Weapons of Mass Destruction

1. Weapons of Mass Destruction The Chemical Agents

2. Stevan Cordas DO MPH • Consultant Bioterrorism - Chemical WMD - Texas Department of Health • Local Emergency Planning Committee - Tarrant county (toxicology) • Medical Reserve Corps oversight committee. • Clinical Associate Professor TCOM • Certified internal medicine, allergy immunology, occupational medicine

5. Nerve Agents • Are related to organophosphate pesticides. • Are lethal in small amounts. • Act as cholinesterase inhibitors at receptor sites. • 5 nerve agents are currently recognized – GA or tabun, GB or sarin, GD or soman, GF and VX.

6. Diazinon (Spectracide) Malathion Parathion Chlorfenviphos Dimethoate Ronnel Nerve Gas Agents Pyridostigmine (Mestinon) Physostigmine (Antilirium) Neostigmine (Prostigmine) Cognex and others Sevin Dust, Carbaryl and many others Organophosphates and Carbamyl Agents

7. History of Nerve Gas • First organophosphate –1854 • Tabun (GA) - Schroeder – discovered 1936 • Sarin (GB) – Schroeder – discovered 1937 • Military production of tabun –nazi –1942 • 30,000 tons of tabun produced 1942-45 • Soman (GD) – discovered 1944

8. History of Nerve Gas • GF discovered Schroeder – 1944 • VX discovered Port Down, England –1955 • Russians captured tabun factories and start their own production-1946 • United states and England start their own production. – Edgewood chemical and biologic center. –1950-1970

9. History of Nerve Gas • President Nixon orders all chemical and biologic agents destroyed. – 1969. • Chemical stockpiles partially destroyed in the United States. • Soviet union continued production – 1946-91 - developed Novilchek agents - current production status uncertain.

10. History of Nerve Gas • Iraq develops tabun and uses it against Iran – 1982-1985 . Iraq also used tabun against Kurdish dissidents. • Iraq admits to placing sarin in scuds and artillery 1991- operation desert storm. • Large amounts of chemical containers destroyed by U.S. forces 1991 – 98,900 low level exposures. – Gulf war syndrome emerges.

12. History of Nerve Gas • 1994 - First attack by Japanese cult using sarin gas – 7 dead and 200 injured. • 1995 – Second attack – same cult using sarin in Tokyo subways – 12 dead and 6000 injured. • 1998 – Traces of VX found in Iraqi warheads. • 2001-London police find sarin plans –thwart attack. • 2001- Insecticide bomb found on terrorist in Israel.

13. Sarin • Also known as GB; phosphonofluoridic acid, methyl, isopropyl ester; Isoproposmethylphosphonyl fluoride • Odorless and colorless • Heavier than air – hovers near the ground • More lethal in higher temperature • Degrades faster with rise in humidity • 26 times more deadly than cyanide gas

14. Basic Mechanism • Nerve gases bind to an esterase (ChE) that breaks down acetylcholine after it is released from the nerve end plate. • After a period of time this binding undergoes complex changes and cannot not be reversed – this is called “aging.” • This results in an excess acetylcholine (ACh) syndrome which affects the muscarinic and nicotinic receptors.

15. The ACh Goes to Muscarinic and Nicotinic Receptor Sites.

16. Signs and symptoms of Nerve Gas • Miosis, dim vision, pain in eyes • Severe rhinorrhea, lacrymation • Bronchorrhea • Nausea, Vomiting • Diaphoresis • Memory, fatigue, anxious, impaired judgment

17. Signs and symptoms of Nerve Gas • Increased airways resistance. • Diarrhea and involuntary micturition. • Local or generalized muscle fasciculations. • Muscle fatigue then flaccid paralysis. • Convulsions and Coma. • DUMBELS

18. Clinical Picture When Exposed to Nerve Gas Vapor • In mild cases, miosis, rhinorrhea, slight tightness in chest or bronchospasm,slight dyspnea, increased secretions, ocular pain and frontal headaches. • In moderate cases. An exaggeration of the above symptoms with marked dyspnea, nausea and vomiting.

19. Clinical Picture • In severe cases the same symptoms as for moderate but also confusion, unconsciousness, muscular fasciculations (generalized), involuntary micturition and defecation, apnea, flaccid paralysis, convulsions, arrhythmias.

20. Case 1 • 27 year old male exposed to unknown substance that was lethal to others in the area. • Subjective: Anxiety, nausea, rhinorrhea, mild chest tightness. • Objective: Miosis, diaphoresis, elevated BP, regular heart rate, short onset time, seems stable. RBC cholinesterase 30% of normal.

21. Hazard to Health Professionals • Persons whose skin or clothing is contaminated with nerve agent can contaminate rescuers by direct contact or through off-gassing vapor. Persons whose skin is exposed only to nerve agent vapor pose no risk of secondary contamination; however, clothing can trap vapor.

22. Protect Yourself • Nerve agent vapor is readily absorbed by inhalation and ocular contact and produces rapid local and systemic effects. The liquid is readily absorbed thorough the skin; however, effects may be delayed for several minutes to up to18 hours.

23. Respiratory Protection: Pressure-demand, self-contained breathing apparatus (SCBA) is recommended in response situations that involve exposure to any nerve agent vapor or liquid. • Skin Protection: Chemical-protective clothing and butyl rubber gloves are recommended when skin contact is possible because nerve agent liquid is rapidly absorbed through the skin and may cause systemic toxicity.

24. Chemical casualty triage is based on walking feasibility, respiratory status, age, and additional conventional injuries. The triage officer must know the natural course of a given injury, the medical resources immediately available, the current and likely casualty flow, and the medical evacuation capabilities.

27. Treat ABC • Quickly ensure that the victim has a patent airway. Maintain adequate circulation. If trauma is suspected, maintain cervical immobilization manually and apply a decontaminable cervical collar and a backboard when feasible. Apply direct pressure to stop arterial bleeding, if present.

28. General Principles of Triage for Chemical Exposure • Check triage tag/card for any previous treatment or triage. • Survey for evidence of associated traumatic/blast injuries. • Observe for sweating, labored breathing, coughing/vomiting, secretions. • Severe casualty triaged as immediate if assisted breathing is required.

29. General Principles of Triage for Chemical Exposure • Blast injuries or other trauma, where there is question whether there is chemical exposure, victims must be tagged as immediate in most cases. Blast victims evidence delayed effects such as ARDS, etc. • Mild/moderate casualty: self/buddy aid, triaged as delayed or minimal and release is based on strict follow up and instructions.

30. Hold your breath. Get fresh air as soon as possible. If you have a respirator, put it on. In the military there are three kits – use them all. In the civilian sector the same first three rules apply. If the patient only has miosis 5 or 10 minutes after removal from agent, they probably don’t need treatment. Treatment of Nerve Gas Agents

31. Mark I Kit • If the military Mark I kits containing autoinjectors are available, they provide the best way to administer the antidotes. One autoinjector automatically delivers 2 mg atropine and the other automatically delivers 600 mg 2-PAM Cl.

32. Decontaminate as a Priority • Rapid decontamination is critical to prevent further absorption by the patient and to prevent exposure to others. Decontaminable gurneys and back boards should be used if possible when managing casualties in a contaminated area. Decontaminable gurneys are made of a monofilament polypropylene fabric that allows drainage of liquids, does not absorb chemical agents, and is easily decontaminated.

33. If water supplies are limited, and showers are not available, an alternative form of decontamination is to use 0.5% sodium hypochlorite solution, or absorbent powders such as flour, talcum powder, or Fuller's earth If exposure to vapor only is certain, remove outer clothing and wash exposed skin with soap and water or 0.5% sodium hypochlorite. Place contaminated clothes and personal belongings in a sealed double bag.

34. Specific Therapy for Nerve Gas • Give atropine sulfate 2mg IV and 2 mg IM stat. Manage Airways, breathing and circulation. Early intubation and ventilatory support with oxygenation. Repeat atropine 2mg IM every 5 or 10 minutes and watch for return of copious secretions and increasing dyspnea. For severe sx, 6 mg is given initially. • Follow atropine with Pralidoxime (2-PAM) Protopam in I g vials. 15 to 25 mg/kg or given over 15 minutes IV. • 15 mg/kg IM for mild to moderate cases

35. 2 PAM • 2-PAM Cl solution needs to be prepared from the ampoule containing 1 gram of desiccated 2-PAM Cl: inject 3 ml of saline, 5% distilled or sterile water into ampoule and shake well. Resulting solution is 3.3 ml of 300 mg/ml. Mild/Moderate symptoms include localized sweating, muscle fasciculations, nausea, vomiting, weakness, dyspnea. • Severe symptoms include unconsciousness, convulsions, apnea, flaccid paralysis.

36. Effect of Atropine

37. Treatment (contd.) • Little effect of 2 PAM treatment on Soman (GD) due to rapid aging. • Pyridostigmine pretreatment is most helpful here and has some value with GA. Given orally 30mg every 8 hours. • If the individual is alive 5 minutes after inhaling the vapor they probably can make it with your help.

38. RBC Cholinesterase Levels • With minor adverse effects there is no correlation with RBC-ChE levels. • With vomiting one can suspect that at least inhibition of 50 to 90% of the baseline ChE has occurred. • Often used to verify organophosphate poisonings. Only decreased by pernicious anemia.

39. Late effects of Nerve Gas Attacks • Generally no serious adverse effects 6 months late. • With convulsions and apnea, inability to learn new tasks, memory impairment and retrograde amnesia has occurred. • No clear evidence of peripheral neuropathy or intermediate syndrome.

40. Resource for more information • Agency for Toxic Substances and Disease Registry Division of Toxicology1600 Clifton Road NE, Mailstop F-32Atlanta, GA 30333 Phone: 1-888-42-ATSDR (1-888-422-8737)FAX:   (770)-488-4178Email: ATSDRIC@cdc.gov

42. Blister Gases HD, H, HN2, HN3, CX, L

43. Sulfur Mustard, 2,2, - Di (Chloro-ethyl)-sulfide

44. H and HD • Pure Mustard Gas is HD, impure is H. • Sulfur Mustard is a vesicant and a respiratory irritant. It was the most effective chemical agent in WWI accounting for 85% of the chemical injuries. • Besides being a severe respiratory irritant, it affected the skin like a burn with painful blisters,. The eyes, axilla and scrotum were especially sensitive.

45. History of Blister Gas • 1822- First discovered. • 1860- Ability to produce burns and vesicles proven. • 1917 – Used by Germans for the first time at Ypres, France. Called Yperite by French. Lost by Germans. • Called yellow cross by the allies and later H and HD. H stood for Hun. HD produced 85% of chemical casualties in WWI.

46. History of Blister Gas • French quickly followed as did English. The US troops used French blister canisters and shells. • Captain Lewis’ team discovers lewisite 1918. • US production after WWI begins Pine Bluff and Aberdeen Proving Ground as chemical warfare department under war department forms in latter days of WWI. Especially from 1950 to 1969.

47. History of Blister Gases • No use in WWII, Korea or Viet Nam of blister gases. Bari incident Dec 2 1943. • 1981 Iraq uses HD against Iran. • 1984 Iraq uses HD against Kurds. • 1991 Iraq deploys HD but doesn’t have a chance to use them.

49. WWI Mustard Casualties and % Death

50. Physical Properties • Thick oily amber to brown liquid which freezes/melts at 58° F. • Heavier than air (vapor) or water (liquid). • Persistent. • Penetrates skin in 2 minutes. • Causes cellular damage in 5 minutes. • Delayed onset of clinical effects. 2-48 hours.