96-64-0 Usage
Description
Soman, a synthetic organophosphate compound, was first synthesized in 1944 by German chemist Richard Kuhn. It belongs to a family of related nerve agents, including tabun (GA) and sarin (GB), which were developed for chemical warfare during World War II. Soman is a colorless liquid that evolves odorless gas and is known for its high toxicity.
Uses
Soman is primarily intended for use as a chemical warfare agent. Due to its high toxicity and rapid action, it poses a significant threat when used in this context. However, it is important to note that the production, stockpiling, and use of chemical weapons, including soman, have been banned by the Chemical Weapons Convention (CWC) since 1997. The CWC is implemented by the Organisation for the Prohibition of Chemical Weapons (OPCW), which requires the destruction of existing chemical weapons stockpiles. As of 2012, nearly all nations are members of the OPCW, and the destruction of existing chemical weapons stockpiles is an ongoing process.
Air & Water Reactions
Hydrolyzed by water, rapidly hydrolyzed by dilute aqueous sodium hydroxide. Water alone removes Fluoride atom producing nontoxic acid.
Reactivity Profile
Acidic conditions produce hydrogen fluoride; alkaline conditions produce isopropyl alcohol and polymers. When heated to decomposition or reacted with steam, Soman. emits very toxic fumes of fluorides and oxides of phosphorus. Slightly corrosive to steel. Hydrolyzed by water.
Hazard
Highly toxic by ingestion, inhalation, and
skin absorption; may be fatal on short exposure;
cholinesterase inhibitor; military nerve gas; fatal
dose (man) 0.01 mg/kg.
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, essentially cumulative. (ANSER)
Health Hazard
Soman is the most toxic of all the nerve agents. It is extremely toxic by all routes of exposure. The symptoms of toxic effects are those of organophosphate insecticides, but the severity of poisoning is much greater.An oral dose of 0.01 mg/kg in humans couldbefatal.Inanimals,somantoxicityvaried among species; the LD50 values by subcutaneous administration were 20, 28, and 126 μg/kg for rabbits, guinea pigs, and rats, respectively (Maxwell et al. 1988). Exposure to a concentration of 21 mg/m3 soman caused a large inhibition of the activities of the enzyme carboxylesterase in bronchi, lungs, and blood tissues in rats (Aas et al. 1985). There was an increase in soman toxicity by 70% following subcutaneous pretreatment with tri-o-cresyl phosphate, a carboxylesterase inhibitor. This study indicates that carboxylesterase is important as a detoxifying enzyme.Jimmerson and coworkers (1989a) reported the 24-hour subcutaneous LD50 value in rats as 118.2 μg/kg. Soman-inhibited carboxylesterase activity in plasma and cholinesterase activity in brain regions in a dose-related manner. Such cholinesterase inhibitionandelevationofacetylcholineinthe brainareverysimilartothosecausedbysarin, DFP, paraoxon, and other organophosphates. However, organophosphates are dissimilar in their effects on choline levels, neuronal activity, and phospholipase A activity. These differential effects are attributed to the differences in the neurotoxicity of soman and other organophosphates (Wecker 1986). Intravenous injection of soman in rats (by six times the LD50 amount) followed by isolation of diaphragms 1 or 2 hours after the injection showed detectable amounts of soman P(-)isomerindiaphragmtissue(VanDongenet al. 1986). Pretreatment of the rats with pinacolyl dimethylphosphinate prevented the storage of soman in diaphragm tissue.A relation between soman toxicity and the aging process has been suggested by many investigators. Sterri and coworkers (1985) measured the activity of the enzymes carboxylesterase and cholinesterase in the plasma, liver, and lung of young rats 5–31 days old. Soman was six- to sevenfold higher in toxicity in 5-day-old rats than in 30day-old animals. The decrease in toxicity was attributed to the increase in plasma carboxylesterase. Plasma and brain regional cholinesterase activity profiles have been investigated by Shih and coworkers (1987) in four groups of male rats of 30, 60, 120, and 240 days old. The calculated 24-hour intramuscular LD50 values were 110.0, 87.2, 66.1, and 48.6 μg/kg, respectively. Young rats showed a less severe initial weight loss and a more rapid and sustained recovery of growth than older animals. These data indicate the relationship between the toxicity of soman to age-related changes of cholinesterase in certain brain areas. In a latter paper, Shih and coworkers (1990) reported that survivors from the two oldest groups of the studied animals did not recover to baseline body weights by the end of the observation period. The activity of plasma cholinesterase did not change significantly with age, while brain regional cholinesterase showed distinct patterns of age dependence. These data further correlate between soman toxicity and the aging process. However, no definite relationship could be established from these studies between the toxicity and the cholinesterase activity in the blood and brain of the test animals.Pretreatment with certain substances showed potentiation in soman toxicity in test animals. Pretreating rats with cresylbenzodioxaphosphorin oxide (CBDP) by 1 mg/kg reduced the 24-hour subcutaneous LD50 value by approximately sixfold (Jimmerson et al. 1989b). CBDP blocks tissue carboxylesterase sites that serve to detoxify soman. This enhances soman-induced inhibition of cholinesterase in the central nervous system, potentiating its lethality. Similar potentiating effects from CBDP pretreatment were reported earlier in other animals, such as mice, guinea pigs, and rabbits (Maxwell et al. 1987). Pretreatment with tri-o-cresyl phosphate, another inhibitor, decreased the LD50 dose of soman in rats (Tekvani and Srivastava 1989).Wheeler (1989) observed that the toxicity of soman in rats increased during exposure of the species to either cold or hot environments and after removal from the cold temperatures. Such an increase in toxicity under cold environmental temperatures was attributed to a generalized adrenocortical stress response. .
Toxicity evaluation
Like other chemical warfare nerve agents, soman is an irreversible
cholinesterase inhibitor. The clinical effects of soman
exposure result primarily from its inhibition of acetylcholinesterase
(AChE), although it does inhibit other cholinesterases
as well, including butyrylcholinesterase (BuChE). The most
important biological function of AChE is the degradation of
acetylcholine, an important neurotransmitter that is found in
nerve terminals in both the peripheral and central nervous
systems. Generally, acetylcholine stimulates secretion of bodily
fluids and contraction of skeletal muscles in the periphery and
affects a multitude of neural pathways in the central nervous
system. Normally, the actions of acetylcholine on its receptors
are terminated when it is hydrolyzed by AChE, thus preventing
continual overstimulation of the receptors. Inhibition of AChE
blocks its ability to degrade acetylcholine, resulting in an
accumulation of acetylcholine and cholinergic overstimulation
of the target tissues. Effects of AChE inhibition include involuntary
muscle contractions and increased fluid secretion (e.g.,
tears, saliva) resulting from acetylcholine accumulation in the
peripheral nervous system and seizures resulting from acetylcholine
accumulation in the central nervous system. The cause
of death is typically respiratory dysfunction resulting from
paralyzation of the respiratory muscles, buildup of pulmonary
secretions, and depression of the brain’s respiratory center.
The binding of soman to AChE is generally considered
irreversible unless removed by therapy. This removal is called
reactivation, which can be accomplished by the use of oximes
prior to ‘aging’. Aging is the biochemical process by which the
agent–enzyme complex becomes refractory to reactivation.
Spontaneous reactivation in the absence of oximes is possible
but is unlikely to occur at a high enough incidence to be clinically
important. Soman ages more rapidly than any other
chemical warfare nerve agent, with an aging half-time of
approximately 2 min.
Circulating cholinesterases in the blood act as effective scavengers
of soman, and blood cholinesterase levelsmay be used to
approximate tissue levels of functional AChE following an exposure
to soman or another cholinesterase inhibitor. Red blood cell
cholinesterase (RBC-ChE) and BuChE are both found in blood,
the latter in the plasma and the former in erythrocytes. RBC-ChE
enzyme activity is restored at the rate of red blood cell turnover,
which is ~1% 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.
Although cholinesterase inhibition is the primary mechanism
of toxicity following exposure to OP nerve agents, recent
investigations have assessed noncholinergic effects of OP nerve
agent poisoning, including changes in the levels of neurotransmitters
other than acetylcholine. These changes may be due to a compensatorymechanismin response to overstimulation of the
cholinergic system, direct action of the OP on the proteins
responsible for noncholinergic neurotransmission, or perhaps
both. It has been reported that OPs inhibit serine esterases that
degrade a number of noncholinergic neuropeptides, and it is
possible that this inhibitionresults in altered levels of a numberof
neurotransmitters other than acetylcholine. Recent studies have
also suggested that neuroinflammation is one putative mechanism
for noncholinergic neurotoxicity of OP nerve agents. Some
toxicity to the pulmonary and cardiovascular systems may result
from direct toxicity to the organs; OP cholinesterase inhibitors
have been reported to cause secondary pneumonia and pulmonary
edema as well as cardiac arrhythmias and lesions. The
etiology of these toxic effects is not well understood and could be
due to the cholinergic disruption that follows cholinesterase
inhibition and/or other mechanisms that have yet to be identified.
It is worth mentioning that mice lacking AChE are actually
more sensitive to OP poisoning than wild-type mice, supporting
the notion that OP cholinesterase inhibitors exert their toxic
effects throughothermechanisms in additiontoAChE inhibition.
Check Digit Verification of cas no
The CAS Registry Mumber 96-64-0 includes 5 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 2 digits, 9 and 6 respectively; the second part has 2 digits, 6 and 4 respectively.
Calculate Digit Verification of CAS Registry Number 96-64:
(4*9)+(3*6)+(2*6)+(1*4)=70
70 % 10 = 0
So 96-64-0 is a valid CAS Registry Number.
InChI:InChI=1/C7H16FO2P/c1-6(7(2,3)4)5-11(8,9)10/h6H,5H2,1-4H3,(H,9,10)/p-1
