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| | cyclohexyl methylphosphonofluoridate Basic information |
| Product Name: | cyclohexyl methylphosphonofluoridate | | Synonyms: | cyclohexyl methylphosphonofluoridate;O-CYCLOHEXYL-METHYLPHOSPHONOFLUORIDATE;AGENTGF;Methyl cyclohexylfluorophosphonate: (GF);Phosphonofluoridic acid, P-methyl-, cyclohexyl ester | | CAS: | 329-99-7 | | MF: | C7H14FO2P | | MW: | 180.16 | | EINECS: | | | Product Categories: | | | Mol File: | 329-99-7.mol |  |
| | cyclohexyl methylphosphonofluoridate Chemical Properties |
| | cyclohexyl methylphosphonofluoridate Usage And Synthesis |
| Description | Cyclosarin was the fourth of the G-series of nerve agents to be
described following the development of tabun (GA), the first
G-agent to be discovered in 1938. Cyclosarin was given the
designation GF, reflective of the order in which it was
discovered.
As with the other G-agents, after learning of its properties
the German Ministry of Defense began studying cyclosarin
along with the United States and United Kingdom following
World War II. Cyclosarin, unlike other G-agents, was not
selected for mass production by any nations at that time
possibly due to the cost of reagents required for cyclosarin
production. After the Gulf War, it was discovered that Iraq
had stockpiled G-agents including cyclosarin. Rockets containing
both sarin and cyclosarin were found and destroyed
by the US forces at the Khamisiyah weapons depot resulting
in exposure to these two agents. One possible reason why
Iraq stockpiled cyclosarin despite the fact that no other
nation had done so, is that the precursor chemicals for sarin
production, but not cyclosarin were embargoed making it
a more desirable selection. Additionally, cyclosarin is the
most persistent of the G-agents potentially making it
a greater threat.
In 1997, the Chemical Weapons Convention (CWC) was
enacted that banned the production, stockpiling, and use of
chemical weapons (including cyclosarin) and called for the
destruction of existing chemical weapons stockpiles. The CWC
is administered by the Organisation for the Prohibition of
Chemical Weapons, of which nearly all world nations are
a part. | | Chemical Properties | Cyclosarin (GF) is a liquid nerve agent/organ-
ophosphate containing fluoride. GF is a colorless liquid.
The odor is variously described as nondescript, sweet, fruit-
like. Odor threshold is about 12 milligram per cubic meter. | | Uses | Cyclosarin is a synthetic organophosphate (OP) compound
used in chemical warfare and terrorism. | | Definition | A highly toxic colourlessliquid, C7H14FO2P; r.d. 1.13; m.p.–30°C; b.p. 239°C. it is a fluorinatedorganophosphorus compound,(fluoromethylphosphoryl)oxycyclohexane.Cyclosarin was discovered in1949 and belongs to the G-series ofnerve agents (GF). | | General Description | Colorless liquid, odorless to fruity. | | Air & Water Reactions | Likely hydrolyzed by water, rapidly hydrolyzed by dilute aqueous sodium hydroxide. | | Reactivity Profile | Acidic conditions produce hydrogen fluoride; alkaline conditions produce isopropyl alcohol and polymers. When heated to decomposition or reacted with steam, cyclohexyl methylphosphonofluoridate emits very toxic fumes of fluorides and oxides of phosphorus. Slightly corrosive to steel. Hydrolyzed by water. | | Health Hazard | GF is a highly toxic nerve agent. It is a potent inhibitor of acetylcholinesterase and a neurotoxicant. The toxic symptoms are characteristics of sarin and other similar organophosphates. The toxicity is lower than GA, GB, GD, and VX.
LD50 value, subcutaneous (guinea pigs): 0.1 mg/kg (NIOSH 1986)
LD50 value,subcutaneous(rats):0.225mg/kg (NIOSH 1986). | | Health Hazard | Median lethal dose (mg-min/m3): 2500 by skin (vapor) or 350 (liquid); 35 inhaled. Median incapacitating dose: 25 inhaled. Eye/skin toxicity: Very high. Rate of action: Very rapid. Physiological action: Cessation of breath-death may follow. Detoxification rate: Low. (ANSER) | | Potential Exposure | A quick-acting and lethal cholinester-
ase inhibitor and casualty agent. Females appear to be more
susceptible to nerve agent effects. Small percentages of
general population have genetic traits that may increase
susceptibility. | | First aid | The immediate treatment for nerve agent intoxication is intravenous injection of 2 mg atropine sulfate(intramuscular injection should be considered if the patientis hypoxic and ventilation cannot be initiated, as there is arisk of ventricular fibrillation). This should be followed byadditional injections of atropine at 10-15-min intervals,continuing until bradycardia has been reversed (e.g., untilthe heart rate is at 90 beats/minute). If breathing hasstopped, a mechanical respirator should be used to ventilate the patient. Do not attempt mouth-to-mouth resuscitation. If possible, oxygen or oxygen-enriched air should beused for ventilation. If possible, monitor cardiac activity.Notes for physician and medical personnel: Oximes (pralidoxime salts, obidoxime) may be of use in restoring acetylcholinesterase activity. Obidoxime may be used to treat GFintoxication; however, it may cause liver damage. Animalstudies indicate that the oxime Hi-6 may be significantlysuperior to other oximes in the treatment of GF intoxication,but it is not widely available. Therefore pralidoxime saltsshould be used, with a slow intravenous infusion of 500 mgto 1 g being given initially. Diazepam may be administeredto control convulsions. It also has value in controlling thevictim’s fear. An initial dose of=mg may be followed byadditional doses at 15-min intervals up to a total of15 mg.[CDC]
Other effective antidote: National Response Team (NRT)lists atropine and (if more severe) 2-PAM Chloride injections; atropine eye drops.[NRT] | | storage | Reasonably stable in steel at normal temperatures.Prior to working with this chemical you should be trainedon its proper handling and storage. Store in tightly closedcontainers in a cool, well-ventilated area away from strongoxidizers. Where possible, automatically transfer materialfrom drums or other storage containers to process containers. Sources of ignition, such as smoking and open flames,are prohibited where this chemical is handled, used, orstored. Metal containers involving the transfer of this chemical should be grounded and bonded. Wherever this chemical is used, handled, manufactured, or stored, useexplosion-proof electrical equipment and fittings. | | Shipping | UN2810 Toxic liquids, organic, n.o.s., Hazard
Class: 6.1; Labels: 6.1-Poisonous materials, Technical
Name Required. | | Toxicity evaluation | Cyclosarin 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
the degradation of 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 cyclosarin, the t1/2 for AChE
is ～7 h and for RBC-ChE is ～2.2 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
upon 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
the fact that inhibition of AChE is not the only cause of
toxic effects.
One of the noncholinergic effects that results from treatment
with OP nerve agents is changes in the levels of neurotransmitters
other than acetylcholine. These include g-amino-butyric
acid, 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. Specifically, OP-induced disruption of mitochondrial
oxidative phosphorylation occurs through a variety of
mechanisms including reduction of electron transport chain
enzyme complexes, reduction in ATP synthesis, increased
hydrolysis of ATP, and disruption of the mitochondrial
membrane potential. Accumulation of reactive oxygen species
induces oxidative damage and cell death via caspase-induced
apoptosis.
The pharmacological and toxicological effects of the nerve
agents are dependent on their stability, rates of absorption by
the various routes of exposure, distribution, ability to cross the
blood–brain barrier, and rate of reaction. | | Incompatibilities | Fairly stable. Cyclo-sarin (GF) is hydro-
lyzed by water; rapidly hydrolyzed in the presence of heat
and alkalies; by dilute solution of aqueous sodium hydrox-
ide. Contact with alkaline conditions produce isopropyl
alcohol and polymer substances. Contact with acid condi-
tions produce HF; alkaline conditions produce isopropyl
alcohol and polymers. Reasonably stable when stored in
steel at normal temperatures; slightly corrosive to steel
when heated. | | Waste Disposal | Principles and methods for
destruction of chemical weapons: “Destruction of chemical
weapons” means a process by which chemicals are con-
verted 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 con-
structed 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.
(Organization for the Prohibition of Chemical Weapons;
Convention on the Prohibition of the Development,
Production, Stockpiling and Use of Chemical Weapons and
Their Destruction). Grossly liquid-contaminated materials
should be decontaminated and containerized and labeled in
accordance with DOT and EPA requirements as a hazwaste.
Wastewater solution from decon should be analyzed to
ensure no residual agent is present. The National Response
Plan, ESF-3 designates United States Army Corps of
Engineers (USACE) as the primary agency to manage con-
taminated debris. USACE and the Department of Defence
(DOD) typically use safety procedures prior to transport that
include “head space” (off gas) monitoring around containers
prior to shipment to ensure no leakage/off-gassing. Typically
waste will be transported in accordance with state require-
ments to a designated disposal facility, such as a RCRA-
permitted hazardous waste facility (typically an incinerator).
Wastewater solution from the decontamination process will
be analyzed to ensure no residual agent is present. It is likely
that the solution will not contain residual agents and there-
fore not need to be classified as a hazardous waste but sam-
pling must be used to verify. Chlorinated wastewater may
need to be treated/neutralized prior to disposal
. United
States munitions stockpiles of G-agent are/have undergone
destruction/disposal in the states of Utah, Oregon, Arkansas,
Alabama, and Kentucky. State/local plans to address poten-
tial releases from United States Army properties are in place
at these sites. |
| | cyclohexyl methylphosphonofluoridate Preparation Products And Raw materials |
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