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Office of Public Health & Environmental Hazards Pesticides, Sarin Gas & Antidotes Was I Exposed? Was the Cure Worse? Omowunmi (Wunmi) Osinubi, MD, M.Sc.,

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Presentation on theme: "Office of Public Health & Environmental Hazards Pesticides, Sarin Gas & Antidotes Was I Exposed? Was the Cure Worse? Omowunmi (Wunmi) Osinubi, MD, M.Sc.,"— Presentation transcript:

1 Office of Public Health & Environmental Hazards Pesticides, Sarin Gas & Antidotes Was I Exposed? Was the Cure Worse? Omowunmi (Wunmi) Osinubi, MD, M.Sc., MBA, FRCA. Associate Professor (Adjunct) Department of Occupational and Environmental Health University of Medicine and Dentistry of New Jersey -School of Public Health Occupational & Environmental Health Physician War Related Illness and Injury Study Center

2 On a nightly basis, we would spray our uniforms with pesticides…. We had to hang them outside so that the excess spray would dissipate in the air…. We were not supposed to put them on immediately after spraying them. …The sand fleas were a problem. We used to put flea collars around the legs of our cots, or we would put flea powder on the floor around our cots to try to keep the sand fleas away from us while we were sleeping…We slept with nets over us to keep the flies off….The flies were ungodly --SSgt TS, Gulf War veteran (GRAC Report, 2008)

3 Pesticides? Chemical substances used to control and destroy pests that interfere with mans agricultural, environmental or amenity requirements. First use of synthetic pesticides –1940 Consumption increasing worldwide 2.26 million tons of active ingredients used in 2001 As of 1999 – 74% of all US used at least one pesticide in the home. Utility based on selective toxicity Environmental toxins intentionally introduced to the environment

4 Pesticides – Benefits Crop protection Food preservation Material Preservation Disease control

5 Persistent Organic Pollutants (POPs) Risks Adverse impact on environment & ecosystems Travel long distances Low water & high fat solubility Persist & bio-concentrate Concentrate in marine animals Accumulate in the food chain May produce toxic human effects Economic Poison

6 Pesticides – Classification by Use Chemicals designed to kill, reduce, or repel pests Fumigants Wood preservatives HerbicidesInsecticides Rats, mice, moles Insects MouldsWeeds RodenticidesFungicides Insect repellants

7 Pesticides – Classification By Use & Chemical Structure Different chemicals used for different purposes INSECTICIDES Pyrethroids Organophosphorus Carbamates Organochlorine Manganese compounds HERBICIDES Bipyridyls Chlorophenoxy Glyphosate Acetanilides Triazines FUNGICIDES Thiocarbamates Dithiocarbamates Cupric salts Tiabendazoles Triazoles Dicarboximides Dinitrophenoles Organotin compounds Miscellaneous RODENTICIDES Warfarines Indanodiones FUMIGANTS Aluminium & zinc phosphide Methyl bromide Ethylene dibromide INSECT REPELLENTS Diethyltoluamide (DEET)

8 Routes of Exposure Ingestion BreastfeedingAccidental ingestion Residues in foodMouthing Inhalation Indoor and outdoor spraying Occupational exposure Dermal absorption Accidental contact Occupational exposure Residues on surfaces Contaminated clothing Medical use: scabies, head lice Transplacental

9 Use of Pesticides in Gulf War Desert is home to large numbers of flying & biting insects and other pests Control of disease-carrying pests is an important part of force protection & readiness in deployed settings Military personnel issued pesticide creams, liquids, sprays to use on skin, uniforms & beddings; and pest strips, baits & sprays used in living quarters Personal repellants – 33% cream or 75% liquid DEET on the skin, 0.5% Permathrine sprayed on uniforms Troops self-acquired pesticides –flea collars, citronella products, OFF e.t.c. Organochlorine – Lindane used for delousing in processing more than 87,000 enemy prisoners & US Army personnel for personal use.

10 US military preventive medicine specialists & field sanitation teams did environmental spraying & fogging using various concentrations in areas were troops lived, ate & worked. OPs- Chlorpyrifos, diazinon & malathion Carbamates – propoxur & bendiocarb Local pest control services by host nations ?information on pesticides used U.S. troops had available for use, at least 64 pesticides/related products 37 active ingredients; 15 of which are pesticides of concern Pest control program was highly successful low rates of arthropod borne illnesses.

11 Routes of Exposure Ingestion BreastfeedingAccidental ingestion Residues in foodMouthing Inhalation Indoor and outdoor spraying Occupational exposure Dermal absorption Accidental contact Occupational exposure Residues on surfaces Contaminated clothing Medical use: scabies, head lice Transplacental

12 Mechanisms of Pesticide Toxicity Local irritation Most pesticides Allergic sensitization Fungicides Enzyme inhibition (cholinesterases) Organophosphates (OPs) & carbamates Neurotransmission altered (Calcium & GABA) Organochlorines Oxidative damage Paraquat Uncoupling of oxidative phosphorylation Glyphosate

13 Acute Pesticide-related Illness Dermal & ocular irritation or allergic response Upper and lower respiratory tract irritation Allergic responses/asthma Gastrointestinal symptoms Specific Syndromes Cholinergic crises (organophosphates &carbamates) Bleeding (warfarin-based rodenticides) Caustic lesions & pulmonary fibrosis (herbicide & paraquat)

14 Anti-Cholinesterases Organophosphates & Carbamates Commonly used as animal flea & tick powders, foggers, shampoos & dips, flea collars, household, garden & farm insecticides Marketed under a variety of names OPs - Chlopyrifos, parathion, diazinon, malathion Carbamates - carbofuran, aldicarb, and carbaryl Fat soluble – easily absorbed through the skin Readily transported throughout the body

15 Mechanism of Action Organophosphates & Carbamates Inhibit the enzyme, acetylcholinesterase (AChE) which normally functions to degrade acetylcholine in nerve synapses Buildup of acetylcholine (ACh) Overstimulation of ACh receptors. Effects of multiple exposures are additive (flea collar, insect repellant, home & lawn treatment) Effects can be long-lasting Highly toxic to animals, pets, livestock & humans

16 Nerve Agents Muscarinic effects Postganglionic parasympathetic Nicotinic effects Preganglionic sympathetic & parasympathetic Neuromuscular junction Excess Ach in CNS Spinal Cord Ganglia NEJ NMJ Ganglia Autonomic Nervous System Somatic Nervous System ACh Epl- Sympathetic Parasympathetic NE

17 Effects of Cholinesterase Inhibition (Nerve Agents) MuscarinicNicotinic DiarrheaSalivationTachycardia Hypertension Mydriasis Neuromuscular junction** Fasciculation Weakness Paralysis UrinationLacrimation Miosis**Urination BradycardiaDefecation BronchorrheaGI symptoms BronchospasmEmesis Lacrimation ** Most important effects after exposure to nerve agent(s) CNS Anxiety, confusion, ataxia, dysarthria, Seizures** Respiratory depression** Coma

18 Nerve Agent Effects Based on Route of Exposure Route & OnsetMildModerateSevere Vapor/Aerosol Immediate Rhinorrhea, secretions, slight dyspnea Miosis, eye pain, dim vision, pronounced dyspnea Coma, convulsions, fasciculations, paralysis Topical Immediate or Delayed Localized sweating & fasciculations Vomiting, diarrhea, secretions Miosis, coma, convulsions, generalized fasciculations

19 Management of Nerve Agent Acute Toxindromes PESTICIDEACUTE SYMPTOMS DIAGNOSISTREATMENT Organophosphates Clorpyriphos Diazinon Azinphos Parathion "Irreversible" cholinesterase inhibition Cholinergic crisis: - nausea, vomiting - hypersecretion - miosis - fasciculations - coma Low cholinesterase levels in red blood cells - Decontamination - IV Atropine - Supportive care - Oximes (pralidoxime) Carbamates Carbaryl Aldicarb Reversible cholinesterase inhibition Low cholinesterase levels in RBC -Decontamination -IV Atropine - Supportive care - NO Oximes

20 Chemical Warfare Nerve Agents Anti-cholinesterases similar to OPs Readily absorbed by inhalation, ingestion & dermal contact Rapidly fatal systemic effects may occur Most toxic chemical warfare agents G-Type Nerve Agents Clear colorless liquids, volatile at ambient temp Tabun (GA); Sarin (GB); Soman (GD) V-Type Nerve Agents Amber liquid, low volatility unless high temp VX

21 Sarin Discovered in 1938 in Germany by 2 scientists attempting to create stronger OPs Most toxic of the G-agents made by Germany Named in honor of its discovers Schrader Ambros Rudiger & Vand der LINde WWW II - large amounts incorporated into artillery shells Nazi Germany ultimately decided not to use sarin against allied targets

22 M190 Honest John chemical warhead section containing demonstration M134 GB (Sarin) bomblets. Sarin [(CH3)2CHO]CH3P(O)F 2-(Fluoro-methylphosphoryl)oxypropane

23 Shelf-life several weeks to months Shortened by impurities Extended by addition of certain oils, stabilizers or petroleum products Binary chemical weapons Two precursors are stored separately in the same shell Mixed to form agent immediately before or when shell is in flight Dual benefit –solves problems of stability & safety of sarin munitions

24 Sarin Health Effects Highly volatile & toxic cholinesterase inhibitor Vapors penetrate the skin & non-lethal dose causes permanent neurological damage 500 X toxicity of cyanide, death within 1 min Health effects similar to OPs & carbamates Acetylcholine builds up at nerve endings Runny nose, chest tightness, pupillary constriction, difficulty breathing, nausea, drooling, vomiting, defecation, urination, twitching, jerking, comatose, convulsive spasms & death Treatment IV atropine – muscarinic symptoms of poisoning only Pralidoxime - regenerates cholinesterases if given 5 hours

25 Sarin as Chemical Warfare Agent Early 1950s – NATO adopted sarin as a standard chemical weapon U.S.S.R and US produced sarin for military purposes 1953 – 20 yr old Royal Air Force Engineer died in human testing of sarin - told he was participating in a test to cure the common cold Classified as weapon of mass destruction in UN Resolution 687 Production & stockpiling of sarin outlawed by the Chemical Weapons Convention of 1993

26 Sarin & Terrorism Matsumoto: 1994 Japanese religious sect released impure sarin in a residential neighborhood Hospital visits - 500; Fatalities -7 Tokyo: 1995 Aum Shinrikyo sect released impure sarin in the subway system in rush hour Hospital visits - > 5000; Fatalities -12

27 Tokyo ph png /_ _attack203.jpg /Biot171PhotoA.jpg

28 Sarin in the Persian Gulf : Iraq used sarin against Iran during the Iraq-Iran war 1988: Ethnic Kurd City of Halabja in Northern Iraq, was bombarded over 2 days with chemical cluster bombs including sarin 5,000 died; 11,000 injured; Thousands more died of complications, diseases and birth defects years after the attack Gulf War, Iraq still had large stockpiles of sarin, discovered by coalition forces

29 Aftermath of the Halabja Chemical Attack

30 Sarin in Iraq On May 14, 2004, Iraq insurgency fighters detonated a 155 mm shell with several liters of binary precursors of sarin. Shell designed to mix chemicals as it spins during flight Detonated shell released small amount of sarin gas Two US soldiers were treated after displaying early symptoms of exposure to sarin.

31 My unit arrived in the Gulf the day before the air war started. We spent about 1 month in Saudi Arabia. Our chemical alarms went off several times during that month…we had to go to MOPP – level four... …While in Saudi Arabia, we started taking PB pills…about 3 days after, my eyes were jittery, my vision was jumping, I was seeing double, & I was nauseated. By the 4 th day, I was vomiting a little blood, so I went to sick call, they told me to cut the dose in half…nothing to worry about…others in the unit had similar vision problems --SSgt TS, Gulf War veteran (GRAC Report, 2008)

32 Exposure to PGW Chemical Weapons Iraqis had chemical weapons, US troops had successfully destroyed most of the chemical manufacturing & storage targets in an air offensive Iraq did not use nerve agents in PGW March Army detonated large caches of stored munitions in Khamisiyah area. Troops were potentially exposed to low-levels of nerve agents. No reports of high-level exposures with large number of soldiers with symptoms of nerve agent poisoning.

33 Protecting the Troops from Chemical Warfare Nerve Agents 1.Chemical agent detection & monitoring alarm systems 2.Personal protective equipment 3.Nerve agent prophylaxis 4.Post-exposure treatment

34 Multi-level Chemical Detection & Monitoring systems M8A1 – initial alarm, troops instructed to wear protective gear, detects nerve agents only at levels high enough to cause symptoms False alarm in the presence of screening smokes, signaling smokes, engine exhaust, rocket/missile propellant smokes, and electromagnetic pulse (EMP). Repeated false alarms ignoring and/or disabling the systems M256A1 detector kit: 20 – 25 mins to complete test, not useful as early warning monitor, less false positives, used to verify chemical agents Armored FOX NBC Reconnaissance vehicles M43A1 chemical agent detector, MM-1 mobile mass spectrometer

35 The M256A1 kit can manually detect & classify nerve, blister, and blood agents in vapor or liquid form. Chemical detection equipment. A soldier using an Improved Chemical Agent Monitor (ICAM). Automatic Chemical Agent Detector Alarm (ACADA)

36 Personal Protection Gear Mission Oriented Protective Posture (MOPP) Protective garments worn in a possible chemical event Protective mask (a.k.a. gas mask), filters chemical, biological & irradiated particles Mask carrier – protects mask from damage, contains spare parts & nerve agent antidotes Over garments- worn over uniform, maximum airflow for cooling, prevents agents from reaching skin, smx with charcoal lining, strips of M9 detection paper Gloves & boots – highly durable rubber

37 Nerve Agent Prophylaxis

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