VX (nerve agent)

From Wikipedia, the free encyclopedia
  (Redirected from 'VX nerve agent')
Jump to: navigation, search
VX[1]
Stereo structural formula VX ((S)-phosphinate)
SP-(−)-VX enantiomer
Ball and stick model of VX ((R)-phosphinate)
VX-S-enantiomer-3D-vdW.png
Names
IUPAC name
Ethyl ({2-[bis(propan-2-yl)amino]ethyl}sulfanyl)(methyl)phosphinate
Systematic IUPAC name
Ethyl ({2-[bis(propan-2-yl)amino]ethyl}sulfanyl)(methyl)phosphinate
Other names
[2-(Diisopropylamino)ethyl]-O-ethyl methylphosphonothioate
Ethyl {[2-(diisopropylamino)ethyl]sulfanyl}(methyl)phosphinate
Ethyl N-2-diisopropylaminoethyl methylphosphonothiolate
Identifiers
3D model (JSmol)
ChEBI
ChemSpider
MeSH VX
Properties
C11H26NO2PS
Molar mass 267.37 g·mol−1
Density 1.0083 g cm−3
Melting point −3.90 °C (24.98 °F; 269.25 K)
Boiling point 300 °C (572 °F; 573 K)
log P 2.047
Vapor pressure 0.09 Pa
Hazards
NFPA 704
Flammability code 1: Must be pre-heated before ignition can occur. Flash point over 93 °C (200 °F). E.g., canola oil Health code 4: Very short exposure could cause death or major residual injury. E.g., VX gas Reactivity code 1: Normally stable, but can become unstable at elevated temperatures and pressures. E.g., calcium Special hazards (white): no codeNFPA 704 four-colored diamond
Flash point 159 °C (318 °F; 432 K) [3]
Lethal dose or concentration (LD, LC):
7 µg/kg (intravenous, rat)[2]
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
N verify (what is YesYN ?)
Infobox references

VX is an extremely toxic synthetic chemical compound in the organophosphorus class, specifically, a thiophosphonate. In the class of nerve agents, it was developed for military use in chemical warfare after translation of earlier discoveries of organophosphate toxicity in pesticide research. In its pure form, VX is a colorless, relatively non-volatile liquid, taking on a yellowish to brown color when impure,[4] because of its low volatility, VX persists in environments where it is dispersed.[4]

VX, short for "venomous agent X",[5] is the best known of Tammelin's esters, named for the member of the Swedish National Defence Research Institute who first studied them. Now one of a broader V-series of agents, they are classified as nerve agents and have been used as a chemical weapon in various recorded deadly attacks. VX fatalities occur with exposure to tens of milligram quantities via inhalation or absorption through skin; VX is thus more potent than sarin, another nerve agent with a similar mechanism of action. On such exposure, these agents severely disrupt the body's signaling between the nervous and muscular systems, leading to a prolonged neuromuscular blockade, flaccid paralysis of all the muscles in the body including the diaphragm, and death by asphyxiation.[6]

The danger of VX, in particular, lies in direct exposure to the chemical agent persisting where it was dispersed, and not through its evaporating and being distributed as a vapor (i.e., it is not a "vapor hazard"). VX is considered an area denial weapon due to these physical and biochemical characteristics,[7] as a chemical weapon, it is categorized as a weapon of mass destruction and is banned by the Chemical Weapons Convention of 1993,[8] where production and stockpiling of VX exceeding 100 grams (3.53 oz) per year is outlawed. The only exception is for "research, medical or pharmaceutical purposes outside a single small-scale facility in aggregate quantities not exceeding 10 kg [22 lb] per year per facility".[9]

Physical properties[edit]

VX is of low molecular weight (FW 267), a liquid under standard and ambient temperate and tropical environmental conditions at most times (m.p. about −51 °C),[10] with a density about that of water.[11] It is relatively hydrophobic—with about 100-fold more partitioning into octanol, over water[citation needed]—and has a relatively high boiling point (about 300 °C).[12] In this regard, as a chemical warfare agent, its physical properties are considered somewhat exceptional, in that for instance its low volatility gives it a high persistence in the environment.[13]

VX is odorless and tasteless,[14] and can be dispersed as a liquid, as an aerosol, or as a mixture with a clay or talc in the form of a thickened agent.[13]

Mechanism of action[edit]

VX is an acetylcholinesterase inhibitor,[15] it works by blocking the function of acetylcholinesterase (AChE). Normally, when a motor neuron is stimulated, it releases the neurotransmitter acetylcholine (ACh) into the space between the neuron and an adjacent muscle cell. When acetylcholine is taken up by the muscle cell, it stimulates muscle contraction. To avoid a state of constant muscle contraction, the acetylcholine is then broken down (hydrolysed) into the inactive substances acetic acid and choline by AChE. VX blocks the action of AChE, resulting in an accumulation of acetylcholine in the space between the neuron and muscle cell, on a molecular level, this leads to this ongoing stimulation and eventual fatigue of all affected muscarinic and nicotinic ACh receptors. This results in initial violent contractions, followed by "sustained supercontraction restricted to the fluid (sarcoplasm) of the subjunctional endplate and prolonged, depolarizing neuromuscular blockade."[this quote needs a citation] The prolonged blockade results in flaccid paralysis of all the muscles in the body, and it is such sustained paralysis of the diaphragm muscle that causes death by asphyxiation.[citation needed]

Accumulation of acetylcholine in the brain also causes neuronal excitotoxicity, due to activation of nicotinic receptors and glutamate release.[16]

Chemistry[edit]

Synthesis[edit]

VX is chiral at its phosporus atom, the individual enantiomers are identified as SP-(−)-VX, and RP-(+)-VX (where the "P" subscript highlights that the chirality is at phosphorus).[1]

VX is produced via the transester process, which gives a racemic mixture of the two enantiomers, this entails a series of steps whereby phosphorus trichloride is methylated to produce methyl phosphonous dichloride. The resulting material is reacted with ethanol to form a diester, this is then transesterified with N,N-diisopropylaminoethanol to produce the mixed phosphonite. Finally, this immediate precursor is reacted with sulfur to form VX.

VX TransesterProcess.png

VX can also be delivered in binary chemical weapons which mix in-flight to form the agent prior to release. Binary VX is referred to as VX2,[17] and is created by mixing O-(2-diisopropylaminoethyl) O′-ethyl methylphosphonite (Agent QL) with elemental sulfur (Agent NE) as is done in the Bigeye aerial chemical bomb. It may also be produced by mixing with sulfur compounds, as with the liquid dimethyl polysulfide mixture (Agent NM) in the canceled XM736 8-inch projectile program.[18]

Solvolysis[edit]

Like other organophosphorus nerve agents, VX may be destroyed by reaction with strong nucleophiles, the reaction of VX with concentrated aqueous sodium hydroxide results in two competing solvolysis reactions: cleavage of either the P–O or P–S esters. Although the P–S cleavage is the dominant pathway, the product of P–O bond cleavage is the toxic phosphonic thioester EA 2192 and both reactions are slow.[19] In contrast, reaction with the hydroperoxide anion (hydroperoxidolysis) leads to exclusive cleavage of the P–S bond and a more rapid overall reaction.[19][20]

P–S cleavage (non-toxic products)
P-O cleavage (EA 2192 product is still toxic)

Medical aspects[edit]

Symptoms of exposure[edit]

Early symptoms of percutaneous exposure (skin contact) include local sweating and muscular twitching at the area of exposure, followed by nausea or vomiting. Early symptoms of exposure to VX vapor include rhinorrhea (runny nose) and/or tightness in the chest with shortness of breath (bronchial constriction). Miosis (pinpointing of the pupils) may be an early sign of agent exposure, but is not usually used as the only indicator of exposure.[21]

Toxicology[edit]

VX is a "particularly toxic nerve agent", the potentially fatal dose is only slightly higher than the dose having any effect at all, and the effects of a fatal dose are so rapid that there is little time for treatment.[4]}} The median lethal dose (LD50)—the exposure required to kill half of a tested population—as estimated for 70 kg human males via exposure to the skin is reported to be 10 mg (0.00035 oz), and the lethal concentration time (LCt50), measuring the concentration of the vapor per length of time exposed, is estimated for VX to be 30–50 mg·min/m3.[4]

Treatment[edit]

When treating VX exposure, primary consideration is given to removal of the liquid agent from the skin, before removal of the individual to an uncontaminated area or atmosphere.[citation needed] After this, the victim is decontaminated by washing the contaminated areas with household bleach and flushing with clean water, followed by removal of contaminated clothing and further skin decontamination.[citation needed] When possible, decontamination is completed before the casualty is taken for further medical treatment.[citation needed]

An individual known to have been exposed to a nerve-agent, or who exhibits definite signs or symptoms of nerve-agent exposure is generally given the antidotes atropine and pralidoxime (2-PAM), as well an injected sedative/antiepileptic such as diazepam.[citation needed] In several nations the nerve agent antidotes are issued for military personnel in the form of an autoinjector such as the United States military Mark I NAAK.[21]

Atropine blocks a subset of acetylcholine receptors known as muscarinic acetylcholine receptors (mAchRs), so that the buildup of acetylcholine produced by loss of the acetylcholinesterase function has a reduced effect on their target receptor.[citation needed] 2-PAM reactivates the acetylcholinesterase enzyme (AChE), thus reversing the effects of VX.[citation needed][22]

However, if 2-PAM is not given soon enough, the inactivated enzyme will "age", resulting in a much stronger AChE-phosphate binding, that 2-PAM treatment cannot reverse,[23] the basis of this "aging" process in protein structure—a possible conformational isomerism—has been studied using X-ray crystallography focused on the AChE active site of relevant enzymes, where possible implications for the two enantiomers in the VX chemical agent are also discussed.[24]

Diagnostic tests[edit]

Ethyl methylphosphonic acid. R1 = ethyl, R2 = methyl.

Controlled studies in humans have shown that minimally toxic doses cause 70–75% depression of erythrocyte cholinesterase within several hours of exposure, the serum level of ethyl methylphosphonic acid (EMPA), a VX hydrolysis product, was measured to confirm exposure in one poisoning victim. There also exist procedures for determination of VX hydrolysis products in urine and of VX adducts to albumin in blood.[25]

History[edit]

Discovery[edit]

The chemists Ranajit Ghosh and J.F. Newman discovered the V-series nerve agents at the British firm ICI in 1952, patenting diethyl S-2-diethylaminoethyl phosphono- thioate (agent VG) in November 1952. Further commercial research on similar compounds ceased in 1955 when its lethality to humans was discovered, the U.S. went into production of large amounts of VX in 1961 at Newport Chemical Depot.

The discovery occurred when the chemists were investigating a class of organophosphate compounds (organophosphate esters of substituted aminoethanethiols).[26] Like Gerhard Schrader, an earlier investigator of organophosphates, Ghosh found that they were quite effective pesticides; in 1954, ICI put one of them on the market under the trade name Amiton. It was subsequently withdrawn, as it was too toxic for safe use, the toxicity did not go unnoticed, and samples of it had been sent to the British Armed Forces research facility at Porton Down for evaluation. After the evaluation was complete, several members of this class of compounds became a new group of nerve agents, the V agents, the best-known of these is probably VX, assigned the UK Rainbow Code Purple Possum, with the Russian V-Agent (VR) coming a close second (Amiton is largely forgotten as VG). This class of compounds is also sometimes known as Tammelin's esters, after Lars-Erik Tammelin of the Swedish National Defence Research Institute. Tammelin was also conducting research on this class of compounds in 1952, but did not widely publicize his work, the name is a contraction of the words "venomous agent X".[27]

Beginning in 1959, the United States Army began volunteer testing of VX in humans. Dr. Van M. Sim underwent an intravenous infusion of VX to evaluate its effects and to establish a baseline for future experimentation, after approximately 3.5 hours following initial administration of the agent, Dr. Sim suddenly became pale and delirious, the experiment was immediately terminated to preserve his life. In their conclusion, the researchers estimated that 2.12 μg/kg of VX delivered intravenously over the course of several hours would be the maximum tolerable dosage and that any more would risk death in a human subject.[28]

Instances of VX use[edit]

There was evidence of a combination of chemical agents having been used by Iraq against the Kurds in the Halabja chemical attack in 1988 under Saddam Hussein.[29] Hussein later testified to UNSCOM that Iraq had researched VX, but had failed to weaponize the agent due to production failure, after U.S. and allied forces had invaded Iraq, no VX agent or production facilities were found. However, UNSCOM laboratories detected traces of VX on warhead remnants.[30][31]

In December 1994 and January 1995, Masami Tsuchiya of Aum Shinrikyo synthesized 100 to 200 grams (3.5 to 7.1 oz) of VX which was used to attack three people. Two people were injured and one 28-year-old man died, who was the first victim of VX ever documented in the world at that time, the VX victim, whom Shoko Asahara had suspected as a spy, was attacked at 7:00 am on December 12, 1994 on the street in Osaka by Tomomitsu Niimi and another AUM member, who sprinkled the nerve agent on his neck. He chased them for about 90 metres (100 yd) before collapsing, dying 10 days later without ever coming out of a deep coma. Doctors in the hospital suspected at the time he had been poisoned with an organophosphate pesticide, but the cause of death was pinned down only after cult members arrested for the subway attack confessed to the killing. Metabolites of VX such as ethyl methylphosphonate, methylphosphonic acid and diisopropyl-2-(methylthio)ethylamine were later found in samples of the victim's blood seven months after his murder.[32] Unlike the cases for sarin gas (the Matsumoto incident and the attack on the Tokyo subway), VX was not used for mass murder.

On February 13, 2017, Kim Jong-nam, half-brother of North Korean leader Kim Jong-un, died after an assault in Kuala Lumpur International Airport in Malaysia. According to the authorities he was murdered by poisoning with VX which was found on his face,[33][34] the authorities further reported that one of the women suspected of applying the nerve agent experienced some physical symptoms of VX-poisoning.[35] The director of a non-proliferation research program of the Middlebury Institute of International Studies at Monterey stated that VX fumes would have killed the suspected attackers even if they had been wearing gloves, suggesting that the VX was applied as two non-lethal components that would mix to form VX only on the victim's face.[36]

Worldwide stockpiles[edit]

Some countries known to possess VX are the United States, Russia,[37] North Korea, Israel[citation needed] and Syria.[38] A Sudanese pharmaceutical facility, the Al-Shifa pharmaceutical factory, was bombed by the U.S. in 1998 acting on information that it produced VX and that the origin of the agent was associated with both Iraq and Al Qaeda.[30] The U.S. had obtained soil samples identified as containing O-ethyl hydrogen methylphosphonothioate (EMPTA), a chemical used in the production of VX which may also have commercial applications. Chemical weapons experts later suggested that the widely used fonofos organophosphate insecticide could have been mistaken for EMPTA.[39]

In 1969, the U.S. government canceled its chemical weapons programs, banned the production of VX in the United States, and began the destruction of its stockpiles of agents by a variety of methods. Early disposal included the U.S. Army's CHASE (Cut Holes And Sink 'Em) program, in which old ships were filled with chemical weapons stockpiles and then scuttled. CHASE 8 was conducted on June 15, 1967, in which the steamship Cpl. Eric G. Gibson was filled with 7,380 VX rockets and scuttled in 2,200 m (7,200 ft) of water off the coast of Atlantic City, New Jersey. Incineration was used for VX stockpile destruction starting in 1990 with Johnston Atoll Chemical Agent Disposal System in the North Pacific with other incineration plants following at Deseret Chemical Depot, Pine Bluff Arsenal, Umatilla Chemical Depot and Anniston Army Depot with the last of the VX inventory destroyed on December 24, 2008.[40]

Stockpile elimination[edit]

Worldwide, VX disposal has continued since 1997 under the mandate of the Chemical Weapons Convention. When the convention entered force, the parties declared worldwide stockpiles of 19,586 tonnes (21,590 short tons) of VX, as of December 2015, 98% of the stockpiles had been destroyed.[41]

In fiscal year 2008, the U.S. Department of Defense released a study finding that the United States had dumped at least 112 tonnes (124 short tons) of VX into the Atlantic Ocean off the coasts of New York/New Jersey and Florida between 1969 and 1970. This material consisted of nearly 22,000 M55 rockets, 19 bulk containers holding 640 kg (1,400 lb) each, and one M23 chemical landmine.[42]

The Newport Chemical Depot began VX stockpile elimination using chemical neutralization in 2005. VX was hydrolyzed to much less toxic byproducts by using concentrated caustic solution, and the resulting waste was then shipped off-site for further processing. Technical and political issues regarding this secondary byproduct resulted in delays, but the depot completed their VX stockpile destruction in August 2008.[43]

The remaining VX stockpile in the U.S. will be treated by the Blue Grass Chemical Agent-Destruction Pilot Plant in Kentucky, part of the Program Executive Office, Assembled Chemical Weapons Alternatives program. The program was established as an alternative to the incineration process successfully used by the Army Chemical Materials Agency, which completed its stockpile destruction activities in March 2012, the Blue Grass Pilot Plant has been plagued by repeated cost over-runs and schedule slippages since its inception.[44]

In Russia, the U.S. is providing support for these destruction activities with the Nunn-Lugar Global Cooperation Initiative.[45] The Initiative has been able to convert a former chemical weapons depot at Shchuchye, Kurgan Oblast, into a facility to destroy those chemical weapons, the new facility, which opened in May 2009, has been working on eliminating the nearly 5,400 tonnes (5,950 short tons) of nerve agents held at the former storage complex. However, this facility only holds about 14% of Russian chemical weapons, which are stored at seven sites.[46]

Popular culture[edit]

One of the best-known references to VX in popular culture is its use in the 1996 film The Rock,[47][48] which centers on a threatened VX attack on San Francisco from the island of Alcatraz. The film uses artistic license, notably with VX being ascribed corrosive powers it does not possess, permitting an early scene in which a VX victim is shown with his face melting, rather than dying through asphyxiation, it also shows the hero applying an intracardiac injection of atropine as a defense against VX contamination, rather than the more usual intramuscular injection (e.g. into the thigh) of a combination of atropine and pralidoxime.

In the BBC One spy drama Spooks, an episode named "I Spy Apocalypse" (Series 2, Episode 5) features an EERE (Extreme Emergency Response Exercise) turned real life emergency. A dirty bomb was reported to have exploded in Parliament Square and later the Morningside area of Edinburgh. The bomb was confirmed to have dispersed VX in quantities that exceeded the lethal dose across much of the southeast of England, it is later found that the emergency is a well constructed and believable exercise designed to test the MI5 officers to their limits.[citation needed]

In the CBS American science-based drama television series Eleventh Hour, an episode named Subway (Episode 16); Dr Hood, a science advisor to the FBI is called in to determine the cause of a poison cluster, which is killing people in Philadelphia.[49]

VX agent was featured on the History Channel's television series Modern Marvels in the episode Deadliest Weapons (Season 11, Episode 10).[50]

See also[edit]

References[edit]

  1. ^ a b John H, Balszuweit F, Kehe K, Worek F & Thiermann H (2015). "Toxicokinetic Aspects of Nerve Agents and Vesicants". In Gupta, Ramesh C. Handbook of Toxicology of Chemical Warfare Agents (2nd ed.). Cambridge, MA: Academic Press. pp. 817–856, esp. 823 [Fig.56.1]. ISBN 0128004940. Retrieved March 22, 2017. 
  2. ^ a b c d e Chambers, Michael. "Substance Name: VX". ChemIDplus. U.S. National Library of Medicine, National Institutes of Health. Retrieved 24 February 2017. 
  3. ^ "Material Safety Data Sheet: Nerve Agent (VX)". ilpi.com. Interactive Learning Paradigms Incorporated. December 22, 2000 [1998]. Retrieved October 25, 2007. 
  4. ^ a b c d FAS Staff (2013). "Types of Chemical Weapons: Nerve Agents [Table. Toxicological Data]". Washington, DC: Federation of American Scientists [FAS]. Archived from the original on November 26, 2016. Retrieved March 22, 2017. 
  5. ^ "Detoxifying VX". Chemical & Engineering News. 94 (38): 10–11. September 26, 2016. doi:10.1021/cen-09438-scicon001. 
  6. ^ Sidell, Frederick R. (1997). "Chapter 5: Nerve Agents" (PDF). Medical Aspects of Chemical and Biological Warfare. p. 142ff. 
  7. ^ Takafuji, Ernest T.; Kok, Allart B. (1997). "Chapter 4: The Chemical Warfare Threat and the Military Healthcare Provider" (PDF). Medical Aspects of Chemical and Biological Warfare. p. 123. Given favorable weather conditions, the use of persistent agents such as mustard and VX may pose a threat for many days. Such agents can deny or interfere with enemy occupation of terrain or use of equipment 
  8. ^ "Convention on the Prohibition of the Development, Production, Stockpiling and Use of Chemical Weapons and on their Destruction. Annex on Chemicals". United Nations Organisation for the Prohibition of Chemical Weapons. 
  9. ^ OPCW (2005). "Convention on the Prohibition of the Development, Production, Stockpiling and Use of Chemical Weapons and on their Destruction" (PDF). OPCW.org. Organization for the Prohibition of Chemical Weapons (OPCW). p. 122. Retrieved 26 August 2016. 
  10. ^ "Tx 60 | C11H26NO2PS". PubChem. Retrieved 2017-04-13. 
  11. ^ "Tx 60 | C11H26NO2PS". PubChem. Retrieved 2017-04-13. 
  12. ^ "Tx 60 | C11H26NO2PS". PubChem. Retrieved 2017-04-13. 
  13. ^ a b Croddy, Eric (October 1, 2002). "Dusty Agents and the Iraqi Chemical Weapons Arsenal". Nuclear Threat Initiative [NTI]. Washington, DC and Monterey, CA: Middlebury Institute of International Studies, James Martin Center for Nonproliferation Studies. Retrieved March 22, 2017 – via NTI.org. 
  14. ^ Bradley, David (February 24, 2017). "VX Nerve Agent in North Korean's Murder: How Does It Work?". Scientific American. Retrieved March 22, 2017. 
  15. ^ McDowall, Jennifer (November 2005). "Acetylcholine Recepetors". European Molecular Biology Laboratory/European Bioinformatics Institute. 
  16. ^ Chen Y (2012). "Organophosphate-induced brain damage: mechanisms, neuropsychiatric and neurological consequences, and potential therapeutic strategies". Neurotoxicology. 33: 391–400. doi:10.1016/j.neuro.2012.03.011. PMID 22498093. 
  17. ^ Ellison, D. Hank (2007). Handbook of Chemical and Biological Agents. New York: CRC Press. p. 47. ISBN 0-8493-1434-8. Retrieved 2014-02-21. 
  18. ^ Adams, Robert W. "Chemical Warfare in Future Military Operations", Command and Staff College, United States Navy, via Globalsecurity.org, April 6, 1984.
  19. ^ a b Yang, Yu-Chu (1999). "Chemical Detoxification of Nerve Agent VX". Acc. Chem. Res. 32 (2): 109–15. doi:10.1021/ar970154s. 
  20. ^ Daniel, Kelly; Kopff, Laura A.; Patterson, Eric V.; et al. (2008). "Computational studies on the solvolysis of the chemical warfare agent VX". J. Phys. Org. Chem. 21 (4): 321–28. doi:10.1002/poc.1333. 
  21. ^ a b "US Army Toxic Chemical Agent Safety Standards" (PDF). DA PAM 385-61. Section 7-8 Self/Buddy Aid Procedures. US Army. Archived from the original (PDF) on December 24, 2003. Retrieved December 15, 2007. 
  22. ^ VX and other organophosphates block AChE activity by binding to and covalently inactivating the enzyme via transfer of the phosphonate moiety from VX to the active site of AChE; this inactivates AChE and produces an inactive bybroduct from the remaining portion of the VX molecule.[citation needed] Pralidoxime (2-PAM) removes this phosphate group.[citation needed]
  23. ^ "Cholinesterase Inhibitors – Management of the Cholinergic Toxidrome – Medications: 2-PAM (2-Pyridine Aldoxime Methylchloride) (Pralidoxime)". ATSDR – Environmental Health and Medicine Education. Centers for Disease Control and Prevention – Agency for Toxic Substances and Disease Registry. 
  24. ^ Wandhammer, Marielle; Carletti, Eugénie; Schans, Marcel Van der; Gillon, Emilie; Nicolet, Yvain; Masson, Patrick; Goeldner, Maurice; Noort, Daan; Nachon, Florian (13 May 2011). "Structural Study of the Complex Stereoselectivity of Human Butyrylcholinesterase for the Neurotoxic V-agents". J. Biol. Chem. 286 (19): 16783–16789. doi:10.1074/jbc.M110.209569. PMC 3089521Freely accessible. PMID 21454498. Retrieved 22 March 2017 – via www.jbc.org. 
  25. ^ R. Baselt (2017). Disposition of Toxic Drugs and Chemicals in Man (11th ed.). Seal Beach, CA: Biomedical Publications. pp. 2264–65. 
  26. ^ Ghosh, R.; Newman, J.E. (Jan 29, 1955). "A new group of organophosphorus pesticides". Chemistry and Industry: 118. 
  27. ^ 01:45 (2016-12-19). "BBC Four – Inside Porton Down: Britain's Secret Weapons Research Facility". Bbc.co.uk. Retrieved 2017-02-24. 
  28. ^ Kazuo K. Kimura, Bernard P. McNamara, Van M. Sim (1960-07-01). "Intravenous Administration of VX in Man". Retrieved 2017-03-25. 
  29. ^ BBC (March 16, 1988). "1988: Thousands die in Halabja gas attack". Retrieved March 1, 2012. 
  30. ^ a b John Pike. "Iraq Survey Group Final Report". Globalsecurity.org. Retrieved March 1, 2012. 
  31. ^ CIA (May 2, 2007). "Intelligence Update: Chemical Warfare Agent Issues Chemical Warfare Issues During the Persian Gulf War". Retrieved Oct 22, 2012. 
  32. ^ Pamela Zurer. "Japanese cult used VX to slay member". Chemical and Engineering News. 1998, Vol 76 (no. 35), 7.
  33. ^ Paddock, Richard C.; Sang-hun, Choe (2017-02-23). "Kim Jong-nam Was Killed by VX Nerve Agent, Malaysians Say". The New York Times. ISSN 0362-4331. Retrieved 2017-02-24. 
  34. ^ "Kim Jong-nam killing: VX nerve agent 'found on his face'". BBC News. 24 February 2017. Retrieved 2017-02-24. 
  35. ^ One suspect in Kim Jong Nam murder suffered effects of VX agent. The Star. 2017-2-24. Retrieved February 23, 2017.
  36. ^ McCurry, Justin (2017-02-20). "What is the VX nerve agent that killed North Korean Kim Jong-nam?". The Guardian. Retrieved 2017-02-25. 
  37. ^ "VX". Council on Foreign Relations. Retrieved June 12, 2007. 
  38. ^ "Synthèse nationale de renseignement déclassifié" [National synthesis of declassified intelligence] (PDF) (in French). Retrieved 2014-01-03. 
  39. ^ Claudine McCarthy (2005). "EMPTA (O-Ethyl methylphosphonothioic acid)". In Eric Croddy; James J. Wirtz. Weapons of mass destruction: an encyclopedia of worldwide policy, technology, and history (Google Books excerpt). pp. 123–24. ISBN 1-85109-490-3. Retrieved 2014-02-21. 
  40. ^ "VX Destruction Milestone". U.S. Army Chemical Materials Agency. March 20, 2009. Archived from the original on 2009-03-27. 
  41. ^ Organisation for the Prohibition of Chemical Weapons (30 November 2016). "Annex 3". Report of the OPCW on the Implementation of the Convention on the Prohibition of the Development, Production, Stockpiling and Use of Chemical Weapons and on Their Destruction in 2015 (Report). p. 42. Retrieved 8 March 2017. 
  42. ^ "App_Q_Sea_Disposal_final" (PDF). denix.osd.mil. Retrieved September 7, 2009. 
  43. ^ "Depot Confirms VX Stockpile Eliminated". U.S. Army Chemical Materials Agency. Retrieved January 7, 2013. 
  44. ^ Schneidmiller, Chris (April 18, 2001). "U.S. Chemical Weapons Disposal Slippage "No Surprise," Expert Says". Nuclear Threat Initiative. Retrieved Oct 11, 2012. 
  45. ^ "Nunn-Lugar Global Cooperation Initiative|". Defense Threat Reduction Agency and USSTRATCOM Center for Combating WMD. Retrieved 23 May 2012. 
  46. ^ Levy, Clifford J. (May 27, 2009). "In Siberia, the Death Knell of a Complex Holding a Deadly Stockpile". The New York Times. Retrieved April 9, 2010. 
  47. ^ Royal Society of Chemistry, 31 January 2012, Molecular dynamics to combat chemical terrorism
  48. ^ Ilan Ben Zion, Times of Israel, 29 August 2013, Vital sarin antidote missing from gas mask kits
  49. ^ Wolff, Eric (March 6, 2009). "Eleventh Hour: VX Gas And How to Survive it". Discover Magazine. Retrieved October 17, 2016.
  50. ^ Modern Marvels Season 12, Episode 17 (March 16, 2005). Deadliest Weapons "...Finally, we examine VX nerve gas, thought by many to be the deadliest chemical agent ever created ..". History Channel. Retrieved October 17, 2016.

External links[edit]