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Blood agents are absorbed into the body primarily by breathing. These agents poison an enzyme called cytochrome oxidase, blocking the use of oxygen in every cell. By preventing the normal transfer of oxygen from the blood to body tissues, the agent rapidly affects all tissues, especially the central nervous system.
The very high volatility of the blood agents makes them less useful as CW, but their low persistency also has its advantages. If used on a battlefield, not much time is needed for the agent to disperse to safe levels, enabling the attacking force to enter the target area. The blood agents hydrogen cyanide (AC) and cyanogen chloride (CK) have been studied extensively and were used sporadically during World War I.
Arsine, also called Arthur, is a gas with a mild, garlic-like odor. Often used as a delayed-action casualty agent, arsine interferes with the functioning of the blood and damages the liver and kidneys. Slight exposure results in headaches and uneasiness. Increased exposure causes chills, nausea and vomiting. Severe exposure damages the blood and causes anemia. A dose of 5,000mg-min/m3 is lethal to 50 percent of exposed adults. It is estimated that 2 milligrams of SA per kilogram of body weight would be lethal to humans. Arsine was studied extensively during World War I, but because of its high volatility and chemical instability, weaponization of arsine was abandoned. Arsine is used today for industrial processing of gallium arsenide chips in the semiconductor industry.
Cyanogen chloride is a colorless, highly volatile liquid with a pungent, biting odor. The odor is usually unnoticed because the agent causes instant irritation to the mucous membranes and tearing to the eyes. Although cyanogen chloride quickly evaporates, vapors may persist in forest or jungle environments for quite some time under suitable weather conditions. Cyanogen chloride irritates the respiratory tract in a manner similar to phosgene, but fluid will accumulate in the lungs much faster than in phosgene poisoning. A dose of 11,000mg-min/m3 is lethal to 50 percent of exposed individuals. While the process of interfering with use of oxygen by body tissues is similar to that of hydrogen cyanide, cyanogen cyanide has strong irritating and choking effects and slows breathing. High concentrations of cyanogen chloride could degrade the effectiveness of a mask.
Hydrogen Cyanide can be readily synthesized in large quantities and is commercially available. Also known to the Germans as Zyklon B, hydrogen cyanide was used by the Nazis in World War II for mass executions of Jews and other prisoners. The Soviet Union perfected the use of hydrogen cyanide, including munitions and spray tanks for low altitude dissemination. Japan also investigated the use of hydrogen cyanide, but the agent was never to become a staple of its chemical arsenal. There were reports that the Japanese army employed hydrogen cyanide against during attacks on China. The United States issued cyanide pills (L pills) to its intelligence agents during World War II to be ingested in the event of capture. Unfortunately, when taken in pill form, hydrogen cyanide produces painful death-throes, which may last for several minutes. Use of hydrogen cyanide in modern battlefield situations is unsubstantiated, but reports in the 1980s suggest that hydrogen cyanide was used by the Syrian government against an uprising in Hama, Syria, in an Iraqi military attack on the Kurdish town of Halabja, Iraq, in 1988, and in Shahabad, Iran, during the Iran-Iraq War. Hydrogen cyanide has a faint bitter almond or peach kernel odor and is a colorless liquid. It is often undetectable even in lethal concentrations. A lethal dose of hydrogen cyanide varies widely with concentration. At 200mg/m3, 2,000mg-min/m3 is lethal to 50 percent of exposed adults, whereas at 150mg/m3, 4,500mg-min/m3 is lethal to 50 percent of individuals exposed. Hydrogen cyanide is a rapid-acting agent. Incapacitation can occur within one to two minutes of exposure, depending upon the concentration of the dose. Death can occur within 15 minutes after exposure to a lethal dose. Hydrogen cyanide is very unstable in storage unless in its pure form. After extended periods in storage, hydrogen cyanide forms an explosive polymer.
This section contains reference information on choking or lung irritant agents. Choking agents were among the first CW armaments produced in large quantities, and were used extensively in World War I. Inhaled in sufficient quantities, choking agents produce pulmonary edema, ultimately suffocating the victim in his own fluids.
Of the choking agents, chlorine and phosgene are the best known. Both chlorine and phosgene are used in many chemical industrial processes that make control of these compounds problematic. The technology and knowledge used to make these first-generation agents are widely available, but for several reasons they are now less attractive for military operations. First, many have a strong odor and create an irritation that alerts the victim to their presence-which gives the victim time to don protective gear or leave the area. Second, compounds such as chlorine and phosgene require large concentrations to deliver a lethal dose. Third, the modern military utility of choking agents is reduced by their tendency to dissipate quickly.
Of the 70,552 American soldiers poisoned with gasses during World War I, 1,842 were exposed to chlorine gas. First used as a chemical weapon at Ypres, France in 1915, chlorine gas acts a pulmonary irritant that causes acute damage in the upper and lower respiratory tract. By the end of World War I, Germany, France and the United Kingdom had all used chlorine gas. Not very efficient and in low concentrations, it was observed that even rudimentary protection would prevent a soldier from succumbing to its full effects. Its use, however, was still enough to cause "gas hysteria" during an attack. Chlorine is a greenish-yellow, noncombustible gas at room temperature and atmospheric pressure. The intermediate water solubility may not cause upper airway symptoms for several minutes. In addition, the density of the gas is greater than that of air, causing it to remain near ground level and increasing exposure time. Chlorine can be detected by odor at 0.3 to 0.5 parts per million, but distinguishing toxic air levels would be difficult until irritative symptoms are present.
Frequent exposure to chlorine gas can degrade an individual's sense of smell; workers with occupational exposure to the gas are at greater risk of inhalational damage in later years. Low concentrations of chlorine gas irritate the nasal passages and constrict the chest. In larger amounts, chlorine gas causes death by asphyxiation. Approximately 19,000mg-min/m3 is lethal dose to 50 percent of exposed adults. Though not currently considered a battlefield weapon, there have been reports of its use in recent times. In the late 1990s, media sources quoted Bosnian soldiers as bragging they possessed gas grenades and other mortar weapons against Serbian forces. Croatia's UN mission issued a press statement confirming that the Bosnian Muslim forces were using gasses and that the agent was most likely chlorine gas. Chlorine is not listed as a Scheduled Chemical in the CWC.
John Stenhouse, a Scottish chemist and inventor synthesized chloropicrin in 1848. Chloropicrin is currently used as a soil fumigant used for its broad biocidal and fungicidal properties. As a CW agent, chlorpicrin was first used by Russia during World War I, and was eventually delivered in artillery shell sand cylinders by all sides. Known to the British as "vomiting gas," the French as "Aquinite," and "Klop" by the Germans, chloropicrin has an intense odor, which is a distinctive warning property. During World War I, its use was often coupled with other agents because the agent often broke through gas mask filters, making soldiers vulnerable to other gasses. Chloropicrin is a colorless-to-light green oily liquid that is an irritant to all body surfaces. At 1 part per million (ppm), the victim experiences irritation with pain in the eyes; at 4 ppm exposed individuals are incapacitated; and at 20 ppm the victim has definite bronchial or pulmonary lesions. Overexposure leads to irritation of the nose and throat leading to coughing, labored breathing, sore throat, dizziness, bluish skin, vomiting and in some instances chemical pneumonitis and pulmonary edema. Skin contact can lead to chemical burns-exposure through damaged skin causes similar symptoms as those resulting from inhalation and prolonged eye exposure can result in blindness. Because of its strong odor, wide use in commercial applications and being one-fourth less toxic than phosgene, chloropicrin has not received the same attention as more potent CW agents. Although not flammable, chloropicrin presents a significant explosion hazard if involved in a fire and bulk containers are shock sensitive and can detonate. Chloropicrin decomposes in the environment.
Liquid at room temperature, diphosgene is easier to handle than phosgene and is more persistent than chlorine or phosgene. The German army first used diphosgene during World War I in May 1916. Diphosgene is a colorless liquid that emits an odor similar to green corn or new mown hay. A lethal dose is 3,000mg-min/m3 for 50 percent of resting adults exposed to the gas. Symptoms can be delayed three hours or more, though immediate symptoms may appear after exposure to high concentrations of diphosgene. Essentially, the body turns diphosgene into phosgene, producing the same results as if the victim were exposed to phosgene gas. Because diphosgene has a strong tearing effect, it has less surprise value than phosgene when used on troops. In addition, its lower volatility makes it more difficult to set up an effective surprise concentration.
Perfluoroisobutylene is an industrial gas that is a byproduct of the overheating and during the production of Teflon. PFIB has the potential to be an asphyxiating weapon, causing pulmonary edema even in low concentrations. The effects of exposure of PFIB, called "polymer fume fever," begin to appear one to two hours after exposure and is often mistaken for influenza. Like phosgene, however, severe symptoms appear suddenly over 24 to 48 hours after exposure. Exposure to PFIB can result in pulmonary edema. Because of its high toxicity the United Kingdom brought PFIB to the attention of the Conference on Disarmament in 1989 and it was entered as a restricted chemical under the CWC.
Phosgene-also called collognite or D-Stoff-was first used in the dye industry before it was used as a battlefield weapon. The first recorded use of phosgene was in the early hours of 19 December 1915, when the Germans released phosgene gas against British positions in Ypres, France. The attack resulted in 1,069 casualties, of which 116 were fatal. Within a year of the first attack with phosgene, the British were manufacturing supplies of phosgene gas at Porton Down. It was filled into artillery shells for British gunners for use in the Second Battle of the Somme in June 1916. By some estimates, over 80 percent of chemical agent fatalities in World War I were caused by phosgene. Phosgene gas will incapacitate a man within a few seconds if exposed to 100 parts per 10 million. Fatalities occur if he is exposed to concentrations of 200 parts per 10 million for one or two minutes. Phosgene kills any breathing thing by attacking the lung capillaries and then the membranes of the lung sacs, causing them to flood with watery fluids. Following exposure, death may follow within hours or up to a day. Phosgene is particularly dangerous because it does not detoxify naturally, has a cumulative effect on its victims and may persist in sheltered areas and buildings. Britain unilaterally destroyed its phosgene stocks after World War II. Phosgene was also produced and stockpiled by the Soviet Union and the United States. Egypt used Soviet-supplied phosgene stocks in the Yemeni civil war between 1963 and 1969.
This section contains reference information on nerve agents. Research into nerve agents began in the early 1930s. Nerve agents are extremely toxic chemicals that were developed in secrecy before and during World War II, primarily for military use. Related substances are used in medicine and other purposes - such as pesticides - but lack the potency of the military agents. These agents vary in persistence, with some compounds creating a short-term battlefield hazard and other compounds lingering for days or weeks. The agents in the "G" series allegedly were given the code letter G because they originated in Germany; the "V" allegedly stands for venomous.
Nerve agents kill by paralyzing the respiratory musculature and can cause death in minutes. Nerve agents inhibit acetylcholinesterase (AChE), a key enzyme to normal autonomic functions and muscular contractions. When AChE makes contact with acetylcholine, muscle fibers return to their relaxed state. When nerve agents block AChE and prevent the necessary reaction with acetylcholine that leads to relaxation, muscles that are fatigued from constant twitching weaken. More demands are made on the muscles - particularly the lungs - than the muscles can provide, causing severe fatigue. Additionally, the build up of acetylcholine leads to the constriction of smooth muscle in the respiratory tree, as well as copious amounts of mucosal and salivary excretions, which effectively smother the victim. These, in combination with the involvement of the central nervous system, finally stop respiration completely.
Dr. Gerhard Schrader, who had given the German army Tabun, became an employee of the army at the new Elberfeld facility in the Ruhr. In 1938, he developed Sarin, it's name an acronym for the development team's names: Schrader, Ambrose, Rudriger and van der Linde. Tests conducted on laboratory animals in June 1939 showed that Sarin was 10 times more effective than Tabun. During the closing stages of World War II, the Allies were surprised to have captured prototype Sarin munitions. The Soviets dismantled a Sarin plant at Falkenhagen and shipped it back to the USSR. After World War II, Sarin was also produced in Canada, the United States and the United Kingdom. In March 1995, the Japanese doomsday cult, Aum Shinrikyo, attacked Tokyo subway commuters with impure Sarin-resulting in the deaths of 12 individuals and affecting more than 5,000 other passengers. Follow-up investigations revealed that Aum Shinrikyo had sufficient material to manufacture a further 5.6 tons of Sarin. Sarin is both odorless and colorless in its liquid and vapor forms, but is described as smelling similar to rotting fruit in its impure state. Not very persistent, Sarin will linger in the environment for two to 24 hours at 5C-25C. When inhaled directly, Sarin causes death within one minute. A dose as small as 100mg-min/m3 will cause death in 50 percent of individuals exposed. If Sarin is absorbed through the skin, death results within ten minutes. Skin exposure of 1.7g on the skin of a man weighing 70 kilograms (roughly 150 pounds) is fatal to 50 percent of exposed individuals. Sarin is five times as heavy as air and represents no fire or explosion hazard. This makes Sarin an ideal agent for delivery by artillery, rockets or aerial spray. Because Sarin is very volatile and non-persistent, it is often thickened with oils or other petroleum products when filled in munitions to leave low-level residues.
Soman was the last of the German nerve agents to be developed. Its name might have been either derived from the Greek verb "to sleep" or the Latin stem for "to bludgeon." Soman combines features of both Sarin and Tabun. In 1945, the archives on Soman research were captured by a Soviet task force. Under the direction of chemical warfare expert Professor Colonel Kargin, the material was shipped to the Karpov Institute in Moscow. A year later, Soman production was under way in the USSR. Soman has a lower evaporation rate than Sarin, remaining effective for about a day, which means that air movement will create a down-wind hazard - a cone-shaped plume of the agent blowing away from the point of delivery. A dose of 50mg-min/m3 of vapor is lethal to 50 percent of those exposed; 350mg of Soman liquid on the skin of a man weighing 70 kilograms (roughly 150 pounds) is fatal to 50 percent of individuals exposed. Though it requires 30 percent more exposure than Sarin to have a lethal effect, it is more readily absorbed into the bloodstream and more readily active with neural tissue - particularly the brain. Soman prevents the formation of cholinesterase in the neural synapses. The peripheral and central nervous systems stimulate themselves to their own destruction in 10 to fifteen minutes. This process includes violent muscle activity and malfunctioning major organs. The brain is the most profoundly affected and ceases to function before the bodily convulsions stop. Soman resembles a clear, heavy solvent or light machine oil and smells initially like over-ripe peaches and changes to a camphor-like odor as the concentration increases. Soman is less of a hazard to exposed skin in the open, but the membranes of the eyes and any open wounds are easy access points that cause rapid death. Soman is 6.5 times as heavy as air, and easily flows into low-lying areas. As a result, it can be used to "flood" subterranean field positions, tunnels and basements, producing long-term contamination. In 1955, the Soviets accidentally created a thickened version of Soman, designated VR-55, in their quest to perfect VX gas. (It was only later discovered that VR-55 compound and VX were different compounds). It was believed that the thickening process involved synthetic polymers and was designed to reduce evaporation and increase the agent's persistency and skin absorption rate.
Tabun, also known as Trilon-83, was isolated accidentally in January 1937 by German doctor Gerhard Schrader while he was engaged in the search for new pesticides at IG Farben. Controlled tests of the substance in laboratory animals revealed that death could occur within 20 minutes of exposure. Experiments were later conducted on German death camp inmates. Schrader reported his discovery to the Wehrmacht chemical laboratory at Berlin Spandau and within a year, Tabun was adopted as a nerve agent and the first nerve gas went into production at Elberfeld in the Ruhr. Production was relocated to Dyhernfurth-am-Oder in 1940. During World War II, the plant produced 12,000 tons of Tabun, of which 2,000 tons were filled into shells and 10,000 into bombs. At least one Tabun factory was captured by the Soviets, giving them a head start on the CW race. The Western allies considered Tabun production in the 1950s, but it was rejected in favor of the more powerful Sarin nerve agent. Tabun manufacture must be conducted under tightly controlled conditions, with high-speed ventilation and atmospheric filtration. Tabun is a rapidly acting lethal nerve agent that is either absorbed through the skin as a liquid or inhaled as a vapor. It is a pale to dark amber that gives off a colorless vapor. There is very little odor in its pure state, but emits a "rotting fruit" smell as it oxidizes. A vapor dose of approximately 400 mg-min/m3 will kill 50 percent of exposed individuals. A 1.0-gram dose of Tabun on the skin of a man weighing 70 kilograms (roughly 150 pounds) is fatal to 50 percent of exposed individuals. Autopsies of Tabun poisoning victims show massive congestion of body enzymes and fluids in all major organs.
VX was developed at the ICI Protection Laboratory, when British chemist Dr. R. Ghosh discovered an organophosphate/sulphur compound, which was immediately toxic to mammals as well as insects. The research was originally intended to derive a replacement for the insecticide DDT, but as it was too lethal to employ as a pesticide, the compound was passed to the Chemical and Biological Weapons Facility at Porton Down. The British, however, were already committed to Sarin and Tabun production and passed the compound on to the United States and Canada. Knowledge of VX production somehow leaked, and the Soviets developed their own version of VX in 1955, which they designated VR-55. However it was later discovered that VR-55 was only a thickened version of Soman. It was believed that the thickening process involved synthetic polymers and was designed to reduce evaporation and increase the agent's persistency and skin absorption rate. In 1960, the United States established a small VX plant in Newport, Indiana that was capable of producing 1,300 pounds of VX a year. In 1968, 20 pounds of VX leaked from an aerial spray tank, which was believed empty, and drifted across Skull Valley over the borders of Dugway Proving Ground, Utah, and killed 6,000 sheep. In 1969, it was discovered that canisters of VX stored on the island of Okinawa were leaking and had contaminated U.S. military personnel. As a direct result of these accidents, President Nixon issued an executive order in 1969 to halt U.S. production and development of CW. VX is designed to create casualties through skin absorption or from mist formed by aerial sprays, airburst rockets or artillery munitions. A dose of 10mg-min/m3 of vapor is sufficient to cause death to 50 percent of individuals exposed, while 10mg of VX liquid on the skin of a man weighing 70 kilograms (roughly 150 pounds) is fatal to 50 percent of individuals exposed. Within 15 minutes of exposure to a moderate dose, spasmodic symptoms will present, including twitching and loss of control of the bowels and bladder. Victims of a heavy dose die quickly, their nervous systems and heart, lungs and brain functions shut down, causing the body to cease functioning.
This section contains reference information on vesicant or "blister" agents. Vesicants are the most widely used and stockpiled CW agent and include the best-known CW agents: Mustard and Lewisite. Vesicants also include the organic arsenicals. These agents are likely to be used both to produce casualties and to force opposing troops to wear full protective equipment thus degrading fighting efficiency, rather than to kill, although exposure to such agents can be fatal. Vesicants can be thickened in order to contaminate terrain, ships, aircraft, vehicles or equipment with a persistent hazard.
These agents burn and blister the skin or any other part of the body they contact, acting on the eyes, mucous membranes, lungs, skin and blood-forming organs. The agent damages the respiratory tract when inhaled and causes vomiting and diarrhea when ingested.
Ethyldichloroarsine, also called "Dick" by the Germans-meaning fat or thick, was developed for weapon use by German chemists during World War I. This organic arsenical was produced in anticipation of a military offensive planned for the spring of 1918 to support German infantry operations. Despite serious efforts made to weaponize this compound, little literature exists on the effectiveness and history of its use. Fast acting-compared to mustard or phosgene - ethyldichloroarsine has multiple effects on the body sharing characteristics of both vesicant and choking agents. Ethyldichloroarsine is a colorless liquid that smells like rotting fruit. Possessing a high volatility at room temperature, ethyldichloroarsine poses a significant vapor threat to exposed personnel. Within seconds of contact with the skin, the agent fixes itself to the epidermis and dermis causing immediate pain. The agent penetrates deeper into the skin layers causing the destruction of subcutaneous tissue. Fluid-filled blisters form only after prolonged exposure; ethyldichloroarsine has one-twentieth the blistering action of Lewisite. Inhalation can cause pulmonary edema or "dry-land drowning." A lethal exposure, however, depends upon the period of exposure. A dose of 3,000 to 5,000 mg-min/m3 is generally a lethal dose. Because the body detoxifies ethyldichloroarsine at an appreciable rate, the product of concentration and time is not a constant. For instance, as time increases, concentration does not decrease proportionately. Therefore, exposure to 40 mg-min/m3 for 75 minutes might have an effect similar to that produced by exposure to 30 mg-min/m3 for 166 minutes. Alarmingly, organic arsenicals are simple to produce. Any nation or terrorist group with access to a basic pesticide production facility can produce these agents with relative ease.
Lewisite (2-chlorovinyldichloroarsine) is an arsenical vesicant. U.S. Army Captain W. L. Lewis is credited with first synthesizing Lewisite in 1918 though German scientists had studied it earlier. It is similar to sulfur mustard in that it damages the skin, eyes and airways, however, it differs from mustard in its clinical effects, which appear within seconds of exposure. An antidote, British anti-Lewisite (BAL) can ameliorate the effects of Lewisite if promptly administered after exposure. Pure Lewisite is an oily, colorless liquid and impure Lewisite is amber to black in color. Lewisite has a geranium-like odor and is much more volatile and persistent in colder temperatures than mustard. Lewisite remains fluid at lower temperatures, making it an ideal agent for winter conditions, however, it hydrolyzes rapidly, and on a humid day, maintaining a biologically active concentration of vapor is difficult. Highly toxic, 15,000mg-min/m3 will kill 50 percent of those exposed by inhalation. Vesication is caused by 14µg of liquid, and 30mg of liquid on skin will cause death in 50 percent of those exposed. Large quantities of Lewisite were manufactured by the United States for use in Europe in World War I, but the war ended while the ship was en route and the vessel was sunk. There has been no verified use of Lewisite on a battlefield, though Japan may have used Lewisite against China between 1933 and 1944. Lewisite is sometimes mixed with mustard to lower the freezing point of mustard. Russia uses this mixture.
Sulfur mustard (HD), called LOST (derived from the names of researchers Lommel and Steinkopf) and Yeprite, is more an oily liquid than a gas. First used in World War I, sulfur mustard is yellow-brown in color and has a garlic-like odor. Sulfur mustard is a persistent agent with low volatility at cool temperatures, but becomes a vapor hazard at high ambient temperatures. Exposure to mustard vapor, not liquid, is of primary medical concern. More than 80 percent of mustard casualties in World War I were caused by exposure to mustard vapor. Mustard vapor is three times more toxic than a similar concentration of cyanide gas, but mustard liquid is also quite toxic. Skin exposure to as little as 7 grams is lethal to 50 percent of adults. There are three forms of nitrogen mustard compound, NH1, NH2 and NH3. Nitrogen mustard (NH), a derivative of sulfur mustard, has never been used on a battlefield and is generally not considered a military agent. Similar to sulfur mustard, nitrogen mustards seem to cause more severe systemic effects, particularly in the central nervous system. Nitrogen mustard was one of the first chemotherapy agents.
Not to be confused with the choking gas phosgene (CG), phosgene oxime (CX) is not a true vesicant because it does not produce blisters. Rather it causes redness of the skin (erythema), wheals and irregular hives (urticaria). Its lesions have been compared with those caused by nettle stings, which gives this agent its nickname: "nettle gas." Because it causes extensive tissue damage, it has also been characterized as a corrosive gas. Pure phosgene oxime (dichloroformoxime) is a colorless, crystalline solid. The munitions-grade compound is a yellowish-brown liquid. Phosgene oxime has a melting point of 35C to 40C. The solid material can produce enough vapor to cause symptoms. German scientists first synthesized phosgene oxime in 1929 and both Russia and Germany had developed it prior to World War II. It is possible that both countries may have developed weapons for this agent. The United States also studied phosgene oxime, but rejected it because of its lack of biological effects and its instability. The apparent lack of biological effects was later found to be due to the low concentrations (1% to 2%) used in pre-World War II studies. Later studies indicated that a concentration less than 8 percent had little or inconsistent effects. Though phosgene oxime is not known to have been used on the battlefield, it is of military interest for several reasons. First, it penetrates garments and rubber more quickly than many other chemical agents. Secondly, it produces a rapid onset of severe and prolonged effects. Third, when mixed with other chemical agents (e.g., VX) the rapid skin damage caused by phosgene oxime will render the skin more susceptible to the second agent. Finally, if an unmasked soldier were exposed to phosgene oxime before donning his mask, the pain caused by exposure to the agent will prompt him to unmask again.
