Medical Aspects of Chemical Warfare (2008) - The Black Vault

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Cyanide Poisoningbitol, and other B vitamins. Its presence in serum caninterfere with some laboratory measurements. Largevolumes of hydroxocobalamin may cause significantamounts of cobalt to be released later, similar to theeffect of cobalt EDTA.Cobalt SaltsA commercial preparation of the cobalt salt ofEDTA, Kelocyanor, is available in Europe but not inthe United States. Cobalt salts, which are chelatingagents, directly bind cyanide in the periphery butlikely also cross the blood-brain barrier. Cobalt EDTAis administered intravenously. 251 In comparison studiesagainst nitrite and hyposulfite, cobalt EDTA wasthought to be superior 64 ; however, in other studiesthe nitrite-thiosulfate combination was found to besuperior. 252 No human volunteer studies or clinicaltrials of cobalt EDTA have been done. Followingadministration of cobalt EDTA, cyanide is excretedwith cobalt in the urine; no follow-on treatment withthiosulfate is required.The drawback of cobalt compounds is their severetoxicity, particularly when administered in the absenceof confirmed cyanide intoxication. Massive urticariawith swelling of the face, lips and neck; convulsions;chest pains; dyspnea; and hypotension have beenreported. Severe toxicity from cobalt can be seen evenafter initial recovery from acute cyanide poisoning.The usual dose of cobalt EDTA is one ampule followedby 50 mL of dextrose solution (500 g/L). Cobalt EDTAhas a shelf life of 3 years at temperatures under 25 °C.It should be stored in the dark; if stored in the light, itscolor lightens, but it is otherwise unchanged.SUMMARYCyanide is often associated with murders andassassinations. Because of the high amount neededto cause death and the inefficient weapons in whichit was used, cyanide was not an effective chemicalweapon in World War I. During World War II it wasdeployed effectively by the Nazi regime againstinternal enemies. It may have been used by Iraqagainst the Kurds in the Iran-Iraq War during the late1980s, although no objective evidence supports thispremise. Cyanide’s widespread industrial use andready availability provide the major opportunity forhuman injury today, particularly for exposure to largepopulations. Muslim extremists worldwide have beenintercepted multiple times with cyanide and specificplans for its deployment.Cyanide causes intracellular hypoxia by inhibitingthe intracellular electron transport mechanism viabinding to cytochrome-c-oxidase. This action stopsaerobic metabolism and forces a shift to anaerobicmetabolism. The nervous system and the heart areparticularly intolerant of ATP deficiency. The liver isparticularly tolerant of cyanide exposure, probablybecause of its generous supply of rhodanese. Cyanideadditionally binds multiple other enzymes and nonenzymaticproteins, although the clinical consequences ofthese actions are less well understood. The dose toxitycurve for cyanide is steep, with very large exposures,particularly respiratory, causing rapid onset of centralnervous system toxicity with the potential for deathwithin several minutes.Rapid removal from further exposure, administrationof general support measures including 100%oxygen, and administration of specific antidotes incritically impaired casualties effectively reverse theeffects of exposure. Multiple antidotes are availableworldwide. The most widely used are nitrites withthiosulfate. This combination has demonstrated efficacy.Hydroxocobalamin, used in France and a fewother countries, has now been introduced into the USformulary. Cobalt EDTA is falling out of favor becauseof its high side-effect profile. The only antidote formulatedfor use by nonphysician emergency respondersis amyl nitrite. No antidotes are currently carried byUS military medics or corpsmen. Current researchefforts are focused on improving the understandingof cyanide’s mechanisms of toxicity and developingimproved antidotes, with better safety profiles andutility in spartan environments.AcknowledgmentThe authors thank MAJ Thomas T Talbot, MC, CPT Denise Millhorn, and Dr Brain Logue of South DakotaState University for reviewing the chapter; Peter Hurst for artwork; LTC Todd Villnes and MAJ ThorMarkwood for their review of cardiac electrophysiology; Paula Digenakis for library assistance; and JohnPortmann of Duke University for computer program aid.397
Medical Aspects of Chemical WarfareREFERENCES1. Smith S. Poisons and poisoners through the ages. Med Leg J. 1952;20:153–167.2. Sykes AH. Early studies on the toxicology of cyanide. In: Vennesland B, Conn EE, Knowles CJ, Westley J, Wissing F,eds. Cyanide in Biology. New York, NY: Academic Press; 1981: 1–9.3. Weider B. The assassination of Napoleon. Georgian J Napoleonic Hist. 2000;(Jan):138–139.4. Maddern T. Poisoning by laurel leaves. Philos Trans R Soc Lond Biol Sci. 1731;37:84–99.5. Prentiss AM. Chemicals in War: A Treatise on Chemical War. New York, NY: McGraw-Hill; 1937: 171–175.6. Baskin SI. Zyklon. In: La Cleuer W, ed. Encyclopedia of the Holocaust. New Haven, Conn: Yale University Press; 2001.7. Robinson JP. The problem of chemical and biological warfare. Vol 1. In: Robinson JP, ed. The Rise of CB Weapons: AStudy of the Historical, Technical, Military, Legal and Political Aspects of CBW, and Possible Disarmament Measures. NewYork, NY: Humanities Press; 1971: 155–156.8. Lang JS, Mullin D, Fenyvesi C, Rosenberg R, Barnes J. Is the “protector of lions” losing his touch? US News & WorldReport. November 1986;10:29.9. Heylin M. US decries apparent chemical arms attack. Chem Eng News. 1988;23.10. Medical expert reports use of chemical weapons in Iran-Iraq War. UN Chronicle. 1985;22:24–26.11. Wolnick KA, Fricke FL, Bonnin E, Gaston CM, Satzger RD. The Tylenol tempering incident—tracing the source. AnalChem. 1984;56:466A-470A, 474A.12. Sidell FR. Chemical casualty consultant, Bel Air, Md. Personal communication, May 1996.13. Walrath J, Li FP, Hoar SK, Mead MW, Fraumeni JF. Causes of death among female chemists. Am J Public Health.1985;75:883–885.14. Thompson RL, Manders WW, Cowan RW. Postmortem findings of the victims of the Jonestown tragedy. J Forensic Sci.1987;32:433–443.15. Toxicological Profile for Cyanide. Atlanta, Ga: US Department of Health and Human Services, Agency for Toxic Substancesand Disease Registry; 2004.16. Cicerone RJ, Zellner R. The atmospheric chemistry of hydrogen cyanide (HCN). J Geophys Res. 1983;88:689–696.17. Li Q, Jacob DJ, Bey I, et al. Atmospheric hydrogen cyanide (HCN): Biomass burning source, ocean sink? Geophys ResLett. 2000;27;357–360.18. Vetter J. Plant cyanogenic glycosides. Toxicon. 2000;38:11–36.19. Way JL. Cyanide intoxication and its mechanism of antagonism. Annu Rev Pharmacol Toxicol. 1984;24:451–481.20. Towill LE, Drury JS, Whitfield BL, Lewis EB, Galyan EL. Review of the Environmental Effects of Pollutants: V. Cyanide.Washington DC: US Environmental Protection Agency; 1978.21. Solomonson LP. Cyanide as a metabolic inhibitor. In: Vennesland B, Conn EE, Knowles CJ, Westley J, Wissing F, eds.Cyanide in Biology. New York, NY: Academic Press; 1981: 11–28.22. Beasley V. Toxicants that inhibit the function of cytochromes. In: Beasley V, ed. Veterinary Toxicology. Ithaca, NY: InternationalVeterinary Information Service; 1999.398
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The Coat of Arms1818Medical Departm
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Textbooks of Military MedicinePubli
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MEDICAL ASPECTS o fCHEMICAL WARFARE
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ContentsContributorsForeword by The
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ContributorsMICHAEL ADLER, PhDResea
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DONALD M. MAXWELL, MSResearch Chemi
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ForewordThe US military has been co
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PrefaceA significant concern for th
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PrologueThe original edition of Med
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xxii
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Medical Aspects of Chemical Warfare
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Nerve AgentsChapter 5NERVE AGENTSFR
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Nerve AgentsAbout 10,000 to 30,000
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Nerve Agentsphorofluoridate (DFP) w
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Nerve AgentsFig. 5-2. This schemati
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Nerve AgentsExhibit 5-1 continuedis
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Nerve Agentsactivity but only 15% t
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Nerve AgentsTABLE 5-3CHEMICAL, PHYS
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Nerve AgentsTABLE 5-4EFFECTS OF EXP
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Nerve Agentsaffecting the other eye
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Nerve Agentsmay cause severe rhinor
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Nerve Agentsof jerks and tremor.Cen
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Nerve Agentsand they were decreased
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Nerve Agentsnerve agent toxicity on
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Nerve Agentspatient. Decontaminatio
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Nerve AgentsFig. 5-5. The Mark I ki
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Nerve Agentsadministered intramuscu
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Nerve Agentsthat hydroxamine reacti
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Nerve AgentsOral administration may
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Nerve AgentsTABLE 5-7RECOMMENDED TH
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Nerve Agentsimpairment such as whee
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Nerve Agentssuboptimal, manner. The
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Nerve Agentsthan those who did not.
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Nerve Agentssible for binding nerve
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Nerve Agentsfor comparison was not
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Nerve AgentsTABLE 5-11EFFECTS OF PY
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Nerve Agentstivity of smooth muscle
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Nerve Agents38. Grob D, Lilienthal
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Nerve Agents77. McDonough JH, Shih
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Nerve Agents117. McLeod CG Jr, Sing
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Nerve Agents154. Tryphonas l, Veino
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Nerve Agents193. Funckes AJ. Treatm
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Nerve Agents235. Suzuki T, Morita H
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Nerve Agents274. Pellegrini JE, Bak
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Page 369 and 370: Medical Aspects of Chemical Warfare
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Triage of Chemical CasualtiesChapte
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Triage of Chemical Casualtiesreceiv
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Triage of Chemical Casualtiesentran
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Triage of Chemical Casualtiescatego
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Triage of Chemical CasualtiesIn a f
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Triage of Chemical Casualtiesnose)
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Triage of Chemical CasualtiesWith n
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Triage of Chemical Casualties14. Sa
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Decontamination of Chemical Casualt
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• Analyze using GC-MS with methan
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Abbreviations and AcronymsAbBreviat
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Abbreviations and AcronymsPADPRP: p
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