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Except where otherwise noted, data are given for materials in their (at 25 °C 77 °F, 100 kPa).N ( Y N?)VX is an extremely toxic in the class, specifically, a. In the class of, it was developed for military use in after of earlier discoveries of toxicity in research. In its pure form, VX is an oily, relatively, liquid that is amber-like in color. Because of its low volatility, VX persists in environments where it is dispersed.VX, short for 'venomous agent X', is one of the best known of the V nerve agents and was first discovered at in England during the early 1950s based on research first done by Dr. Schrader, a chemist working for IG Farben in Germany during the 1930s. Now one of a broader V-series of agents, they are classified as and have been used as a 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, another nerve agent with a similar.
On such exposure, these agents severely disrupt the body's signaling between the and, leading to a prolonged, of all the muscles in the body including the, and death by.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 due to these physical and biochemical characteristics. As a, it is categorized as a and is banned by the of 1993, 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'. Contents.Physical properties VX is an odorless and tasteless chiral organophosphorous chemical with a molecular weight of 267.37 g/mol. Under standard conditions it is an amber-colored liquid with a boiling point of 298 °C (568 °F), and a freezing point of −51 °C (−60 °F). Its density is similar to that of water.
It has a value of 2.047, meaning it is relatively hydrophobic with an about 100-fold more partitioning into octanol, over water. Its low of 0.09 pascals (1.3 ×10 −5 psi) gives it a low volatility, resulting in a high persistence in the environment.When weaponized, it can be dispersed as a liquid, aerosol, or as a mixture with a clay or talc in the form of a thickened agent. Mechanism of action VX is an.It works by blocking the function of (AChE). Normally, when a is stimulated, it releases the neurotransmitter (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 into the inactive substances and 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 the ongoing stimulation and eventual fatigue of all affected and ACh receptors. This results in initial violent contractions, followed by 'sustained supercontraction restricted to the fluid of the subjunctional and prolonged, depolarizing.' The prolonged blockade results in flaccid paralysis of all the muscles in the body, and it is such sustained paralysis of the that causes death. Accumulation of acetylcholine in the brain also causes neuronal, due to activation of receptors and release.The extreme toxicity of VX is partly due to the fact that the inhibitor was designed to be an excellent structural mimic for the transition state of the natural substrate (acetylcholine) of acetylcholinesterase.
VX has a very high 'on-rate' to react with the target enzyme and form a stable P-O-C bond (phosphorylation). However, compared with other highly toxic nerve agents like soman or sarin, VX undergoes relatively slow 'aging.'
Aging is a time-dependent side reaction (loss of an alkoxyl group) that occurs on nerve agents after phosphonylation and renders the nerve agent-acetylcholinesterase complex highly resistant to regeneration by any known antidote. Slower aging by VX suggests it should be possible to develop more effective antidotes and treatments.The reaction products of acetylcholinesterase with VX before and after the 'aging' reaction were solved near atomic resolution by X-ray crystallography to aid in antidote development. The X-ray structures revealed the specific parts of the VX molecule that interact with key residues and sub-sites of the target enzyme. The structural kinetic of phosphonylation followed by aging also showed an unexpected conformational change in the catalytic triad suggestive of an 'induced fit' between the VX molecule and acetylcholinesterase.Chemistry Synthesis VX is at its atom. The individual are identified as S P-(−)-VX, and R P-(+)-VX (where the 'P' subscript highlights that the chirality is at phosphorus).VX is produced via the, which gives a mixture of the two enantiomers. This entails a series of steps whereby is to produce. The resulting material is reacted with to form a.
This is then with to produce the mixed. Finally, this immediate precursor is reacted with sulfur to form VX. VX can also be delivered in 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 with elemental sulfur (Agent NE) as is done in the. It may also be produced by mixing with sulfur compounds, as with the liquid dimethyl polysulfide mixture (Agent NM) in the canceled program. Solvolysis Like other nerve agents, VX may be destroyed by reaction with strong nucleophiles.
The reaction of VX with concentrated aqueous results in two competing 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 and both reactions are slow. In contrast, reaction with the anion (hydroperoxidolysis) leads to exclusive cleavage of the P–S bond and a more rapid overall reaction. US Army Nerve Agent Weapons Experiments on Rabbits & effects of antidotes.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 (runny nose) and/or tightness in the chest with shortness of breath (bronchial constriction). (pinpointing of the pupils) may be an early sign of agent exposure, but is not usually used as the only indicator of exposure. Toxicology 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.
The (LD 50)—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 (LCt 50), measuring the concentration of the vapor per length of time exposed, is estimated for VX to be 30–50 mgmin/m 3. Treatment 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. 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. When possible, decontamination is completed before the casualty is taken for further medical treatment. 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 and (2-PAM), as well an injected sedative/antiepileptic such as. In several nations the nerve agent antidotes are issued for military personnel in the form of an such as the United States military.Atropine blocks a subset of acetylcholine receptors known as (mAchRs), so that the buildup of acetylcholine produced by loss of the acetylcholinesterase function has a reduced effect on their target receptor.
2-PAM reactivates the acetylcholinesterase enzyme (AChE), thus reversing the effects of VX. VX and other organophosphates block AChE activity by binding to and the enzyme via transfer of the moiety from VX to the of AChE; this inactivates AChE and produces an inactive bybroduct from the remaining portion of the VX molecule. Pralidoxime (2-PAM) removes this phosphate group.
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Diagnostic tests. Further information: Discovery The chemists Ranajit Ghosh and J. Newman discovered the V-series nerve agents at the British firm in 1952, patenting diethyl S-2-diethylaminoethyl phosphonothioate in November 1952. Further commercial research on similar compounds ceased in 1955 when its lethality to humans was discovered. Started production of large amounts of VX in 1961 at.The discovery occurred when the chemists were investigating a class of compounds (organophosphate of substituted aminoethanethiols).
Like, an earlier investigator of organophosphates, Ghosh found that they were quite effective. 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 were sent to the British Armed Forces research facility at 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 Purple Possum, with the (VR) coming a close second (Amiton is largely forgotten as VG). The name is a contraction of the words 'venomous agent X'.Beginning in 1959, the United States Army began volunteer testing of VX in humans. 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, 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.
Use as a weapon In 1988, a United Nations inquiry established that was responsible for deploying VX against Angolan insurgents during the. UN toxicologists obtained trace elements of VX from soil, water, and plant samples taken from areas where Cuban troops had recently carried out counter-insurgency operations. Patients demonstrating symptoms of exposure to nerve agents first began appearing in Angolan hospitals around 1984.There was evidence of a combination of chemical agents having been used by against the Kurds in the in 1988 under, including VX. Hussein later testified to that Iraq had researched VX, but had failed to weaponize the agent due to production failure. And allied forces invaded Iraq, no VX agent or production facilities were found. However, UNSCOM laboratories detected traces of VX on warhead remnants.In December 1994 and January 1995, Masami Tsuchiya of 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 had suspected as a spy, was attacked at 7:00 am on 12 December 1994 on the street in Osaka by and another AUM member, who sprinkled the nerve agent on his neck. He chased them for about 90 metres (100 yd) before collapsing, dying ten 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 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. Unlike the cases for gas (the and ), VX was not used for mass murder.On 13 February 2017, half-brother of North Korean leader, died after in in. According to the authorities he was with VX which was found on his face. The authorities further reported that one of the women suspected of applying the nerve agent experienced some physical symptoms of VX-poisoning. The director of a non- research program of the stated that VX fumes would have killed the suspected attackers even if they had been wearing gloves, suggesting that the VX was applied as that would mix to form VX only on the victim's face.
Worldwide stockpiles Some countries known to possess VX are the United States, the United Kingdom, Russia, North Korea, and Syria. A pharmaceutical facility, the, 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. Had obtained soil samples identified as containing (EMPTA), a chemical used in the production of VX which may also have commercial applications.
Chemical weapons experts later suggested that the widely used organophosphate insecticide could have been mistaken for EMPTA. Cuba obtained VX during the 1980s and deployed it during its.In 1969, the U.S. Government cancelled 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 (Cut Holes And Sink 'Em) program, in which old ships were filled with chemical weapons stockpiles and then. CHASE 8 was conducted on 15 June 1967, in which the steamship Cpl. Gibson was filled with 7,380 VX rockets and scuttled in 2,200 m (7,200 ft) of water off the coast of.
Was used for VX stockpile destruction starting in 1990 with in the North Pacific with other incineration plants following at, and with the last of the VX inventory destroyed on 24 December 2008. Stockpile elimination Worldwide, VX disposal has continued since 1997 under the mandate of the.
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.In fiscal year 2008, the 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, 19 bulk containers holding 640 kg (1,400 lb) each, and one.The 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.The remaining VX stockpile in the U.S. Will be treated by the in Kentucky, part of the program. The program was established as an alternative to the incineration process successfully used by the, 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.In Russia, the U.S. Is providing support for these destruction activities with the. The Initiative has been able to convert a former chemical weapons depot at, 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, which are stored at seven sites. In popular culture One of the best-known references to VX in popular culture is its use in the 1996 film, which centers on a threatened VX attack on from the island of.
The film uses, 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.See also. Inhibitors: Reversible: Carbamates:.; Stigmines:.; Others:. Irreversible: Organophosphates:.; Others:.
(, ). ( ). Unsorted:.
Reactivators:.
Updated: with so many new iPhones now in the spotlight, and with the, you might be left wondering how the, compares to the most conservative member of the new guard, theCan the new base iPhone be considered an upgrade over last year’s flagship, or are those already in possession of an iPhone X better to stick with or instead consider the XR’s more potent companions – the and?It’s also worth noting Apple have discontinued the iPhone X, replacing it with the XS, but that doesn’t mean you have to make the jump. So what do we think?Related: iPhone XR vs iPhone X – DesignThe has the iPhone X to thank for its good looks. Last year’s flagship iPhone signified a fork in Apple’s smartphone design language, most notably with the adoption of an elongated display and the characteristic notch – a feature that became commonplace in 2018. The X and XR both take the form of a sandwich of curved glass with a metal frame bordering the face and back – polished stainless steel on the iPhone X, colour-matched matte 7000 series aluminium on the XR. Whichever handset you pick, there’s no headphone jack here, just the company’s own Lightning connector at the base.