타분

For information on chemical warfare nerve agents see the ERG Criminal or Terrorist Use of CBR Agents. (ERG, 2024)

- Tabun is combustible.

TIH (Toxic Inhalation Hazard) - Term used to describe gases and volatile liquids that are toxic when inhaled. Some are TIH materials themselves, e.g., chlorine, and some release TIH gases when spilled in water, e.g., chlorosilanes. [ERG 2016].

Tabun is a combustible liquid. Extinguish with alcohol foam, carbon dioxide, or dry chemical. Complete protection required; have available decontaminants (bleach, alkali) and atropine. Bleaching powder (chlorinated line) destroys tabun but gives rise to cyanogen chloride. Poisonous gases including phosphorus oxides, cyanide and nitrogen oxides are produced in fire. Vapors are heavier than air and will collect in low areas. Containers may explode in fire. Storage containers and parts of containers may rocket great distances, in many directions. If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Notify local health and fire officials and pollution control agencies. From a secure, explosion-proof location, use water spray to cool exposed containers. If cooling streams are ineffective (venting sound increases in volume and pitch, tank discolors, or shows any signs of deforming), withdraw immediately to a secure position. If employees are expected to fight fires, they must be trained and equipped in OSHA 1910.156.

Store in tightly closed containers in a cool, well vented area away from strong oxidizers. Where possible, automatically transfer material from drums or other storage containers to process containers. Sources of ignition such as smoking and open flames are prohibited where this chemical is used, handled, or stored. Metal containers involving the transfer of this chemical should be grounded and bonded. Drums must be equipped with self-closing valves, pressure vacuum bungs, and flame arresters. Wherever this chemical is used, handled, manufactured, or stored, use explosion-proof electrical equipment and fittings.

Decontamination: Liquid: Small Areas: Puddles of liquid must be contained by covering with vermiculite, diatomaceous earth, clay, fine sand, sponges, or towels. Place the absorbed material into containers with a high density polyethylene liner. Decontaminate the area with copious amounts of aqueous sodium hydroxide solution (a minimum of 10 percent by weight). If sodium hydroxide solution is not available, then sodium carbonate may be used. Removal of porous material, including painted surfaces, that may have absorbed Nerve Agent liquid may be required as these materials could continue to re-release liquid and/or vapor after exposure has ceased. /"G" Series Nerve Agents/

Decontamination: Vapor: Small Areas: Ventilation. In heavily contaminated areas, decontamination with copious amounts of aqueous sodium hydroxide solution (a minimum of 10 percent by weight) may be required. If sodium hydroxide solution is not available, then sodium carbonate may be used. Removal of porous material, including painted surfaces, that may have absorbed Nerve Agent vapor may be required as these materials could continue to re-release vapor after exposure has ceased. /"G" Series Nerve Agents/

... Absorb liquids in vermiculite, dry sand, earth, peat, carbon, or a similar material and deposit in sealed containers. Keep this chemical out of confined spaces, such as a sewer, because of the possibility of an explosion, unless the sewer is designed to prevent the build up of explosive concentrations. ...

If decontamination cannot be left to natural processes, chemical neutralizers or removal must be used. ... Decontaminating agent DS2 is a general purpose decontaminant. It consists of 70% diethylenetriamine, 28% ethylene glycol monomethyl ether & 2% sodium hydroxide. DS2 reacts with both the nerve agents & blister agents to effectively reduce their hazards. ... Important limitations in the use of DS2 are: (a) personnel must remain masked because of the vapor; (b) rubber gloves must be worn to protect the hands; (c) it is a combustible liq, therefore it must not be allowed to get on hot metal surfaces such as running engines or exhaust pipes. /Chemicals in war/

Protection: Evacuation: Immediately isolate an area around any liquid or solid contamination for at least 700 feet in all directions. If possible, identify the agent and develop a downwind hazard diagram (see Table 3.2). Adjust the initial isolation distance as appropriate. Based on the type of release, amount of material aerosolized, persistence of the agent and local conditions (e.g., weather, population density, time of day), shelter in place until the initial cloud passes may be the most appropriate course of action since timely evacuation of the threatened downwind population may not be possible. Depending on the persistence of the agent and the potential for condensation of agent from the cloud, evacuation of the threatened population after passage of the initial cloud may be appropriate. /"G" Series Nerve Agents/

Principles and methods for destruction of chemical weapons: ... "Destruction of chemical weapons" means a process by which chemicals are converted in an essentially irreversible way to a form unsuitable for production of chemical weapons, and which in an irreversible manner renders munitions and other devices unusable as such. ... Each /nation/ shall determine how it shall destroy chemical weapons, except that the following processes may not be used: dumping in any body of water, land burial, or open-pit burning. It shall destroy chemical weapons only at specifically designated and appropriately designed and equipped facilities. ... Each /nation/ shall ensure that its chemical weapons destruction facilities are constructed and operated in a manner to ensure the destruction of the chemical weapons; and that the destruction process can be verified under the provisions of this Convention.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Any chemical release will have its maximum harmful effect against unprotected individuals, so those who self-evacuate and the rapidly rescued will generally have the best survival and recovery prospects. Planners and incident commanders should bear in mind that by the time rescue efforts are mounted survivors are generally unlikely to be found in environments or circumstances that demand the wearing of self-contained respiratory protection. Health plans should also recognize that the level of meaningful assessment or treatment that can be carried out in the ... hot zone... will be very limited. ... Rapid rescue from the hot zone represents the most practical and effective operational approach and in most major releases the most effective health response is likely to be focused in the more lightly contaminated ("warm") and uncontaminated ("cold") zones. There - and at receiving hospitals - the main emphasis should be on providing the type of respiratory and physical protection for staff so that secondary contamination is prevented. Unprotected staff should not come into contact with undecontaminated patients. /Chemical warfare agents/

Identifying the chemical(s) involved and measuring its concentration would obviously be helpful... but may not prove possible until more specialist support arrives and so responders are likely to be reliant on environmental indicators and/or the signs and symptoms displayed by victims. In practice, information gathered during clinical examination may be most useful. /Chemical warfare agents/

Decontaminating "non-ambulatory" patients is very staff-intensive and time-consuming but should generally be the primary focus of health effort at the scene. ... Dealing with those who are "ambulatory" is a quicker process as they should normally be able to carry out their own decontamination under supervision ... /Chemical warfare agents/

Current recommendations for decontamination of civilians exposed to chemicals as a result of release of such substances by terrorists. ... decontamination of the entire body - not just, for example, the hands and face, should be undertaken. All clothing should be removed and placed in sealed polythene bags. Jewelry, watches, money and other personal possessions should be collected and placed in labeled polythene bags. Two approaches to decontamination are feasible: the "bucket and sponge" method taking one patient at a time, or the mass decontamination approach with attendants supervising the passage of a queue of people through some communal shower unit. Patients who have been injured or are unable to help themselves should be decontaminated by trained attendants using a system in which a stretcher is placed on a table equipped with rollers that allows transfer of the decontaminated patient to a clean stretcher, and ambulance and to hospital. Some authorities have argued for the addition of liquid soap to the water used in automated decontamination units. This will speed the process of material but the interaction of water and soap leading to foaming when passed through a jet should be considered. Whatever means of decontamination are used it should be thorough. This means that each patient will need some minutes of attention: up to 15 or so minutes may be needed to deal with an incapacitated patient. Whatever system is used, plans for dealing with waste water and any decontaminants used should be devised and practiced in advance of an incident occurring. Waste water may be collected inside an area protected by inflatable "bunds". ...If waste water is to be allowed to run into drains, the local water company should be informed. ...Suitable towels and clothing must be provided, modesty should be preserved and consideration given to how people are to make their way home. /Chemical warfare agents/

Limited data are available on chronic or repeated exposure to tabun. The available data however, suggest that tabun is not a human carcinogen, reproductive toxin, or developmental toxin. Limited data suggest that chronic or repeated exposure to tabun may result in a delayed postural sway and/or impaired psychomotor performance (neuropathy).

0.00042 [ppm]

0.0053 [ppm]

0.039 [ppm]

These experiments were performed on a rat model. The rats were divided into eight groups and consequently exposed to either a saline solution (control), atropine or a combination of atropine and tabun. The reactivation efficacy of the oximes was estimated on the rats exposed to tabun, atropine and a reactivator of AChE. The oximes HI-6, obidoxime, trimedoxime, K203 and KR-22836 were used as representative compounds of commonly available and new AChE reactivators. Besides the positive effect of the administered reactivators on blood AChE activity, the sizable modulation of low molecular weight antioxidant (LMWA) levels was also determined. The LMWA levels in the the animals treated with the oxime reactivators were decreased in comparison with the animals treated by atropine alone. It was found that the levels of LMWA returned to the level found in the control animals when either trimedoxime, K203 or KR-22836 were administered. ...

Two guinea pig models were used to study the anticonvulsant potency of diazepam, midazolam, and scopolamine against seizures induced by the nerve agents tabun, sarin, soman, cyclosarin, O-ethyl S-(2-(diisopropylamino)ethyl)methylphosphonothioate (VX), and O-isobutyl S-(2-diethylamino)ethyl)-methyl phosphonothioate (VR). Animals instrumented for electroencephalogram recording were pretreated with pyridostigmine bromide (0.026 mg/kg im) 30 min before challenge with 2 x LD50 (s.c.) of a nerve agent. In model A, atropine sulfate (2.0 mg/kg im) and pyridine-2-aldoxime methylchloride (2-PAM; 25.0 mg/kg im) were given 1 min after nerve agent challenge, and the tested anticonvulsant was given (im) 5 min after seizure onset. In model B, a lower dose of atropine sulfate (0.1 mg/kg im) was given along with 2-PAM 1 min after nerve agent challenge, and the anticonvulsant was given at seizure onset. With the lower dose of atropine, seizure occurrence increased to virtually 100% for all agents; the time to seizure onset decreased for sarin, cyclosarin, and VX; the signs of nerve agent intoxication were more severe; and coma resulted frequently with cyclosarin. The anticonvulsant ED50 doses for scopolamine or diazepam were, in general, not different between the two models, whereas the anticonvulsant ED50 values of midazolam increased 3- to 17-fold with the lower atropine dose. Seizure termination times were not systematically effected by the different doses of atropine. The order of anticonvulsant effectiveness within each model was scopolamine > or = midazolam > diazepam. The findings indicate that the dose of atropine given as antidotal therapy can significantly influence measures of nerve agent toxicity and responsiveness to anticonvulsant therapy.

Female Pirbright-white guinea-pigs were anesthetized with urethane (1.8 g/kg) and the carotid artery, jugular vein and trachea were cannulated. After baseline measurements the animals received tabun, 60, 180 or 300 ug/kg, and 2 min later the antidotes (all iv): obidoxine, HLo 7, or HI 6 (30 or 100 umol/kg, each) or atropine 10 mg/kg or a combination of atropine and one of the oximes. Respiratory and circulatory parameters were recorded for 60 min or until the death of the animal. Erythrocyte, brain and diaphragm AChE activity was determined in every animal after the experiment. Poisoning by tabun resulted in a rapid deterioration of respiratory function and respiratory arrest within 5 min. Atropine treatment was very effective in improving the respiratory function after tabun 60 ug/kg but was ineffective after tabun 300 ug/kg. However, circulatory parameters were restored almost completely in all atropine therapy groups. Therapy of tabun 300 ug/kg poisoned animals with atropine plus oxime (30 umol/kg) improved respiration to a variable extent and restored circulation.

The effect of pyridostigmine on cardiorespiratory function after oxime + atropine injection was investigated in tabun poisoned guinea-pigs and without tabun poisoning. The trachea, a carotid artery and jugular vein were cannulated in female urethane-anesthetised Pirbright-white guinea-pigs. After baseline measurements the animals received pyridostigmine (0.05 umol/kg) and 30 min later atropine (29.5 umol/kg) plus obidoxime, HI 6 or HLo 7 (30 or 100 umol/kg) or tabun (1.85 umol/kg = 5 x LD50) followed by oxime + atropine treatment (all iv). Erythrocyte, brain and diaphragm acetylcholinesterase (AChE) activity were determined. Similar groups without pretreatment were included for comparison. Pyridostigmine aggravated the oxime + atropine induced hypotension and prevented the increase in heart rate but not the respiratory stimulation. The pyridostigmine inhibited AChE recovered only in the 100 umol/kg oxime groups at the end of the experiment. In tabun poisoning, pyridostigmine reduced the oxime + atropine induced circulatory recovery and decreased the survival time and rate. It did not affect the therapeutic oxime + atropine effect on respiratory function. These results suggest that pyridostigmine enhances oxime + atropine related circulatory depression which may be the reason for the reduced efficacy of oxime + atropine treatment in tabun poisoning...

For more Interactions (Complete) data for TABUN (17 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 39(SRC), determined from a log Kow of 0.38(2) and a regression-derived equation(3), indicates that tabun is expected to have very high mobility in soil(SRC). Volatilization of tabun from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.5X10-7 atm-cu m/mole(SRC), derived from its vapor pressure, 0.07 mm Hg(4), and water solubility, 9.8X10+4 mg/L(5). Hydrolysis in moist soil will attenuate the importance of volatilization under wet conditions(SRC). Persistence depends on moisture and weather conditions. Liquid tabun may persist for 1 to 2 days under average weather conditions and it evaporates about 20 times more slowly than water(2). In a Norwegian study, tabun was found to volatilize from snow slowly; tabun was present 2 weeks after being sprayed on snow, but was not measurable after 4 weeks(2). In another field study, the disappearance of tabun applied to snow found that <0.1% remained after 14 days(6). Tabun hydrolyzes in water at neutral or slightly acid pH and more rapidly under strong acid or alkaline conditions(7). Field studies measuring the evaporation rate of tabun at ambient temperatures from soil found that 50% of applied tabun evaporated in 1.71 hr and that 90% evaporated in 4.66 hr(8). Several species of bacteria, such as Alteromonas sp. and Flavobacterium sp. are capable of degrading G-type agents(9), but data are not available to assess the environmental importance of biodegradation(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 39(SRC), determined from a log Kow of 0.38(2) and a regression-derived equation(3), indicates that tabun is not expected to adsorb to suspended solids and sediment(SRC). Tabun hydrolyzes in water at neutral or slightly acid pH and more rapidly under strong acid or alkaline conditions(2). The rate of hydrolysis also increases with increasing temperature(2). At neutral pH and 25 °C, tabun persists in water for 14 to 28 hours; the half-life at 20 °C and pH 7.4 is approximately 8 hours. The half-life in seawater at 20 °C is shorter (4.5 hours) than in freshwater(2). Volatilization from water surfaces is not expected(4) based upon an estimated Henry's Law constant of 1.5X10-7 atm-cu m/mole(SRC), derived from its vapor pressure, 0.07 mm Hg(2), and water solubility, 9.8X10+4 mg/L(5) and tabun's susceptibility to hydrolysis. According to a classification scheme(6), an estimated BCF of 3(SRC), from its log Kow(2) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Several species of bacteria, such as Alteromonas sp. and Flavobacterium sp. are capable of degrading G-type agents(7), but data are not available to assess the environmental importance of biodegradation(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), tabun, which has a vapor pressure of 0.07 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase tabun is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 8 hours(SRC), calculated from its rate constant of 4.9X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). The UV absorption spectra of tabun in cyclohexane solution does not exhibit any absorption above 295 nm(4); therefore, tabun is not expected to be susceptible to direct photolysis by sunlight(SRC).

Toxicology: Effects: Nerve agents are the most toxic of the known chemical agents. Liquids or vapors from these agents are hazardous and can cause death within minutes after exposure. Nerve agents disrupt the function of the nervous system by interfering with the enzyme acetylcholinesterase. The major effects will be on skeletal muscles, certain organs, and the central nervous system. These compounds are similar to, but much more deadly than, agricultural organophosphate pesticides. Pathways: "G" series nerve agents are hazardous through inhalation, skin and eye exposure, ingestion, and abraded skin (e.g., breaks in the skin or penetration of skin by debris). /"G" Series Nerve Agents/

- Contracted or pinpoint pupils (miosis), redness of the membranes (conjunctiva), pain in and around the eye, dim and/or blurred vision, a sensation of pressure with heaviness, and reflex nausea and vomiting (emesis).

- Nausea, vomiting (emesis), diarrhea, abdominal pain, and cramping.

- Mild to moderate: Contracted or pinpoint pupils (miosis), runny nose (rhinorrhea), narrowing of the large airways (bronchoconstriction), fluid build up within the airways of the lungs, slight to moderate difficulty breathing or shortness of breath (dyspnea).

- Mild to moderate: Health effects may be immediate or may be delayed up to 18 hours. Profuse sweating (diaphoresis) and muscular twitching (fasciculations) at the site of contact, nausea, vomiting (emesis), diarrhea, and weakness (malaise).

Effects from skin exposure to liquid nerve agent may not develop for up to 18 hours following exposure. Patients who have inhalation exposure and who complain of chest pain, chest tightness, or cough should be observed and examined periodically for 6 to 12 hours to detect delayed-onset bronchitis, pneumonia, pulmonary edema, or respiratory failure. Patients who have severe exposure should be evaluated for persistent CNS sequelae. Patients should be advised to avoid organophosphate insecticide exposure until sequential RBC cholinesterase activity (measured at weekly to monthly intervals) has stabilized in the normal range, a process that may take 3 to 4 months after severe poisoning. /Nerve agents/

Routine laboratory studies for all admitted patients include CBC, glucose, and serum electrolyte determinations. Chest X-ray and pulse oximetry (or ABG measurements) are recommended for severe exposures. Symptomatic and asymptomatic patients suspected of significant exposure should have determinations of red blood cell (RBC) cholinesterase activity, the most useful test for nerve agent poisoning. Severe symptoms of toxicity are usually present when more than 70% of RBC cholinesterase is inhibited. However, there is no correlation between cholinesterase activity and severity of topical signs and symptoms (e.g., miosis, rhinorrhea, dyspnea). If this test is not available, plasma cholinesterase can be measured. /Nerve Agents/

Laboratory criteria for diagnosis. Biologic: A case in which nerve agents in urine are detected, as determined by CDC or one of five LRN laboratories that have this capacity. Decreased plasma or red blood cell cholinesterase levels based on a specific commercial laboratory reference range might indicate a nerve agent or organophosphate exposure; however, the normal range levels for cholinesterase are wide, which makes interpretation of levels difficult without a baseline measurement or repeat measurements over time. -OR - Environmental: Detection of organophosphate pesticides in environmental samples, as determined by FDA. However, a confirmation test for nerve agents in environmental samples is not available. /Nerve agents/

/HUMAN EXPOSURE STUDIES/ 49 /human/ subjects were exposed to tabun vapor at Cts of 0.7-21 mg min/cu m /Ct is the product of concentration of vapor or aerosol and time of exposure/... The effects included miosis, frontal headache, retrobulbar pain, engorgement of vessels in the eye, rhinorrhea, nausea and vomiting, and complaints of tightness in the chest and blurring ov vision. The signs and symptoms were at their maximal at 24-48 hr after exposure. No changes in near or far visual acuity were noted ... /and/ topical atropine in the eye relieved most of the symptoms...

/HUMAN EXPOSURE STUDIES/ 22 infantry soldiers, 2 officers and 5 civilian scientists were exposed to a Ct of 28 mg min/cum of tabun vapor/Ct is the product of concentration of vapor or aerosol and time of exposure/. The soldiers then performed a number of military field tasks at 2, 5, 24 and 30 hr after exposure and also at twilight (about 10 hr after exposure)... The scientists performed their usual work. All 29 had miosis, disturbances of vision and headache; these effects were most severe at 24 hr. Of the 29, 22 vomited, 24 had poor or no sleep, 22 had tiredness or lassitude and 26 felt depressed. Their average far vision changed from 6/6 (m) before exposure to 6/24 (m) and recovered gradually over a week. Rhinorrhea was common, but there is no mention of lower airway complaints. ...

/HUMAN EXPOSURE STUDIES/ ... Tabun, 50-400 mg in 0.5-mg droplets was placed on the volar aspects of forearm skin of six subjects. The droplets evaporated in 18-167 min, and the maximal inhibition of erythrocyte cholinesterase activity was 34% (in a subject who received 400 ug/kg). Sweating, a feeling of coolness and blanching occurred at the site after exposure, and localized sweating persisted for 8-95 days. Ambient temperatures were about 24 °C, relative humidities about 40%, and wind speed about 1 mile per hour ... .

/HUMAN EXPOSURE STUDIES/ One arm of each of four subjects was put into a chamber and exposed to concentration x times (Cts) of 1000-8000 mg min/cu m of tabun. There were no effects or changes in plasma cholinesterase activity. Later, 16 subjects dressed in shoes, shorts and protective masks were exposed to Cts of 520-2000 mg min/cu m of tabun (roughly 5-10 times the estimated LCt50 of tabun by inhalation /LCt50 is lethal concentration & time required to kill half the members of a tested population after a specified test duration/). The cholinesterase activity was inhibited more at 1 hour after exposure than at 15 min after exposure, but at neither time was it markedly inhibited. There was a slight but statistically significant difference between the cholinesterase activity of the group exposed to 520-970 mg min/cu m (between 90% and 100% of control) and that of the group exposed to 1320-2000 mg min/cu m (80-90%). There were no signs or symptoms, and electrocardiograms and blood pressures were normal.

For more Human Toxicity Excerpts (Complete) data for TABUN (23 total), please visit the HSDB record page.

AEROBIC: Generally few microorganisms found in soil can break down the C-P bond which is essential for the metabolism of some nerve chemical warfare agents(1); the biodegradation is assumed to be promoted by warm soil temperatures, adequate moisture and the presence of organic matter(1). Several species of bacteria, such as Alteromonas sp. and Flavobacterium sp. are capable of degrading G-type agents(2).

An estimated BCF of 3 was calculated in fish for tabun(SRC), using a log Kow of 0.38(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Releases of CERCLA hazardous substances are subject to the release reporting requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to the requirements of 40 CFR part 355. Tabun is an extremely hazardous substance (EHS) subject to reporting requirements when stored in amounts in excess of its threshold planning quantity (TPQ) of 10 lbs.

Tabun

CUM 100g

CUM 100g

Chemical Weapons/Chemical Weapons Precursors chemical material that, if stolen or diverted, can be converted into weapons using simple chemistry, equipment, or techniques.

Chemical warfare

Chemical warfare agent

Tabun (military designation GA) is one of the nerve agents, which are the most toxic of the known chemical warfare agents. It has a fruity odor reminiscent of bitter almonds. Exposure to tabun can cause death in minutes. A fraction of an ounce (1 to 10 mL) of tabun on the skin can be fatal. Nerve agents are chemically similar to organophosphate pesticides and exert their effects by interfering with the normal function of the nervous system.

Phosphoramidocyanidic acid, N,N-dimethyl-, ethyl ester: ACTIVE

Tabun is listed in the CWC /Chemical Weapons Convention/ Annex on Chemicals under Schedule 1.

/The Chemical Weapons Convention (CWC) is an international treaty which bans the development, production, stockpiling, and transfer or use of chemical weapons. The Convention mandates the destruction and prohibition of chemical weapons and related facilities and provides for restrictions on international trade in toxic chemicals and precursors./ The Convention's monitoring and verification measures involve submission of declarations regarding ... /Schedule 1, 2, and 3 chemicals/ and inspections by the Organization for the Prohibition of Chemical Weapons of the facilities where these chemicals are produced. ... Schedule 1 lists chemicals considered to pose a high risk to the object and purpose of the Convention by virtue of their high potential for use in activities prohibited by the CWC. These chemicals have little or no use for peaceful purposes in commercial or industrial trade. ... Schedule 1 also lists precursor chemicals that may be used in the final single technological stage of production of any of the toxic chemicals listed in the schedule.

The three most active G-agents are tabun, ethyl phosphorodimethylamidocyanidate ... (Chemical Agent Symbol GA) ... ; sarin, isopropyl methylphosphonofluoridate ... (GB) ... ; and soman, pinacolyl methylphosphonofluoridate ... (GD). ... The G-agent liquids under ordinary atmospheric conditions have sufficiently high volatility to permit dissemination in vapor form. They are generally colorless, odorless or nearly so, and are readily absorbable through not only the lungs and eyes but also the skin and intestinal tract without producing any irritation or other sensation on the part of the exposed individual. These agents are sufficiently potent so that even a brief exposure may be fatal. Death may occur in 1-10 min, or be delayed for 1-2 hr depending on the concentration of the agent.

Discovery of nerve agents in Germany led to the availability of a class of compounds at least one order of magnitude more lethal than previously known where death might occur in a matter of minutes instead of hours. Nerve agents are part of a class known as organophosphorus compounds, and were first synthesized in 1854, but their development as warfare agents did not occur until 80 years later. The first military nerve agent, ethyl phosphorodimethylamidocyanidate, known as tabun, or chemical agent symbol GA, was synthesized in 1936 by Schrader while searching for more effective agricultural organophosphorate insecticides at the German chemical firm of IG Farbenindustrie. Two years later, he synthesized a second nerve agent, isopropyl methylphosphonofluoridate, now known as Sarin or GB. In 1944, a third nerve agent, pinacolyl methylphosphonofuoridate, now known as Soman or GD, was synthesized.

For more General Manufacturing Information (Complete) data for TABUN (9 total), please visit the HSDB record page.