scaling up the manufacturing process. After the war, other nations including the United States, United Kingdom, and former Soviet Union were also quick to realize the weaponization potential of OP nerve agents and establish research and development programs of their own. Soman was never mass produced by the United States due to the difficulty and cost of large-scale production as well as concerns over the lack of effective antidotes (compared to tabun and sarin). However, it was manufactured in large quantities and loaded into munitions by the former Soviet Union beginning in the 1960s. In the 1990s, the production, stockpiling, and use of chemical weapons (including soman) by nations were banned by the Chemical Weapons Convention (CWC), an international agreement that entered into force in 1997. The CWC is implemented by the Organisation for the Prohibition of Chemical Weapons (OPCW) and requires the destruction of existing chemical weapons stockpiles. Nearly all of the nations in the world are members of the OPCW, and destruction of existing chemical weapons stockpiles was ongoing at the time of this writing in 2012.

Soman (GD), a fluorinated organophosphorus compound. Exposure to soman can cause death in minutes. A fraction of an ounce (1 to 10 mL) of soman on the skin can be fatal. When pure, GD is a colorless liquid with fruity odor. With impurities, or upon aging, GD is an amber to dark brown oily liquid with an odor of rotten fruit or camphor (like Vicks Vapo-Rub). Do not rely on odor for detection; not everyone can smell low concentrations of this chemical.

Colorless liquid. Evolves odorless gas.

Chemical warfare agent.

Soman is a synthetic nerve agent intended for use in chemical warfare.

ChEBI: Soman is a phosphonic ester.

Colorless liquid, odorless to fruity.

Hydrolyzed by water, rapidly hydrolyzed by dilute aqueous sodium hydroxide. Water alone removes Fluoride atom producing nontoxic acid.

Acidic conditions produce hydrogen fluoride; alkaline conditions produce isopropyl alcohol and polymers. When heated to decomposition or reacted with steam, Soman. emits very toxic fumes of fluorides and oxides of phosphorus. Slightly corrosive to steel. Hydrolyzed by water.

Highly toxic by ingestion, inhalation, and skin absorption; may be fatal on short exposure; cholinesterase inhibitor; military nerve gas; fatal dose (man) 0.01 mg/kg.

Soman is the most toxic of all the nerve agents. It is extremely toxic by all routes of exposure. The symptoms of toxic effects are those of organophosphate insecticides, but the severity of poisoning is much greater.
An oral dose of 0.01 mg/kg in humans couldbefatal.Inanimals,somantoxicityvaried among species; the LD50 values by subcutaneous administration were 20, 28, and 126 μg/kg for rabbits, guinea pigs, and rats, respectively (Maxwell et al. 1988). Exposure to a concentration of 21 mg/m³ soman caused a large inhibition of the activities of the enzyme carboxylesterase in bronchi, lungs, and blood tissues in rats (Aas et al. 1985). There was an increase in soman toxicity by 70% following subcutaneous pretreatment with tri-o-cresyl phosphate, a carboxylesterase inhibitor. This study indicates that carboxylesterase is important as a detoxifying enzyme.
Jimmerson and coworkers (1989a) reported the 24-hour subcutaneous LD50 value in rats as 118.2 μg/kg. Soman-inhibited carboxylesterase activity in plasma and cholinesterase activity in brain regions in a dose-related manner. Such cholinesterase inhibitionandelevationofacetylcholineinthe brainareverysimilartothosecausedbysarin, DFP, paraoxon, and other organophosphates. However, organophosphates are dissimilar in their effects on choline levels, neuronal activity, and phospholipase A activity. These differential effects are attributed to the differences in the neurotoxicity of soman and other organophosphates (Wecker 1986). Intravenous injection of soman in rats (by six times the LD50 amount) followed by isolation of diaphragms 1 or 2 hours after the injection showed detectable amounts of soman P(-)isomerindiaphragmtissue(VanDongenet al. 1986). Pretreatment of the rats with pinacolyl dimethylphosphinate prevented the storage of soman in diaphragm tissue.
A relation between soman toxicity and the aging process has been suggested by many investigators. Sterri and coworkers (1985) measured the activity of the enzymes carboxylesterase and cholinesterase in the plasma, liver, and lung of young rats 5–31 days old. Soman was six- to sevenfold higher in toxicity in 5-day-old rats than in 30day-old animals. The decrease in toxicity was attributed to the increase in plasma carboxylesterase. Plasma and brain regional cholinesterase activity profiles have been investigated by Shih and coworkers (1987) in four groups of male rats of 30, 60, 120, and 240 days old. The calculated 24-hour intramuscular LD50 values were 110.0, 87.2, 66.1, and 48.6 μg/kg, respectively. Young rats showed a less severe initial weight loss and a more rapid and sustained recovery of growth than older animals. These data indicate the relationship between the toxicity of soman to age-related changes of cholinesterase in certain brain areas. In a latter paper, Shih and coworkers (1990) reported that survivors from the two oldest groups of the studied animals did not recover to baseline body weights by the end of the observation period. The activity of plasma cholinesterase did not change significantly with age, while brain regional cholinesterase showed distinct patterns of age dependence. These data further correlate between soman toxicity and the aging process. However, no definite relationship could be established from these studies between the toxicity and the cholinesterase activity in the blood and brain of the test animals.
Pretreatment with certain substances showed potentiation in soman toxicity in test animals. Pretreating rats with cresylbenzodioxaphosphorin oxide (CBDP) by 1 mg/kg reduced the 24-hour subcutaneous LD50 value by approximately sixfold (Jimmerson et al. 1989b). CBDP blocks tissue carboxylesterase sites that serve to detoxify soman. This enhances soman-induced inhibition of cholinesterase in the central nervous system, potentiating its lethality. Similar potentiating effects from CBDP pretreatment were reported earlier in other animals, such as mice, guinea pigs, and rabbits (Maxwell et al. 1987). Pretreatment with tri-o-cresyl phosphate, another inhibitor, decreased the LD50 dose of soman in rats (Tekvani and Srivastava 1989).
Wheeler (1989) observed that the toxicity of soman in rats increased during exposure of the species to either cold or hot environments and after removal from the cold temperatures. Such an increase in toxicity under cold environmental temperatures was attributed to a generalized adrenocortical stress response. .

Median lethal dose (mg-min/m3): 2500 by skin (vapor) or 350 (liquid); 35 inhaled. Median incapacitating dose: 25 inhaled. Eye/skin toxicity: Very high. Rate of action: Very rapid. Physiological action: Cessation of breath-death may follow. Detoxification rate: Low, essentially cumulative. (ANSER)

Agent GD, an organic fluoride compound, is a quick-acting chemical warfare nerve agent (nerve gas). Medical treatment of soman is difficult because it permanently binds to receptors in the body in minutes. Large amounts of the vapor or liquid can hurt you in minutes, and can quickly lead to death.

UN2810 Toxic liquids, organic, n.o.s., Hazard Class: 6.1; Labels: 6.1-Poison Inhalation Hazard, Technical Name Required. Military driver shall be given full and complete information regarding shipment and conditions in case of emergency. AR 50-6 deals specifically with the shipment of chemical agents. Shipments of agent will be escorted in accordance with AR 740-32

Like other chemical warfare nerve agents, soman is an irreversible cholinesterase inhibitor. The clinical effects of soman exposure result primarily from its inhibition of acetylcholinesterase (AChE), although it does inhibit other cholinesterases as well, including butyrylcholinesterase (BuChE). The most important biological function of AChE is the degradation of acetylcholine, an important neurotransmitter that is found in nerve terminals in both the peripheral and central nervous systems. Generally, acetylcholine stimulates secretion of bodily fluids and contraction of skeletal muscles in the periphery and affects a multitude of neural pathways in the central nervous system. Normally, the actions of acetylcholine on its receptors are terminated when it is hydrolyzed by AChE, thus preventing continual overstimulation of the receptors. Inhibition of AChE blocks its ability to degrade acetylcholine, resulting in an accumulation of acetylcholine and cholinergic overstimulation of the target tissues. Effects of AChE inhibition include involuntary muscle contractions and increased fluid secretion (e.g., tears, saliva) resulting from acetylcholine accumulation in the peripheral nervous system and seizures resulting from acetylcholine accumulation in the central nervous system. The cause of death is typically respiratory dysfunction resulting from paralyzation of the respiratory muscles, buildup of pulmonary secretions, and depression of the brain’s respiratory center.
The binding of soman to AChE is generally considered irreversible unless removed by therapy. This removal is called reactivation, which can be accomplished by the use of oximes prior to ‘aging’. Aging is the biochemical process by which the agent–enzyme complex becomes refractory to reactivation. Spontaneous reactivation in the absence of oximes is possible but is unlikely to occur at a high enough incidence to be clinically important. Soman ages more rapidly than any other chemical warfare nerve agent, with an aging half-time of approximately 2 min.
Circulating cholinesterases in the blood act as effective scavengers of soman, and blood cholinesterase levelsmay be used to approximate tissue levels of functional AChE following an exposure to soman or another cholinesterase inhibitor. Red blood cell cholinesterase (RBC-ChE) and BuChE are both found in blood, the latter in the plasma and the former in erythrocytes. RBC-ChE enzyme activity is restored at the rate of red blood cell turnover, which is ~1% per day. Tissue AChE and plasma BuChE activities return with synthesis of new enzymes, the rate of which differs between plasma and tissues as well as between different tissues.
Although cholinesterase inhibition is the primary mechanism of toxicity following exposure to OP nerve agents, recent investigations have assessed noncholinergic effects of OP nerve agent poisoning, including changes in the levels of neurotransmitters other than acetylcholine. These changes may be due to a compensatorymechanismin response to overstimulation of the cholinergic system, direct action of the OP on the proteins responsible for noncholinergic neurotransmission, or perhaps both. It has been reported that OPs inhibit serine esterases that degrade a number of noncholinergic neuropeptides, and it is possible that this inhibitionresults in altered levels of a numberof neurotransmitters other than acetylcholine. Recent studies have also suggested that neuroinflammation is one putative mechanism for noncholinergic neurotoxicity of OP nerve agents. Some toxicity to the pulmonary and cardiovascular systems may result from direct toxicity to the organs; OP cholinesterase inhibitors have been reported to cause secondary pneumonia and pulmonary edema as well as cardiac arrhythmias and lesions. The etiology of these toxic effects is not well understood and could be due to the cholinergic disruption that follows cholinesterase inhibition and/or other mechanisms that have yet to be identified. It is worth mentioning that mice lacking AChE are actually more sensitive to OP poisoning than wild-type mice, supporting the notion that OP cholinesterase inhibitors exert their toxic effects throughothermechanisms in additiontoAChE inhibition.

Hydrolyzed by water to form hydrogen fluoride and the nontoxic phosphonic acid derivative. It is rapidly hydrolyzed by dilute aqueous NaOH Stable after storage in steel for 3 months @ 65 C. Raising the pH increases the rate of decomposition significantly. GD decomposes slowly in water; will hydrolyze to form HF-H-H-O-CH3 and (CH3)3-C-C-O-P-OH. GD reacts readily with bases and weak acids. Under acid conditions, GD hydrolyzes, forming hydrofluoric acid (HF). Flammable hydrogen gas produced by the corrosive vapors reacting with metals, concrete, etc., may be present. Corrosive to steel and possibly other ferrous metals. GD corrodes steel at the rate of 1×10-5 in/month. When heated to decomposition or on contact with steam, it emits very toxic fumes of fluorides and oxides of phosphorus.

Principles and methods for destruction of chemical weapons: “Destruction of chemical weapons” means a process by which chemicals are converted in an essentially irreversible way to a form unsuitable for production of chemical weapons, and which in an irreversible manner renders munitions and other devices unusable as such. Each nation shall determine how it shall destroy chemical weapons, except that the following processes may not be used: dumping in any body of water, land burial, or open-pit burning. It shall destroy chemical weapons only at specifically designated and appropriately designed and equipped facilities. Each nation/shall ensure that its chemical weapons destruction facilities are constructed and operated in a manner to ensure the destruction of the chemical weapons; and that the destruction process can be verified under the provisions of this Convention . A minimum of 55 g of decontamination solution is required per gram of soman (GD). A minimum of 65 g of decontamination fluid per gram of soman (GD) is allowed to agitate for a minimum of 1 hour. Agitation is not necessary following the first hour provided a single phase is obtained. At the end of the first hour the pH should be checked and adjusted Up to 11.5 with additional NaOH as required. An alternate solution for the decontamination of soman (gd) is 10% sodium carbonate in place of the 10% NaOH solution above. Continue with 55 g of decon per gram of gd. Agitate for 1 hour and allow to react for 3 hours. At the end of the third hour, adjust the pH to above 10. It is also permitted to substitute 5.25% sodium hypochlorite for the 10% NaOH solution above. Continue with 55 g of decon per gram of soman (GD). Agitate for 1 hour and allow to react for 3 hours, then adjust the pH to above 10. Scoop up all material and place in a fully removable head and a high density polyethylene liner. Cover the contents with additional decontaminating solution before affixing the drum head. After sealing the head, the exterior of the drum shall be decontaminated and then labeled in accordance with IAW EPA, and DOT regulations. All contaminated clothing will be placed in a fully removable head drum with a high density polyethylene liner. Cover the contents of the drum with decontaminating solution as above before affixing the drum head. After sealing the head, the exterior of the drum shall be decontaminated and then labeled per IAW EPA, and DOT regulations. All leaking containers shall be overpacked with vermiculite placed between the interior and exterior containers. Decontaminate and label in accordance with IAW EPA, and DOT regulations. Conduct general area monitoring to confirm that the atmospheric concentrations do not exceed the exposure limits. Waste disposal method: Open pit burning or burying of soman (GD) or items containing or contaminated with soman (GD) in any quantity is prohibited. The detoxified soman (GD) (using procedures above) can be thermally destroyed by incineration in an EPA approved incinerator in accordance with appropriate provisions of federal, state and local RCRA regulations. NOTE: Several states define decontaminated surety material as a RCRA Hazardous Waste.