Soman inhalation

Allon, N., Raveh, L., Gilat, E., Cohen, E., Grunwald, J., Ashani, Y. (1998). Prophylaxis against soman inhalation toxicity in guinea pigs by pretreatment alone with human serum hutyr-ylcholinesterase. Toxicol. Sci. 43 121-8. 

IV. Prophylaxis against Soman Inhalation Toxicity in Guinea Pigs with Human Butyrylcholinesterase (HuBChE)... 

IV. PROPHYLAXIS AGAINST SOMAN INHALATION TOXICITY IN GUINEA PIGS WITH HUMAN BUTYRYLCHOLINESTERASE (HuBChE)... 

H-oximes used in combination with atropine sulfate against a background of the intramuscular or inhalation administration of soman are able to protect animals (dogs, monkeys) from 4-5 DL50 of this poison [9],... 

Drug solutions and implantation of osmotic mini-pumps Physostigmine hemisulphate and procyclidine hydrochlorid were obtained from Sigma (St.Louis, U.S.A.), scopolamine hydrobromid from Merck (Darmstadt, Germany), atropine sulphate was obtained from ACF (Amsterdam, The Netherlands), and diazepam from Roche (The Netherlands). HI-6 was made available by the Defence Research Establishment, Suffield, Canada. Soman (O-pinacolyl methylphosphonofluoridate) was synthesised at TNO. Alzet Osmotic Mini-pumps with a constant delivery rate of 0.55 pl/hr (Model 2002, Alza Corp., Palo Alto, USA) were used to deliver PYR, PHY and SCO. The vehicle consisted of 20% propylene glycol, 10% ethanol and 70% water. The pumps were implanted subcutaneously under isoflurane/02 inhalation anesthesia. 

Soman (pinacolyl methylphosphonofluoridate), called GD in the United States, is a moderately volatile substance that can be taken by inhalation or skin contact. 

Nerve Agent Substances that interfere with the central nervous system. Organic esters of phosphoric acid used as a chemical warfare agent because of their extreme toxicity (tabun-GA, sarin-GB, soman-GD, GF, and VX). All are potent inhibitors of the enzyme, acetylcholinesterase, which is responsible for the degradation of the neurotransmitter, acetylcholine in neuronal synapses or myoneural junctions. Nerve agents are readily absorbed by inhalation and/or through intact skin. 

Nerve agent Chemical agent inhaled, absorbed through the skin, or ingested that causes interference with the neural synapses and overstimulation of the nervous system, which in turn leads to overreactivity in the muscles and malfunctioning of various organs. The primary agents are tabun, sarin, soman, and VX. 

Soman (GD) Pinoacolyl methylphosphonogluoridate fastest-killing nerve gas, produced in 1944 for the first time at I.G. Farben, Germany kills both through inhalation and skin contact. 

Dahisch, P.A., Davis, E.A., Renner, J.A., Jakuhowski, E.M., Mioduszewski, R.J., Thomson, S.A. (2008h). Biomarkers oflow-level exposure to soman vapor comparison of fluoride regeneration to acetylcholinesterase inhibition. Inhal. Toxicol. 20 149-56. 

Walday, P., Aas, P., Fonniun, F. (1991). Inhibition of serine esterases in different rat tissues following inhalation of soman. Biochem. Pharmacol. 41 151-3. 

Langenberg, J.P., Spruit, H.E.T., Van der Wiel, H.J., Trap, H.C., Helmich, R.B., Bergers, W.W.A., Vanhelden, H.P.M., Benschop, H.P. (1998a). Inhalation toxicokinetics of soman stereoisomers in the atropinized guinea pig with nose-only exposure to soman vapor. Toxicol. Appl. Pharmacol. 151 79-87. 

Sarin is absorbed both through the skin and via respiration. It is more soluble in water than the other nerve agents (soman (GD) and VX) its solubility is directly related to temperature. The half-life of sarin, however, is inversely related to temperature and pH. In water the half-life of sarin is 15 min at 30°C and at pH 7.6. Nerve agents inhaled as vapors or aerosols enter the systemic circulation, resulting in toxic manifestations within seconds to 5 min of inhalation. 

Casualties are caused primarily by inhalation but can occur following percutaneous and ocular exposure, as well as by ingestion and injection. Soman mixes easily with water, and people could be exposed by drinking contaminated water or via dermal contact with contaminated water. People could be exposed by eating contaminated food. Clothing can release soman for 30 min, which could lead to exposure of other people. Soman vapor is heavier than air, and can sink to low-lying areas. 

An LCt5o of 30mgminm was reported in rats following a 30-min inhalation exposure to soman. The acute toxicities by other routes of exposure in various animal species are presented in Table 1. 

Physical Properties. Pure soman is a colorless liquid with a somewhat fruity odor. It has density 1.01 g/mL (20°C), vapor pressure of 0.27 mm/Hg (20°C), mp of —80°C, and bp of 190°C (85°C at 15 mm/Hg). Distillation is accompanied by decomposition that begins near 130°C. Soman s solubility in water is about 20% at 25°C. It is only about 20% as soluble in water as is tabun. With two different chiral centers, it exists as four stereoisomers (Benschop et al., 1985), each with a different toxicity. The lethal concentration (inhalation) in humans is estimated at approximately 25-50 mg min/m (Somani et al., 1992). 

Recently, Olson et al. (2000) and Benschop et al. (1998) have provided reports of animal studies of effects of repeated low-level exposure to nerve CWA. In rats, Olson et al. determined the LOAEL and NOEL of subacute dosages of sarin, administered, i.m. They found that the dose of sarin (GB) needed to produce a low but measurable blood ChE inhibition was 0.75 p-g/kg once a day for 4 days. Thus, the exposure in Olson s study would be described as subclinical. GB was paired with a variety of other chemicals to include chlorpyrifos, DEET (A,A-diethyl-m-toluamide), carbaryl, and PB. No neurobehavioral or neuropathologic effects could be attributable to dosing with GB alone or in any combination with the other chemicals. Rats were also evaluated using a functional observational battery (EOB) and a Eigure 8 Activity Monitor with no significant behavioral effects reported. Benschop et al. (1998) reported on the toxicokinetics of low-level inhalation exposure to soman in... 

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