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Battlefield Chemical Inhalation Injury
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Synonyms for Sarin (GB) include T46, Trilon 46, methylfluorophosphoric acid isopropyl ester, isopropyl methanefluorophosphonate (MFI), isopropyl methylphosphonofluoridate, and isopropoxy-methylphosphoryl fluoride. Its formula is C4H10FO2P; vapor density 4.8; specific gravity 1.09; boiling point 158°C. Sarin is a colorless and odorless substance that may be disseminated by spray or explosion (in liquid form). Although it has a soil persistence of up to 14 days, it is generally regarded as a relatively nonpersistent agent when it contaminates hard surfaces.
Toxicokinetics of Nerve Agents
Published in Brian J. Lukey, James A. Romano, Salem Harry, Chemical Warfare Agents, 2019
Marcel J. van der Schans, Hendrik P. Benschop, Christopher E. Whalley
Analysis of regenerated sarin from binding sites has provided more insight into the elimination pathways of nerve agents. This is especially true for the lungs and the eyes, which appeared to contain many binding sites for nerve agents following whole-body exposure. Both organs are also the porte d’entrée for the agent, and for the eyes, it cannot be excluded that the amount of measured sarin partly consists of intact sarin. Exposure studies at lower levels (occupational exposure) are near the lower limit of what can be reached with regard to toxicokinetics based on in vivo measurement of the intact nerve agent. Ultra-low-level exposure can only be studied after the analysis of fluoride-regenerated nerve agents (Van Helden et al., 2003). With these studies, it is possible to quantify the link between external and internal dosages, which is highly relevant in the area of regulatory toxicology.
Toxic cyanobacteria *
Published in Jamie Bartram, Rachel Baum, Peter A. Coclanis, David M. Gute, David Kay, Stéphanie McFadyen, Katherine Pond, William Robertson, Michael J. Rouse, Routledge Handbook of Water and Health, 2015
Anatoxin-a(s) is a naturally occurring organophosphate produced principally by species of Dolichospermum (formerly Anabaena) (Table 9.1). Like other organophosphates including paraoxon (the active metabolite of the parathion insecticide) and the chemical-warfare nerve agent sarin, anatoxin-a(s) irreversibly binds to and inhibits acetylcholinesterase (Mahmood and Carmichael, 1986). Although anatoxin-a(s) is chemically unrelated to anatoxin-a, both toxins result in similar over-stimulation of the post-synaptic membrane, blocking subsequent nerve impulse leading ultimately to fatigue and paralysis (Carmichael, 1994). Anatoxin-a(s) is highly toxic to mammals and causes symptoms consistent with that of synthetic organophosphates exposure such as hyper-salivation [the ‘s’ in anatoxin-a(s) was coined for excessive salivation occurring in intoxicated animals and is consistent with symptoms in humans exposed to sarin nerve agent] lacrimation, urinary incontinence, defecation and convulsions. Death by respiratory arrest/asphyxiation can be rapid when respiratory muscles are affected. Like anatoxin-a, anatoxin-a(s) degrades relatively quickly in the environment, but the rate is influenced by pH – it would be expected to decompose more quickly in alkaline waters as opposed to neutral or acidic conditions. This characteristic, along with the lack of commercially available standards required for analytical assessment are reasons anatoxin-a(s) is infrequently monitored in surface waters and few countries have implemented water quality guidelines.
Influence of experimental end point on the therapeutic efficacy of the antinicotinic compounds MB408, MB442 and MB444 in treating nerve agent poisoned mice – a comparison with oxime-based treatment
Published in Toxicology Mechanisms and Methods, 2020
Jiri Kassa, Christopher M. Timperley, Mike Bird, A. Christopher Green, John E. H. Tattersall
The dependence of the therapeutic efficacy of the antidotes studied on the experimental end point in the case of sarin poisoning is summarized in Table 1. Sarin-poisoned mice showed a wide spectrum of clinical signs of poisoning including salivation, lachrymation, nose secretion and tonic-clonic convulsions within a few minutes. The distribution of times to death differed between treatment groups. Antidotal treatment involving MB compounds prevented some deaths before more than 6 h, especially in the case of MB408. On the contrary, in the other groups (atropine alone, atropine in combination with obidoxime), all deaths occurred within the first 6 h after poisoning. Atropine alone increased the LD50 value of sarin 1.21-fold and atropine in combination with obidoxime increased the LD50 value of sarin 1.86-fold, regardless of time of the end point. The therapeutic efficacy of all MB compounds in combination with atropine depended on the end point (Table 1).
Lung damage following whole body, but not intramuscular, exposure to median lethality dose of sarin: findings in rats and guinea pigs
Published in Inhalation Toxicology, 2019
Shira Chapman, Shlomi Lazar, Rellie Gez, Ishai Rabinovitz, Guy Yaakov, Ettie Grauer
Sarin is a highly toxic, volatile warfare agent hazardous mostly through inhalation exposure. It is an irreversible organophosphate (OP) cholinesterase (ChE) inhibitor and its exposure results in a dose-dependent hyper-secretion, fasciculation, tremor, convulsions, respiratory failure, and death (Munro 1994). Sarin was used in the terror attacks in Japan (Okumura et al. 2003) and, more recently, in the civil war in Syria (Eisenkraft et al. 2014; Rosman et al. 2014). Although intermediate and severe OP injuries were associated with inhalation (Niven and Roop 2004), animal studies seldom focus on airway injuries. G-agents such as sarin and soman, induce a dose-dependent, wide spread and specific brain damage (Kadar et al. 1995; McDonough and Shih 1997; Lazar et al. 2016), the severity of which was found to correlate with the extent and duration of convulsions (McLeod et al. 1984; Chapman et al. 2006; Carpentier et al. 2008; de Araujo Furtado et al. 2010).
Comparative evaluation of antidotal efficacy of 2-PAM and HNK-102 oximes during inhalation of sarin vapor in Swiss albino mice
Published in Inhalation Toxicology, 2018
Devyani Swami, Ruchi Yadav, A.S.B. Bhaskar, A. Soni, D.P. Nagar, J. Acharya, H.N. Karade, K.P. Singh, Pravin Kumar
Animals exposed to sub-lethal concentration (0.8 × LCt50 or 605 mg/min/m3) of sarin vapor showed nicotinic receptors over stimulation mediated signs like mild intermittent tremors and scattered fasciculations (Taylor, 2011) within 3–4 min, whereas those exposed to higher concentrations, i.e., multiples of LCt50 showed continuous tremors, excessive excitement followed by loss of righting reflex and generalized seizures within 1–2 min and open-mouthed gasping culminated in death. Treatment either with atropine alone or in combination with oxime (2-PAM or HNK-102), could not prevent sarin-induced aforesaid most of the signs of acute toxicity; however, animals survived.