Was I Exposed Was the Cure Worse Omowunmi Wunmi Osinubi MD MSc MBA FRCA Associate Professor Adjunct Department of Occupational and Environmental Health University of Medicine and Dentistry of New Jersey School of Public Health ID: 702623
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Slide1
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 CenterSlide2
“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)Slide3
Pesticides?Chemical substances used to control and destroy pests that interfere with man’s 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 environmentSlide4
Pesticides – BenefitsCrop protectionFood preservationMaterial PreservationDisease controlSlide5
Persistent Organic Pollutants (POPs)RisksAdverse impact on environment & ecosystemsTravel long distances
Low water & high fat solubility
Persist & bio-concentrate
Concentrate in marine animals
Accumulate in the food chainMay produce toxic human effects
Economic PoisonSlide6
Pesticides – Classification by Use Chemicals designed to kill, reduce, or repel pests
Fumigants
Wood preservatives
Herbicides
Insecticides
Rats, mice, moles
Insects
Moulds
Weeds
Rodenticides
Fungicides
Insect repellantsSlide7
Pesticides – Classification By Use & Chemical StructureDifferent 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 & zincphosphide•
Methyl bromide
•
Ethylene
dibromide
INSECT REPELLENTS
•
Diethyltoluamide
(DEET)Slide8
Routes of ExposureSlide9
Use of Pesticides in Gulf WarDesert is home to large numbers of flying & biting insects and other pestsControl 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 uniformsTroops 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.Slide10
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 & bendiocarbLocal 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.Slide11
Routes of ExposureSlide12
Mechanisms of Pesticide ToxicityLocal irritationMost pesticidesAllergic sensitizationFungicides
Enzyme inhibition (
cholinesterases
)
Organophosphates (OPs) & carbamatesNeurotransmission altered (Calcium & GABA)Organochlorines
Oxidative damage
Paraquat
Uncoupling of oxidative
phosphorylation
GlyphosateSlide13
Acute Pesticide-related IllnessDermal & ocular irritation or allergic responseUpper and lower respiratory tract irritationAllergic responses/asthma
Gastrointestinal symptoms
Specific Syndromes
Cholinergic crises (organophosphates &
carbamates)Bleeding (warfarin
-based
rodenticides
)
Caustic lesions & pulmonary fibrosis (herbicide &
paraquat
)Slide14
Anti-CholinesterasesOrganophosphates & 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 skinReadily transported throughout the bodySlide15
Mechanism of Action Organophosphates & Carbamates
Inhibit the enzyme,
acetylcholinesterase
(
AChE) which normally functions to degrade acetylcholine in nerve synapsesBuildup 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 & humansSlide16
Nerve AgentsMuscarinic effects
Postganglionic parasympathetic
Nicotinic effects
Preganglionic
sympathetic & parasympatheticNeuromuscular junctionExcess Ach in CNS
Spinal Cord
Ganglia
NEJ
NMJ
Ganglia
Autonomic Nervous System
Somatic Nervous System
ACh
ACh
ACh
ACh
ACh
Epl
-
Sympathetic
Parasympathetic
NESlide17
Effects of Cholinesterase Inhibition (Nerve Agents)
Muscarinic
Nicotinic
D
iarrhea
S
alivation
Tachycardia
Hypertension
Mydriasis
Neuromuscular junction**
Fasciculation
Weakness
Paralysis
U
rination
L
acrimation
M
iosis
**
U
rination
B
radycardia
D
efecation
B
ronchorrhea
G
I symptoms
B
ronchospasm
E
mesis
E
mesis
L
acrimation
** Most important effects
after exposure to nerve agent(s)
CNS
Anxiety,
confusion, ataxia,
dysarthria
,
Seizures**
Respiratory depression**
ComaSlide18
Nerve Agent Effects Based on Route of Exposure
Route & Onset
Mild
Moderate
Severe
Vapor/Aerosol
Immediate
Rhinorrhea
,
secretions,
slight
dyspnea
Miosis
, eye pain,
dim vision,
pronounced
dyspnea
Coma,
convulsions,
fasciculations
,paralysisTopical
Immediate or DelayedLocalized
sweating &fasciculations
Vomiting,diarrhea,secretions
Miosis, coma,convulsions,generalized
fasciculationsSlide19
Management of Nerve Agent Acute Toxindromes
PESTICIDE
ACUTE
SYMPTOMS
DIAGNOSIS
TREATMENT
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
OximesSlide20
Chemical Warfare Nerve AgentsAnti-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 AgentsClear colorless liquids, volatile at ambient tempTabun
(GA);
Sarin (GB)
;
Soman
(GD)
V-Type Nerve Agents
Amber liquid, low volatility unless high temp
VXSlide21
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
S
chrader Ambros
R
udiger
&
Vand
der
L
IN
de
WWW II - large amounts incorporated into artillery shells
Nazi Germany ultimately decided not to use
sarin
against allied targetsSlide22
M190 Honest John chemical warhead section containing demonstration M134 GB (Sarin) bomblets.
Sarin
[(CH3)2CHO]CH3P(O)F
2-(Fluoro-methylphosphoryl)oxypropaneSlide23
Shelf-life several weeks to monthsShortened by impuritiesExtended by addition of certain oils, stabilizers or petroleum productsBinary chemical weaponsTwo 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
munitionsSlide24
Sarin Health EffectsHighly volatile & toxic cholinesterase inhibitorVapors 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 endingsRunny 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 hoursSlide25
Sarin as Chemical Warfare AgentEarly 1950’s – NATO adopted sarin
as a standard chemical weapon
U.S.S.R and US produced
sarin
for military purposes1953 – 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 1993Slide26
Sarin & TerrorismMatsumoto: 1994Japanese religious sect released impure
sarin
in a residential neighborhood
Hospital visits - 500; Fatalities -7
Tokyo: 1995Aum Shinrikyo sect released impure sarin
in the subway system in rush hour
Hospital visits - > 5000; Fatalities -12Slide27
Tokyo 1995
http://www.npa.go.jp/hakusyo/h16/hakusho/h16/image/ph200025.png
http://newsimg.bbc.co.uk/media/images/39504000/jpg/_39504695_attack203.jpg
http://www.semp.us/_images/biots/Biot171PhotoA.jpgSlide28
Sarin in the Persian Gulf1980-88: 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
sarin5,000 died; 11,000 injured;Thousands more died of complications, diseases and birth defects years after the attack1990-91 Gulf War, Iraq still had large stockpiles of
sarin
, discovered by coalition forcesSlide29
Aftermath of the Halabja Chemical AttackSlide30
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 flightDetonated shell released small amount of sarin gasTwo US soldiers were treated after displaying early symptoms of exposure to
sarin
.Slide31
“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)Slide32
Exposure to PGW Chemical WeaponsIraqis 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 1991- 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.Slide33
Protecting the Troops from Chemical Warfare Nerve Agents Chemical agent detection & monitoring alarm systems
Personal protective equipment
Nerve agent prophylaxis
Post-exposure treatmentSlide34
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 spectrometerSlide35
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)Slide36
Personal Protection GearMission
O
riented
P
rotective Posture (MOPP) Protective garments worn in a possible chemical eventProtective mask (a.k.a. gas mask), filters chemical, biological & irradiated particlesMask 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 rubberSlide37
Nerve Agent Prophylaxis