96-64-0

Colorless liquid. Evolves odorless gas.

Chemical warfare agent.

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.

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)

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.

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.

Inhalation: Hold breath until respiratory protective mask is donned. If severe signs of agent exposure appear (chest tightens; pupil constriction; a lack of coordination; etc.); immediately administer, in rapid succession,all three Nerve Agent Antidote Kit(s); Mark I injectors (or atropine if directed by the local physician). Injections using the Mark I kit injectors may be repeated @ 5 to 20 minute intervals if signs and symptoms are progressing until three series of injections have been administered. No more injections will be given unless directed by medical personnel. In addition, a record will be maintained of all injections given. If breathing has stopped, give artificial respiration. Mouthto-mouth resuscitation should be used when approved mask-bag of oxygen delivery systems are not available. Do not use mouth-to-mouth resuscitation when facial contamination exists. If breathing is difficult, administer oxygen. Seek medical attention Immediately.
Eye contact: Immediately flush eyes with water for 10 15 minutes, then don respiratory protective mask. Although miosis (pinpointing of the pupils) may be an early sign of agent exposure, an injection will not be administered when miosis is the only sign present. Instead, the individual will be taken immediately to the medical treatment facility for observation. Skin contact: Don respiratory protective mask and remove contaminated clothing. Immediately wash contaminated skin with copious amounts of soap and water; 10% sodium carbonate solution, or 5% liquid household bleach. Rinse well with water to remove decontaminant. Administer nerve agent antidote kit, Mark I, only if local sweating and muscular twitching symptoms are present. Seek medical attention Immediately. Ingestion: Do not induce vomiting. First symptoms are likely to be gastrointestinal. Immediately administer Nerve Agent Antidote kit, Mark I. Seek medical attention immediately. If there is no apparent breathing, artificial resuscitation will be started immediately, but do not use mouth-to-mouth resuscitation when facial contamination exists; in this case, use mechanical resuscitator. The situation will dictate method of choice. When appropriate and trained personnel are available, CPR may be necessary.
Notes for physician and qualified medical personnel: An individual who has received a known agent exposure or who exhibits definite signs or symptoms of agent exposure shall be given an intramuscular injection immediately with the MARK I kit auto-injectors. Some of the early symptoms of a vapor exposure may be rhinorrhea (runny nose) and/or tightness in the chest with shortness of breath (bronchial constriction). Some of the early symptoms of a percutaneous exposure may be local muscular twitching or sweating at the area of exposure followed by nausea or vomiting. Although myosis (pin-pointing of the pupils) may be an early sign of agent exposure, an injection shall not be administered when myosis is the only sign present. Instead, the individual shall be taken immediately to the medical facility for observation. Injections using the MARK I kit injectors (or atropine only if directed by the local physician) may be repeated @ 5 to 20 minutes intervals if signs and symptoms are progressing until three series of injections have been administered. No more injections will be given unless directed by medical personnel. In addition, a record will be maintained of all injections given. Administer, in rapid succession, all three MARK I kit injectors (or atropine if directed by the local physician) in the case of SEVERE signs of agent exposure. If indicated, CPR should be started immediately. Mouth-to-mouth resuscitation should be used when approved mask-bag or oxygen delivery systems are not available. Do not use mouth-to-mouth resuscitation when facial contamination exists. CAUTION: atropine does not act as a prophylactic and shall not be administered until an agent exposure has been ascertained.

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

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.

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.

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.

ChEBI: Soman is a phosphonic ester.

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.