Soman

Soman. · AGENTGD · GRXKLBBBQUKJJZ-UHFFFAOYSA-N · PINACOLYLMETHYLPHOSPHONOFLUORIDATE · O-PINACOLYLMETHYLPHOSPHONOFLUORIDATE · PINACOLYHEXYLMETHYLPHOSPHONOFLURIDATE · 1,2,2-TRIMETHYLPROPYLESTER,PHOSPHONOFLUORIDATE · [fluoro(1,2,2-trimethylpropoxy)phosphoryl]methane

https://huagongshe.com/de/chemical/7305

Identifikatoren & physikalische Daten

CAS No.	96-64-0
Summenformel	CH3PO(F)OCH(CH3)C(CH3)3
Durchschnittliche Molmasse	182,17 g/mol
Monoisotopische Masse	182,0871946 g/mol
SMILES	CC(OP(C)(=O)F)C(C)(C)C
InChIKey	GRXKLBBBQUKJJZ-UHFFFAOYSA-N
PubChem CID	7305
ChEMBL	CHEMBL15910
ChEBI	CHEBI:9195
DTXSID	DTXSID2031906

Chemische & physikalische Eigenschaften

XLogP	2,1
Polarare Oberfläche (TPSA)	26,3
H-Brücken-Donoren	0
H-Brücken-Akzeptoren	3
Frei drehbare Bindungen	3
Schwere Atome	11
Formalladung	0
Komplexität	174
Stoffklassen	Toxic Gases & Vapors -> Chemical Weapons-> NIOSH Emergency Response Categories
LogP (Verteilungskoeffizient)	log Kow = 1.78
Geruch	Evolves odorless gasWhen pure: fruity odorwith impurities: oil of camphor odorAromatic odor of camphorWill have an odor similar to rotting fruitwith impurities may have a camphor-like smell
Dichte	1.0222 g/mL at 25 °CDensity: 1.026 at 20 °C1.022 @ 20°C1.0222 g/cm3(Temp: 25 °C)
Color/Form	Colorless liquidColorless transparent liquidColorless liquid which gives off a colorless vaporWhen pure, colorless liquidwith impurities, amber or dark brown
Löslichkeit	In water, 2.1X10+4 mg/L at 20 °CMiscible with both polar and nonpolar solvents
Corrosivity	Corrodes steel at the rate of 1X10-5 inch/month
Siedepunkt	198 °C198 °C @760 [mm Hg]182.5°C
Decomposition	When heated to decomposition, can emit highly toxic fumes of /phosphorus oxides/.
Schmelzpunkt	-42 °C-41.9°C
Dampfdichte	6.3 (Air = 1)
Geruchsschwelle	About 50% of 34 subjects (22 male and 12 female laboratory workers) detected the odor of soman in concentrations of 3.3-7.0 mg/cu m and described it as sweet, fruity or nutty. About 65% of the subjects had mild nasal and airway symptoms from the agent.Although soman has a camphor or fruity odor, the odor may not be noticeable enough to give people sufficient warning against a toxic exposure.
Aggregatzustand	liquid
Henry-Konstante	2.1×100 mol/(m3Pa) at 25℃, HSDB (2015)
EPA chemische Informationen	Phosphonofluoridic acid, methyl-, 1,2,2-trimethylpropyl ester (96-64-0)

Sicherheit & Vorschriften

Weitere Sicherheitsinformationen	- Indoor Air: Soman can be released into indoor air as a liquid spray (aerosol) or as a vapor.
Brandgefahren	For information on chemical warfare nerve agents see the ERG Criminal or Terrorist Use of CBR Agents. (ERG, 2024)
Brandpotenzial	Fire: "G" series Nerve Agents may be volatilized during a fire or be spread by efforts to extinguish the fire. Agents may be decomposed by heat to produce other toxic and/or corrosive gases. In addition, "G" series Nerve Agents may react with steam or water during a fire to produce toxic and/or corrosive vapors. Hydrogen produced by the action of the corrosive vapors on metals or other corrodible materials may be present. /"G" Series Nerve Agents/
Gesundheitsgefahren	For information on chemical warfare nerve agents see the ERG Criminal or Terrorist Use of CBR Agents. (ERG, 2024)
Gefahrenübersicht	Soman a colorless liquid with a fruity or oil of camphor odor and a vapor pressure of 0.4 mm Hg at 77 degrees F. It is relatively persistent in the soil. [Jane, p. 85-6] The LD50 on skin is 50 mg. The LCt50 is 70 mg-min/m3. Soman undergoes 'aging' in about two minutes. Treatment of casualties is more difficult than for other nerve agents that take longer to age. After two minutes, the usefulness of oximes is reduced. [USAMRICD, p. 107, 110] As little as one drop of VX on the skin can be fatal and 1 to 10 mL of GA, GB, or GD can be fatal. [ATSDR Medical Management] A potent cholinesterase inhibitor[Merck Index] See the disease, Organophosphate & carbamates, acute poisoning.
Reaktive Gruppe	Sulfonates, Phosphonates, and Thiophosphonates, Organic
Explosion Hazards	- When heated, vapors may form explosive mixtures with air, presenting an explosion hazard indoors, outdoors, and in sewers.
Special Reports	Gupta RC, ed. Handbook of Toxicology of Chemical Warfare Agents. Amsterdam: Academic Press (2009). This handbook provides in-depth information on chemical warfare agents and covers every aspect of deadly toxic chemicals used as weapons of mass destruction and employed in conflicts, warfare and terrorism.Marrs TC et alChemical Warfare Agents Toxicology and Treatment. 2nd edition Chichester, West Sussex, England: (2007) This book provides a comprehensive review of chemical warfare agents, assessing all available evidence regarding the medical, technical and legal aspects of their use.Langford RE: Introduction to Weapons of Mass Destruction: Radiological, Chemical, and Biological . New York, NY: John Wiley and Sons, Inc. (2004). This handbook provides the detailed information on nuclear, biological, and chemical weapons of mass destruction (WMD) that is required for policy decisions, response planning, and accurate presentation of information to the general public.National Research Council, Board on Environmental Studies and ToxicologyReview of the U.S. Army's Health Risk Assessments for Oral Exposure to Six Chemical-Warfare Agents (1999). National Academies Press, Washington, DC. The U.S. ARMY is under a congressional mandate and the Chemical Weapons Convention of January 1993 to destroy its entire stockpile of chemical munitions. To ensure that chemical contamination is reduced to safe concentrations at stockpile and NSCM sites before they are used for residential, occupational, or wildlife purposes, the U.S. Army requested that health-based exposure limits for GA, GB, GD, VX, sulfur mustard, and lewisite be developed to protect the public and the environment. The National Research Council subcommittee determined that the Army's interim RfDs for GA, GB, GD, and sulfur mustard were scientifically valid but concluded that the RfDs for VX and lewisite and the SF for sulfur mustard were too high. The bases for those conclusions are described in this report.[Available from, as of July 3, 2007: http://books.nap.edu/catalog.php?record_id=9644]For more Special Reports (Complete) data for SOMAN (11 total), please visit the HSDB record page.
Reactivity Alerts	Water-Reactive
Reactivity Profile	Acidic conditions produce hydrogen fluoridealkaline conditions produce isopropyl alcohol and polymers. When heated to decomposition or reacted with steam, it emits very toxic fumes of fluorides and oxides of phosphorus. Slightly corrosive to steel. Hydrolyzed by water.
Chemical Dangers	- Under acid conditions, soman hydrolyzes to form hydrofluoric acid (HF). See the emergency response card for hydrofluoric acid.
Physical Dangers	- Vapors are heavier than air. They will spread along the ground and collect and stay in poorly-ventilated, low-lying, or confined areas (e.g., sewers, basements, and tanks).
Brandbekämpfung	For information on chemical warfare nerve agents see the ERG Criminal or Terrorist Use of CBR Agents. (ERG, 2024)- Soman is combustible.
Erste Hilfe	For information on chemical warfare nerve agents see the ERG Criminal or Terrorist Use of CBR Agents. (ERG, 2024)
Firefighting Hazards	React with steam or water to produce toxic and corrosive vapors.
Expositionsschutz und Persönliche Schutzausrüstung	TIH (Toxic Inhalation Hazard) - Term used to describe gases and volatile liquids that are toxic when inhaled. Some are TIH materials themselves, e.g., chlorine, and some release TIH gases when spilled in water, e.g., chlorosilanes. [ERG 2016].
Brandbekämpfungsverfahren	Water mist, fog, and foam, CO2. Avoid using extinguishing methods that will cause splashing or spreading. ... Fire-fighting personnel should wear full protective clothing and respiratory protection during fire-fighting and rescue.
Reinigungsverfahren	Decontamination: Liquid:Small Areas: Puddles of liquid must be contained by covering with vermiculite, diatomaceous earth, clay, fine sand, sponges, or towels. Place the absorbed material into containers with a high density polyethylene liner. Decontaminate the area with copious amounts of aqueous sodium hydroxide solution (a minimum of 10 percent by weight). If sodium hydroxide solution is not available, then sodium carbonate may be used. Removal of porous material, including painted surfaces, that may have absorbed Nerve Agent liquid may be required as these materials could continue to re-release liquid and/or vapor after exposure has ceased. /"G" Series Nerve Agents/Decontamination: Solids, powders and solutions containing various types of bleach (NaOCl or Ca(OCl)2)DS2 (2% NaOH, 70% diethylenetriamine, 28% ethylene glycol monomethyl ether)towelettes moistened with NaOH dissolved in water, phenol, ethanol, and ammoniaDecontamination: Vapor: Small Areas: Ventilation. In heavily contaminated areas, decontamination with copious amounts of aqueous sodium hydroxide solution (a minimum of 10 percent by weight) may be required. If sodium hydroxide solution is not available, then sodium carbonate may be used. Removal of porous material, including painted surfaces, that may have absorbed Nerve Agent vapor may be required as these materials could continue to re-release vapor after exposure has ceased. /"G" Series Nerve Agents/Commercial ammonia-containing cleaners are also shown to be effective surface decontaminants for GD, but not for VX or HD.For more Cleanup Methods (Complete) data for SOMAN (6 total), please visit the HSDB record page.
Freisetung ohne Brand	For information on chemical warfare nerve agents see the ERG Criminal or Terrorist Use of CBR Agents. (ERG, 2024)
Entsorgungsverfahren	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 weaponsand that the destruction process can be verified under the provisions of this Convention. /Chemical warfare agents/Cover /spills/ with vermiculite, diatomaceous earth, clay, fine sand, sponges, and paper or cloth towels. Treat with large amounts of aqueous sodium hydroxide solution (minimum 10 % by weight). Scoop decontaminated material and place in approved container. After sealing, decontaminate the exterior and label. All leaking containers will be over packed with sorbent (e.g. vermiculite) placed between the interior and exterior containers. Label and dispose according to regulations. Conduct general area monitoring. If aqueous sodium hydroxide is not available, use following in the order of preference: Decontaminating Agent (DS2), Sodium Carbonate, and Supertropical Bleach Slurry (STB).SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.
Preventive Measures	Any chemical release will have its maximum harmful effect against unprotected individuals, so those who self-evacuate and the rapidly rescued will generally have the best survival and recovery prospects. Planners and incident commanders should bear in mind that by the time rescue efforts are mounted survivors are generally unlikely to be found in environments or circumstances that demand the wearing of self-contained respiratory protection. Health plans should also recognize that the level of meaningful assessment or treatment that can be carried out in the ... hot zone... will be very limited. ... Rapid rescue from the hot zone represents the most practical and effective operational approach and in most major releases the most effective health response is likely to be focused in the more lightly contaminated ("warm") and uncontaminated ("cold") zones. There - and at receiving hospitals - the main emphasis should be on providing the type of respiratory and physical protection for staff so that secondary contamination is prevented. Unprotected staff should not come into contact with undecontaminated patients. /Chemical warfare agents/Identifying the chemical(s) involved and measuring its concentration would obviously be helpful... but may not prove possible until more specialist support arrives and so responders are likely to be reliant on environmental indicators and/or the signs and symptoms displayed by victims. In practice, information gathered during clinical examination may be most useful. /Chemical warfare agents/Decontaminating "non-ambulatory" patients is very staff-intensive and time-consuming but should generally be the primary focus of health effort at the scene. ... Dealing with those who are "ambulatory" is a quicker process as they should normally be able to carry out their own decontamination under supervision ... /Chemical warfare agents/Current recommendations for decontamination of civilians exposed to chemicals as a result of release of such substances by terrorists. ... decontamination of the entire body - not just, for example, the hands and face, should be undertaken. All clothing should be removed and placed in sealed polythene bags. Jewelry, watches, money and other personal possessions should be collected and placed in labeled polythene bags. Two approaches to decontamination are feasible: the "bucket and sponge" method taking one patient at a time, or the mass decontamination approach with attendants supervising the passage of a queue of people through some communal shower unit. Patients who have been injured or are unable to help themselves should be decontaminated by trained attendants using a system in which a stretcher is placed on a table equipped with rollers that allows transfer of the decontaminated patient to a clean stretcher, and ambulance and to hospital. Some authorities have argued for the addition of liquid soap to the water used in automated decontamination units. This will speed the process of material but the interaction of water and soap leading to foaming when passed through a jet should be considered. Whatever means of decontamination are used it should be thorough. This means that each patient will need some minutes of attention: up to 15 or so minutes may be needed to deal with an incapacitated patient. Whatever system is used, plans for dealing with waste water and any decontaminants used should be devised and practiced in advance of an incident occurring. Waste water may be collected inside an area protected by inflatable "bunds". ...If waste water is to be allowed to run into drains, the local water company should be informed. ...Suitable towels and clothing must be provided, modesty should be preserved and consideration given to how people are to make their way home. /Chemical warfare agents/For more Preventive Measures (Complete) data for SOMAN (15 total), please visit the HSDB record page.
Isolation and Evacuation	For initial isolation and protective action distances for chemical warfare nerve agents see the Chemical Warfare Agents table in the ERG Criminal or Terrorist Use of CBR Agents. (ERG, 2024)
Effects of Short Term Exposure	Limited data are available on chronic or repeated exposure to soman. The available data however, suggest that soman is not a human carcinogen, reproductive toxin, or developmental toxin. Limited data suggest that chronic or repeated exposure to soman may result in a delayed postural sway and/or impaired psychomotor performance (neuropathy).
Protective Action Criteria (PAC)	0.00018 [ppm]0.0022 [ppm]0.017 [ppm]
Wechselwirkungen	To date, treatment of organophosphate (OP) poisoning shows several shortcomings, and OP-victims might suffer from lasting cognitive deficits and sleep-wake disturbances. In the present study, long-term effects of soman poisoning on learning ability, memory and neurogenesis were investigated in rats, treated with the anticholinergic atropine and the oxime HI-6 for reactivation of soman-inhibited acetylcholinesterase. /The authors/ also investigated whether sub-chronic treatment with the reported neurogenesis enhancer olanzapine would stimulate neurogenesis and possibly normalize the anticipated long-term deleterious effects of soman intoxication. Animals were treated with HI-6 (125 mg/kg i.p.), followed after 30 min by soman (200 ug/kg s.c.) and atropine sulphate (16 mg/kg i.m.) 1 min thereafter. Soman poisoning led to an elevation of extracellular acetylcholine levels to 1500% over baseline values as assessed by striatal microdialysis. Brain acetylcholinesterase was inhibited over 95%. This was accompanied by short recurrent seizures lasting for 40 min. Osmotic minipumps releasing olanzapine (7.5 mg/kg/day) or vehicle were subcutaneously implanted 24 hr post-intoxication. After drug delivery for 4 weeks, newborn cells were BrdU labeled. Learning and memory performance were assessed 8 weeks after soman poisoning, followed by analysis of surviving newborn cells (BrdU) and neurogenesis (doublecortin, DCX). Eight weeks after soman-intoxication a significantly impaired learning ability was found that was paralleled by significantly lower numbers of DCX-positive cells but no changes in the number of BrdU-labeled cells. Apparently, the present Olanzapine regime was ineffective. /The authors/ conclude that soman poisoning has long lasting effects on learning ability, a finding that was accompanied by impaired neurogenesis. /They/ confirm a correlation between impaired neurogenesis and cognitive deficits...Nerve agents irreversibly inhibit acetylcholinesterase (AChE), leading to cholinergic crisis and death at acute exposure levels. The complexity, delayed onset, and persistent nature of nerve agent induced CNS effects need to be elucidated to block their multiple effects. In the present study gene expression and phosphoprotein profile of certain key neuronal proteins were studied after soman exposure. Quantitative real time PCR analysis of c-Fos, Bax, CREB and caspase 3 genes in the hippocampus, cortex and cerebellum showed that only c-Fos and Bax mRNA expression was increased significantly. Western blot analysis also confirmed the induction of c-Fos at early time points both at 0.5 and 1.0 LD(50) dose of soman exposure. Acute soman exposure caused perturbations in the phosphorylation status of ERK, JNK, p38 MAPK, CREB, c-Jun and NF-?B in all the three brain regions. The primary target for soman toxicity, AChE was inhibited in blood and brain up to 90%. Therapeutic treatment comprising of HI-6, atropine and diazepam has completely protected animals from death and reactivated soman inhibited AChE up to 40% in the plasma and RBC. This therapeutic regime also reduced soman induced Bax expression to near control levels, but could not reverse the soman induced changes in c-Fos expression and phosphorylation levels completely. Results suggest that exposure to soman caused persistent changes in these key brain proteins, which could lead to the development of complex neurotoxic effects and there is an urgent need for development of better drugs to stop multiple effects of nerve agents poisoning.Two guinea pig models were used to study the anticonvulsant potency of diazepam, midazolam, and scopolamine against seizures induced by the nerve agents tabun, sarin, soman, cyclosarin, O-ethyl S-(2-(diisopropylamino)ethyl)methylphosphonothioate (VX), and O-isobutyl S-(2-diethylamino)ethyl)-methyl phosphonothioate (VR). Animals instrumented for electroencephalogram recording were pretreated with pyridostigmine bromide (0.026 mg/kg im) 30 min before challenge with 2 x LD50 (s.c.) of a nerve agent. In model A, atropine sulfate (2.0 mg/kg im) and pyridine-2-aldoxime methylchloride (2-PAM25.0 mg/kg im) were given 1 min after nerve agent challenge, and the tested anticonvulsant was given (im) 5 min after seizure onset. In model B, a lower dose of atropine sulfate (0.1 mg/kg im) was given along with 2-PAM 1 min after nerve agent challenge, and the anticonvulsant was given at seizure onset. With the lower dose of atropine, seizure occurrence increased to virtually 100% for all agentsthe time to seizure onset decreased for sarin, cyclosarin, and VXthe signs of nerve agent intoxication were more severeand coma resulted frequently with cyclosarin. The anticonvulsant ED50 doses for scopolamine or diazepam were, in general, not different between the two models, whereas the anticonvulsant ED50 values of midazolam increased 3- to 17-fold with the lower atropine dose. Seizure termination times were not systematically affected by the different doses of atropine. The order of anticonvulsant effectiveness within each model was scopolamine > or = midazolam > diazepam. The findings indicate that the dose of atropine given as antidotal therapy can significantly influence measures of nerve agent toxicity and responsiveness to anticonvulsant therapy.The current treatment for soman-intoxication is the oxime HI 6 together with the anticholinergic drug atropine. This antidote combination is known to have effects on seizures, respiratory system, blood pressure and animal survival in experiments. ... This paper ... /focuses/ on the cytokine IL-1beta induction in the rat brain after soman-intoxication (1.0 x LD50 and 1.1 x LD50) and during antidote treatment. ... IL-1beta levels in rat brain /were analyzed/ to determine the effects of time of antidote HI 6 and atropinethe effects of different combinations of HI 6 and atropineand also the effects of antidotes diazepam and atropine following soman-intoxication. ... The initiation of the antidote combination of HI 6 and atropine following soman-intoxication was crucial for successful treatment. The study also demonstrated that atropine alone was more effective against IL-1beta up-regulation after soman-intoxication within the 2-hr time frame, than the combination of the HI 6 and atropine, the therapy of choice in many countries. Furthermore, treatment with a combination of diazepam and atropine maintained IL-1beta levels at normal when administered at the onset of the seizures following soman exposure. Soman-intoxicated groups without seizures did not have an elevated cytokine level. ...For more Interactions (Complete) data for SOMAN (43 total), please visit the HSDB record page.
Ökotoxizitätswerte	LD50 Frog ip 251 ug/kg /from table/
Umweltverhalten	TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 103(SRC), determined from a log Kow of 1.78(2) and a regression-derived equation(3), indicates that soman is expected to have high mobility in soil(SRC). Soil sorption studies using different soil types noted that soman applied to the surface can adsorb to soil with increasing resistance to desorption in the absence of sufficient moisture and water(4)simulated rainfall events were shown to desorb the soman resulting in volatilization to the atmosphere(4). Volatilization of soman from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 4.7X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 0.41 mm Hg(5), and water solubility, 2.1X10+4 mg/L(6). Soman has been observed to volatilize from both wet and dry surfaces(7,8). Soman has an aqueous hydrolysis half-life of about 60 hours at pH 6 and 25 °C(7). Soman decomposes in soil via hydrolysis and is most stable in the medium pH range from 4 to 6 and is self-buffering in that range(9). Extrapolation of aqueous hydrolysis rates to soil must be used with caution(4)susceptibility to hydrolysis on soil surfaces can depend upon dissemination method to the soil, soil properties, degree of adsorption, organic matter content, pH, and moisture content(4). However, hydrolysis is expected to be an important fate process in soil(4). The persistence of soman on soil under different weather conditions was found as follows(10): 15 °C, sunshine and a slight wind, soman persisted in soil 2.5 to 5 daysat 10 °C, rainfall and foul weather, soman persisted in soil 3 to 36 hoursat -10 °C, sunshine and calm on snow, soman persisted in soil 1 to 6 weeks(10). Another soil study found that the persistence of soman in soil may be expected for days-to-months timeframe depending upon soil type(4). Several species of bacteria, such as Alteromonas sp. and Flavobacterium sp. are capable of degrading G-type nerve agents(7), but data are not available to assess the environmental importance of biodegradation(SRC).AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 103(SRC), determined from a log Kow of 1.78(2) and a regression-derived equation(3), indicates that soman is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(4) based upon an estimated Henry's Law constant of 4.7X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 0.41 mm Hg(5), and water solubility, 2.1X10+4 mg/l(6). Using this Henry's Law constant and an estimation method(4), volatilization half-lives for a model river and model lake are 11 and 82 days, respectively(SRC). Soman hydrolyzes in water at neutral or slightly acid pH and more rapidly under strong acid or alkaline conditions(7). The half-life of soman in water at pH 7, 20 °C and 30 °C has been reported as 82 and 22 hours, respectivelythe half-life of soman in water at pH 7.6, 20 and 30 °C has been reported as 41 and 9.6 hours, respectively(8). According to a classification scheme(9), an estimated BCF of 7(SRC), from its log Kow(2) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is low. Biodegradation data in water were not available(SRC,2013).ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), soman, which has a vapor pressure of 0.41 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase soman is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC)the half-life for this reaction in air is estimated to be 8 hours(SRC), calculated from its rate constant of 5.0X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). The UV absorption spectrum of soman in cyclohexane solution exhibits little to no absorption above 290 nm(4)therefore, direct photolysis by sunlight in the environment is not expected to be an important fate process(SRC). Soman vapor pressure studies attempting to incorporate ambient humidity found that soman vapor reacted with water vapor probably through hydrolysis(5)therefore, reaction of soman vapor with water vapor may be an important fate process in the atmosphere(SRC).
Unerwünschte Wirkungen	Other Poison - Organophosphate
Expositionspfade	Soman can be absorbed into the body by inhalation, ingestion, skin contact, or eye contact. Ingestion is an uncommon route of exposure.
Toxizitätsübersicht	Toxicology: Effects: Nerve Agents are the most toxic of the known chemical agents. Liquids or vapors from these agents are hazardous and can cause death within minutes after exposure. Nerve Agents disrupt the function of the nervous system by interfering with the enzyme acetylcholinesterase. The major effects will be on skeletal muscles, certain organs, and the central nervous system. These compounds are similar to, but much more deadly than, agricultural organophosphate pesticides. Pathways: "G" series Nerve Agents are hazardous through inhalation, skin and eye exposure, ingestion, and abraded skin (e.g., breaks in the skin or penetration of skin by debris). /"G" Series Nerve Agents/
Signs and Symptoms	- Contracted or pinpoint pupils (miosis), redness of the membranes (conjunctiva), pain in and around the eye, dim and/or blurred vision, sensation of pressure with heaviness, reflex nausea and vomiting (emesis).- Nausea, vomiting (emesis), diarrhea, abdominal pain, cramping.- Mild to moderate: Health effects may be immediate or may be delayed up to 18 hours. Profuse sweating (diaphoresis) and muscular twitching (fasciculations) at the site of contact, nausea, vomiting (emesis), diarrhea, and weakness (malaise).
Medical Surveillance	Laboratory criteria for diagnosis. Biologic: A case in which nerve agents in urine are detected, as determined by CDC or one of five LRN laboratories that have this capacity. Decreased plasma or red blood cell cholinesterase levels based on a specific commercial laboratory reference range might indicate a nerve agent or organophosphate exposurehowever, the normal range levels for cholinesterase are wide, which makes interpretation of levels difficult without a baseline measurement or repeat measurements over time. -OR - Environmental: Detection of organophosphate pesticides in environmental samples, as determined by FDA. However, a confirmation test for nerve agents in environmental samples is not available. /Nerve Agents/Routine laboratory studies for all admitted patients include CBC, glucose, and serum electrolyte determinations. Chest X-ray and pulse oximetry (or ABG measurements) are recommended for severe exposures. Symptomatic and asymptomatic patients suspected of significant exposure should have determinations of red blood cell (RBC) cholinesterase activity, the most useful test for nerve agent poisoning. Severe symptoms of toxicity are usually present when more than 70% of RBC cholinesterase is inhibited. However, there is no correlation between cholinesterase activity and severity of topical signs and symptoms (e.g., miosis, rhinorrhea, dyspnea). If this test is not available, plasma cholinesterase can be measured.Effects from skin exposure to liquid nerve agent may not develop for up to 18 hours following exposure. Patients who have inhalation exposure and who complain of chest pain, chest tightness, or cough should be observed and examined periodically for 6 to 12 hours to detect delayed-onset bronchitis, pneumonia, pulmonary edema, or respiratory failure. Patients who have severe exposure should be evaluated for persistent CNS sequelae. Patients should be advised to avoid organophosphate insecticide exposure until sequential RBC cholinesterase activity (measured at weekly to monthly intervals) has stabilized in the normal range, a process that may take 3 to 4 months after severe poisoning.
Soil Adsorption/Mobility	The Koc of soman is estimated as 103(SRC), using a log Kow of 1.78(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that soman is expected to have high mobility in soil. Clay converted to a calcium form and dehydrated at 105 °C adsorbed 30.0 mg soman(4). At 2.0, 2.3, 3.0 and 9.1 percent moisture, soman sorption in the clay was 91.2, 94.4, 91.3, and 43.1 mg/g(4). If soman is sorbed while soil is wet, desorption occurs quicklyif the soil is dry for 2 or 3 days after uptake, desorption is much more difficult. An increase in soil temperature generally leads to a decrease in adsorption of soman(5). Soil sorption studies using different soil types noted that soman applied to the surface can adsorb to soil with increasing resistance to desorption in the absence of sufficient moisture and water(6)simulated rainfall events were shown to desorb the soman resulting in volatilization to the atmosphere(6).
Human Toxicity Excerpts	/HUMAN EXPOSURE STUDIES/ ... Soman, 10-40 mg in 0.5-mg droplets, was placed on the forearms of 32 subjects. The mean erythrocyte cholinesterase inhibition increased from 13% to 27% as the dose increased./HUMAN EXPOSURE STUDIES/ ... 0.2-6.1 mg of soman was placed on the forearms of subjects in an open ward. Several subjects and the investigators had eye effects from agent vapor, but there were no systemic effects or inhibition of erythrocyte cholinesterase./HUMAN EXPOSURE STUDIES/ ... 2.0-7.8 mg /soman/ was applied to the forearm skin of 25 subjects. Most had localized sweating at the site of application. On several days of the study when the ambient temp was over 80 °F (27 °C) and relative humidity over 85%, the cholinesterase activity inhibition was slightly greater than on the other days when temp and humidity were lower. Otherwise, maximal inhibition of erythrocyte cholinesterase activity occurred between 2 and 24 hour after exposure, and the maximal inhibition was to 69% of baseline./SIGNS AND SYMPTOMS/ Latency Period: Vapor: Effects from vapor exposure begin to appear 30 seconds to 2 minutes after exposure. Liquid: There is almost always a latent period with no visible effects between the time of exposure and the onset of symptoms. Effects from liquid exposure begin to appear from several minutes up to 18 hours after exposure. Onset of symptoms from exposure to large amounts of liquid agent may appear as rapidly as 1 minute after exposure. Generally, the more rapid the onset of symptoms, the larger the amount of agent involved in the exposure. /"G" Series Nerve Agents/For more Human Toxicity Excerpts (Complete) data for SOMAN (27 total), please visit the HSDB record page.
Artificial Pollution Sources	Soman's production may result in its release to the environment through various waste streamsits use as a military nerve gas(1) and chemical warfare agent(2) will result in its direct release to the environment(SRC).
Environmental Biodegradation	AEROBIC: Data were not available on the biodegradation of soman under environmental conditions(1). Pseudomonas melophthora and Pseudomonas testosteroni were found capable of degrading O-pinacolyl hydrogen methylphosphonate, a primary metabolite of soman. Generally, few microorganisms found in soil can break down the C-P bond in soman. The biodegradation process is assumed to be promoted by warm soil temperatures, adequate moisture and the presence of organic matter(2). The enzymes parathion hydrolase, squid hepatopancreas, and Alteromonas sp. JD6.5 were found to have specific activity for soman at 5, 60 and 600 umol/min/mg, respectively, conditions unknown(3). Soman can be biotransformed via O-dealkylation and C-dealkylationhowever, the final products would remain toxic(4). Several species of bacteria, such as Alteromonas sp. and Flavobacterium sp. are capable of degrading G-type nerve agents(5).
DHS Chemicals of Interest (COI)	SomanCUM 100gChemical Weapons/Chemical Weapons Precursors chemical material that, if stolen or diverted, can be converted into weapons using simple chemistry, equipment, or techniques.
UN-Transportnummer	2810
Toxizität	LD50 in mice (mg/100 g): 0.062 i.p.0.78 dermally (Loomis, Salafsky)
Gefahrenklasse	6.1(a)
Verpackungsgruppe	I
Gefahrstoffdaten	96-64-0(Hazardous Substances Data)

Anwendungen & Verwendung

Beschreibung

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.

Verwenden

Chemical warfare agent.