107-44-8

liquid

Chemical warfare agent.

A colorless, odorless liquid. Almost no odor in pure state. Used as a quick-acting military chemical nerve agent. Chemical warfare agent.

Hydrolyzed by water, rapidly hydrolyzed by dilute aqueous sodium hydroxide. Water alone removes Fluoride atom producing nontoxic acid [Merck 11th ed. 1989].

Acidic conditions produce hydrogen fluoride; alkaline conditions produce isopropyl alcohol and polymers. When heated to decomposition or reacted with steam, Sarin. emits very toxic fumes of fluorides and oxides of phosphorus. Slightly corrosive to steel. Hydrolyzed by water [EPA, 1998].

Extremely toxic; lethal dose in humans may be as low as 0.01 mg/kg. Extremely active cholinesterase inhibitor. Toxic effects similar to, but more severe than those of parathion. Death within 15 minutes after fatal dose is absorbed.

Non-flammable. Acidic conditions produce hydrogen fluoride; alkaline conditions produce isopropyl alcohol and polymers. When heated to decomposition or reacted with steam, Sarin. emits very toxic fumes of fluorides and oxides of phosphorus. Slightly corrosive to steel. Hydrolyzed by water.

GB is used as a quick-acting chemical warfare nerve agent; nerve gas. Both the liquid and the vapor can kill you. Very small amounts can hurt you in one minute or less, and can quickly lead to death. A single drop, if vaporized, can kill everyone in a room ! Sarin is 26 times more deadly than cyanide gas and 20 times more deadly than Potassium cyanide.

Administration of antidotes is a critical step in managing a patient/victim. However, this may be difficult to achieve in the Red Zone, because the antidotes may not be readily available, and procedures or policies for their administration in the Red Zone may be lacking. Do not administer antidotes preventatively; there is no benefit to doing so. Diazepam (or other benzodiazepines) should be administered when there is evidence of seizures, usually seen in cases of moderate to severe exposure to a nerve agent. Remember, physical findings of localized exposure often precede systemic exposure and physical findings . Inhalation: Hold breath until respiratory protective mask is donned. If severe signs of agent exposure appear (chest tightens, pupil constriction; a lack of coordination; etc.), immediately administer, in rapid succession, all three Nerve Agent Antidote Kit(s), Mark I injectors (or atropine if directed by the local physician). Injections using the Mark I kit injectors may be repeated @ 5 to 20 minutes intervals if signs and symptoms are progressing until three series of injections have been administered. No more injec- tions will be given unless directed by medical personnel. In addition, a record will be maintained of all injections given. If breathing has stopped, give artificial respiration. Mouth- to-mouth resuscitation should be used when approved mask-bag or oxygen delivery systems are not available. Do not use mouth-to-mouth resuscitation when facial contami- nation exists. If breathing is difficult, administer oxygen. Seek medical attention immediately. Eye contact: Immediately flush eyes with water for 10?15 minutes, then don respiratory protective mask. Although miosis (pinpoint- ing of the pupils) may be an early sign of agent exposure, an injection will not be administered when miosis is the only sign present. Instead, the individual will be taken immediately to the medical treatment facility for observa- tion. Skin contact: Don respiratory protective mask and remove contaminated clothing. Immediately wash contaminated skin with copious amounts of soap and water, 10% sodium carbonate solution, or 5% liquid household bleach. Rinse well with water to remove decon- taminant. Administer an intramuscular injection with the Mark I Kit injectors only if local sweating and muscular twitching symptoms are observed. Seek medical attention immediately.

UN2810 Toxic liquids, organic, n.o.s., Hazard Class: 6.1; Labels: 6.1-Poison Inhalation Hazard, Technical Name Required. Driver shall be given full and complete information regarding shipment and conditions in case of emergency. AR 50-6 deals specifically with the shipment of chemical agents. Shipments of agent will be escorted in accordance with AR 740-32. Passenger aircraft/rail: FORBIDDEN; Cargo aircraft only: FORBIDDEN. The packaging and shipping of samples are subject to strict regulations established by the Department of Transportation (DOT), Center for Disease Control, United States Postal Service, OSHA, and International Air Transport Association). Military driver shall be given full and complete information regarding shipment and condi- tions in case of emergency. AR 50-6 deals specifically with the shipment of chemical agents. Shipments of agent will be escorted in accordance with AR 740-32.

Attacks tin, magnesium, cadmium plated steel; and some aluminums. GB decomposes tin, magne- sium, cadmium-plated steel, and aluminum. Slightly corro- sive to brass, copper, and lead. No attack on 1020 steel, Inconel, and K-Monel. Hydrolyzed by water. In acid condi- tions, GB hydrolyzes, forming hydrofluoric acid (HF). Rapidly hydrolyzed by dilute aqueous sodium hydroxide (NaOH), or sodium carbonate, forming relatively nontoxic products of polymers and isopropyl alcohol. Contact with metals may evolve flammable hydrogen gas.

ChEBI: Isopropyl methylphosphonofluoridate is a phosphinic ester that is the isopropyl ester of methylphosphonofluoridic acid. It is a phosphinic ester and a fluorine molecular entity.

Sarin and other nerve agents are irreversible cholinesterase inhibitors. Clinical effects of exposure result primarily from inhibition of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE). Normally, AChE is responsible for degradation of the neurotransmitter acetylcholine in both the peripheral and central nervous systems (CNS). Acetylcholine stimulates contraction of skeletal muscles, and hydrolysis by AChE prevents continual overstimulation of the acetylcholine receptors. Inhibition of AChE blocks degradation of acetylcholine, resulting in an accumulation of acetylcholine and cholinergic overstimulation of the target tissues. AChE inhibition can have muscarinic, nicotinic, and CNS effects, resulting in a variety of symptoms, including involuntary muscle contractions, seizures, and increased fluid secretion (e.g., tears, saliva). The cause of death is typically respiratory dysfunction resulting from paralysis of the respiratory muscles, bronchoconstriction, buildup of pulmonary secretions, and depression of the brain’s respiratory center.
Cholinesterases in the blood are often used to approximate AChE tissue levels following exposure to a nerve agent. Red blood cell cholinesterase (RBC-ChE) is found on erythrocytes and BuChE in blood plasma. Affinities of cholinesterase inhibitors for BuChE or RBC-ChE vary. The turnover rate for RBC-ChE enzyme activity is the same as that for red blood cell turnover at w1% per day. Tissue AChE and plasma BuChE activities return with synthesis of new enzymes, the rate of which differs between plasma and tissues as well as between different tissues.
Binding of nerve agents to AChE is generally considered to be irreversible unless removed by therapy. Oximes are used as therapeutics to reactivate the enzyme prior to ‘aging’ or the point at which the agent–enzyme complex is covalently linked and the enzyme cannot be reactivated. Spontaneous reactivation in the absence of oximes is possible but is unlikely to occur at a rate sufficient to be clinically important. The time required for 50% of the enzyme to become resistant to reactivation varies by nerve agent. For sarin, the t1/2 for AChE is w3 h and for RBC-ChE w5 h.
It is known that OP cholinesterase inhibitors exert their toxic effects through mechanisms other than AChE inhibition. A 1978 study by Van Meter, Karczamar, and Fiscus showed that administering a second dose of sarin to rabbits still induced seizures even though the brain AChE was already inhibited by the previous dose of sarin. Further, pretreatment protection of AChE with physostigmine still resulted in death after high-dose treatment with nerve agent. Finally, it has been shown that mice lacking AChE are actually more sensitive to OP poisoning (including sarin) than wild type mice, supporting that fact that inhibition of AChE is not the only cause of toxic effects.
One of the noncholinergic effects resultant from treatment with OP nerve agents is changes in the levels of neurotransmitters other than acetylcholine. These include g-amino-butyric acid (GABA), dopamine, serotonin, and norepinephrine. While the exact mechanism by which nerve agent exposure alters the levels of these neurotransmitters is not known, it is thought that these changes may be due to a compensatory mechanism in response to overstimulation of the cholinergic system, direct action of the OP on the proteins responsible for noncholinergic neurotransmission, or perhaps both. Nerve agents have also been shown to inhibit a family of enzymes called serine esterases, which play an important role in the metabolism and persistence of neuropeptides such as endorphins and enkephalins. Neuroinflammation as a result of nerve agent exposure is another possible mechanism for noncholinergic toxicity effects. OPs have also been shown to have direct toxic effects on cells via induction of cellular oxidative stress and mitochondrial dysfunction.

It is dissolved in a combustible solvent and burned in a chemical incinerator equipped with an afterburner and scrubber. Sarin may also be destroyed by the Shultz process of molten metal reduction (Shultz 1987). Molten aluminum, aluminum alloys, recovered scrap metal, or eutectic melts may be used at 780－1000°C (1436-1832°F). Sarin is reduced to phosphorus, alkenes, and hydrogen. The hydrocarbon products may be used in preheating the feed.
Worley (1989) reported decomposition of sarin,soman,VX,andother chemicalwarfare agentsbyoxidizingwith1,3-dibromo-4,4,5,5tetramethyl-2-imidazolidinoneorotherN,N0dihalo-2-imidazolidinone. The reaction is carriedoutinanaqueousemulsioncontaining tetrachloroethylene or a similar organic solvent.
Sarin and other nerve agents may be removed from cleaning organic solvents (trichlorotrifluoroethane and its mixtures) by such adsorbents as Fuller’s earth, activated alumina, silica gel, and silica gel impregnated with a metal salt (Fowler and McIlvaine 1989). Hydrolysis with water or dilute alkaliesshould yieldproductsof low toxicity. .