Wikipedia

Sarin

For other uses, seeSarin (disambiguation).
Not to be confused withserine,sarrin,orsaran.

Sarin(NATOdesignationGB[short forG-series,"B" ]) is an extremely toxicorganophosphorus compound.[4]A colourless, odourlessliquid,it is used as achemical weapondue to its extreme potency as anerve agent.Exposure can be lethal even at very low concentrations, where death can occur within one to ten minutes after direct inhalation of a lethal dose,[5][6]due to suffocation from respiratory paralysis, unless antidotes are quickly administered.[4]People who absorb a non-lethal dose and do not receive immediate medical treatment may suffer permanent neurological damage.[citation needed]

Sarin[1]
S-Sarin
Names
Pronunciation /ˈsɑːrɪn/
Preferred IUPAC name
Propan-2-yl methylphosphonofluoridate
Other names
(RS)-O-Isopropyl methylphosphonofluoridate; IMPF;
GB;[2]
2-(Fluoro-methylphosphoryl)oxypropane;
Phosphonofluoridic acid,P-methyl-, 1-methylethyl ester
EA-1208
TL-1618
T-144
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
UNII
  • InChI=1S/C4H10FO2P/c1-4(2)7-8(3,5)6/h4H,1-3H3checkY
    Key: DYAHQFWOVKZOOW-UHFFFAOYSA-NcheckY
  • InChI=1/C4H10FO2P/c1-4(2)7-8(3,5)6/h4H,1-3H3
  • InChI=1/C4H10FO2P/c1-4(2)7-8(3,5)6/h4H,1-3H3
    Key: DYAHQFWOVKZOOW-UHFFFAOYAY
  • FP(=O)(OC(C)C)C
Properties
C4H10FO2P
Molar mass 140.094g·mol−1
Appearance Clear colourless liquid, brownish if impure
Odor Odourless in pure form. Impure sarin can smell like mustard or burned rubber.
Density 1.0887 g/cm3(25 °C)
1.102 g/cm3(20 °C)
Melting point −56 °C (−69 °F; 217 K)
Boiling point 158 °C (316 °F; 431 K)
Miscible
logP 0.30
Hazards
Occupational safety and health(OHS/OSH):
Main hazards
 Extremely lethalcholinergicagent.
GHSlabelling:
GHS06: Toxic
NFPA 704(fire diamond)
NFPA 704 four-colored diamondHealth 4: Very short exposure could cause death or major residual injury. E.g. VX gasFlammability 1: Must be pre-heated before ignition can occur. Flash point over 93 °C (200 °F). E.g. canola oilInstability 1: Normally stable, but can become unstable at elevated temperatures and pressures. E.g. calciumSpecial hazards (white): no code
4
1
1
0.00003 mg/m3(TWA), 0.0001 mg/m3(STEL)
Lethal doseor concentration (LD, LC):
39 μg/kg (intravenous, rat)[3]
NIOSH(US health exposure limits):
IDLH(Immediate danger)
 0.1 mg/m3
Safety data sheet(SDS) Lethal Nerve Agent Sarin (GB)
Except where otherwise noted, data are given for materials in theirstandard state(at 25 °C [77 °F], 100 kPa).

Sarin is widely considered aweapon of mass destruction.Production and stockpiling of sarin was outlawed as of April 1997 by theChemical Weapons Conventionof 1993, and it is classified as aSchedule 1 substance.

Health effects

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Biological effects of sarin in the neuromuscular junction. Sarin (red), acetylcholinesterase (yellow), acetylcholine (blue)[clarification needed]
For broader coverage of this topic, seeOrganophosphate poisoning.

Like some other nerve agents that affect theneurotransmitteracetylcholine,sarin attacks thenervous systemby interfering with the degradation of the neurotransmitter acetylcholine atneuromuscular junctions.Death usually occurs as a result ofasphyxiadue to the inability to control the muscles involved in breathing.[7]

Initial symptoms following exposure to sarin are arunny nose,tightness in the chest, andconstriction of the pupils.Soon after, the person will have difficulty breathing and experiencenauseaand drooling. This progresses to losing control of bodily functions, which may cause the person to vomit, defecate, and urinate. This phase is followed bytwitchingand jerking. Ultimately, the person becomes comatose and suffocates in a series of convulsivespasms.Common mnemonics for the symptomatology of organophosphate poisoning, including sarin, are the "killer Bs" ofbronchorrheaandbronchospasmbecause they are the leading cause of death,[8]andSLUDGE– salivation,lacrimation,urination, defecation, gastrointestinal distress, and emesis (vomiting). Death may follow in one to ten minutes after direct inhalation, but may also occur after a delay ranging from hours to several weeks, in cases where exposure is limited but no antidote is applied.[7]

Sarin has a highvolatility(ease with which a liquid can turn into vapour) relative to similar nerve agents, making inhalation very easy, and may even absorb through the skin. A person's clothing can release sarin for about 30 minutes after it has come in contact with sarin gas, which can lead to exposure of other people.[9]

Management

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Treatment measures have been described.[9]Treatment is typically with theantidotesatropineandpralidoxime.[4]Atropine, anantagonisttomuscarinic acetylcholine receptors,is given to treat the physiological symptoms of poisoning. Since muscular response to acetylcholine is mediated throughnicotinic acetylcholine receptors,atropine does not counteract the muscular symptoms. Pralidoxime can regeneratecholinesterasesif administered within approximately five hours.Biperiden,a syntheticacetylcholine antagonist,has been suggested as an alternative to atropine due to its betterblood–brain barrierpenetration and higher efficacy.[10]

Mechanism of action

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Sarin is a potentinhibitor of acetylcholinesterase,[11]an enzyme that degrades theneurotransmitteracetylcholineafter it is released into thesynaptic cleft.In vertebrates, acetylcholine is the neurotransmitter used at the neuromuscular junction, where signals are transmitted betweenneuronsfrom thecentral nervous systemto muscle fibres. Normally, acetylcholine is released from the neuron to stimulate the muscle, after which it is degraded byacetylcholinesterase,allowing the muscle to relax. A build-up of acetylcholine in thesynaptic cleft,due to the inhibition of acetylcholinesterase, means the neurotransmitter continues to act on the muscle fibre, so that any nerve impulses are effectively continually transmitted.

Sarin acts on acetylcholinesterase by forming acovalent bondwith the particularserineresidue at the active site. Fluoride is theleaving group,and the resulting organo-phosphoester is robust andbiologically inactive.[12][13]

Its mechanism of action resembles that of some commonly usedinsecticides,such asmalathion.In terms of biological activity, it resemblescarbamateinsecticides, such asSevin,and the medicinespyridostigmine,neostigmine,andphysostigmine.

Diagnostic tests

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Controlled studies in healthy men have shown that a nontoxic 0.43 mg oral dose administered in several portions over a 3-day interval caused average maximum depressions of 22 and 30%, respectively, in plasma and erythrocyte acetylcholinesterase levels. A single acute 0.5 mg dose caused mild symptoms of intoxication and an average reduction of 38% in both measures of acetylcholinesterase activity. Sarin in blood is rapidly degraded eitherin vivoorin vitro.Its primary inactivemetaboliteshavein vivoserum half-lives of approximately 24 hours. The serum level of unbound isopropyl methylphosphonic acid (IMPA), a sarinhydrolysisproduct, ranged from 2–135 μg/L in survivors of a terrorist attack during the first four hours post-exposure. Sarin or its metabolites may be determined in blood or urine by gas or liquidchromatography,while acetylcholinesterase activity is usually measured by enzymatic methods.[14]

A newer method called "fluoride regeneration" or "fluoride reactivation" detects the presence of nerve agents for a longer period after exposure than the methods described above. Fluoride reactivation is a technique that has been explored since at least the early 2000s. This technique obviates some of the deficiencies of older procedures. Sarin not only reacts with the water in the blood plasma through hydrolysis (forming so-called 'free metabolites'), but also reacts with various proteins to form 'protein adducts'. These protein adducts are not so easily removed from the body, and remain for a longer period of time than the free metabolites. One clear advantage of this process is that the period, post-exposure, for determination of sarin exposure is much longer, possibly five to eight weeks according to at least one study.[15][16]

Toxicity

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As a nerve gas, sarin in its purest form is estimated to be 26 times more deadly thancyanide.[17]TheLD50ofsubcutaneously injectedsarin in mice is 172 μg/kg.[18]

Sarin is highly toxic, whether by contact with the skin or breathed in. The toxicity of sarin in humans is largely based on calculations from studies with animals. The lethal concentration of sarin in air is approximately 28–35 mg per cubic meter per minute for a two-minute exposure time by a healthy adult breathing normally (exchanging 15 liters of air per minute, lower 28 mg/m3value is for general population).[19]This number represents the estimated lethal concentration for 50% of exposed victims, theLCt50value. TheLCt95orLCt100value is estimated to be 40–83 mg per cubic meter for exposure time of two minutes.[20][21]Calculating effects for different exposure times and concentrations requires following specific toxic load models. In general, brief exposures to higher concentrations are more lethal than comparable long time exposures to low concentrations.[22]There are many ways to make relative comparisons between toxic substances. The list below compares sarin to some current and historic chemical warfare agents, with a direct comparison to the respiratory LCt50:

Production and structure

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Sarin is achiralmolecule because it has four chemically distinctsubstituentsattached to thetetrahedralphosphorus center.[25]TheSPform (the(–) optical isomer) is the more activeenantiomerdue to its greaterbinding affinitytoacetylcholinesterase.[26][27]The P-F bond is easily broken bynucleophilicagents, such as water and hydroxide. At highpH,sarin decomposes rapidly to nontoxicphosphonic acidderivatives.[28]

It is almost always manufactured as aracemic mixture(a 1:1 mixture of its enantiomeric forms) as this involves a much simplersynthesiswhile providing an adequate weapon.[26][27]

A number of production pathways can be used to create sarin. The final reaction typically involves attachment of the isopropoxy group to the phosphorus with analcoholysiswithisopropyl alcohol.Two variants of this final step are common. One is the reaction ofmethylphosphonyl difluoridewith isopropyl alcohol, which produces a racemic mixture of sarin enantiomers withhydrofluoric acidas a byproduct:[28]

The second process, known as the "Di-Di" process, uses equimolar quantities ofmethylphosphonyl difluoride(Difluoro) andmethylphosphonyl dichloride(Dichloro). This reaction gives sarin,hydrochloric acidand others minors byproducts. The Di-Di process was used by the United States for the production of its unitary sarin stockpile.[28]

The scheme below shows a generic example that employs the Di-Di method as the final esterification step; in reality, the selection of reagents and reaction conditions dictate both product structure and yield. The choice of enantiomer of the mixed chloro fluoro intermediate displayed in the diagram is arbitrary, but the final substitution is selective for chloro over fluoro as theleaving group.Inert atmosphere and anhydrous conditions (Schlenk techniques) are used for synthesis of sarin and other organophosphates.[28]

An example of "di-di" process using arbitrary reagents.

As both reactions leave considerable acid in the product, sarin produced in bulk by these methods has a short half life without further processing, and would be corrosive to containers and damaging to weapons systems. Various methods have been tried to resolve these problems. In addition to industrialrefiningtechniques to purify the chemical itself, various additives have been tried to combat the effects of the acid, such as:

Another byproduct of these two chemical processes isdiisopropyl methylphosphonate,formed when a second isopropyl alcohol reacts with the sarin itself and from disproportionation of sarin, when distilled incorrectly. The factor of its formation in esterification is that as the concentration of DF-DCl decreases, the concentration of sarin increases, the probability of DIMP formation is greater. DIMP is a natural impurity of sarin, that is almost impossible to be eliminated, mathematically, when the reaction is a 1 mol-1 mol "one-stream".[35]

This chemical degrades into isopropyl methylphosphonic acid.[36]

Degradation and shelf life

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Rabbit used to check for leaks at former sarin production plant (Rocky Mountain Arsenal), 1970

The most important chemical reactions of phosphoryl halides is the hydrolysis of the bond between phosphorus and the fluoride. This P-F bond is easily broken by nucleophilic agents, such as water andhydroxide.At highpH,sarin decomposes rapidly to nontoxicphosphonic acidderivatives.[37][38]The initial breakdown of sarin is into isopropyl methylphosphonic acid (IMPA), a chemical that is not commonly found in nature except as a breakdown product of sarin (this is useful for detecting the recent deployment of sarin as a weapon). IMPA then degrades intomethylphosphonic acid(MPA), which can also be produced by other organophosphates.[39]

Sarin with residual acid degrades after a period of several weeks to several months. The shelf life can be shortened by impurities inprecursor materials.According to theCIA,someIraqi sarinhad a shelf life of only a few weeks, owing mostly to impure precursors.[40]

Along with nerve agents such astabunandVX,sarin can have a short shelf life. Therefore, it is usually stored as two separate precursors that produce sarin when combined.[41]Sarin's shelf life can be extended by increasing the purity of the precursor and intermediates and incorporatingstabilizerssuch astributylamine.In some formulations, tributylamine is replaced bydiisopropylcarbodiimide(DIC), allowing sarin to be stored inaluminiumcasings. Inbinary chemical weapons,the two precursors are stored separately in the sameshelland mixed to form the agent immediately before or when the shell is in flight. This approach has the dual benefit of solving the stability issue and increasing the safety of sarin munitions.

History

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Sarin was discovered in 1938 inWuppertal-Elberfeld in Germany by scientists atIG Farbenwho were attempting to create stronger pesticides; it is the most toxic of the fourG-Series nerve agentsmade by Germany. The compound, which followed the discovery of thenerve agenttabun,was named in honor of its discoverers: chemistGerhardSchrader,chemistOttoAmbros,chemistGerhardRitter[de],and fromHeereswaffenamtHans-Jürgen von der Linde.[42]

Use as a weapon

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In mid-1939, the formula for the agent was passed to thechemical warfaresection of theGerman Army Weapons Office,which ordered that it be brought into mass production for wartime use. Pilot plants were built, and a production facility was under construction (but was not finished) by the end ofWorld War II.Estimates for total sarin production byNazi Germanyrange from 500 kg to 10 tons.[43]

Though sarin,tabun,andsomanwere incorporated intoartilleryshells, Germany did not use nerve agents againstAlliedtargets.Adolf Hitlerrefused to initiate the use of gases such as sarin as weapons.[44]

U.S.Honest John missilewarhead cutaway, showingM134Sarin bomblets (c. 1960)
Sarin gas used against animals in a weapons experiment
  • 1950s (early):NATOadopted sarin as a standard chemical weapon. The USSR and the United States produced sarin for military purposes.
  • 1953: 20-year-oldRonald Maddison,aRoyal Air Forceengineer fromConsett,County Durham,died in human testing of sarin at thePorton Downchemical warfare testing facility inWiltshire,England. Ten days after his death aninquestwas held in secret which returned a verdict ofmisadventure.In 2004, the inquest was reopened and, after a 64-day inquest hearing, the jury ruled that Maddison had been unlawfully killed by the "application of a nerve agent in a non-therapeutic experiment".[45]
  • 1957: Regular production of sarin chemical weapons ceased in the United States, though existing stocks of bulk sarin were re-distilled until 1970.[29]
  • 1976: Chile's intelligence service,DINA,assigned biochemistEugenio Berríosto develop Sarin gas within its programProyecto Andrea,to be used as a weapon against its opponents.[46]One of DINA's goals was to package it in spray cans for easy use, which, according to testimony by former DINA agentMichael Townley,was one of the planned procedures in the 1976assassination of Orlando Letelier.[46]Berríos later testified that it was used in a number of assassinations and it was planned to be used to kill inhabitants, through poisoning the water supply ofArgentinecapitalBuenos Aires,in caseOperation Soberaníatook place.[47][48]
  • March 1988:Halabja chemical attack;Over two days in March, the ethnicKurdishcity ofHalabjain northern Iraq (population 70,000) was bombarded bySaddam Hussein'sIraqi Air Forcejets with chemical bombs including sarin. An estimated 5,000 people died, almost all civilians.[49]
  • April 1988: Iraq used Sarin four times against Iranian soldiers at the end of theIran–Iraq War,helping Iraqi forces to retake control of theal-Faw Peninsuladuring theSecond Battle of al-Faw.
  • 1993: The United NationsChemical Weapons Conventionwas signed by 162 member countries, banning the production and stockpiling of many chemical weapons, including sarin. It went into effect on April 29, 1997, and called for the complete destruction of all specified stockpiles of chemical weapons by April 2007.[50]When the convention entered force, the parties declared worldwide stockpiles of 15,047 tonnes of sarin. As of November 28, 2019, 98% of the stockpiles have been destroyed.[51]
  • 1994:Matsumoto incident;the Japanese religious sectAum Shinrikyoreleased an impure form of sarin inMatsumoto, Nagano,killing eight people and harming over 500. The Australian sheep stationBanjawarnwas a testing ground.
  • 1995:Tokyo subway sarin attack;theAum Shinrikyosect released an impure form of sarin in theTokyo Metro.Twelve people died, and over 6,200 people received injuries.[52][53]
  • 2002: Pro-ChechenmilitantIbn al-Khattabmay have been assassinated with sarin by the Russian government.[54][55]
  • May 2004:Iraqi insurgentsdetonated a 155 mm shell containing binary precursors for sarin near a U.S. convoy inIraq.The shell was designed to mix the chemicals as it spun during flight. The detonated shell released only a small amount of sarin gas, either because the explosion failed to mix the binary agents properly or because the chemicals inside the shell had degraded with age. Two United States soldiers were treated after displaying the early symptoms of exposure to sarin.[56]
  • March 2013:Khan al-Assal chemical attack;Sarin was used in an attack on a town west ofAleppocity inSyria,killing 28 and wounding 124.[57]
  • August 2013:Ghouta chemical attack;Sarin was used in multiple simultaneous attacks in theGhoutaregion of theRif DimashqGovernorate of Syria during theSyrian Civil War.[58]Varying[59]sources gave a death toll of 322[60]to 1,729.[61]
  • April 2017:Khan Shaykhun chemical attack:TheSyrian Air Forcereleased sarin gas in rebel-held Idlib Province in Syria during anairstrike.[62][63]
  • April 2018: Victims of theDouma chemical attackin Syria reported to have symptoms consistent with exposure to sarin and other agents. On July 6, 2018, the Fact-Finding Mission (FFM) of the OPCW published their interim report. The report stated that, "The results show that no organophosphorous [sarin] nerve agents or their degradation products were detected in the environmental samples or in the plasma samples taken from alleged casualties". The chemical agent used in the attack was later identified as elementalchlorine.[64]
  • July 2023: The U.S. destroyed the last of its declared chemical weapons, a sarin nerve agent-filledM55 rocket,on July 7, 2023.[65]

See also

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References

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