VX

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VX is a type of chemical weapon called a nerve agent. It is a very toxic chemical. Because it is so toxic, it cannot be used as anything other than a chemical weapon. The United Nations classifies VX as a weapon of mass destruction.[1]

VX is the most toxic nerve agent ever created.[2] The Council on Foreign Relations says: "A fraction of a drop of VX, absorbed through the skin, can fatally disrupt the nervous system."[2]

The Chemical Weapons Convention of 1993, an international law, made it illegal for countries to use chemical weapons like VX. It also made it illegal to make or keep more than 100 grams of VX. It allows some scientists to make and use amounts under 100 grams only if they are trying to create an antidote, or doing medical research.[3]

Creation[change | change source]

VX is one of the "V-series nerve agents," which were made in the 1950s by the United Kingdom's military researchers.[4] Nobody agrees on why these nerve agents are called "V-series." Different people say the V stands for "Victory," "Venomous" (poisonous), or "Viscous" (thick liquid).[4]

VX as a weapon[change | change source]

VX is a liquid that cannot be smelled or tasted. It is a thick liquid with the texture of motor oil. As a weapon, it can be used as a liquid or an aerosol. It could be spread by air, through water, or through food.[5]

Making VX is difficult and very dangerous. Many toxic and dangerous chemicals are used in the process.[2]

VX works the same way other nerve agents do. It blocks nerve signals from getting from the brain to the body. Normally, a neurotransmitter (chemical messenger) called acetylcholine tells the body's muscles to tighten up when they need to. When it is time for the muscles to relax, an enzyme called acetylcholinesterase destroys acetylcholine, so the muscles stop getting the signal to relax.[6]

VX blocks acetylcholinesterase. Acetylcholine builds up, because it is not getting destroyed by acetylcholinesterase. The muscles get tighter and tighter, because the extra acetylcholine keeps telling them to. The extra acetylcholine also signals the parasympathetic nervous system to work extra hard. These changes in the body cause the signs and symptoms of VX poisoning.[7]

Signs and symptoms[change | change source]

The earliest symptoms of VX poisoning depend on how a person was exposed to VX. If VX got on a person's skin, their first symptoms might be sweating or twitching muscles near where the VX was. If the person breathed in VX, their first symptoms might be a runny nose and trouble breathing, caused by the bronchi (the tubes that bring air to the lungs) getting narrower.[7]

To breathe, a person's diaphragm muscle (shown in green) has to tighten and then relax. VX can stop the diaphragm from being able to relax, and stop a person from breathing.

All nerve agents have the same symptoms, because they work the same way. They make the parasympathetic nervous system work too hard. They also keep signals from the brain from getting through to the body, so the brain cannot tell the muscles to relax. This causes a group of unique symptoms:[8][9]

  • The person's nose will run, tears will come out of their eyes, and they will drool because their body is making so much extra saliva (spit)
  • As the brain loses control over the body's muscles, the person will not be able to stop themselves from urinating and defecating
  • The person will have nausea, vomiting, and abdominal pain
  • The person's heart rate will be slow
  • The bronchi will get narrower, causing trouble breathing
  • The body will make a lot of extra mucus, which can build up in the lungs and make breathing even harder

People with VX poisoning can have seizures and go into status epilepticus. They can die because their breathing muscles get so tight that they do not work.[7]

Treatment[change | change source]

Nerve agent antidote kits used by the U.S. military, containing atropine and pralidoximine

If a person got VX on their skin, the first step is to wash away the VX with bleach and water. This is called decontamination. Removing clothing that the VX touched is also part of decontamination.[5][10]p.30

There are antidotes for nerve agent poisoning. They have to be given together.[11]

  1. Atropine keeps extra acetylcholine from having any more effects on the body
  2. Pralidoxime (2-PAM) reverses the effects of VX. It does this by attaching to the VX in the body. With pralidoxime attached to it, VX cannot keep blocking acetylcholinesterase. Acetylcholinesterase starts working again, and can destroy the extra acetylcholine that has built up in the body.

However, nerve agents like VX work very quickly. Antidotes usually have to be given within a few minutes after a person was exposed to VX. If pralidoxime is not given soon enough, it cannot reverse VX's effects.[10]p.6

Usually, a sedative like diazepam (Valium) is also given. This will help the body's muscles relax, and can prevent seizures.[12]

Related pages[change | change source]

References[change | change source]

  1. "United Nations Security Council Resolution 687 (1991)" (PDF). UN.org. The United Nations. April 3, 1991. Retrieved February 10, 2016.
  2. 2.0 2.1 2.2 "VX". Council on Foreign Relations. January 1, 2006. Retrieved February 10, 2016.
  3. "Convention on the Prohibition of the Development, Production, Stockpiling, and use of Chemical Weapons and on their Destruction (Chemical Weapons Convention)" (PDF). opcw.org. Organisation for the Prohibition of Chemical Weapons. 1993. Retrieved February 10, 2016.
  4. 4.0 4.1 "Nerve Agents". emergency.cdc.gov. United States Centers for Disease Control and Prevention (CDC). April 19, 2013. Retrieved December 26, 2015.
  5. 5.0 5.1 "VX: Nerve Agent". National Institute for Occupational Safety and Health. United States Centers for Disease Control and Prevention. May 26, 2015. Missing or empty |url= (help); |access-date= requires |url= (help)
  6. Mistovich, Joseph J.; Karren, Keith J.; Hafen, Brent (July 18, 2013). Prehospital Emergency Care (10th ed.). Prentice Hall. ISBN 978-0133369137.
  7. 7.0 7.1 7.2 Sidell, Frederick R.; Takafuji, Ernest T; Franz, David R. (eds.) (1997). Medical Aspects of Chemical and Biological Warfare. Washington, D.C.: Office of the Surgeon General at TMM Publications. pp. 129–179. Unknown parameter |Chapter= ignored (|chapter= suggested) (help)
  8. Wagner, Mary J.; Promes, Susan B. (January 1, 2007). Last Minute Emergency Medicine: A Concise Review for the Specialty Boards. McGraw Hill Professional. p. 12. ISBN 978-0-07-150975-6.
  9. "EMS Subspecialty Certification Review Course: Organophosphates" (PDF). UTSW.ws. University of Texas Southwestern Medical Center. September 5, 2013. Retrieved February 9, 2016.
  10. 10.0 10.1 Department of the Army (November 13, 2012). Toxic Chemical Agent Safety Standards (PDF) (Report). United States Army. Retrieved February 10, 2016.
  11. "Cholinesterase Inhibitors: Including Insecticides and Chemical Warfare Nerve Agents, Part 4 - Section 11, Management Strategy 3: Medications - 2-PAM (2-Pyridine Aldoxime Methylchloride) (Pralidoxime)". Agency for Toxic Substances and Disease Registry. United States Centers for Disease Control and Prevention. October 16, 2010. Retrieved February 10, 2016.
  12. Marrs TC 2004. "The role of diazepam in the treatment of nerve agent poisoning in a civilian population". Critical Reviews in Toxicology 23 (3): 145-157. PMID 15862082.