소만

Toxic Gases & Vapors -> Chemical Weapons

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log Kow = 1.78

1.78

Evolves odorless gas

When pure: fruity odor; with impurities: oil of camphor odor

Aromatic odor of camphor

Will have an odor similar to rotting fruit; with impurities may have a camphor-like smell

1.0222 g/mL at 25 °C

Density: 1.026 at 20 °C

1.022 @ 20°C

Colorless liquid

Colorless transparent liquid

Colorless liquid which gives off a colorless vapor

When pure, colorless liquid; with impurities, amber or dark brown

In water, 2.1X10+4 mg/L at 20 °C

Miscible with both polar and nonpolar solvents

198 °C

198 °C @760 [mm Hg]

-42 °C

-42 °C

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.

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/

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.

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 al; Chemical 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 Toxicology; Review 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.

Acidic conditions produce hydrogen fluoride; alkaline 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.

For information on chemical warfare nerve agents see the ERG Criminal or Terrorist Use of CBR Agents. (ERG, 2024)

- Soman is combustible.

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].

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 ammonia

Decontamination: 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.

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. /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.

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.

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).

0.00018 [ppm]

0.0022 [ppm]

0.017 [ppm]

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-PAM; 25.0 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 agents; the time to seizure onset decreased for sarin, cyclosarin, and VX; the signs of nerve agent intoxication were more severe; and 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 atropine; the effects of different combinations of HI 6 and atropine; and 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.

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 days; at 10 °C, rainfall and foul weather, soman persisted in soil 3 to 36 hours; at -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, respectively; the 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).

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/

- 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).

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 exposure; however, 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.

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 quickly; if 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 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.

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-dealkylation; however, 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).

Soman

CUM 100g

CUM 100g

Chemical Weapons/Chemical Weapons Precursors chemical material that, if stolen or diverted, can be converted into weapons using simple chemistry, equipment, or techniques.

Exposure to nerve agents and other organophosphorus acetylcholinesterases used in industry and agriculture can cause death, or brain damage, producing long-term cognitive and behavioral deficits. Brain damage is primarily caused by the intense seizure activity induced by these agents. Identifying the brain regions that respond most intensely to nerve agents, in terms of generating and spreading seizure activity, along with knowledge of the physiology and biochemistry of these regions, can facilitate the development of pharmacological treatments that will effectively control seizures even if administered when seizures are well underway. Here, /investigators/ contrast the pathological (neuronal damage) and pathophysiological (neuronal activity) findings of responses to nerve agents in the amygdala and the hippocampus, the two brain structures that play a central role in the generation and spread of seizures. The evidence so far suggests that exposure to nerve agents causes significantly more damage in the amygdala than in the hippocampus. Furthermore, in in vitro brain slices, the amygdala generates prolonged, seizure-like neuronal discharges in response to the nerve agent soman, at a time when the hippocampus generates only interictal-like activity. In vivo experiments are now required to confirm the primary role that the amygdala seems to play in nerve agent-induced seizure generation.

Chronic low dose exposure to organophosphorus poisons (OP) results in cognitive impairment. Studies in rats have shown that OP interfere with microtubule polymerization. Since microtubules are required for transport of nutrients from the nerve cell body to the nerve synapse, it has been suggested that disruption of microtubule function could explain the learning and memory deficits associated with OP exposure. Tubulin is a major constituent of microtubules. /Investigators/ tested the hypothesis that OP bind to tubulin by treating purified bovine tubulin with sarin, soman, chlorpyrifos oxon, diisopropylfluorophosphate, and 10-fluoroethoxyphosphinyl-N-biotinamidopentyldecanamide (FP-biotin). Tryptic peptides were isolated and analyzed by mass spectrometry. It was found that OP bound to tyrosine 83 of alpha tubulin in peptide TGTYR, tyrosine 59 in beta tubulin peptide YVPR, tyrosine 281 in beta tubulin peptide GSQQYR, and tyrosine 159 in beta tubulin peptide EEYPDR. The OP reactive tyrosines are located either near the GTP binding site or within loops that interact laterally with protofilaments. It is concluded that OP bind covalently to tubulin, and that this binding could explain cognitive impairment associated with OP exposure.

Some organophosphorus compounds are toxic because they inhibit acetylcholinesterase (AChE) by phosphylation of the active site serine, forming a stable conjugate: Ser-O-P(O)-(Y)-(XR) (where X can be O, N, or S and Y can be methyl, OR, or SR). The inhibited enzyme can undergo an aging process, during which the X-R moiety is dealkylated by breaking either the P-X or the X-R bond depending on the specific compound, leading to a nonreactivatable enzyme. Aging mechanisms have been studied primarily using AChE. However, some recent studies have indicated that organophosphate-inhibited butyrylcholinesterase (BChE) may age through an alternative pathway. /This/ work utilized matrix-assisted laser desorption/ionization-time-of-flight mass spectrometry to study the aging mechanism of human BChE inhibited by dichlorvos, echothiophate, diisopropylfluorophosphate (DFP), isomalathion, soman, sarin, cyclohexyl sarin, VX, and VR. Inhibited BChE was aged in the presence of H2(18)O to allow incorporation of (18)O, if cleavage was at the P-X bond. Tryptic-peptide organophosphate conjugates were identified through peptide mass mapping. /The/ results showed no aging of VX- and VR-treated BChE at 25 degrees C, pH 7.0. However, BChE inhibited by dichlorvos, echothiophate, DFP, soman, sarin, and cyclohexyl sarin aged exclusively through O-C bond cleavage, i.e., the classical X-R scission pathway. In contrast, isomalathion aged through both X-R and P-X pathways; the main aged product resulted from P-S bond cleavage and a minor product resulted from O-C and/or S-C bond cleavage.

Nerve agents phosphonylate a serine hydroxyl group in the active site of the enzyme, acetylcholinesterase (AChE), which results in accumulation of acetylcholine and, in turn, causes enhancement and prolongation of cholinergic effects and depolarisation blockade. The rate of spontaneous reactivation of AChE is variable, which partly accounts for differences in acute toxicity between the nerve agents. With soman in particular, an additional reaction occurs known as 'aging'. This consists of monodealkylation of the dialkylphosphonyl enzyme, which is then resistant to spontaneous hydrolysis and reactivation by oximes. Monodealkylation occurs to some extent with all dialkylphosphonylated AChE complexes; however, in general, is only of clinical importance in relation to the treatment of soman poisoning, where it is a very serious problem. With soman, aging occurs so fast that no clinically relevant spontaneous reactivation of AChE occurs before aging has taken place. Hence, recovery of function depends on resynthesis of AChE. As a result, it is important that an oxime is administered as soon after soman exposure as possible so that some reactivation of AChE occurs before all the enzyme becomes aged. Even though aging occurs more slowly and reactivation occurs relatively rapidly in the case of nerve agents other than soman, early oxime administration is still clinically important in patients poisoned with these agents.

For more Mechanism of Action (Complete) data for SOMAN (15 total), please visit the HSDB record page.

The toxicokinetics of the four stereoisomers of the nerve agent C(+ or -)P(+ or -)-soman was analysed in cerebrospinal fluid (CSF) and blood in anaesthetized, spontaneously breathing pigs during a 90-min period after injection of soman. All four isomers of soman were detected in both blood and CSF samples. The relatively non-toxic C(+ or -)P(+) isomers disappeared from the blood stream and cerebrospinal fluid within the first minute, whereas the levels of the highly toxic C(+ or -)P(-) isomers could be followed for longer, depending on the dose.

Chemicals that are used to cause the disturbance, disease, or death of humans during WARFARE.

Drugs that inhibit cholinesterases. The neurotransmitter ACETYLCHOLINE is rapidly hydrolyzed, and thereby inactivated, by cholinesterases. When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. Cholinesterase inhibitors are widely used clinically for their potentiation of cholinergic inputs to the gastrointestinal tract and urinary bladder, the eye, and skeletal muscles; they are also used for their effects on the heart and the central nervous system.

Substances that act in the brain stem or spinal cord to produce tonic or clonic convulsions, often by removing normal inhibitory tone. They were formerly used to stimulate respiration or as antidotes to barbiturate overdose. They are now most commonly used as experimental tools.

/G-agents/ are ... readily absorbable through not only the lung and eyes but also the skin and intestinal tract without producing any irritation or other sensation on the part of the exposed individual. /G-agents, SRP: such as soman/

Most organophosphate compounds are ... absorbed from skin, conjunctiva, gastrointestinal tract, & lung. /Organophosphate compounds/

Blood levels of the four stereoisomers of the nerve agent C(+/-)P(+/-)-soman were analyzed gas chromatographically in anesthetized, artificially respirated and atropinized rats, guinea pigs and marmosets at iv doses of C(+/-)P(+/-)-soman corresponding with 1-6 LD50. The relatively nontoxic C(+/-)P(+/-)-isomers disappear within a few minutes from the blood stream of all three species, whereas the levels of the highly toxic C(+/-)P(-)-isomers remain toxicologically relevant for periods of 50-100 min in three species of doses of 2-3 LD50. Elimination pathways were quantified using carbon-14 labeled soman stereoisomers. Whereas the C(+/-)P(+)-isomers are largely eliminated by way of enzymatic hydrolysis, the major elimination pathway for the C(+/-)P(-)-isomers is binding to various proteins, in competition with binding to target acetylcholinesterase. Intraspecies nonlinearity with dose in the toxicokinetics of the C(+/-)P(-)-isomers is related to heterogeneous reactivity of the binding sites. Interspecies nonlinearity is probably due to decreasing amounts of binding sites in the order rats greater than guinea pigs greater than primates, leading to increasing "toxico-availability" in the reversed order.

Incubation of both sarin and soman with human plasma has shown that binding occurs to a tyrosine residue. Similar binding occurs when sarin and soman are incubated with human serum albumin. This binding may provide an important biological marker, which retains full structural information concerning the identity of the agent, in cases of allegations of chemical warfare use.

For more Absorption, Distribution and Excretion (Complete) data for SOMAN (6 total), please visit the HSDB record page.

Chemical warfare

Chemical warfare agent

Military nerve gas

Soman (military designation GD) is one of the nerve agents, which are the most toxic of the known chemical warfare agents. It has an odor like camphor or rotting fruit. 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. Nerve agents are chemically similar to organophosphate pesticides and exert their effects by interfering with the normal function of the nervous system.

Soman is listed in the CWC /Chemical Weapons Convention/ Annex on Chemicals under Schedule 1.

/The Chemical Weapons Convention (CWC) is an international treaty which bans the development, production, stockpiling, and transfer or use of chemical weapons. The Convention mandates the destruction and prohibition of chemical weapons and related facilities and provides for restrictions on international trade in toxic chemicals and precursors./ The Convention's monitoring and verification measures involve submission of declarations regarding ... /Schedule 1, 2, and 3 chemicals/ and inspections by the Organization for the Prohibition of Chemical Weapons of the facilities where these chemicals are produced. ... Schedule 1 lists chemicals considered to pose a high risk to the object and purpose of the Convention by virtue of their high potential for use in activities prohibited by the CWC. These chemicals have little or no use for peaceful purposes in commercial or industrial trade. ... Schedule 1 also lists precursor chemicals that may be used in the final single technological stage of production of any of the toxic chemicals listed in the schedule.

The three most active G-agents are tabun, ethyl phosphorodimethylamidocyanidate ... (Chemical Agent Symbol GA) ... ; sarin, isopropyl methylphosphonofluoridate ... (GB) ... ; and soman, pinacolyl methylphosphonofluoridate ... (GD). ... The G-agent liquids under ordinary atmospheric conditions have sufficiently high volatility to permit dissemination in vapor form. They are generally colorless, odorless or nearly so, and are readily absorbable through not only the lungs and eyes but also the skin and intestinal tract without producing any irritation or other sensation on the part of the exposed individual. These agents are sufficiently potent so that even a brief exposure may be fatal. Death may occur in 1-10 min, or be delayed for 1-2 hr depending on the concentration of the agent.

Discovery of nerve agents in Germany led to the availability of a class of compounds at least one order of magnitude more lethal than previously known where death might occur in a matter of minutes instead of hours. Nerve agents are part of a class known as organophosphorus compounds, and were first synthesized in 1854, but their development as warfare agents did not occur until 80 years later. The first military nerve agent, ethyl phosphorodimethylamidocyanidate, known as tabun, or chemical agent symbol GA, was synthesized in 1936 by Schrader while searching for more effective agricultural organophosphorate insecticides at the German chemical firm of IG Farbenindustrie. Two years later, he synthesized a second nerve agent, isopropyl methylphosphonofluoridate, now known as Sarin or GB. In 1944, a third nerve agent, pinacolyl methylphosphonofuoridate, now known as Soman or GD, was synthesized.

For more General Manufacturing Information (Complete) data for SOMAN (10 total), please visit the HSDB record page.