| Product Name: | VX. | | Synonyms: | VX.;S-(2-DIISOPROPYLAMINOETHYL)-O-ETHYLMETHYLPHOSPHONOTHIOLATE;AGENTVX;ORTHO-ETHYLS-(2-DIISOPROPYLAMINOETHYL)METHYLPHOSPHONOTHIOATE;ETHYLS-2-DIISOPROPYLAMINOETHYLMETHYLPHOSPHOROTHIOLATE;ETHYLS-2-DIISOPROPYLAMINOETHYLMETHYLPHOSPHONOTHIOLATE;Ethyl-S-dimethylaminoethyl methylphosphonothiolate: (VX nerve agent);Methylphosphonothioic acid O-ethyl S-[2-(diisopropylamino)ethyl] ester | | CAS: | 50782-69-9 | | MF: | C11H26NO2PS | | MW: | 267.37 | | EINECS: | | | Product Categories: | | | Mol File: | 50782-69-9.mol |  |
| 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. Preparation Products And Raw materials |
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