VX. Chemical Properties

Melting point:

-38.9°C

Boiling point:

299°C

Density 

1.0080

form 

liquid

pka

7.9(at 25℃)

EPA Substance Registry System

O-Ethyl S-(2-diisopropylaminoethyl) methylphosphonothioate (50782-69-9)

Safety Information

RIDADR 

2810

HazardClass 

6.1(a)

PackingGroup 

I

Hazardous Substances Data

50782-69-9(Hazardous Substances Data)

Toxicity

LD50 s.c. in rabbits: 15.4 mg/kg (Gordon, Leadbeater)

VX. Usage And Synthesis

Chemical Properties

VX, a sulfinated organophosphorus compound, is a nerve agent, and the most toxic of all known chemical warfare agents. VX can cause death in minutes. As little as one drop of VX on the skin can be fatal. VX is a colorless, to straw to amber-colored, odorless liquid. Looks like motor oil.

Uses

Chemical warfare agent.

Definition

ChEBI: VX nerve agent is a organic thiophosphate that is the ethyl ester of S-{2-[di(propan-2-yl)amino]ethyl} O hydrogen methylphosphonothioate. A toxic nerve agent used in chemical warfare. It has a role as an EC 3.1.1.7 (acetylcholinesterase) inhibitor and a neurotoxin. It is an organic thiophosphate and a tertiary amino compound.

General Description

Odorless liquid, with an amber color. Used as a quick-acting military chemical nerve agent.

Reactivity Profile

Organophosphates are susceptible to formation of highly toxic and flammable phosphine gas in the presence of strong reducing agents such as hydrides. Partial oxidation by oxidizing agents may result in the release of toxic phosphorus oxides.

Health Hazard

Cholinesterase inhibitor. Lowest toxic oral dose (TDLO) to humans is 4 mg/kg; lowest lethal skin dose to humans (LDLO) is 86 mg/kg. Death within 15 minutes after fatal dose is absorbed.

Health Hazard

VX is an extremely toxic organophosphorus compound. Like soman and sarin, it is a highly potent cholinesterase inhibitor, a property that results in severe toxicity. Its toxic effects in humans may become moderate to severe from oral intake of about 5 μg/kg. The symptoms may be nausea, vomiting, hypermotility, and diarrhea. Higher dosages can cause difficulty in breathing, bronchial constriction, tremor, convulsions, and death.
Intramuscular injections of VX at 2– 20 μg/kg in hens increased the levels of plasma enzymes such as creatine kinase,causing tissue damage (Wilson et al. 1988). There was depression of plasma acetylcholinesterase but not butyrylcholinesterase 2 hours after injections. Goldman and coworkers (1988) performed in vitro and in vivo tests to determine any possible genotoxic, teratogenic, and reproductive effects of exposure to VX. Mutagenicity was tested using the Ames Salmonella assay. There were no mutations induced in any of these assays. Exposure to concentrations up to 100 μg VX/mL failed to increase the recombinant activity in the yeast Saccharomyces cerevisiae. Chilcott et al. (2003) observed clinical manifestations of VX poisoning from percutaneous exposure in the domestic white pig. Application of 120 μg/kg VX produced mastication followed by miosis, salivation, fasciculations, and apnea. Although there was no correlation of cholinesterase activity with the onset of signs, mastication, however, preceded substantial cholinesterase inhibition, while the symptoms of miosis, fasciculations, and apnea arose after maximum acetylcholinesterase inhibition had been attained (5-10% of normal). The study indicated that there was a lateral diffusion of the initial droplet of VX substantially over the application site. The authors suggested that when decontaminating exposed skin attention should also be directed to the areas on the skin peripheral to the original site of contact.
Hamilton et al. (2004) have investigated percutaneous poisoning from topical application of VX on domestic swine and the effects of application site and decontamination. VX applied to the surface of the ear rapidly produced toxicity from cholinergic effect, causing apnea and death. On the other hand, VX on epigastrium markedly delayed and reduced toxicity. Skin decontamination 15 minutes after application of VX on the ear prevented any further cholinesterase inhibition and death.
Wilson and coworkers (1988) reported the antidote properties of atropine and 2pralidoxime against VX, paraoxon, and DFPin hens. The birds tolerated 150 μg/kg (five times the LD50) dose when atropine and 2pralidoxime were given before and immediately after subcutaneous injections of VX. Methylthioobidoxime and methylthio-TMB 4 given together with atropine showed protection against VX and sarin poisoning in mice (Bevandic et al. 1985). An effective antidote against VX and other nerve agents is the enzyme fetal bovine serum acetylcholinesterase. This enzyme has been reported to protect mice from multiple LD50 doses (Wolfe et al. 1987). .

Fire Hazard

Highly toxic nitrogen oxides and sulfur oxides. Avoid extreme heat.

Safety Profile

Human poison by skin contact. Experimental poison by intraperitoneal and subcutaneous routes. An experimental teratogen. Other experimental reproductive effects. Human systemic effects by ingestion and intravenous routes: hallucinations and distorted perceptions, blood pressure increase, hypermotihty, diarrhea, nausea and vomiting, visual field changes, sleep disturbance. A chemical warfare agent. A combustible liquid. When heated to decomposition it emits very toxic fumes of SOx and NOx.

Potential Exposure

VX is a quick-acting, military chemical nerve agent. VX is the most potent of all chemical warfare agents. It attacks the nervous system, causing the muscles to convulse uncontrollably. The nerve agent works similarly to pesticide and was originally developed in the early 1950s. Highly persistent, it can be dangerous for weeks and remains a liquid for more than 24 hours. It poses little vapor hazard. The least volatile of the nerve agents, VX, is very slow to evaporate; about as slowly as motor oil. VX is highly efficient at skin penetration, more than any other of the “G” agents. It is used in the M-23 land mine. VX was never used in combat by the United States and all stockpiles of approximately 4400 t of the Agent were destroyed in 2008 by the United States Army Chemical Materials Agency (CMA).

Shipping

UN2810 Toxic liquids, organic, n.o.s., Hazard Class: 6.1; Labels: 6.1-Poison Inhalation Hazard, Technical Name Required. Military driver shall be given full and complete information regarding shipment and conditions in case of emergency. AR 50-6 deals specifically with the shipment of chemical agents. Shipments of agent will be escorted in accordance with AR 740-32. Packing Group: 1.

Incompatibilities

Relatively stable at room temperature. Unstabilized VX of 95% purity decomposed at a rate of 5% a month @ 71℃. Relatively stable at room temperature. Unstabilized VX of 95% purity decomposes at a rate of 5% a month @ 71℃. At pH 12, the toxic by-product has a halflife of about 14 days and in 90 days there is about a 64-fold reduction. Organophosphates are susceptible to formation of highly toxic and flammable phosphine gas in the presence of strong reducing agents such as hydrideds and active metals. Partial oxidation by oxidizing agents may result in the release of toxic phosphorus oxides Contact with metals may evolve flammable hydrogen gas.

Waste Disposal

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 . Recommended field procedures (for quantities greater than 50 g): NOTE: These procedures can only be used with the approval of a qualified expert or safety officer. An alcoholic calcium HTH mixture is prepared by adding 100 mL of denatured ethanol to a 900 mL slurry of 10% calcium HTH in water. This mixture should be made just prior to use since the HTH can react with the ethanol. Fourteen grams of alcoholic calcium HTH solution is used for each gram of VX. Agitate the contamination mixture as the VX is added. Continue the agitation for a minimum of 1 hour. This reaction is reasonable exothermic and evolves substantial off gassing. The evolved reaction gases should be routed through a decontaminate filled scrubber prior to release through filtration systems. After completion of the one hour minimum agitation, 10% sodium hydroxide is added in a quantity equal to that necessary to assure that a pH of 12.5 is maintained for a period not less than 24 hours. Hold the material at a pH between 10 and 12 for a period not less than 90 days to ensure that a hazardous intermediate material is not formed. After sealing the head, the exterior of the drum shall be decontaminated and then labeled in accordance with IAW, EPA, and DOT regulations. All leaking containers shall be overpacked with vermiculite placed between the interior and exterior containers. Decontaminate and label per IAW EPA and DOT regulations. Conduct general area monitoring to confirm that the atmospheric concentrations do not exceed the airborne exposure limit. If the alcoholic calcium HTH mixture is not available then the following decontaminates may be used instead and are listed in the order of preference: Decontaminating Solution No. 2 , Supertropical Bleach Slurry (STB), and sodium HTH. Open pit burning or burying of VX or items containing or contaminated with VX in any quantity is prohibited. The detoxified VX (using procedures above) can be thermally destroyed by incineration in an EPA approved incinerator in accordance with appropriate provisions of federal, state and local RCRA regulations. Note: Several states define decontaminated surety material as a RCRA Hazardous Waste.
Recommended laboratory procedures (for quantities less than 50 g): If the active chlorine of the calcium HTH is at least 55%, then 80 g of a 10% slurry is required for each gram of VX. Proportionally more HTH is required if the chlorine activity of the HTH is lower than 55%. The mixture is agitated as the VX is added and the agitation is maintained for a minimum of one hour. If phasing of the VX/deconsolution continues after 5 minutes, an amount of denatured ethanol equal to a 10 wt.% of the total agent/decon shall be added to assist miscibility. Note: Ethanol should be minimized to prevent the formation of a hazardous waste. Upon completion of the one hour agitation the decon mixture shall be adjusted to a pH between 10 and 11. Conduct general area monitoring to confirm that the atmospheric concentrations do not exceed the airborne exposure limit.

VX.(50782-69-9)Related Product Information

• O-ETHYL METHYLPHOSPHONOTHIOATE
• VX.
• O,S-DIETHYL METHYLPHOSPHONOTHIOATE
• O,S-Dimethyl methylphosphonothioate
• O-ethyl S-(2-dimethylaminoethyl) methylphosphonothioate