Tabun
Tabun
Tabun (or “GA”) is one of a group of synthetic chemicals that were developed in Germany during the 1930s and 1940s (Tabun was developed in 1936). The original intent of these compounds, including tabun, was to control insects. These pesticides were similar to organophosphates in their action on the nervous system. However, Tabun and the other human-made nerve agents proved to be much more potent than the organophosphates, and so quickly became attractive as chemical weapons.
Tabun is one of the G-type nerve agents, along with Sarin and Soman. They are all clear, colorless, and tasteless. As a result, Tabun mixes readily with water, and so can be used as a water-poisoning agent. Food can also be contaminated. The fluid form of Tabun can also be absorbed through the skin.
When in water, Tabun loses its potency relatively quickly, compared to airborne vapors, which can remain potent for a few days. The vapors can even bind to clothing, where they will subsequently be released for 30 minutes or so. People close to the contaminated person can themselves be affected by the vapor. Tabun vapors tend to be denser than air and so settle into low-lying depressions or valleys. People in such regions are especially susceptible.
Like the other members of the G series, Tabun is a nerve agent. Specifically, it inhibits an enzyme called cholinesterase. The enzyme breaks apart a compound that acts as a communication bridge between adjacent nerve cells. Normally, the transient formation and destruction of the bridge allows a control over the transmission of nerve impulses. But, the permanent presence of the bridging compound means that nerves ‘fire’ constantly, which causes muscles to tire and eventually stop functioning. In the case of the lungs, this can be fatal.
Symptoms of Tabun poisoning, which can begin within minutes of exposure, include runny nose, watery and painful eyes, drooling, excessive sweating, rapid breathing, heart beat abnormalities, and, in severe cases, convulsions, paralysis, and even fatal respiratory failure.
Treatment for the inhalation of Tabun consists of three timed injections of a nerve agent antidote such as atropine. Since this may or may not be successful, prevention remains the most prudent strategy. Protective clothing including a gas mask is a wise precaution for those who are in an environment where the deployment of Tabun is suspected.
While the United States once had an active chemical weapons development program that included the weaponization of Tabun, this program was halted decades ago. Other countries may still be engaged in such weapons development. For example, Iraq is suspected of having used Tabun against Iranians during the Iran-Iraq war in the 1980s.
See also Biological warfare; Decontamination methods; Forensic science; Nerve gas.
Resources
BOOKS
Government of the United States. 21st Century Complete Guide to Chemical Weapons and Chemical Terrorism - U.S. Demilitarization Program, Stockpile Destruction Emergency Plans, Nerve Gas and Blister Agent Civilian Treatement and First Aid, Home Sheltering Plans. Washington, DC: Progressive Management, 2002.
OTHER
Agency for Toxic Substances and Disease Registry. “Facts About Tabun.” Division of Toxicology, Centers for Disease Control and Prevention. March 7, 2003. <http://www.bt.cdc.gov/agent/tabun/basics/facts.asp> (accessed October 19, 2006).
Agency for Toxic Substances and Disease Registry. “Nerve Agents (GA, GB, GD, VX).” Division of Toxicology, Centers for Disease Control and Prevention. March 13, 2003. <http://www.atsdr.cdc.gov/tfactsd4.html> (accessed October 19, 2006).
Tabun
Tabun
Tabun (or "GA") is one of a group of synthetic chemicals that were developed in Germany during the 1930s and 1940s (Tabun was developed in 1936). The original intent of these compounds, including tabun, was to control insects. These pesticides were similar to organophosphates in their action on the nervous system. However, Tabun and the other human-made nerve agents proved to be much more potent than the organophosphates, and so quickly became attractive as chemical weapons.
Tabun is one of the G-type nerve agents, along with Sarin and Soman. They are all clear, colorless, and tasteless. As a result, Tabun mixes readily with water, and so can be used as a water-poisoning agent. Food can also be contaminated. The fluid form of Tabun can also be absorbed through the skin.
When in water, Tabun loses its potency relatively quickly, compared to airborne vapors, which can remain potent for a few days. The vapors can even bind to clothing, where they will subsequently be released for 30 minutes or so. People close to the contaminated person can themselves be affected by the vapor. Tabun vapors tend to be denser than air and so settle into low-lying depressions or valleys. People in such regions are especially susceptible.
Like the other members of the G series, Tabun is a nerve agent. Specifically, it inhibits an enzyme called cholinesterase. The enzyme breaks apart a compound that acts as a communication bridge between adjacent nerve cells. Normally, the transient formation and destruction of the bridge allows a control over the transmission of nerve impulses. But, the permanent presence of the bridging compound means that nerves "fire" constantly, which causes muscles to tire and eventually stop functioning. In the case of the lungs, this can be fatal.
Symptoms of Tabun poisoning, which can begin within minutes of exposure, include runny nose, watery and painful eyes, drooling, excessive sweating, rapid breathing, heart beat abnormalities, and, in severe cases, convulsions, paralysis, and even fatal respiratory failure.
Treatment for the inhalation of Tabun consists of three timed injections of a nerve agent antidote such as atropine. Since this may or may not be successful, prevention remains the most prudent strategy. Protective clothing including a gas mask is a wise precaution for those who are in an environment where the deployment of Tabun is suspected.
While the United States once had an active chemical weapons development program that included the weaponization of Tabun, this program was halted decades ago. Other countries may still be engaged in such weapons development. For example, Iraq is suspected of having used Tabun against Iranians during the Iran-Iraq war in the 1980s.
█ FURTHER READING:
BOOKS:
Government of the United States. 21st Century Complete Guide to Chemical Weapons and Chemical Terrorism—U.S. Demilitarization Program, Stockpile Destruction Emergency Plans, Nerve Gas and Blister Agent Civilian Treatement and First Aid, Home Sheltering Plans. Washington, DC: Progressive Management, 2002.
ELECTRONIC:
Agency for Toxic Substances and Disease Registry. "Nerve Agents (GA, GB, GD, VX)." Division of Toxicology, Centers for Disease Control and Prevention. March 13, 2003. <http://www.atsdr.cdc.gov/tfactsd4.html>(April 10, 2003).
Agency for Toxic Substances and Disease Registry. "Facts about Tabun." Division of Toxicology, Centers for Disease Control and Prevention. March 7, 2003. <http://www.bt.cdc.gov/agent/tabun/basics/facts.asp>(April 10, 2003).
SEE ALSO
Chemical Warfare
Mustard Gas
Sarin Gas
Tabun
Tabun
Tabun (or "GA") is one of a group of synthetic chemicals that were developed in Germany during the 1930s and 1940s. (Tabun was developed in 1936.) The original intent of these compounds, including tabun, was to control insects. These pesticides were similar to organophosphates (pesticides that contain phosphorus and act as nerve poisons on most animals) in their action on the nervous system. However, tabun and the other human-made nerve agents proved to be much more potent than the organophosphates, and so quickly became attractive as chemical weapons.
Tabun is one of the G-type nerve agents, along with sarin and soman. They are all clear, colorless, and tasteless. As a result, tabun mixes readily with water, and so can be used as a water-poisoning agent. Food can also be contaminated. The fluid form of tabun can also be absorbed through the skin.
When in water, tabun loses its potency relatively quickly, compared to airborne vapors, which can remain potent for a few days. The vapors can even bind to clothing, where they will subsequently be released for 30 minutes or so. People close to the contaminated person can themselves be affected by the vapor. Tabun vapors tend to be denser than air and so settle into low-lying depressions or valleys. People in such regions are especially susceptible.
Like the other members of the G series, tabun is a nerve agent. Specifically, it inhibits an enzyme called cholinesterase. This enzyme breaks apart a compound that acts as a communication bridge between adjacent nerve cells. Normally, the transient formation and destruction of the bridge allows a control over the transmission of nerve impulses. But, the permanent presence of the bridging compound means that nerves "fire" constantly, which causes muscles to tire and eventually stop functioning. In the case of the lungs, this can be fatal.
Symptoms of tabun poisoning, which can begin within minutes of exposure, include runny nose, watery and painful eyes, drooling, excessive sweating, rapid breathing, heart beat abnormalities, and, in severe cases, convulsions, paralysis, and even fatal respiratory failure.
Treatment for the inhalation of tabun consists of three timed injections of a nerve agent antidote such as atropine. Since this may or may not be successful, prevention remains the most prudent strategy. Protective clothing including a gas mask is a wise precaution for forensic investigators who are in an environment where the deployment of tabun is suspected.
see also Chemical warfare; Sarin gas.