Sarin Gas
Sarin Gas
History and global production of sarin
Sarin gas (O-Isopropyl methylphosphonofluori-date), also called GB, is one of the most dangerous and toxic chemicals known. It belongs to a class of chemical weapons known as nerve agents, all of which are organophosphates. The G nerve agents (including tabun, sarin, and soman) are all extremely toxic, but not very persistent in the environment. Pure sarin is a colorless and odorless gas, that is extremely volatile, and can spread quickly through the air. A lethal dose of sarin is about 0.5 milligrams; it is approximately 500 times more deadly than cyanide.
History and global production of sarin
Sarin was first synthesized in 1938 by a group of German scientists researching new pesticides. Its name is derived from the names of the chemists involved in its creation: Schrader, Ambros, Rudriger and van der Linde. A pilot plant to study the use of sarin was built in Dyernfurth. Although they produced between 500 kg and 10 tons of sarin, the German government decided not to use chemical weapons in artillery during World War II. The Soviet army captured the plant at Dyernfurth at the end of the war and resumed production of sarin in 1946.
Between about 1950 and 1956, the United States produced sarin. Several other countries also have confirmed or suspected stocks of sarin.
Sarin as a weapon
Iraq produced sarin between 1984 and 1985, when weapons inspectors were ordered to leave the country. Prior to Operation Iraqi Freedom in 2003, Iraq had admitted to once having at least 790 tons of the nerve agent. In 1987 and 1988, the United Nations confirmed that Iraq used a combination of organo-phosphorous nerve agents against Kurds in northern Iraq. It is estimated that 5,000 people were killed and 65,000 others were wounded in these attacks. There was also extreme environmental damage.
On March 20, 1995, the Aum Shinrikyo doomsday cult released the nerve agent sarin in a Tokyo subway. This incident killed 11 and injured more than 5,500 people. Members of the cult left soft drink containers and lunch boxes filled with the toxin on the floor of subway trains. They punctured the containers with umbrellas just as they exited the cars. The attack was timed for rush hour, so as to affect as many people as possible. Because the sarin was of low quality and the affected cars were quickly sealed once the sarin was detected, the magnitude of the attack was suppressed.
Sarin poisoning
Like other organophosphate nerve agents, sarin inhibits the break down of the enzyme acetyl-cholinesterase. Under normal conditions, this enzyme hydrolyzes the neurotransmitteracetylcholine. When sarin is present, the build up of acetyl-cholinesterase results in the accumulation of excessive concentrations of acetyl-choline in nerve synapses. This overstimulates para-sympathetic nerves in the smooth muscle of the eyes, respiratory tract, gastrointestinal tract, sweat glands, cardiac muscles, and blood vessels.
After exposure to sarin, symptoms begin within minutes. If a person survives for a few hours after exposure, he or she will likely recover from the poisoning. The first symptoms of sarin poisoning include a runny nose, blurred vision, sweating and muscle twitches. Longer exposures result in tightness of the chest, headache, cramps, nausea, vomiting, involuntary defecation and urination, convulsions, coma, and respiratory arrest.
Atropine acts an antidote for nerve agent, including sarin. Atropine binds to one type of acetylcholine receptor on the post-synaptic nerve. A second antidote is pralidoxime iodide (PAM), which blocks sarin from binding to any free acetyl-cholinesterase. Both should be administered as soon as possible following exposure to the toxin. Diazapam can also be used to prevent seizures and convulsions. Soldiers fighting in regions where chemical weapons are likely to be deployed are now equipped with a Mark I antidote kit containing both atropine and PAM.
Resources
BOOKS
Bollinger, Matt. Recognizing and Treating Exposure to Anthrax, Smallpox, Nerve Gas, Radiation, and other Likely Agents of Terrorist Attack. Boulder: Paladin Press, 2004.
Crawford, John. The Last True Story I’ll Every Tell: An Accidental Soldier’s Account of the War in Iraq. New York: Penguin, 2006.
OTHER
Centers for Disease Control and Prevention. “Facts About Sarin” <http://www.bt.cdc.gov/agent/sarin/basics/facts.asp> (accessed November 1, 2006).
Council on Foreign Relations. Terrorism Questions and Answers, “Sarin” <http://www.terrorismanswers.com/weapons/sarin.html> (accessed November 1, 2006).
Juli Berwald
Sarin Gas
Sarin Gas
█ JULI BERWALD
Sarin gas (O-Isopropyl methylphosphonofluoridate), also called GB, is one of the most dangerous and toxic chemicals known. It belongs to a class of chemical weapons known as nerve agents, all of which are organophosphates. The G nerve agents, including tabun, sarin and soman, are all extremely toxic, but not very persistent in the environment. Pure sarin is a colorless and odorless gas, and since it is extremely volatile, and can spread quickly through the air. A lethal dose of sarin is about 0.5 milligrams; it is approximately 500 times more deadly than cyanide.
History and global production of sarin. Sarin was first synthesized in 1938 by a group of German scientists researching new pesticides. Its name is derived from the names of the chemists involved in its creation: Schrader, Ambros, Rudriger, and van der Linde. A pilot plant to study the use of sarin was built in Dyernfurth. Although they produced between 500 kg and 10 tons of sarin, the German government decided not to use chemical weapons in artillery during World War II. The Soviet army captured the plant at Dyernfurth at the end of the war and resumed production of sarin in 1946. The Russian government currently has about 11,700 tons of sarin.
Between about 1950 and 1956, the United States produced sarin. It is estimated to have stockpiles totaling 5,000 tons of the nerve agent stored in different parts of the country. Several other countries including Syria, Egypt,
Iran, Libya, North Korea, and Iraq have confirmed or suspects stocks of sarin.
Sarin as a weapon. Iraq produced sarin between 1984 and 1985, when weapons inspectors were ordered to leave the country. Prior to Operation Iraqi Freedom, Iraq had admitted to once having at least 790 tons of the nerve agent. In 1987 and 1988, the United Nations confirmed that Iraq used a combination of organo-phosphorous nerve agents against Kurds in northern Iraq. It is estimated that 5,000 people were killed and 65,000 others were wounded in these attacks. There was also extreme environmental damage.
On March 20, 1995, the Aum Shinrikyo doomsday cult released the nerve agent sarin in a Tokyo subway. This incident killed 11 and injured more than 5,500 people. Members of the cult left soft drink containers and lunch boxes filled with the toxin on the floor of subway trains. They punctured the containers with umbrellas just as they exited the cars. The attack was timed for rush hour, so as to affect as many people as possible. Because the sarin was of low quality and the affected cars were quickly sealed once the sarin was detected, the magnitude of the attack was suppressed.
Sarin poisoning. Like other organophosphate nerve agents, sarin inhibits the break down of the enzyme acetylcholinesterase. Under normal conditions, this enzyme hydrolyzes the neurotransmitter acetylcholine. When sarin is present, the build up of acetyl-cholinesterase results in the accumulation of excessive concentrations of acetylcholine in nerve synapses. This overstimulates parasympathetic nerves in the smooth muscle of the eyes, respiratory tract, gastrointestinal tract, sweat glands, cardiac muscles, and blood vessels.
After exposure to sarin, symptoms begin within minutes. If a person survives for a few hours after exposure, he or she will likely recover from the poisoning. The first symptoms of sarin poisoning include a runny nose, blurred vision, sweating, and muscle twitches. Longer exposures result in tightness of the chest, headache, cramps, nausea, vomiting, involuntary defecation and urination, convulsions, coma, and respiratory arrest.
Atropine acts an antidote for nerve agent, including sarin. Atropine binds to one type of acetylcholine receptor on the post-synaptic nerve. A second antidote is pralidoxime iodide (PAM), which blocks sarin from binding to any free acetyl-cholinesterase. Both should be administered as soon as possible following exposure to the toxin. Diazapam can also be used to prevent seizures and convulsions. Soldiers fighting in regions where chemical weapons are likely to be deployed are now equipped with a Mark I antidote kit containing both atropine and PAM.
█ FURTHER READING:
ELECTRONIC:
Centers for Disease Control and Prevention: "Facts About Sarin" <http://www.bt.cdc.gov/agent/sarin/basics/facts.asp> (March 25, 2003).
Council on Foreign Relations: Terrorism Questions and Answers, "Sarin" <http://www.terrorismanswers.com/weapons/sarin.html> (March 25, 2003).
"Sarin Poisoning on Tokyo Subway" <http://www.sma.org/smj/97june3.htm> (March 25, 2003).
SEE ALSO
Biological Warfare
Nerve Gas
Toxins
Sarin Gas
Sarin gas
Sarin gas (O-Isopropyl methylphosphonofluoridate), also called GB, is one of the most dangerous and toxic chemicals known. It belongs to a class of chemical weapons known as nerve agents, all of which are organophosphates. The G nerve agents (including tabun, sarin and soman), are all extremely toxic, but not very persistent in the environment. Pure sarin is a colorless and odorless gas, and since it is extremely volatile, and can spread quickly through the air. A lethal dose of sarin is about 0.5 milligrams; it is approximately 500 times more deadly than cyanide.
History and global production of sarin
Sarin was first synthesized in 1938 by a group German scientists researching new pesticides . Its name is derived from the names of the chemists involved in its creation: Schrader, Ambros, Rudriger and van der Linde. A pilot plant to study the use of sarin was built in Dyernfurth. Although they produced between 500 kg and 10 tons of sarin, the German government decided not to use chemical weapons in artillery during World War II. The Soviet army captured the plant at Dyernfurth at the end of the war and resumed production of sarin in 1946. The Russian government currently has about 11,700 tons of sarin.
Between about 1950 and 1956, the United States produced sarin. It is estimated to have stockpiles totaling 5,000 tons of the nerve agent stored in different parts of the country. Several other countries including Syria, Egypt, Iran, Libya, North Korea, and Iraq have confirmed or suspected stock of sarin.
Sarin as a weapon
Iraq produced sarin between 1984 and 1985, when weapons inspectors were ordered to leave the country. Prior to Operation Iraqi Freedom in 2003, Iraq had admitted to once having at least 790 tons of the nerve agent. In 1987 and 1988, the United Nations confirmed that Iraq used a combination of organo-phosphorous nerve agents against Kurds in northern Iraq. It is estimated that 5,000 people were killed and 65,000 others were wounded in these attacks. There was also extreme environmental damage.
On March 20, 1995, the Aum Shinrikyo doomsday cult released the nerve agent sarin in a Tokyo subway. This incident killed 11 and injured more than 5,500 people. Members of the cult left soft drink containers and lunch boxes filled with the toxin on the floor of subway trains. They punctured the containers with umbrellas just as they exited the cars. The attack was timed for rush hour, so as to affect as many people as possible. Because the sarin was of low quality and the affected cars were quickly sealed once the sarin was detected, the magnitude of the attack was suppressed.
Sarin poisoning
Like other organophosphate nerve agents, sarin inhibits the break down of the enzyme acetyl-cholinesterase. Under normal conditions, this enzyme hydrolyzes the neurotransmitter acetylcholine . When sarin is present, the build up of acetyl-cholinesterase results in the accumulation of excessive concentrations of acetylcholine in nerve synapses. This overstimulates parasympathetic nerves in the smooth muscle of the eyes, respiratory tract, gastrointestinal tract, sweat glands , cardiac muscles and blood vessels.
After exposure to sarin, symptoms begin within minutes. If a person survives for a few hours after exposure, he or she will likely recover from the poisoning. The first symptoms of sarin poisoning include a runny nose, blurred vision , sweating and muscle twitches. Longer exposures result in tightness of the chest, headache, cramps, nausea, vomiting, involuntary defecation and urination, convulsions, coma and respiratory arrest.
Atropine acts an antidote for nerve agent, including sarin. Atropine binds to one type of acetylcholine receptor on the post-synaptic nerve. A second antidote is pralidoxime iodide (PAM), which blocks sarin from binding to any free acetyl-cholinesterase. Both should be administered as soon as possible following exposure to the toxin. Diazapam can also be used to prevent seizures and convulsions. Soldiers fighting in regions where chemical weapons are likely to be deployed are now equipped with a Mark I antidote kit containing both atropine and PAM.
See also Bioterrorism.
Resources
organizations
Centers for Disease Control and Prevention. "Facts About Sarin" [cited March 25, 2003]. <http://www.bt.cdc.gov/agent/sarin/basics/facts.asp>.
Council on Foreign Relations. Terrorism Questions and Answers, "Sarin" [cited March 25, 2003]. <http://www.terrorismanswers.com/weapons/sarin.html>.
other
"Sarin Poisoning on Tokyo Subway" [cited March 25, 2003]. <http://www.sma.org/smj/97june3.htm>.
Juli Berwald
Sarin Gas
Sarin Gas
Sarin gas (O-Isopropyl methylphosphonofluoridate), also called GB, is one of the most dangerous and toxic chemicals known. It belongs to a class of chemical weapons known as nerve agents, all of which are organophosphates. The G nerve agents, including tabun , sarin, and soman, are all extremely toxic, but not very persistent in the environment. Pure sarin is a colorless and odorless gas, and since it is extremely volatile, can spread quickly through the air. A lethal dose of sarin is about 0.5 milligrams; it is approximately 500 times more deadly than cyanide.
Sarin, which has become infamous in contemporary times from its use in Iraq, and by the Aum Shinrikyo doomsday cult, was first synthesized in 1938 by a group of German scientists researching new pesticides. Its name is derived from the names of the chemists involved in its creation: Schrader, Ambros, Rudriger, and van der Linde. A pilot plant to study the use of sarin was built in Dyernfurth. Although they produced between 500 kg and 10 tons of sarin, the German government decided not to use chemical weapons in artillery during World War II. The Soviet army captured the plant at Dyernfurth at the end of the war and resumed production of sarin in 1946. The Russian government currently has about 11,700 tons of sarin.
Between about 1950 and 1956, the United States produced sarin. It is estimated to have stockpiles totaling 5,000 tons of the nerve agent stored in different parts of the country. Several other countries including Syria, Egypt, Iran, Libya, and North Korea have confirmed or suspected stocks of sarin.
Like other organophosphate nerve agents, sarin inhibits the break down of the enzyme acetyl-cholinesterase. Under normal conditions, this enzyme hydrolyzes the neurotransmitter acetylcholine. When sarin is present, the build up of acetyl-cholinesterase results in the accumulation of excessive concentrations of acetylcholine in nerve synapses. This overstimulates parasympathetic nerves in the smooth muscle of the eyes, respiratory tract, gastrointestinal tract, sweat glands, cardiac muscles, and blood vessels.
After exposure to sarin, symptoms begin within minutes. If a person survives for a few hours after exposure, he or she will likely recover from the poisoning. The first symptoms of sarin poisoning include a runny nose, blurred vision, sweating, and muscle twitches. Longer exposures result in tightness of the chest, headache, cramps, nausea, vomiting, involuntary defecation and urination, convulsions, coma, and respiratory arrest.
Atropine acts an antidote for nerve agent, including sarin. Atropine binds to one type of acetylcholine receptor on the post-synaptic nerve. A second antidote is pralidoxime iodide (PAM), which blocks sarin from binding to any free acetyl-cholinesterase. Both should be administered as soon as possible following exposure to the toxin. Diazapam can also be used to prevent seizures and convulsions.
see also Toxicological analysis; Toxicology.