Path: utzoo!utgpu!news-server.csri.toronto.edu!cs.utexas.edu!tut.cis.ohio-state.edu!att!cbnews!military From: djm@castle.ed.ac.uk (D Murphy) Newsgroups: sci.military Subject: Re: Our chem vs Iraqi Chem Message-ID: <1990Aug28.030524.21113@cbnews.att.com> Date: 28 Aug 90 03:05:24 GMT References: <1990Aug22.025307.16138@cbnews.att.com> Sender: military@cbnews.att.com (William B. Thacker) Organization: Edinburgh University Chemistry Lines: 101 Approved: military@att.att.com From: D Murphy In article <1990Aug22.025307.16138@cbnews.att.com> sysmgr@KING.ENG.UMD.EDU (Doug Mohney) writes: > > >From: sysmgr@KING.ENG.UMD.EDU (Doug Mohney) >Could someone post a summary of the types of chemical weapons we have >in our stockpiles? I am more interested in the fillers than the actual >delivery mechanisms. > There are basically 4 types of chemical weapon available: 1. Lachrymators - an example being CS (or `tear') gas usually used for crowd suppression or riot control (depending who is using it :-). Its use is unlikely here as it is nonlethal in deployable doses unless the target is compromised in some way - e.g. asthmatic - and these people are unlikely to pass military medicals. 2. Blister agents. These are `mustard gases' and nitrosoureas which use highly reactive nitrogen based compounds to corrode the skin - e.g. R2NCH2CH2Cl ---> R2NCH2 skin \| -------> R2NCH2CH2-skin CH2 R = chemical groups chosen to provide desired physical characteristics 3. Hydrogen cyanide - works by chemically binding cyano groups to metal ions in the body - among them the iron in haemoglobin - and preventing them doing their biological jobs properly, as cyano metal complexes are often more stable than the natural complexes. Certainly the Fe(ii)CN produced by reaction of HCN with haemoglobin prevents oxygen uptake. 4. Organophosphorus nerve agents. These are based on the skeleton: R2P=O | F the fluorine provides a reactive `handle'. R is again a chemical group chosen to impart desired characteristics of volatility, environmental stability and biological penetration. I have a list somewhere of the structures of the main ones (the German sarin, soman and tabun, and the UK developed VX). These things are not gases, but viscous liquids deployed from their containers by a small explosive charge as an aerosol. Thickening agents are also sometimes added to increase persistence. >The Iraqis might not want to pick a chemical battle with us; so far as the >press has been advertising, most of the Iraqi nerve agents are of short >(what's short?) duration. I seem to recall we have various long-duration >nerve agents which could contaminate areas for weeks, as do the Soviets. > I don't know how long they'd last in desert conditions. Chemically the blister agents and nerve agents are readily destroyed by heat and water, and by alkalis. >Further, no chemical warfare discussion would be complete without addressing >the capabilities of the French and the British, who are also in the area >and may be called upon for a multi-national response (or, with the French, >a unilateral response should their people get hit). Dunno about the French - they'll probably go their own way as usual. UK forces have no offensive chemical capability (and haven't had for over 30 years), but the protective gear is very good. Antidotes. The antidote used depends on the weapon. Cyanide poisoning is countered by administration of amyl nitrite to increase heart rate and make what oxygen carrying capacity is left in the blood available faster. Cyanide ion sequestrants, which bind CN- better than Fe(ii) and thus pull cyanide off haemoglobin, can also be used. Blister agents cause direct physical damage just as much as fire would. There is little that can be done except the same sort of treatment administered to burns victims. Nerve agents work by tightly binding to the enzyme acetyl cholinesterase in the synapse between nerve endings and muscles. In normal transmission, the nerve signal causes release of acetylcholine which triggers muscle response. The enzyme breaks down the acetylcholine and recycles the choline. When the enzyme is blocked, the muscle becomes desensitised by continual presence of acetylcholine in the synapse. There are 2 ways of countering this: a. Use of a muscle relaxant such as atropine. This relaxes the muscle by affecting receptors in the synapses which cause the opposite effect to acetylcholine (hence belladonna - Italian women used to put it in their eyes to expand the pupil). b. Use of a phosphorus sequestrant. Chemicals based on, e.g. hydroxylamine H2NOH bind the phosphorus better than the available nitrogen atoms in the enzyme which the nerve agent is blocking. This pulls the agent away from the enzyme and free it again. These actually reverse the action of the nerve agent (unlike a. which just counter the effects) but are toxic themselves, so the most likely field treatment would be to administer atropine to keep the victim alive until the antidote can be given under medical supervision. Murff...