VX (nerve agent)

Jump to: navigation, search

Skeletal formula of VX
Ball-and-stick model of VX Space-filling model of VX
Discovered by Ranajit Ghosh
Discovered in 1952
Chemical characteristics
Chemical name O-ethyl S-(2-diisopropylaminoethyl)


Chemical family Organophosphorus compound
Chemical formula C11H26NO2PS
NFPA Rating
NFPA 704.svg
Boiling point 298°C (568.4°F)
Freezing/melting point −50°C (−58°F)
Vapor pressure 0.0007 mm Hg (0.0933256 Pa) at 25 °C
Vapor density (Air=1) 9.2
Liquid density 1.0083 g cm−3
Solubility in water ? g/100 g at 25 °C
? g/100 g at 20 °C
Specific gravity 1.0113
Appearance and color Colorless
Fire and Explosion Data
Flashpoint 159 °C (? °F) / ?°R
Unusual hazards Extremely toxic
Disclaimer and references

VX (O-ethyl-S-[2(diisopropylamino)ethyl] methylphosphonothiolate) is an extremely toxic substance whose sole application is as a nerve agent. As a chemical weapon, it is classified as a weapon of mass destruction by the United Nations in UN Resolution 687. Production and stockpiling of VX was outlawed by the Chemical Weapons Convention of 1993.

The VX nerve agent is the most well-known of the V-series of nerve agents and is considered an area denial weapon due to its physical properties.

Chemical characteristics

With its high viscosity and low volatility, VX has the texture and feel of high-grade motor oil. This makes it especially dangerous, as it has a high persistence in the environment. It is odourless and tasteless, and can be distributed as a liquid or, through evaporation, into small amounts of vapor. It works as a nerve agent by blocking the function of the enzyme acetylcholinesterase. Normally, an electric nerve pulse would cause the release of acetylcholine over a synapse that would stimulate muscle contraction. The acetylcholine is then broken down to non-reactive substances (acetic acid and choline) by the acetylcholinesterase enzyme. If more muscle tension is needed the nerve must release more acetylcholine. VX blocks the action of acetylcholinesterase, thus resulting in sustained contractions of all the muscles in the body. Sustained contraction of the diaphragm muscle causes death by asphyxiation.


VX is produced via the "Transester Process". This entails a complex chemical transition 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 to produce the immediate precursor of VX. Finally, the immediate precursor is reacted with sulfur to form VX.

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, 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 cancelled XM-768 8-inch binary projectile program.


Like other organophosphorus nerve agents, VX may be destroyed by reaction with strong nucleophiles such as pralidoxime. The reaction of VX with concentrated aqueous sodium hydroxide results in competing cleavage of the P-O and P-S esters, with P-S cleavage dominating. This is somewhat problematic, since the product of P-O bond cleavage (named EA 2192) remains toxic. In contrast, reaction with the anion of hydrogen peroxide (hydroperoxidolysis) leads to exclusive cleavage of the P-S bond.[1]

400px P-S cleavage
NaOH(aq) reacts with VX in two ways. It can cleave VX's P-S bond, yielding two relatively nontoxic products...
400px P-O cleavage
...or it can cleave VX's P-O bond, forming ethanol and EA 2192 (shown in red), which has similar toxicity to VX itself

Biological effects

VX is one of the most toxic nerve agents ever synthesized.[2] The median lethal dose (LD50) for 50 percent of an average human population is estimated to be about 10 micrograms through skin contact and the LCt50 for inhalation is estimated to be 30-50 mg•min/m³[3]. If the absorbed dose is not too high, death can be avoided if the appropriate antidote is injected immediately after exposure. The most commonly used antidotes are atropine, pralidoxime (2-PAM), and diazepam which are, in several nations, issued for military personnel in the form of an autoinjector. Atropine works by binding and blocking a subset of acetylcholine receptors (known as muscarinic acetylcholine receptor, mAchR), so that the build up of acetylcholine produced by loss of the acetylcholinesterase function can no longer affect their target. The injection of pralidoxime regenerates bound acetylcholinesterase.


The following is the specific history of VX, which is closely linked to the history of similar nerve agents also discovered in Germany during or soon after World War II. That broader history is detailed in Nerve Agent: History.

The chemists Ranajit Ghosh and J.F. Newman discovered the V-series nerve agents at ICI in 1952, patenting diethyl S-2-diethylaminoethyl phosphor-othiolate (VG) in November, 1952. Further commercial research on similar compounds ceased in 1955 when its lethality to humans was discovered. Information on the substance was passed to Porton Down in 1954 and research there led to VX within a year. This was traded to the United States as the British passed over VX in favour of continuing with sarin as the UK chemical weapon of choice, the reasoning behind the decision is unclear, although the recent completion of a sarin production facility at Nancekuke may have played a part.

Despite creating the agent, the United Kingdom unilaterally renounced chemical and biological weapons in 1956.[citation needed] In 1958 the British government traded their research on VX technology with the United States of America in exchange for information on thermonuclear weapons.[citation needed] The US then went into production of large amounts of VX in 1961.[citation needed]
Iraq under Saddam Hussein admitted to UNSCOM that it had researched VX, but had failed to weaponize the agent due to production failure. After U.S. and allied forces had invaded Iraq, no proof of weaponized VX was found. [1] Subsequent investigation after the 2003 Invasion of Iraq indicates that Iraq had indeed weaponized VX in 1988, and had dropped three VX-filled bombs on Iran. [2]

The only countries known to possess VX are the United States and Russia[2]. However, under Saddam Hussein's regime, Iraq was suspected of buying VX[2]; a Sudanese pharmaceutical facility was bombed by the U.S. in 1998 following allegations that it in some way used VX and that the origin of the agent was associated with both Iraq and Al Qaeda.[4]

VX Stockpile elimination

The US later started the destruction of its stockpiles of the nerve agents (by incineration at Johnston Island in the North Pacific), as mandated by the US accession to the Chemical Weapons Convention. Earlier, pre-treaty disposal included the US 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 S.S. Cpl. Eric G. Gibson was filled with 7,380 VX rockets and scuttled in 7,200 feet of water, off the coast of Atlantic City, New Jersey.

The US is also destroying chemical weapons stockpiles containing VX in nine other locations, one of which is in Russia[citation needed].

On June 12, 2005, it was reported that more than 250,000 US gallons (950 m³) of the chemical weapon are stored at the Newport Chemical Depot in Newport, Indiana, about 30 miles (50 km) north of Terre Haute, Indiana. The VX is in the process of being hydrolyzed to much less toxic byproducts using concentrated caustic solution. The VX hydrolysate produced will contain mainly a phosphonate ester and a thiolamine, with 20 parts per billion or less of residual VX. (Interestingly, 20 ppb is the level of VX in water that is considered permissible for drinking by US combat troops.) A plan was developed to truck the hydrolysate from Indiana to the DuPont Chambers Works Secure Environmental Facility at Deepwater, NJ where it was to be further treated to destroy the phosphonate ester and the thiolamine, and dumped into the Delaware River.[5] The governors of Delaware, New Jersey, Pennsylvania, and New York have opposed this plan and the New Jersey Governor Codey instructed the New Jersey Department of Transportation to deny entry to any trucks carrying the hydrolysate to the Deepwater facility. Prior to the current plan, it had been proposed that the hydrolysate be dumped into the Great Miami River, a tributary of the Ohio River, near Dayton, Ohio but the community there successfully defeated the proposal.

VX hydrolysis began on May 5 2005 and as of June 12 the facility had destroyed 2,894 US gallons (11 m³) of VX. A contained spill of 30 US gallons (100 L) drew attention to the disposal process, but authorities said no agent was released and no one was injured in the spill.

On January 5, 2007, DuPont announced they had abandoned plans to seek the contract for transportation, treatment, and disposal of VX at their Chambersworks Secure Treatment Facility in Deepwater, NJ. They cited lengthy review processes and strong opposition by New Jersey's governor, Jon Corzine, New Jersey senators and congressmen, and environmental groups including NJ Audubon, Delaware Riverkeepers, and the Litoral Society as well as the on-going investigation by the GAO as factors in their decision to withdraw from the plan.

In popular culture


  1. Yang, Yu-Chu (1999). "Chemical Detoxification of Nerve Agent VX". Acc. Chem. Res. p. 109-115.
  2. 2.0 2.1 2.2 "VX". Council on Foreign Relations. 2006-01. Retrieved 2007-03-27. Check date values in: |date= (help)
  3. http://www.fas.org/cw/cwagents.htm
  4. Chomsky, Noam (Oct. 2001). 9-11. Open Media. Check date values in: |date= (help)
  5. Montgomery, Jeff (2006-04-26). "Army backs VX disposal at N.J. facility". The News Journal. p. A2. Check date values in: |date= (help)

External links

ar:في أكس de:VX (Nervenkampfstoff) he:VX hu:VX nl:VX no:VX sl:VX fi:VX sv:VX-gas