Everything about Nerve Agent totally explained
Nerve agents (also being referred to as
nerve gases, though these chemicals are liquid at room temperature) are a class of
phosphorus-containing
organic chemicals (
organophosphates) that disrupt the mechanism by which nerves transfer messages to organs. The disruption is caused by blocking
acetylcholinesterase, an
enzyme that normally relaxes the activity of
acetylcholine, a
neurotransmitter.
As
chemical weapons, they're 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.
Biological effects
As their name suggests, nerve agents attack the
nervous system of the human body. All such agents function the same way: by interrupting the breakdown of the
neurotransmitters that signal muscles to contract, preventing them from relaxing.
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'll involuntarily salivate,
lacrimate, urinate, defecate, and experience gastrointestinal pain and
emesis. 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.
Mechanism of action
When a normally functioning
motor nerve is stimulated it releases the
neurotransmitter acetylcholine, which transmits the impulse to a muscle or organ. Once the impulse is sent, the enzyme
acetylcholine esterase immediately breaks down the acetylcholine in order to allow the muscle or organ to relax.
Nerve agents disrupt the nervous system by inhibiting the
enzyme acetylcholine esterase 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 don't stop.
This same action also occurs at the gland and organ levels, resulting in uncontrolled drooling, tearing of the eyes (lacrimation), and excess production of mucous from the nose (
rhinorrhea).
Antidotes
Atropine and related
anticholinergic drugs act as antidotes to nerve agent poisoning because they block acetylcholine receptors, but they're poisonous in their own right. (Some synthetic anticholinergics, such as
biperiden may counteract the central symptoms of nerve agent poisoning better than
atropine, since they pass the blood-brain barrier better than atropine.) While these drugs will save the life of a person affected with nerve agents, that person may be incapacitated briefly or for an extended period, depending on the amount of exposure. The endpoint of atropine administration is the clearing of bronchial secretions. Atropine for field use by military personnel is often loaded in an
autoinjector, for ease of use in stressful conditions.
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.
Classes
There are two main classes of nerve agents. The members of the two classes share similar properties, and are given both a common name (such as
sarin), and a two-character
NATO identifier (such as GB).
G-Series
The
G-series is thus named because
German scientists first synthesized them. All of the compounds in this class were discovered and synthesized during or soon after World War II, led by Dr.
Gerhard Schrader (later under the employment of
I.G. Farben).
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.
V-Series
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 didn't 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 didn't publicize his work widely.
The
V-series is the second family of nerve agents, and also contains four members:
VE,
VG,
VM,
VX. 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 don't 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.
Novichok agents
The Novichok (Russian for "newcomer") agents are a series of organophosphate compounds developed in the
Soviet Union. The advantage to using new agents is that they've never been previously encountered. As a result:
- potentially, no specific treaties banning their possession or use exist
- existing detection and warning devices can't detect these agents on the battlefield
- existing protective equipment (eg gasmasks) won't protect troops from being poisoned
Insecticides
A number of
insecticides, the
phenothiazines,
organophosphates such as
dichlorvos,
malathion and
parathion, are nerve agents. The metabolism of
insects is sufficiently different from
mammals that these compounds have little effect on humans and other mammals at proper doses; but there's considerable concern about the effects of long-term exposure to these chemicals by farm workers and animals alike. At high enough doses, however,
acute toxicity and death can occur through the same mechanism as other nerve agents. Organophosphate
pesticide poisoning is a major cause of disability in many developing countries, and is often the preferred method of suicide.
History
The discovery of nerve agents
This first class of nerve agents, the so-called
G-Series, was accidentally discovered in
Germany on
December 23,
1936 by a research team headed by
Dr. Gerhard Schrader. Since
1934, Schrader had been in charge of a laboratory in
Leverkusen to develop new types of
insecticides for
IG Farben. While working toward his goal of improved insecticide, Schrader experimented with numerous
fluorine-containing compounds, eventually leading to the preparation of
tabun.
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.
During World War II
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:
Four pipe fitters had liquid tabun drain onto them; they died before their rubber suits could be removed.
A worker had 2 liters of tabun pour down the neck of his rubber suit; he died within 2 minutes.
Seven workers were hit in the face with a stream of tabun of such force that the liquid was forced behind their respirators; only two survived despite heroic resuscitation measures.
The plant produced between 10,000 and 30,000 tons of tabun before its capture by the Soviet Army.
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:
The secret gets out
Towards the end of World War II and during the occupation of Germany, the Allies recovered weapons containing the three German nerve agents of the day, prompting further research into nerve agents by the former Allies. The Red Army captured a factory producing tabun at Dyhernfurth in early 1945, they dismantled the entire site and took it back to Russia. Stocks of tabun, sarin and soman were discovered by all the Allies within Germany; the Anglo-American advance seizing around 250,000 tons of chemical weapons, the subset of nerve agents (totaling around 30,000 tons) was split with the British taking 14,000 tons of tabun-filled bombs and the Americans taking the balance of sarin-filled devices. The fourth G-series nerve agent, cyclosarin, although discovered by German scientists studying organophosphates during WWII was seemingly not found by the Allies, but independently rediscovered in 1949.
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
Since World War II, the only large scale use of chemical weapons, including nerve agents, was Iraq's use of mustard gas against Iranian troops and Kurds (Iran-Iraq war of 1981–1988); the Kurdish village of Halabja was exposed to chemical weapons, possibly mustard gas, and most likely nerve agents by Iraqi forces.
Nerve agents were not used by Iraq in the Gulf War, though 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 nerve gas attack has been proposed as a possible cause of Gulf war syndrome.
One of the most widely publicised uses of nerve agents was the 1995 terrorist attack in which operatives of the Aum Shinrikyo religious group released sarin into the Tokyo subway system.
Ocean disposal of chemical weapons
In 1972, The United States Congress banned the practice of disposing chemical weapons into the ocean. However 32,000 tons of nerve and mustard agents had already been dumped into the ocean waters off the United States by the U.S. Army. According to a 1998 report created by William Brankowitz, a deputy project manager in the U.S. Army Chemical Materials Agency, the Army created at least 26 chemical weapons dumpsites in the ocean off at least 11 states on both the west and east coasts. Additionally due to poor records, currently they only know the rough whereabouts of half of them.
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're 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'll kill every susceptible organism it touches before it breaks down into its nonlethal chemical components.
Footnotes
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