| Identification | Back Directory | [Name]
Sarin. | [CAS]
107-44-8 | [Synonyms]
GB
IMPF
Sarin.
AGENTGB
SARIN-I
SARIN-II
SARINTYPEI
SARINTYPEII
ISOPROPYLMETHYLPHOSPHONOFLUORIDATE
ISOPROPOXYMETHYLPHOSPHORYLFLUORIDE
O-ISOPROPYLMETHYLPHOSPHONOFLUORIDATE
[fluoro(isopropoxy)phosphoryl]methane
Methylfluorophosphinic acid isopropyl
Methylfluorophosphinic acid isopropyl ester
Methyl(fluoro)phosphinic acid isopropyl ester
Isopropyl methanefluorophosphonate: (Sarin: GB) | [Molecular Formula]
C4H10FO2P | [MOL File]
107-44-8.mol | [Molecular Weight]
140.093 |
| Chemical Properties | Back Directory | [Description]
Sarin, also known as "nerve agent Gas B" or GB, is an organophosphorus compound,
a colourless and odourless liquid, and a potent inhibitor of the cholinesterase enzyme.
Sarin reacts with steam or water to produce toxic and corrosive gases. Sarin is incompatible
with tin, magnesium, cadmium-plated steel, and some aluminium and reacts
with copper, brass, and lead. Sarin is the most volatile of the nerve agents, which
means that it can easily and quickly evaporate from a liquid into a vapour and spread
into the environment. People can be exposed to the vapour even if they do not come
in contact with the liquid form of sarin. | [Appearance]
liquid | [Melting point ]
-57° | [Boiling point ]
bp760 147°; bp16 56° | [density ]
d420 1.10 | [form ]
liquid | [Stability:]
Stability | [EPA Substance Registry System]
Sarin (107-44-8) |
| Hazard Information | Back Directory | [Chemical Properties]
liquid | [Uses]
Chemical warfare agent. | [General Description]
A colorless, odorless liquid. Almost no odor in pure state. Used as a quick-acting military chemical nerve agent. Chemical warfare agent. | [Air & Water Reactions]
Hydrolyzed by water, rapidly hydrolyzed by dilute aqueous sodium hydroxide. Water alone removes Fluoride atom producing nontoxic acid [Merck 11th ed. 1989]. | [Reactivity Profile]
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]. | [Health Hazard]
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. | [Fire Hazard]
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. | [Potential Exposure]
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. | [First aid]
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. | [Shipping]
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. | [Incompatibilities]
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. | [Definition]
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. | [Toxicity evaluation]
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. | [Waste Disposal]
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. . |
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