Sarin

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

- Sarin 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].

This chemical is a combustible liquid. Poisonous gases including phosphorus oxides and fluoride are produced in fire. Complete protection required; have available decontaminants (bleach, alkali) and atropine. Use dry chemical, carbon dioxide, or foam extinguishers. Vapors are heavier than air and will collect in low areas. Containers may explode in fire. Storage containers and parts of containers may rocket great distances, in many directions. If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Notify local health and fire officials and pollution control agencies. From a secure, explosion-proof location, use water spray to cool exposed containers. If cooling streams are ineffective (venting sound increases in volume and pitch, tank discolors, or shows any signs of deforming), withdraw immediately to a secure position. If employees are expected to fight fires, they must be trained and equipped in OSHA 1910.156.

Water, fog, foam, CO2. Avoid methods that cause splashing or spreading.

To fight fire, use foam, carbon dioxide, dry chemical.

Where possible automatically pump liquid from drums or other storage containers to process containers. Sources of ignition such as smoking and open flames are prohibited where this chemical is handled, used, or stored. Metal containers involving the transfer of this chemical should be grounded and bonded.

Cover 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: Sodium Carbonate, and Supertropical Bleach Slurry (STB).

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: 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/

Evacuate and restrict persons not wearing protective equipment from area of spill or leak until cleanup is complete. Remove all ignition sources. Ventilate area of spill or leak. Rapidly hydrolyze by dilute aqueous sodium hydroxide or sodium carbonate forming relatively non-toxic acid. Decontaminants include bleach slurry, dilute alkali, hot soapy water, steam and ammonia. Absorb liquids in vermiculite, dry sand, earth, peat, carbon, or a similar material and deposit in sealed containers. Keep this chemical out of confined spaces, such as a sewer, because of the possibility of an explosion, unless the sewer is designed to prevent the build up of explosive concentrations. It may be necessary to contain and dispose of this chemical as a hazardous waste. If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Contact your Department of Environmental Protection or your regional office of the federal EPA for specific recommendations. If employees are required to clean-up spills, they must be properly trained and equipped. OSHA 1910.120(q) may be applicable.

For more Cleanup Methods (Complete) data for SARIN (7 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.

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/

Limited data are available on chronic or repeated exposure to sarin. The available data however, suggest that sarin is not a human carcinogen, reproductive toxin, or developmental toxin. Limited data suggest that chronic or repeated exposure to sarin may result in a delayed postural sway and/or impaired psychomotor performance (neuropathy).

A time-course study was carried out to measure the acetylcholinesterase (AChE) gene expression in the brain of female rats exposed to different doses of sarin and physostigmine. Short-term effects were studied with an acute single subcutaneous dose (s.c.) of 80 ug kg(-1) (0.5 x LD50) sarin. Cortex and cerebellum showed a significant decline in AChE mRNA expression at 2.5, 24 and 72 hr. Biochemical studies showed that plasma butrylcholinesterase (BChE) and brain AChE activities were significantly decreased at 2.5 hr, which came back to near control values by 24 hr in both cases. For long-term chronic studies, three groups of female rats received daily doses of physostigmine (0.1 mg kg(-1) day(-1)) intramuscularly (i.m.), sarin (15 ug kg(-1) day(-1)) s.c. independently and a combined dose of physostigmine (i.m.) (0.1 mg kg(-1) day(-1)) followed by sarin (s.c.) (15 ug kg(-1) day(-1)) continuously for 30 days. Differential AChE mRNA levels in cortex and cerebellum of rat brain were observed after 30 days and after a lag period of another 30 days with no further administration. Plasma (BChE) and brain (AChE) showed irregular inhibition profile in biochemical studies at 30 days and returned to control levels after 60 days. The acute single subcutaneous administration of sarin for short-term as well as chronic long-term studies showed that AChE inhibition alone does not lead to observed changes in mRNA expression of AChE gene. These observations further suggest that route of administration as well as dose exposure regimen also contributes to the regulation of AChE mRNA expression.

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 organophosphorous nerve agent sarin (GB) and the carbamate pyridostigmine bromide (PB) both inhibit acetylcholinesterase (AChE), leading to overstimulation of muscarinic receptors. Both GB and PB produce miosis through stimulation of ocular muscarinic receptors. ... Rats were injected im with saline, 0.04 mg/kg, 0.5 mg/kg, or 1.4 mg/kg of PB twice daily for 8 consecutive days. After day 3, animals injected with 1.4 mg/kg PB developed miotic tolerance. Twenty-four (24) hr following the final PB injection, the rats were exposed to GB vapor (4.0 mg/cu m). A similar magnitude of miosis was observed in all groups after GB exposure. However, the rate of recovery of pupil size in animals pretreated with 0.5 and 1.4 mg/kg PB was significantly increased. Twenty (20) hr following exposure to GB vapor, the pupils of animals pretreated with 1.4 mg/kg PB had recovered to 77% +/- 4% of their pre-exposure baseline, whereas the saline-injected controls had recovered to only 52% +/- 2% of their pre-exposure baseline. The increased rate of recovery does not appear to be a result of protection of pupillary muscarinic receptors by the higher doses of PB, as there was no longer PB present in the animal at the time of GB exposure. These results demonstrate the development of tolerance to the miotic effect of PB following repeated exposures, and also suggest that cross-tolerance between PB and GB occurs. However, because the magnitude of the response was not reduced, the PB pretreatment and its associated miotic cross-tolerance does not appear to diminish the effectiveness of miosis as a biomarker of acute exposure to nerve agent vapor.

The interactions of atropine with the potent anticholinergic agents soman and sarin in the production of neurotoxic effects were investigated in rats. Male Sprague Dawley rats were subcutaneously injected with sublethal doses of soman or sarin, and at various times before and after these treatments, were intravenously injected with different doses of atropine. Atropine alone produced dose dependent limb shake myoclonus, stereotyped sniffing, head movements, and turning. Soman or sarin alone produced tremors, convulsions, chewing movements and hind limb abduction. Pretreatment with atropine inhibited the effects of soman and sarin; however, the effects of atropine were significantly attenuated by sarin. Administration of 5 mg/kg of atropine 6 to 72 hr after exposure to soman or sarin, resulted in significant enhancement of limb shake myoclonus. Atropine induced stereotypes were not affected by soman, but administration of atropine 24 hours after sarin exposure resulted in a significant increase in stereotyped sniffing. The /results suggest/ that brief exposure to potent anticholinergic agents can produce supersensitivity to the effects of low doses of antimuscarinic compounds, and that subjects who are treated with antimuscarinics for anticholinergic poisoning should be observed closely for adverse reactions such as myoclonus.

For more Interactions (Complete) data for SARIN (12 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 16(SRC), determined from a log Kow of 0.30(2) and a regression-derived equation(3), indicates that sarin is expected to have very high mobility in soil(SRC). The importance of leaching in moist soil will be attenuated(SRC) due to sarin's ability to hydrolyze in water(4). Volatilization of sarin from both dry and moist soil surfaces is expected to be an important fate process(SRC) based on results of field and laboratory studies(4). Biodegradation data for sarin were not available(SRC, 2013). Sarin is considered nonpersistent in the environment since it is volatile, soluble in water, and subject to hydrolysis(4).

TERRESTRIAL FATE: Two soil persistence studies conducted by the US Army found that 90% or more of sarin added to soil will be lost in the first five days; one study found that the disappearance rate increased with increases in soil moisture; in humus and loam soils (12.8-36.8% moisture content, pH 6.5), 100% disappearance occurred in 24 hr(1). The persistence times of sarin droplets applied to soil (dry to wet conditions) at 25 °C ranged from 7 to 14 hrs(2). Field studies measuring the disappearance of sarin applied to snow surfaces found that <0.1% remained after 14 days on uncovered snow; persistence times increased when the surface applications were covered by snowfall thereby decreasing the evaporation rates(3).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 16(SRC), determined from a log Kow of 0.30(2) and a regression-derived equation(3), indicates that sarin is not expected to adsorb to suspended solids and sediment(SRC). Aqueous hydrolysis is expected to be the major degradation process for sarin in water forming the products HF and isopropyl methylphosphonic acid(4). The hydrolysis is pH and temperature dependent(4-6); with the fastest rates of hydrolysis occurring below pH 4 and above 6.5(6), the hydrolysis half-life is about 237 hr at 25 °C(6). Hydrolysis takes place faster in seawater than in distilled water due to the presence of metal cations in seawater(5,6); the hydrolysis half-lives in seawater at 25 °C and pHs 7.6 and 7.9 are 58.1 and 25 min, respectively(6); in seawater at 25 °C, the time required to decompose 99.9% of initial sarin is about 8 hr(6); in distilled water, the time required to decompose 99.9% varies from about 750 to 7.5 hr at pHs of 7.0 to 9.0(6). Sarin has been shown to volatilize slowly from water(5) and its estimated Henry Law constant of 5.7X10-7 atm-cu m/mole(SRC) derived from its vapor pressure, 2.86 mm Hg at 25 °C(1), and water solubility, and assigned value for water solubility of 1.0X10+6 mg/L (miscible)(7), also indicates that sarin will volatilize slowly from water surfaces(8). Using this Henry's Law constant and an estimation method(8), volatilization half-lives for a model river and model lake are 76 and 555 days, respectively(SRC). Hydrolysis will attenuate the environmental importance of volatilization(SRC). According to a classification scheme(9), an estimated BCF of 3(SRC), from its log Kow of 0.30(10) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data for sarin were not available(SRC, 2013). Sarin is considered nonpersistent in the environment since it is volatile, soluble in water, and subject to hydrolysis(4).

The increasing threat of nerve agent use for terrorist purposes against civilian and military population calls for effective therapeutic preparedness. At present, administration of atropine and an oxime are recommended, although effectiveness of this treatment is not proved in clinical trials. Here, monitoring of intoxications with organophosphorus (OP) pesticides may be of help, as their actions are closely related to those of nerve agents and intoxication and therapy follow the same principles. To this end, the clinical course of poisoning and the effectiveness of antidotal therapy were investigated in patients requiring artificial ventilation being treated with atropine and obidoxime. However, poisoning with OP pesticides shows extremely heterogeneous pictures of cholinergic crisis frequently associated with clinical complications. To achieve valuable information for the therapy of nerve agent poisoning, cases resembling situations in nerve agent poisoning had to be extracted: (a) intoxication with OPs forming reactivatable OP-AChE-complexes with short persistence of the OP in the body resembling inhalational sarin intoxication; (b) intoxication with OPs resulting rapidly in an aged OP-AChE-complex resembling inhalational soman intoxication; (c) intoxications with OPs forming a reactivatable AChE-OP complex with prolonged persistence of the OP in the body resembling percutaneous VX intoxication. From these cases it was concluded that sufficient reactivation of nerve agent inhibited non-aged AChE should be possible, if the poison load was not too high and the effective oximes were administered early and with an appropriate duration.../Nerve agents/

/AQUATIC SPECIES/ ... Sarin hydrolyzes into isopropyl methylphosphonic acid (IMPA), a compound detected in groundwater from prior chemical warfare agent (CWA) production. This study determined the acute toxicity of IMPA to golden shiner, Notemigonus crysoleucas, and channel catfish, Ictalurus punctatus, eggs and 15-days posthatch (dph) fry. The median lethal concentration (LC50) values at time of hatch for golden shiner and channel catfish eggs were 66.6 mg/L (hatched in 72 hr) and 167.5 mg/L (hatched in 168 hr) IMPA, respectively. The 96-hr LC50 estimates for 15-dph golden shiner and channel catfish fry were 93.9 and 144.1 mg/L IMPA, respectively. The lowest LC50 value from the most sensitive species in this study is approximately 100 times greater than the human adult lifetime drinking water health advisory value, and is approximately 2500 times greater than the critical reporting limit (> or =0.025 mg/L) for IMPA detection in groundwater from CWA production. These results are critical in understanding the toxicological properties of this potential environmental contaminant. /Isopropyl methylphosphonic acid/

- 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, and reflex nausea and vomiting (emesis).

- Nausea, vomiting (emesis), diarrhea, abdominal pain, and cramping.

- Mild to moderate: Contracted or pinpoint pupils (miosis), runny nose (rhinorrhea), narrowing of the large airways (bronchoconstriction), fluid accumulation within the airways of the lungs, and slight to moderate difficulty breathing or shortness of breath (dyspnea).

- 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).

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. /Nerve agents/

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. /Nerve agents/

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 or organophosphates/

Inhibition of blood cholinesterases can be used as a biomarker of exposure to sarin. Although high doses of sarin inhibit both AChE and butrylcholinesterase (BuChE), at lower doses sarin preferentially inhibits AChE, making AChE inhibition a more sensitive biomarker of sarin exposure than BuChE inhibition. Because inhibition of blood cholinesterases is a common feature of sarin, other OP compounds, and some other compounds, cholinesterase inhibition is not a specific biomarker of sarin exposure. Blood esterase activity returns to normal 1-3 months after exposure and this limits its utility as a biomarker to a short time after exposure. ... A more specific biomarker of sarin poisoning by measuring organophosphate-inhibited BuChE in blood has been developed.

/HUMAN EXPOSURE STUDIES/ Between 1958 and 1975, the U.S. Army studied servicemen exposed voluntarily to an array of chemical warfare agents. During the program, the Army investigated only acute short-term effects. Approximately 6,720 soldiers (between the ages of 20 and 25 years) were exposed at Edgewood Arsenal, Maryland, to one or more of 254 chemicals in five classes. About 1,406 of the soldiers were exposed to 15 anticholinesterases. Of this group, 246 were tested with sarin under different conditions (e.g., i.v. or inhalation of sarin vapor)... . In a series of reports, the NRC designed and conducted a follow-up survey and examined soldiers' hospitalization and mortality. ... The NRC results and conclusions were based primarily on anticholinesterases as a class, rather than on sarin or cyclosarin. The NRC questionnaire contained 27 outcome variables relating to health, social adjustment, and reproductive experience of the participants. Mailed survey questionnaires were returned by 64 percent of the overall population of soldiers tested. No long-term health consequences were reported by those responding to the questionnaire, including those exposed to anticholinesterases. Nonrespondents reported having had no health problems to report, when contacted later about their reasons for not returning the questionnaire. Nevertheless, the NRC cautioned that the study had low statistical power and that the exposed group was a highly selected, healthier subset than those who were unexposed. Thus, despite no major identifiable long-term effects, the NRC concluded that "the limited information available from the follow-up on these soldiers does not permit definitive conclusions regarding the nature and extent of possible long-term problems resulting from chemical exposure at Edgewood."

/HUMAN EXPOSURE STUDIES/ One of the clinical syndromes occurring after high exposure to certain OP pesticides is referred to as a delayed intermediate syndrome . It is a life-threatening paralysis of respiratory, neck, and limb muscles. It appears after recovery from the acute cholinergic syndrome, but before the expected time of onset of delayed neuropathy. The symptoms are reversible and disappear within about 2 weeks. ... In one uncontrolled study of male U.K. military volunteers (n = 8) exposed to sarin vapors at 15 mg/min/cu m, soldiers quickly displayed some signs of the acute cholinergic syndrome (e.g., miosis and depressed RBC AChE levels). Although soldiers did not experience muscular weakness, they developed a subclinical change detected by single-fiber electromyography of the forearm muscle, an increased "jitter" at 3 hours postexposure. Jitter refers to a variation in the time of onset of a second action potential within a motor unit after an initial discharge. Jitter is one indication of potential failure of transmission at the neuromuscular junction. The change in jitter in the soldiers was apparent at about 1 year, but disappeared by the second follow-up at about 2 years postexposure. The findings were interpreted by the authors as possibly a subtle indicator of the onset of the intermediate syndrome, but the intermediate syndrome itself did not become manifest.

Releases of CERCLA hazardous substances are subject to the release reporting requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to the requirements of 40 CFR part 355. Sarin is an extremely hazardous substance (EHS) subject to reporting requirements when stored in amounts in excess of its threshold planning quantity (TPQ) of 10 lbs.

Sarin

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.

Chemical warfare

Chemical warfare agent

Sarin is a human-made chemical warfare agent classified as a nerve agent. Nerve agents are the most toxic and rapidly acting of the known chemical warfare agents. They are similar to ... pesticides ... called organophosphates in terms of how they work and what kind of harmful effects they cause. However, nerve agents are much more potent than organophosphate pesticides. Sarin originally was developed in 1938 in Germany as a pesticide.

Sarin (military designation GB) is a nerve agent that is one of the most toxic of the known chemical warfare agents. It is generally odorless and tasteless. Exposure to sarin can cause death in minutes. A fraction of an ounce (1 to 10 mL) of sarin 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.

Phosphonofluoridic acid, P-methyl-, 1-methylethyl ester: ACTIVE

Sarin 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 SARIN (11 total), please visit the HSDB record page.