Soman inhalation exposure

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. 

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... 

Gause, E.M., Hartmann, R.J., Leal, B.Z., et al., 1985. Neurobehavioral effects of repeated sublethal soman in primates. Pharmacol. Biochem. Behav. 23,1003-1012. Genovese, R.F., Benton, B.J., Shippee, S.J., et al, 2006. Effects of low-level inhalation exposure to cyclosarin on learned behaviors in Sprague-Dawley rats. J. 

Katos, A.M., Conti, M., Moran, T.S., et al., 2009. Acute microinstillation inhalation exposure to soman induces changes in respiratory dynamics and functions in guinea pigs. Inhal. Toxicol. 21, 648-657. 

Valiyaveettil, M., Alamneh, Y., Rezk, P, et al., 2011. Recombinant paraoxonase 1 protects against sarin and soman toxicity following microinstillation inhalation exposure in guinea pigs. Toxicol. Lett. 202, 203-208. 

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. 

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. 

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. 

There are only a few reports in the open literature on the effect of oximes in nerve agent-exposed humans. Pralidoxime chloride was very effective in reactivating erythrocyte AChE in individuals exposed to sublethal intravenous or oral VX while this oxime was substantially less effective in humans exposed to IV sarin (Sidell and Groff, 1974). Accidental sarin exposure by inhalation resulted in an initial progressive deterioration (coma, apnea) of the patient despite atropine and 2-PAM treatmentand substantial recovery of erythrocyte AChE activity (Sidell, 1974). It took several hours until the patient s condition improved. Sidell also reported an accidental oral soman exposure. A lethal dose of diluted soman splashed into and around the mouth of an individual, resulting in coma, bronchoconstriction and respiratory depression, which was successfully treated with repeated atropine injections. 2-PAM (2 g IV) had no effect on inhibited erythrocyte AChE. 

VII. Inhalation Toxicokinetics of Soman upon Low-Level Exposure... 

VII. INHALATION TOXICOKINETICS OF SOMAN UPON LOW-LEVEL EXPOSURE... 

The inhibition of AChE activity in nerve tissues of animals at different times after exposure to low-dose nerve agents are depicted in Table 3.3. In most studies, subcutaneous, intravenous, inhalation, and oral routes of exposure were used. AChE activity in whole brain, spinal cord, and brain regions such as cerebral cortex, corpus striatum, meduUa, and cerebellum was significantly decreased in rats, " " mice, and hens, ° hours, days, and weeks after low-dose exposure to nerve agents such as soman, sarin, and tabun. 

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