- bleeding from the nose and mouth
- difficulty breathing
- disturbed sleep and nightmares
- extreme sensitivity to light
- foaming at the mouth
- high fevers
- influenza-like symptoms
- loss of consciousness
- loss of memory
- nausea and vomiting
- post-traumatic stress disorder
- respiratory problems
- uncontrollable trembling
- vision problems, both temporary and permanent
Discovered in the 1930's by German scientists, nerve agents are much more lethal than World War I chemical weapons. They can enter into the body through inhalation or through the skin. They cause damage to the nervous system, leading to loss of muscle control and, more commonly, death as a resuslt of paralysis of the respiratory system. They can cause breathing problems, confusion, convulsions, and ultimately death.
Nerve agents block the action of acetylcholinesterase (AChE), an enzyme required to break down acetylcholine. Acetylcholine is a neurotransmitter used to send messages in the nervous system, particularly for muscle contraction. Without AChe to break down the acetylcholine, the neurotransmitter builds up in the synapses between neurons and causes uncontrollable muscle spasms, which eventually lead to death by suffocation.
Unlike the toxic gases used during World War I, nerve agents have very little odor, making them more viable to cause injury or death before being detected. Fortunately, impurities in the sarin used in the 1995 Tokyo subway attacks caused a foul odor that alerted subway passengers to evacuate.
VX sits stored in 1269 steel containers at the Newport Chemical Depot, Indiana, United States
G-series gases can cause death in 1 to 10 minutes from exposure, compared to 4-24 hours for phosgene. The G-series nerve agents are similar to insecticides.
Sarin is known in the military by the abbreviation GB. It is a highly lethal nerve agent. Only 1.7g of sarin touching the skin or 1 mg in the lungs is required to kill a person. Death may result in one minute after direct ingestion of 10 micrograms per kilogram of body weight. At room temperature, sarin is a colorless, odorless liquid. It has a high vapor pressure, which means it evaporates wuickly.
Initial symptoms after exposure are a runny nose, tightness in the chest, and contraction of the pupils, followed by difficulty breathing, nausea, and drooling. The victim will continue to lose control of bodily functions as he vomits, defecates, and urinates. Twitching and jerking are ultimately followed by a coma and death by suffocation through convulsive spasms. These symptoms are indicative of any nerve gas.
Sarin has a relatively short shelf life. It will degrade after several weeks to several months. Impurities in precursor materials significantly decrease shelf life. The issue of short shelf life can be overcome by purifying the chemicals and by using binary chemical technology, where two precursor chemicals are stored separately in the same shell. Immediately prior to use, the two chemicals are combined. It can be made more persistent by adding oils or certain petroleum products.
Antidotes include atropine and pralidoxime.
Sarin was discovered in 1938 in Wuppertal-Elberfeld, Germany. In an attempt to create stronger pesticides, two German scientists stumbled across sarin, the most toxin of the four G-series nerve agents made by Germany. It was named in honor of the scientists: Gerhard Schrader, Ambros, Rudiger, and Van der Linde. It was mass produced by Germans but never used for fear of Allied retaliation in the form of chemical warfare. Estimates for the aggregate total sarin production by the Nazis range from 500 kg to 10 tons.
Code Red Think Quest Team
Tabun is abbreviated in the military as GA. Depending on purity, it is a colorless to brown liquid. It is relatively volatile, though less than sarin or soman. When pure, tabun is odorless, but it is commonly described as having a faint fruity odor in small quantities and a "fishy" smell in large quantities. Since tabun is easier to produce than other G-series nerve agents and the process is relatively widely understood, newer countries wishing to develop a nerve agent or terrorist organizations often start by producing tabun.
Tabun requires only 1000mg on conact with the skin to kill. Its effects are similar to the effects of all nerve agents.
Tabun was the first chemical nerve agent to be discovered. While conducting research on organophosphate insecticides in 1936, German scientist Gerhard Schrader produced tabun. During World War II, a plant for the manufacture of tabun was built in modern-day Poland. Only about 12,500 tons were produced before the plant was overrun by the Soviet military. The Soviet Union dismantled the plant and took it back with them. Soon, they abandoned tabun for soman and sarin.
Soman is abbreviated in the military as GD. Soman is volatile, corrosive, colorless liquid with a faint odor at room temperature. It is more lethal than sarin and tabun, though its effects are largely the same. Soman was discovered by Richard Kuhn in Germany in 1944.
V-series nerve agents are even more potent than G-agents. Extremely small doses of V-agents can penetrate skin and contaminate the ground, plants, and equipment. If absorbed through the skin, V-series gases are 2000 times more poisonous than mustard gas. "V" signifies long persistence. Unlike G-series gases which dissipate quickly and have only short-term effects, V-series nerve agents persist
V-agents must be manufactured, stored, and delivered in a specific manner, or they will not caused the desired effect.
Only 15mg of VX poison gas in contact with the skin is required to kill its victim. If the victim inhales it, less than half that amount is required. If absorbed in liquid form, it takes 1-2 hours to take effect. When in gaseous form, however, it is far more deadly and acts almost immediately.
Despite its name, it is normally in a liquid state. VX is oderless and is not volatile. Some forms of VX are so adhesive that it is almost impossible to remove from the surface it is in contact with. Thus, a strategic attack on an airfield or enemy base can leave VX stuck to buildings and the ground, which has the potential to kill anyone attempting to use the area.
The LD50 (lethal dose to 50%) is as little as 10 mg for humans. This means that 10mg of VX nerve agent will kill 50% of humans exposed.
VX has not been used in warfare because it is too dangerous to use with wind that could blow the VX back. At present, the only known countries to possess VX nerve gas are the US, Syria, Great Britain, France, and Russia. Great Britain abandoned it for nuclear weapons after discovering it.
The antidote to VX nerve gas is atropine, a toxin itself. It counteracts the effect of VX by blocking acetylcholine receptors to prevent the excess acetylcholine from firing the neurons. It is normally injected into the arm or thigh. For gaseous attacks, which are lethal if not treated immediately, the atropine must go directly into the heart. Full body protection and gas masks are the best prevention to avoid exposure in a VX missile attack.
VX was developed in the Porton Down Chemical Weapons Research Centre, Wiltshire, England in 1952. The chemist Ranajit Ghosh discovered V-series nerve agents, but VX was passed over in facor of continuing with sarin as their chemical weapon of choice. In 1956, Great Britain unilaterally renounced the use of biological and chemical weapons. In 1958, the British traded VX gas technology with the United States for information on thermonuclear weapons.
The US entered into mass production of VX in 1961. Later on, large stockpiles of VX were destroyed by incineration at Johnston Island in the Pacific Ocean as part of accession to the Chemical Weapons Convention.
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Chapter 34, p161.
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