As chemical weapons, they are classified as weapons of mass destruction by the United Nations according to UN Resolution 687, and their production and stockpiling was outlawed by the Chemical Weapons Convention of 1993; the Chemical Weapons Convention officially took effect on April 291997.
Poisoning by a nerve agent leads to contraction of pupils, profuse salivation, convulsions, involuntary urination and defecation, and eventual death by asphyxiation as control is lost over respiratory muscles. Some nerve agents are readily vaporized or aerosolized and the primary portal of entry into the body is the respiratory system. Nerve agents can also be absorbed through the skin, requiring that those likely to be subjected to such agents wear a full body suit in addition to a respirator.
Initial symptoms following exposure to sarin (and other nerve agents) are a runny nose, tightness in the chest and constriction of the pupils. Soon after, the victim will then have difficulty breathing, and will experience nausea and drooling. As the victim continues to lose control of his or her bodily functions, he or she will involuntarily salivate, lacrimate, urinate, defecate, and experience gastrointestinal pain and vomiting. This phase is followed by twitching and jerking, and ultimately the victim will become comatose and suffocate as a consequence of convulsive spasms.
The effects of nerve agents are very long lasting and cumulative (increased successive exposures), and survivors of nerve agent poisoning almost invariably suffer chronic neurological damage.
Nerve agents disrupt the nervous system by inhibiting the function of acetylcholinesterase by forming a covalent bond with the site of the enzyme where acetylcholine normally undergoes hydrolysis (breaks down). The result is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted, and muscle contractions do not stop.
Pralidoxime chloride, also known as 2-PAM chloride, is also used as an antidote. Rather than counteracting the initial effects of the nerve agent on the nervous system like atropine, pralidoxime chloride reactivates the poisoned enzyme (acetylcholinesterase) by scavenging the phosphoryl rest attached on the functional hydroxyl group of the enzyme. Though safer to use, it takes longer to act.
Recent scientific breakthroughs have seen antidotes being produced in the milk of genetically modified goats.
This series is the first and oldest family of nerve agents. The first nerve agent ever synthesised was GA (tabun) in 1936. GB (sarin) was discovered next in 1938, followed by GD (soman) in 1944 and finally the more obscure GF (cyclosarin) in 1949. GB was the only G agent that was fielded by the USA as a munition, specifically in rockets, aerial bombs, howitzer rounds, and gun rounds.
Dr. Ranajit Ghosh, a chemist at the Plant Protection Laboratories of Imperial Chemical Industries was investigating a class of organophosphate compounds (organophosphate esters of substituted aminoethanethiols). Like the earlier investigator of organophosphate, Dr. Schrader, Dr. Ghosh found that they were quite effective pesticides. 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 some of the more toxic materials had in fact been sent to the British Armed Forces research facility at Porton Down for evaluation. After the evaluation was complete, several members of this class of compounds would become a new group of nerve agents, the V agents (depending on who you talk to, the V stands for Victory, Venomous, or Viscous). The best known of these is probably VX, with the Russian V-gas coming a close second (Amiton is largely forgotten as VG). This class of compounds is also sometimes known as Tammelin's esters, after Lars-Erik Tammelin of the Swedish Institute of Defense Research. Dr. Tammelin was also conducting research on this class of compounds in 1952, but for obvious reasons he did not publicize his work widely.
The V-series is the second family of nerve agents, and contains five well known members: VE, VG, VM, VR and VX, along with several more obscure analogues. The most studied agent in this family, VX, was invented in the 1950s at Porton Down in the United Kingdom. The other agents in this series have not been studied extensively, and information about them is limited. It is known, however, that the V-series agents are about 10 times more toxic than the G-agent sarin (GB).
All of the V-agents are persistent agents, meaning that these agents do not degrade or wash away easily, and can therefore remain on clothes and other surfaces for long periods. In use, this allows the V-agents to be used to blanket terrain to guide or curtail the movement of enemy ground forces. The consistency of these agents is similar to oil; as a result, the contact hazard for V-agents is primarily - but not exclusively - dermal. VX was the only V-series agent that was fielded by the USA as a munition, consisting of rockets, artillery shells, airplane spray tanks, and landmines.
In addition to the newly developed "third generation" weapons, binary versions of several Soviet agents were developed and are designated as "Novichok" agents.
In experiments, tabun was extremely potent against insects: as little as 5 ppm of tabun killed all the leaf lice he used in his initial experiment. In January 1937, Schrader observed the effects of nerve agents on human beings first-hand when a drop of tabun spilled onto a lab bench. Within minutes he and his laboratory assistant began to experience miosis (constriction of the pupils of the eyes), dizziness, and severe shortness of breath. It took them three weeks to recover fully.
In 1935 the Nazi government had passed a decree that required all inventions of possible military significance to be reported to the Ministry of War, so in May of 1937 Schrader sent a sample of tabun to the chemical warfare (CW) section of the Army Weapons Office in Berlin-Spandau. Dr. Schrader was summoned to the Wehrmacht chemical lab in Berlin to give a demonstration, after which Schrader's patent application and all related research was classified. Colonel Rüdiger, head of the CW section, ordered the construction of new laboratories for the further investigation of tabun and other organophosphate compounds, and Schrader soon moved to a new laboratory at Wuppertal-Elberfeld in the Ruhr valley to continue his research in secret throughout World War II. The compound was initially codenamed Le-100 and later Trilon-83.
Sarin was discovered by Schrader and his team in 1938 and named after their initials: Schrader, Ambrose, Rudriger, and van der Linde. It was codenamed T-144 or Trilon-46. It was found to be more than ten times as potent as tabun. Soman was discovered by Dr. Richard Kuhn in 1944 as he worked with the existing compounds, the name is derived from either the Greek 'to sleep' or the Latin 'to bludgeon', it was codenamed T-300. Cyclosarin was also discovered during WWII but the details were lost and it was 'discovered' again in 1949. The G-series naming system was created by the United States when it uncovered the German activities, labeling tabun as GA (German Agent A), sarin as GB, and soman as GD. Ethyl sarin was tagged GE and cyclosarin as GF.
In 1939, a pilot plant for tabun production was set up at Munster-Lager, on Luneberg heath near the German Army proving grounds at Raubkammer. In January 1940, construction began on a secret plant, code named "Hochwerk" (High factory), for the production of tabun at Dyherrnfurth an der Oder (now Brzeg Dolny in Poland), on the Oder River 40 km (24.9 miles) from Breslau (now Wrocław) in Silesia.
The plant was large, covering an area of 2.4 by 0.8 km (1.5 by 0.5 miles), and was completely self-contained, synthesizing all intermediates as well as the final product, tabun. The factory even had an underground plant for filling munitions, which were then stored at Krappitz (now Krapkowice) in Upper Silesia. The plant was operated by Anorgana GmbH, a subsidiary of IG Farben, as were all other chemical weapon agent production plants in Germany at the time.
Because of the plant's deep secrecy and the difficult nature of the production process, it took from January 1940 until June 1942 for the plant to become fully operational. Many of tabun's chemical precursors were so corrosive that reaction chambers not lined with quartz or silver soon became useless. Tabun itself was so hazardous that the final processes had to be performed while enclosed in double glass-lined chambers with a stream of pressurized air circulating between the walls.
3,000 German nationals were employed at Hochwerk, all equipped with respirators and clothing constructed of a poly-layered rubber/cloth/rubber sandwich that was destroyed after the tenth wearing. Despite all precautions, there were over 300 accidents before production even began, and at least 10 workers died during the 2.5 years of operation. Some incidents cited in A Higher Form of Killing: The Secret History of Chemical and Biological Warfare are as follows:
The plant produced between 10,000 and 30,000 tons of tabun before its capture by the Soviet Army.
In 1940 the German Army Weapons Office ordered the mass production of sarin for wartime use. A number of pilot plants were built, and a high-production facility was under construction (but was not finished) by the end of World War II. Estimates for total sarin production by Nazi Germany range from 500 kg to 10 tons.
During that time, German intelligence believed that the Allies also knew of these compounds, assuming that because these compounds were not discussed in the Allies' scientific journals information about them was being suppressed. Though sarin, tabun and soman were incorporated into artillery shells, the German government ultimately decided not to use nerve agents against Allied targets. The Allies didn't learn of these agents until shells filled with them were captured towards the end of the war.
This is detailed in Joseph Borkin's book The Crime and Punishment of IG Farben:
In 1952, researchers in Porton Down, England invented the VX nerve agent, inspired by the commercial pesticide Amiton, later reclassified as VG. The UK soon unilaterally abandoned the chemical weapons and chemical weapons research. In 1958 the British government traded their VX technology with the United States of America in exchange for information on thermonuclear weapons; by 1961 the US was producing large amounts of VX, and performed its own nerve agent research. The four agents (VE, VG, VM, VX) are collectively known as the "V-Series" class of nerve agents.
Since World War II, Iraq's use of mustard gas against Iranian troops and Kurds (Iran-Iraq war of 1981–1988) has been the only large-scale use of any chemical weapons. On the scale of the single Kurdish village of Halabja within its own territory, Iraqi forces did expose the populace to some kind of chemical weapons, possibly mustard gas, and most likely nerve agents.
In the Gulf War, no nerve agents (nor other chemical weapons) were used, but a number of U.S. and UK personnel were exposed to them when the Khamisiyah chemical depot was destroyed. This, and the widespread use of anticholinergic drugs as a protective treatment against any possible nerve gas attack, have been proposed as a possible cause of Gulf war syndrome.
It is unknown how these dumps of chemical weapons have affected the ocean ecology—it may be responsible for some of the decline in fish populations over the past decades, but no evidence has yet proved a causal relationship between dumping and fish population decline. The steel containers they are contained within face a variable rate of decay and no one is really certain where or how deep they were dumped. If a nerve agent leaks into the ocean, it can last up to six weeks, during which time it will kill every susceptible organism it touches before it breaks down into its nonlethal chemical components.
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