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Insecticide Poisoning
Organophosphate
Pesticide
Poisoning
POISONING( acute or
chronic) ANY SUBSTANCE CAUSING ADVERSE
EFFECT ON BODY.
 10% OF HOSPITAL ADMISSIONS
 HALF OF THIS IS DUE TO OP
COMPOUND POISONING.(exposure or
ingestion)
 OTHER COMMON POISONING ARE;
ALUMINIUM/ZINC PHOSPHIDE. YELLOW
OLEANDER, METHANOL,, HYPNOTICS,
SEDATIVES, TCAS,PCT, 2
PESTICIDE POISONING
 “”Pest”” means a destructive insect or other
animal that attack plants , crops
 Pesticide means any substance intended for
preventing, destroying, repelling, or mitigating
any pest.
 Poisoning can be;
1 accidental,
2 occupational- respiratory or dermal exposure.
3 suicidal
Pesticides.
 Insecticides
 Fungicides-cuso4
 Herbicides-cuSo4
 Rodenticides –
zn / al phosphide.
DDT.COUMARINS
 Disinfectants
 repellents
4
Insecticides
 Cholinesterase
Inhibitors
 Carbamates
 Organophosphates
 Pyrethrins &
Pyrethroids
 Organochlorines
5
Insecticide--acetyl
Cholinesterase Inhibitors
 Carbamates
 Baygon, aldicarb (Temik), carbofuran (Furadan),
carbaryl (Sevin)
 Organophosphates (OPs)
 chlorpyrifos (Dursban,), Diamethoate ,diazinon,malathion,
 Market names; bay-tax, tick-20, parathion. lycil, Rogor
6
RO O
P OX
RO
R O
N C
R X
Generic structure for N—
methyl carbamates
Generic structure for
organophosphates
Organophosphate Pesticide
Poisoning
Pharmacology of
Cholinomimetics
1. Esters of choline; ach, methanichol,
carbochol, bethochol.
2. Cholinomimetic alkaloids; pilocarpine,
muscarine, arecholine.
3. Cholinesterase inhibitors;
 Reversible; Simple Alcohols; eg edrophonium
Carbamates ; Eg Neostigmine and
Physostigmine
 Irreversible ; Organophosphates; eg Parathion
OP COMPOUND classification
Low volatile
compounds
highly volatile
compounds
 Used in agriculture
 Ex; chlorpyriphos,
dimethoate,
dichlorvos,
methylparathion,
 Used in chemical
warfare
 Ex; sarin, tabun.
9
10
Acetyl Cholinesterase Normal
Function
11
Acetylcholine (ACh)
3. End organ activates in
presence of acetylcholine
Acetylcholinesterase
Choline +
Acetyl
5. Choline reuptake
Acetyl CoA + Choline
Cholinergic Nerve Terminal
2. ACh binds
to receptor
1. Nerve signal releases ACh
4. Choline regeneration
by acetylcholinesterase
Inhibition of acetyl
Cholinesterase
12
Acetylcholine
R1 R2
O==P
O
Cholinergic
Nerve Terminal
3. Activity of end organ does not cease
1. Nerve signal releases ACh
2. ACh binds
to receptor
4. OP binds to
cholinesterase,
preventing
regeneration
Normal Nerve Function
AChACh
Normal Nerve Function
AChACh
Normal Nerve Function
AChACh
AChEAChE
How OP Work:
Reversible & Aged Binding
AChEAChE
AChACh OPOP
Clinical feature;three phases
1) Cholinergic crisis - 0.5-12 hrs after exposure
2) Intermediate syndrome - 1-4 days after
exposure.
3) Delayed neuropathic phase - 2-4wks after
exposure(neurotoxic effects)
4) other effects - CNS, CVS, pancreas ect.
+ Death
 Acute Cholinergic:
 Central
 Peripheral Muscarinic
 Peripheral Nicotinic
 Intermediate Syndrome
 OPIDN: Delayed peripheral neuropathy
 Neurocognitive dysfunction
Clinical Syndrome
Respiratory
failure
}
Neurological
manifestations Neuromuscular weakness/paralysis
 Type I, Type II and Type III paralysis
(OPIDP)
 Neuropsychiatric manifestations -COPIND
 Extrapyramidal manifestations
 Dystonia, resting tremor, rigidity, chorea
 Neuro-ophthalmic manifestations
 Optic neuropathy, retinal degeneration
 Rarer manifestations
 GBS, Ototoxicity, Sphincter involvement
cholinergic phase(24-
72HR)-medical emergency.
 Muscuranic effects;
all postganglonic nerve
endings
 Nicotinic effects;
all autonomic ganglia
and skelatal muscle
endplates.
 Central effects- brain.
Nicotinic, Muscurinic &
Central Syndrome
s/s cholinergic phase –
Muscuranic effects
 Lungs; increased secretion,
tightness in chest, wheezing, dyspnea,
cynosis.
pulmonary edema.
 CVS; bradycardia, hypotension
 GIT; nausea, vomiting, diarrhea, cramps,
incontinence.
 Urinary system; increased frequency,
incontinence.
 Sweat glands; increased sweating
23
cholinergic phase-
nicotinic effects
 Striated muscle; twitching, fasciculation,
cramps, weakness and resp failure.
 Symp ganglia; pallor, tachycardia,
hypertension
central effects
 CNS/BRAIN; giddiness, anxiety, restlessness,
mental alterations, drowsiness ,coma,
respiratory failure, seizure, cardiovascular
collapse.
Commonly-used Acronyms for
Cholinesterase Inhibition
Syndromes(1-phase)
 Salivation
 Lacrimation
 Urination
 Diarrhea
 G
 Emesis
 Diarrhea
 Urination
 Miosis
 Bronchorrhea Bronchospasm
Bradycardia
 Emesis ,
 Lacrimation
 Salivation
 Sweating.
25
Intermediate syndrome-2nd
phase-type 2
paralysis(nicotinic)
 Develops 1-4 days following poisoning.
 Persist for 4-18 days.
 First described in 1987,from srilanka.
 This is due to pathology at N-M junction.
 These are signs prolonged nicotinic
receptors inhibition of Ach
 No prominent muscuranic findings.
 Presented as paralysis of varies groups of
muscles in pts recovering from acute
poisoning.
Intermediate syndrome-type 2
paralysis in op poisoning
 Paralytic s/s;
-weakness of neck, back muscles,
limb muscle(proximal>distal), eyes muscle,
cranial nerve muscle.respiratory
muscle.areflexia
-death.
EMG/NCS- depolarisation block.
28
Chronic Effects
 Organophosphate induced delayed
neuropathy (OPIDN)
 1-3weeks after exposure
 Worsens/persist for several months.
 Peripheral neuropathy
 Axonopathy due to Neuropathy Target Esterases
(NTE)
 Chronic organophosphate induced
neuropsychiatric disorder (COPIND)
Delayed neuropathy-3rd
phase
 Present as chronic predominent motor
peripheral neuropathy due to axonal
degeneration
 s/s are distal weakness of hands and feet,
paraesthesia, wasting of distal muscles.
 Often seen in poisoning of some op
compounds—TOCP, TCP.
 less sever 1 st phase.
 Toxicity due to adulteration in cooking oil.
Lab Tests;
 Cholinesterase blood tests
 Measurement of op compound levels in blood,
and its metabolites in urine.
 Foliage and clothing pesticide residues
 ECG; QTc- prolonged, ST-elevated. T wave-
inverted. PR- PROLONGED. Torsade de
pointes, and complete heart block.
 Diagnosis is primarily clinical
31
Cholinesterase Blood Tests
 Two cholinesterase enzymes
 RBC
“true”/ acetylcholinesterase
 Plasma
“pseudo”/ butyrylcholinesterase
32
Cholinesterase Blood Tests
Interpretation
 20% variability in population “baseline”readings
 Correlation with symptoms unpredictable
 Enzyme activity reversible
 Carbamates
 Sample temperature
 Storage time
33
Diagnosis
 Purely clinical , by history, typical smell
( garlic, pungent odor) from breath, gastric aspirates ,
classical clinical features.
 When to suspect ?
-History of ingestion or spray. typical smell.
-Drowning in own secretions ,like vomiting and diarrhea,
salivation, rhinorrhea, lacrimation, sweating
bronchorrea. pulmonary edema etc.
-Pinpoint pupils. Muscle fasiculations, and proximal
weakness.
Grading of severity.
 MILD - normal consciousness, mild increase
in secretions, and fasciculation.
 SEVERE- impaired consciousness with
copious secretions and multiple
fasciculations.
 LIFE THREATENING- stupor , abnormal cxr,
and PaO2<60 mmhg. Pts needs ventilator
supports.
Specific Management for
Cholinesterase Inhibitor
Poisoning Collect serum, urine, & clothing samples
 Hospitalization and register as MLC
 General measures.
 Specific treatments
 Atropine
 Pralidoxime (2-PAM)--OPs only
 Special measures.
36
Management;
General measures.
 Step I: Identify the nature of the poison
Organophosphate
Carbamate
Chloride
Pyrethroid
Neonicotinoids
Management
 Step II: Decontamination
 Skin decontamination
 Important aspect – not to be
neglected
 Remove contaminated clothing
 Wash with soap and water (soaps
Management
 Step II: Decontamination
 Care to be taken by health personnel to avoid
contamination
 Reports of occupational illness in 3 staff caring for OP
poisoned patients
 Another report 7 of 10 staff who cared for a patient
developed chest tightness or discomfort
Geller RJ, Singleton KL, Tarantino ML, Drenzek CL, Toomey KE. Nosocomial poisoning associated
with emergency department treatment of organophosphate toxicity – Georgia 2000. J Toxicol Clin Toxicol
2001; 39: 109-11.
Management
 Step II: Decontamination
Gastric decontamination
 Forced emesis if patient is awake
 Gastric lavage
 Activated charcoal 25 gm 2
hourly
 Sorbitol as cathartic
Reduce absorption
 Gastric lavage
 Gastric lavage decreases absorption by 42% if
done 20 min and by 16% if performed at 60 min
 Performed by first aspirating the stomach and
then repetitively instilling & aspirating fluid
 Left lateral position better - delays spont.
Absorption
 No evidence that larger tube better
 Simplest, quickest & least expensive way -
funnel
 Choice of fluid is tap water - 5-10 ml/kg
Reduce absorption
 Gastric lavage
 Preferrably done on awake patients
 Presence of an ET tube does not preclude aspiration,
though preferred if GCS is low
Management
 Step III: Airways and Respiration
 Maintain airway
 Ensure adequate oxygenation
 Watch for intermediate syndrome (diplopia, extra-
ocular muscle weakness/neck muscle weakness)
 Monitor respiratory rate/tidal volume/vital capacity
 Blood gas analysis
 Step IV: Cardiac monitoring
 Hemodynamic and monitor for arrhythmias
Management Specific
therapy
 Step V: Specific therapy
 ATROPINE / GLYCOPYRROLATE
 OXIME
Remember
Steps I to V occur
simultaneously
Cholinesterase
Inhibitors:Treatment
Atropine vs.2-PAM
46
Atropine 2-PAM
Drug Class Belladonna
alkaloid
Oxime
Indications Hypersecretion,
bradycardia; OPs
or carbamates
Muscle paralysis,
respiratory failure
OPs only
Mode of
action
Antagonist:
temporarily
blocks binding of
acetylcholine to
receptor
Antidote:
permanently
reverses OP
inhibition of
cholinesterase
Treatment: Atropine
 Reverses SLUDGE, DUMBELSS syndrome
 Intravenous dose:
 Therapeutic;~~50mg/24 hr
 2 mg - 4 mg adult
 0.02-0.08 mg/kg pediatric
 Repeat every 5-10 minutes till atropinisation.
 Then titrate the doses as per signs of atropinisation.
 Total duration 4-7 days
 Given preparably by infusion pump.
47
How Atropine Works
AChEAChE
AChACh OPOP
AtropineAtropine
Scheme of atropinization
(endpoints to be reached)
.
0 5 10 15
0
10
20
30
40
min after first atropine
dose
2 4 8 16 Atropine requirement
Poor air entry into lungs caused by
bronchospasmand bronchorrhoea
Excessive sweating
(Hypotension)
(Bradycardia)
(Miosis)
Atropinization
Clear lungs
Dry axillae
Systol. BP>
80 mmHg
Heart rate>
80/min
No miosis
Atropinisation
Heart rate about 80/mt
Pupils mid position
Bowel sounds just heard
Clear lung fields
Atropine
 Loading
 Doubling dose regime e.g. 2 4 8 16 mgs every 5
minutes
 Maintenance
 Continuous infusion < 3mg/hr
 10-20% of loading dose/hour
 Endpoints; Atropinisation
 Clear chest on auscultation with no wheeze
 Heart rate >80 beats/min
 Pulse and pupil size are not reliable signs for atropine
monitoring
 Withdrawal
 Atropine toxicity
 Clinical Improvement
What if you give too much
Atropine ?
 Anticholinergic Syndrome:
 Hot as hell
 Blind as a bat
 Red as a beet
 Dry as a bone
 Mad as a hatter
 Full syndrome is rare
Treatment: Pralidoxime (2-
PAM),obioxime-Reactivating
agents
 Enzyme aging occurs if
not treated
 Treatment effective
within 48 hours
 2-PAM reactivates
cholinesterase
 Cholinesterase levels
rise
 USE IS
CONTROVERSIAL. 52
AChE--OP
OP 2-PAM
AChE OPAging
Regenerated
enzyme
Permanent bondNo treatment
2-PAM
AChE +
Oximes CONT…………..
 Ineffective in some situations
 Ageing
 Variation between organophosphates
 Effective protocols not established
 Variation in use
 Expensive
 USA $30-600 / gram
 India $6- 9 / gram
 Unlikely to address Non-ACh effects
2-PAM Treatment Regimen
 IV infusion over 30 minutes or longer
 > 12 years
 1.0-2.0 g in 100 mL saline
 < 12 years
 20-50 mg/kg body weight in 100 mL saline
 Repeat doses usually required
 1-2 hours, then 10-12 hour intervals. Max-12g/24hrs
 Treatment side effects
 Arrhythmia
 Hypertension, HEADACHE, blurred vision,dizziness.
54
Treatment-special measures
 CVS; monitor HR, bp,ECG,
-cardiac arrest; CPR
-arrhythmia; antiarrhythmic drugs
 RS; monitor RR,TV ,Pao2,PaCO2.
-airway obstruction; suction, airway maintance.
-depressed ventilation; intubation, ventilation,oxygen
 CNS; monitor level of consciousess.size of pupil,occurances of
seizures.
-coma care.
- restlessness;diazepam.
-convulsion;diazepam.
Treatment- special measures
 Avoid morphine,barbiturates bcoz of
respiratory depression.
 Avoid aminophylline or xanthine bcoz of
seizure.
 Iv fluids, electrolyte maintance and good
nursing care.
Relapse on treatment.
 Person may improve with initial treatment,
but later worsen again
Causes.
 1. due to intermediate syn
 2.failure to continue atropine long enough
 3.release of compound from fat stores.
Mortality-prognosis
 7-12%
organocarbomates
 Less lethal poisoning
 Effects shorter duration
 Less severity
 Rapidly reversible.
 Effects are simillar to op poisoning,muscuranic
signs more marked than nicotinic signs.
 PAM contraindicated as it aggravates toxicity,as
it itself bind to ChE.
 If first few hrs are tide over , one would expect
dramatic recovery.
Insecticides
 Cholinesterase Inhibitors
 Carbamates
 Organophosphates
 Pyrethrins & Pyrethroids
 Organochlorines
60
Insecticides
Pyrethrins & Pyrethroids
 Pyrethrins
 Natural insecticidal extract
 Unstable
 Pyrethroids
 Synthetic derivatives
 Used with piperonyl
butoxide
61
Pyrethrins: Health Effects
 Low systemic toxicity
 Respiratory sensitization
 Asthma
 Skin reactions
 Paresthesia
 Allergic dermatitis
62
C
O
O
CH3 CH3
CHC
CH3
CH3
O
CH3
CH2CH CHCH CH2
Pyrethrin I
Pyrethroid Insecticides
 Use increasing
 Examples of use
 Structural & agricultural
 Pet flea control
 Pediculicide
 Vector control
 West Nile virus
 Aircraft “disinfection”
63
Source: CDC
Pyrethroids: Health Effects
 Skin
 Paresthesia, dermatitis
 Respiratory
 Rhinitis
 Systemic
 Dizziness, headache
 Fasciculations, seizures,
 Hormonal disruption in vitro
64
Pyrethrins & Pyrethroids
Mechanism of Toxicity
 Prolong
inactivation of
nerve membrane
sodium channels
65
Pyrethrin & Pyrethroid
Illness: Treatment
 Decontamination
 Vitamin E cream
 Symptomatic therapy
 Remove from further
exposure if needed
66
Case
Woman Exposed to Flea Bomb
 35 year-old non-pregnant female with skin
burning, itching and chest tightness after
putting on clothes from cupboard.
 Physical exam
 Arms and face bright red
 Vital signs normal
 Lungs clear
67
Woman Exposed to Flea Bomb
Ingredients
 Label
 0.435% permethrin
 0.05% pyrethrins
 0.4% piperonyl butoxide
 99.115% inert ingredients
 Recommended no entry for 4 hours after
fogging
68
Insecticides
 Cholinesterase Inhibitors
 Carbamates
 Organophosphates
 Pyrethrins & Pyrethroids
 Organochlorines
69
Insecticides:
Organochlorines
 DDT (prototype)
 Chlordane
 Lindane (Kwell, etc.)
 Hexachlorobenzene
 (Fungicide)
70
Organochlorine Toxicity ;
acute.
 CNS toxicity
 Headache, dizziness, irritability, incoordination,
tremor, seizures, paresthesia (DDT),
Blood; DIC. MYOGLOBINURIA.
Chronic.
 Carcinogenicity
 Hepatic tumors in rodents . Breast cancer (?)
 Endocrine disruption.
 SPERM ABNORMALITIES.BLOOD DYSCRASIAS.LUECOPENIA.
APLASTIC ANEMIA PANCYTOPENIA. THROMBOCYTOPENIA.
 CNS; MND 71
Skin Effects of
Organochlorines
 DDT
 Chloracne
 Lindane
 Irritant reactions
 Negative in patch
test series
72
Insecticide Illness: Summary
 Occupational and environmental exposure
 Toxicity varies by chemical class
 Specific therapy limited
 Prevent illness by reducing use
73
Source:USDA

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Insecticides and OP Poisoning

  • 2. POISONING( acute or chronic) ANY SUBSTANCE CAUSING ADVERSE EFFECT ON BODY.  10% OF HOSPITAL ADMISSIONS  HALF OF THIS IS DUE TO OP COMPOUND POISONING.(exposure or ingestion)  OTHER COMMON POISONING ARE; ALUMINIUM/ZINC PHOSPHIDE. YELLOW OLEANDER, METHANOL,, HYPNOTICS, SEDATIVES, TCAS,PCT, 2
  • 3. PESTICIDE POISONING  “”Pest”” means a destructive insect or other animal that attack plants , crops  Pesticide means any substance intended for preventing, destroying, repelling, or mitigating any pest.  Poisoning can be; 1 accidental, 2 occupational- respiratory or dermal exposure. 3 suicidal
  • 4. Pesticides.  Insecticides  Fungicides-cuso4  Herbicides-cuSo4  Rodenticides – zn / al phosphide. DDT.COUMARINS  Disinfectants  repellents 4
  • 5. Insecticides  Cholinesterase Inhibitors  Carbamates  Organophosphates  Pyrethrins & Pyrethroids  Organochlorines 5
  • 6. Insecticide--acetyl Cholinesterase Inhibitors  Carbamates  Baygon, aldicarb (Temik), carbofuran (Furadan), carbaryl (Sevin)  Organophosphates (OPs)  chlorpyrifos (Dursban,), Diamethoate ,diazinon,malathion,  Market names; bay-tax, tick-20, parathion. lycil, Rogor 6 RO O P OX RO R O N C R X Generic structure for N— methyl carbamates Generic structure for organophosphates
  • 8. Pharmacology of Cholinomimetics 1. Esters of choline; ach, methanichol, carbochol, bethochol. 2. Cholinomimetic alkaloids; pilocarpine, muscarine, arecholine. 3. Cholinesterase inhibitors;  Reversible; Simple Alcohols; eg edrophonium Carbamates ; Eg Neostigmine and Physostigmine  Irreversible ; Organophosphates; eg Parathion
  • 9. OP COMPOUND classification Low volatile compounds highly volatile compounds  Used in agriculture  Ex; chlorpyriphos, dimethoate, dichlorvos, methylparathion,  Used in chemical warfare  Ex; sarin, tabun. 9
  • 10. 10
  • 11. Acetyl Cholinesterase Normal Function 11 Acetylcholine (ACh) 3. End organ activates in presence of acetylcholine Acetylcholinesterase Choline + Acetyl 5. Choline reuptake Acetyl CoA + Choline Cholinergic Nerve Terminal 2. ACh binds to receptor 1. Nerve signal releases ACh 4. Choline regeneration by acetylcholinesterase
  • 12. Inhibition of acetyl Cholinesterase 12 Acetylcholine R1 R2 O==P O Cholinergic Nerve Terminal 3. Activity of end organ does not cease 1. Nerve signal releases ACh 2. ACh binds to receptor 4. OP binds to cholinesterase, preventing regeneration
  • 16. How OP Work: Reversible & Aged Binding AChEAChE AChACh OPOP
  • 17. Clinical feature;three phases 1) Cholinergic crisis - 0.5-12 hrs after exposure 2) Intermediate syndrome - 1-4 days after exposure. 3) Delayed neuropathic phase - 2-4wks after exposure(neurotoxic effects) 4) other effects - CNS, CVS, pancreas ect.
  • 18. + Death  Acute Cholinergic:  Central  Peripheral Muscarinic  Peripheral Nicotinic  Intermediate Syndrome  OPIDN: Delayed peripheral neuropathy  Neurocognitive dysfunction Clinical Syndrome Respiratory failure }
  • 19. Neurological manifestations Neuromuscular weakness/paralysis  Type I, Type II and Type III paralysis (OPIDP)  Neuropsychiatric manifestations -COPIND  Extrapyramidal manifestations  Dystonia, resting tremor, rigidity, chorea  Neuro-ophthalmic manifestations  Optic neuropathy, retinal degeneration  Rarer manifestations  GBS, Ototoxicity, Sphincter involvement
  • 20. cholinergic phase(24- 72HR)-medical emergency.  Muscuranic effects; all postganglonic nerve endings  Nicotinic effects; all autonomic ganglia and skelatal muscle endplates.  Central effects- brain.
  • 22. s/s cholinergic phase – Muscuranic effects  Lungs; increased secretion, tightness in chest, wheezing, dyspnea, cynosis. pulmonary edema.  CVS; bradycardia, hypotension  GIT; nausea, vomiting, diarrhea, cramps, incontinence.  Urinary system; increased frequency, incontinence.  Sweat glands; increased sweating
  • 23. 23
  • 24. cholinergic phase- nicotinic effects  Striated muscle; twitching, fasciculation, cramps, weakness and resp failure.  Symp ganglia; pallor, tachycardia, hypertension central effects  CNS/BRAIN; giddiness, anxiety, restlessness, mental alterations, drowsiness ,coma, respiratory failure, seizure, cardiovascular collapse.
  • 25. Commonly-used Acronyms for Cholinesterase Inhibition Syndromes(1-phase)  Salivation  Lacrimation  Urination  Diarrhea  G  Emesis  Diarrhea  Urination  Miosis  Bronchorrhea Bronchospasm Bradycardia  Emesis ,  Lacrimation  Salivation  Sweating. 25
  • 26. Intermediate syndrome-2nd phase-type 2 paralysis(nicotinic)  Develops 1-4 days following poisoning.  Persist for 4-18 days.  First described in 1987,from srilanka.  This is due to pathology at N-M junction.  These are signs prolonged nicotinic receptors inhibition of Ach  No prominent muscuranic findings.  Presented as paralysis of varies groups of muscles in pts recovering from acute poisoning.
  • 27. Intermediate syndrome-type 2 paralysis in op poisoning  Paralytic s/s; -weakness of neck, back muscles, limb muscle(proximal>distal), eyes muscle, cranial nerve muscle.respiratory muscle.areflexia -death. EMG/NCS- depolarisation block.
  • 28. 28
  • 29. Chronic Effects  Organophosphate induced delayed neuropathy (OPIDN)  1-3weeks after exposure  Worsens/persist for several months.  Peripheral neuropathy  Axonopathy due to Neuropathy Target Esterases (NTE)  Chronic organophosphate induced neuropsychiatric disorder (COPIND)
  • 30. Delayed neuropathy-3rd phase  Present as chronic predominent motor peripheral neuropathy due to axonal degeneration  s/s are distal weakness of hands and feet, paraesthesia, wasting of distal muscles.  Often seen in poisoning of some op compounds—TOCP, TCP.  less sever 1 st phase.  Toxicity due to adulteration in cooking oil.
  • 31. Lab Tests;  Cholinesterase blood tests  Measurement of op compound levels in blood, and its metabolites in urine.  Foliage and clothing pesticide residues  ECG; QTc- prolonged, ST-elevated. T wave- inverted. PR- PROLONGED. Torsade de pointes, and complete heart block.  Diagnosis is primarily clinical 31
  • 32. Cholinesterase Blood Tests  Two cholinesterase enzymes  RBC “true”/ acetylcholinesterase  Plasma “pseudo”/ butyrylcholinesterase 32
  • 33. Cholinesterase Blood Tests Interpretation  20% variability in population “baseline”readings  Correlation with symptoms unpredictable  Enzyme activity reversible  Carbamates  Sample temperature  Storage time 33
  • 34. Diagnosis  Purely clinical , by history, typical smell ( garlic, pungent odor) from breath, gastric aspirates , classical clinical features.  When to suspect ? -History of ingestion or spray. typical smell. -Drowning in own secretions ,like vomiting and diarrhea, salivation, rhinorrhea, lacrimation, sweating bronchorrea. pulmonary edema etc. -Pinpoint pupils. Muscle fasiculations, and proximal weakness.
  • 35. Grading of severity.  MILD - normal consciousness, mild increase in secretions, and fasciculation.  SEVERE- impaired consciousness with copious secretions and multiple fasciculations.  LIFE THREATENING- stupor , abnormal cxr, and PaO2<60 mmhg. Pts needs ventilator supports.
  • 36. Specific Management for Cholinesterase Inhibitor Poisoning Collect serum, urine, & clothing samples  Hospitalization and register as MLC  General measures.  Specific treatments  Atropine  Pralidoxime (2-PAM)--OPs only  Special measures. 36
  • 37. Management; General measures.  Step I: Identify the nature of the poison Organophosphate Carbamate Chloride Pyrethroid Neonicotinoids
  • 38. Management  Step II: Decontamination  Skin decontamination  Important aspect – not to be neglected  Remove contaminated clothing  Wash with soap and water (soaps
  • 39. Management  Step II: Decontamination  Care to be taken by health personnel to avoid contamination  Reports of occupational illness in 3 staff caring for OP poisoned patients  Another report 7 of 10 staff who cared for a patient developed chest tightness or discomfort Geller RJ, Singleton KL, Tarantino ML, Drenzek CL, Toomey KE. Nosocomial poisoning associated with emergency department treatment of organophosphate toxicity – Georgia 2000. J Toxicol Clin Toxicol 2001; 39: 109-11.
  • 40. Management  Step II: Decontamination Gastric decontamination  Forced emesis if patient is awake  Gastric lavage  Activated charcoal 25 gm 2 hourly  Sorbitol as cathartic
  • 41. Reduce absorption  Gastric lavage  Gastric lavage decreases absorption by 42% if done 20 min and by 16% if performed at 60 min  Performed by first aspirating the stomach and then repetitively instilling & aspirating fluid  Left lateral position better - delays spont. Absorption  No evidence that larger tube better  Simplest, quickest & least expensive way - funnel  Choice of fluid is tap water - 5-10 ml/kg
  • 42. Reduce absorption  Gastric lavage  Preferrably done on awake patients  Presence of an ET tube does not preclude aspiration, though preferred if GCS is low
  • 43. Management  Step III: Airways and Respiration  Maintain airway  Ensure adequate oxygenation  Watch for intermediate syndrome (diplopia, extra- ocular muscle weakness/neck muscle weakness)  Monitor respiratory rate/tidal volume/vital capacity  Blood gas analysis  Step IV: Cardiac monitoring  Hemodynamic and monitor for arrhythmias
  • 44. Management Specific therapy  Step V: Specific therapy  ATROPINE / GLYCOPYRROLATE  OXIME
  • 45. Remember Steps I to V occur simultaneously
  • 46. Cholinesterase Inhibitors:Treatment Atropine vs.2-PAM 46 Atropine 2-PAM Drug Class Belladonna alkaloid Oxime Indications Hypersecretion, bradycardia; OPs or carbamates Muscle paralysis, respiratory failure OPs only Mode of action Antagonist: temporarily blocks binding of acetylcholine to receptor Antidote: permanently reverses OP inhibition of cholinesterase
  • 47. Treatment: Atropine  Reverses SLUDGE, DUMBELSS syndrome  Intravenous dose:  Therapeutic;~~50mg/24 hr  2 mg - 4 mg adult  0.02-0.08 mg/kg pediatric  Repeat every 5-10 minutes till atropinisation.  Then titrate the doses as per signs of atropinisation.  Total duration 4-7 days  Given preparably by infusion pump. 47
  • 48. How Atropine Works AChEAChE AChACh OPOP AtropineAtropine
  • 49. Scheme of atropinization (endpoints to be reached) . 0 5 10 15 0 10 20 30 40 min after first atropine dose 2 4 8 16 Atropine requirement Poor air entry into lungs caused by bronchospasmand bronchorrhoea Excessive sweating (Hypotension) (Bradycardia) (Miosis) Atropinization Clear lungs Dry axillae Systol. BP> 80 mmHg Heart rate> 80/min No miosis Atropinisation Heart rate about 80/mt Pupils mid position Bowel sounds just heard Clear lung fields
  • 50. Atropine  Loading  Doubling dose regime e.g. 2 4 8 16 mgs every 5 minutes  Maintenance  Continuous infusion < 3mg/hr  10-20% of loading dose/hour  Endpoints; Atropinisation  Clear chest on auscultation with no wheeze  Heart rate >80 beats/min  Pulse and pupil size are not reliable signs for atropine monitoring  Withdrawal  Atropine toxicity  Clinical Improvement
  • 51. What if you give too much Atropine ?  Anticholinergic Syndrome:  Hot as hell  Blind as a bat  Red as a beet  Dry as a bone  Mad as a hatter  Full syndrome is rare
  • 52. Treatment: Pralidoxime (2- PAM),obioxime-Reactivating agents  Enzyme aging occurs if not treated  Treatment effective within 48 hours  2-PAM reactivates cholinesterase  Cholinesterase levels rise  USE IS CONTROVERSIAL. 52 AChE--OP OP 2-PAM AChE OPAging Regenerated enzyme Permanent bondNo treatment 2-PAM AChE +
  • 53. Oximes CONT…………..  Ineffective in some situations  Ageing  Variation between organophosphates  Effective protocols not established  Variation in use  Expensive  USA $30-600 / gram  India $6- 9 / gram  Unlikely to address Non-ACh effects
  • 54. 2-PAM Treatment Regimen  IV infusion over 30 minutes or longer  > 12 years  1.0-2.0 g in 100 mL saline  < 12 years  20-50 mg/kg body weight in 100 mL saline  Repeat doses usually required  1-2 hours, then 10-12 hour intervals. Max-12g/24hrs  Treatment side effects  Arrhythmia  Hypertension, HEADACHE, blurred vision,dizziness. 54
  • 55. Treatment-special measures  CVS; monitor HR, bp,ECG, -cardiac arrest; CPR -arrhythmia; antiarrhythmic drugs  RS; monitor RR,TV ,Pao2,PaCO2. -airway obstruction; suction, airway maintance. -depressed ventilation; intubation, ventilation,oxygen  CNS; monitor level of consciousess.size of pupil,occurances of seizures. -coma care. - restlessness;diazepam. -convulsion;diazepam.
  • 56. Treatment- special measures  Avoid morphine,barbiturates bcoz of respiratory depression.  Avoid aminophylline or xanthine bcoz of seizure.  Iv fluids, electrolyte maintance and good nursing care.
  • 57. Relapse on treatment.  Person may improve with initial treatment, but later worsen again Causes.  1. due to intermediate syn  2.failure to continue atropine long enough  3.release of compound from fat stores.
  • 59. organocarbomates  Less lethal poisoning  Effects shorter duration  Less severity  Rapidly reversible.  Effects are simillar to op poisoning,muscuranic signs more marked than nicotinic signs.  PAM contraindicated as it aggravates toxicity,as it itself bind to ChE.  If first few hrs are tide over , one would expect dramatic recovery.
  • 60. Insecticides  Cholinesterase Inhibitors  Carbamates  Organophosphates  Pyrethrins & Pyrethroids  Organochlorines 60
  • 61. Insecticides Pyrethrins & Pyrethroids  Pyrethrins  Natural insecticidal extract  Unstable  Pyrethroids  Synthetic derivatives  Used with piperonyl butoxide 61
  • 62. Pyrethrins: Health Effects  Low systemic toxicity  Respiratory sensitization  Asthma  Skin reactions  Paresthesia  Allergic dermatitis 62 C O O CH3 CH3 CHC CH3 CH3 O CH3 CH2CH CHCH CH2 Pyrethrin I
  • 63. Pyrethroid Insecticides  Use increasing  Examples of use  Structural & agricultural  Pet flea control  Pediculicide  Vector control  West Nile virus  Aircraft “disinfection” 63 Source: CDC
  • 64. Pyrethroids: Health Effects  Skin  Paresthesia, dermatitis  Respiratory  Rhinitis  Systemic  Dizziness, headache  Fasciculations, seizures,  Hormonal disruption in vitro 64
  • 65. Pyrethrins & Pyrethroids Mechanism of Toxicity  Prolong inactivation of nerve membrane sodium channels 65
  • 66. Pyrethrin & Pyrethroid Illness: Treatment  Decontamination  Vitamin E cream  Symptomatic therapy  Remove from further exposure if needed 66
  • 67. Case Woman Exposed to Flea Bomb  35 year-old non-pregnant female with skin burning, itching and chest tightness after putting on clothes from cupboard.  Physical exam  Arms and face bright red  Vital signs normal  Lungs clear 67
  • 68. Woman Exposed to Flea Bomb Ingredients  Label  0.435% permethrin  0.05% pyrethrins  0.4% piperonyl butoxide  99.115% inert ingredients  Recommended no entry for 4 hours after fogging 68
  • 69. Insecticides  Cholinesterase Inhibitors  Carbamates  Organophosphates  Pyrethrins & Pyrethroids  Organochlorines 69
  • 70. Insecticides: Organochlorines  DDT (prototype)  Chlordane  Lindane (Kwell, etc.)  Hexachlorobenzene  (Fungicide) 70
  • 71. Organochlorine Toxicity ; acute.  CNS toxicity  Headache, dizziness, irritability, incoordination, tremor, seizures, paresthesia (DDT), Blood; DIC. MYOGLOBINURIA. Chronic.  Carcinogenicity  Hepatic tumors in rodents . Breast cancer (?)  Endocrine disruption.  SPERM ABNORMALITIES.BLOOD DYSCRASIAS.LUECOPENIA. APLASTIC ANEMIA PANCYTOPENIA. THROMBOCYTOPENIA.  CNS; MND 71
  • 72. Skin Effects of Organochlorines  DDT  Chloracne  Lindane  Irritant reactions  Negative in patch test series 72
  • 73. Insecticide Illness: Summary  Occupational and environmental exposure  Toxicity varies by chemical class  Specific therapy limited  Prevent illness by reducing use 73 Source:USDA

Editor's Notes

  1. The next two sections of the curriculum will present pesticides by functional category. Please refer to the speaker’s notes to supplement the PowerPoint slides.
  2. As with all toxins, pesticide illness is determined by the dose, the exposure route, and the specific pesticide involved. There are many ways to categorize pesticides. In this module, pesticides will be grouped and described by functional category, that is, how they are used. Insecticides are used to kill insects; fumigants are gasses that are toxic to a variety of organisms; fungicides kill fungi; herbicides are used to control plants, namely, weeds; disinfectants kill microbes. Information on all these and some miscellaneous pesticides will be presented.
  3. In each functional group, pesticides may be further classified by structure. In Part 2 of this curriculum, the cholinesterase-inhibiting pesticides, carbamates and organophosphates, pyrethroid pesticides, and organochlorine pesticides will be covered. The cholinesterase-inhibitors will be presented first. Cholinesterase inhibitors were first used as weapons in World War I. In the 1970s, they replaced organochlorines as widely used pesticides.
  4. There are 2 major categories of cholinesterase-inhibiting pesticides: N-methyl carbamates and organophosphates. Generic structures for the 2 categories and some common generic and brand names are shown. The major difference between the 2 categories is that organophosphates produce irreversible cholinesterase inhibition and carbamate-induced cholinesterase inhibition is reversible without treatment. However, carbamates may be quite toxic and exposure may result in significant morbidity or even death. Cholinesterase inhibiting pesticides will be presented in detail for several reasons: (1) Alone or in combination, they account for the majority of reported pesticide illnesses both in the US and worldwide; (2) They have been extensively studied and their mechanism of toxicity is fairly well known; (3) They are one of the only classes of pesticides for which there is a readily available diagnostic test; and (4) They are one of the few pesticides for which there is specific treatment.
  5. In order to understand how cholinesterase-inhibiting pesticides cause illness, it is important to be aware of how the enzyme acetylcholinesterase functions under normal conditions. Nerve signals causes the release of the neurotransmitter acetylcholine into a cholinergic nerve terminal. Acetylcholine travels across the terminal and binds to a cholinergic receptor on the end organ: either smooth or voluntary muscle, or an exocrine gland. This causes the end organ to perform its normal function: muscle contraction or gland secretion. The end organ activity ceases when acetylcholine leaves the receptor and is broken down by the enzyme acetylcholinesterase, located on the surface of the organ. The broken-down acetyl and choline are taken up by the cholinergic nerve and are recycled for the next activity.
  6. Cholinesterase-inhibitors disrupt normal function of the enzyme cholinesterase and cholinergic end organs. Nerve signals cause acetylcholine release and The neurotransmitter binds to receptors on end organs The end organ activates, but because The cholinesterase-inhibiting compound (in this case an organophosphate, OP) binds to acetylcholinesterase, the acetylcholine does not break down, and causes excessive activity of the end organ. Excess receptor activation manifests as the signs and symptoms of cholinesterase-inhibitor poisoning; and the bound enzyme shows up as depressed cholinesterase in lab tests.
  7. Nerves communicate with muscles, organs, and other nerves by releasing chemicals or neurotransmitters at their connection site (synapse). One of the most common neurotransmitters is acetylcholine(ACh), which is released and collects at the receptor site stimulating the end organ to respond and produce a variety of effects: muscle contraction, gland secretion, and nerve-to-nerve conduction. INSTRUCTOR NOTE: The function of nerve conduction, as well as the action of nerve agents and antidotes, can be additionally described by showing a portion of the nerve agent video at this time.
  8. When a nerve impulse reaches the synapse, ACh is released from the nerve ending and diffuses across the synaptic cleft to combine with receptor sites on the next nerve, and the electrical message continues.
  9. To stop further stimulation of the nerve, ACh is rapidly broken down by acetylcholinesterase (AChE), producing choline, acetic acid, and the regenerated enzyme. Thus, a “check and balance” system prevents the accumulation of ACh and the resultant over-stimulation of nerves, muscles, and glands.
  10. Nerve agents work by inhibiting the enzyme AChE, thus allowing the neurotransmitter ACh to accumulate.
  11. A couple of well-known acronyms used as reminders of the effects of cholinesterase-inhibition are SLUD and DUMBELS. However, the best way to remember the effects is to understand the type of organs affected (the information presented in the previous 2 slides).
  12. If the clinical evaluation and other information, such as label and MSDS, indicates that cholinesterase-inhibiting pesticides may be involved, laboratory tests should be obtained for confirmation. In general, pesticide poisoning may be confirmed with blood tests (measurement of physiologic response, parent compound, or metabolites), urine metabolites, and residues on plants, clothing, or other surfaces. The type of test available varies according to the specific pesticide. Currently for most pesticides, clinical tests are not available to detect the presence of the parent compound, metabolites, or physiologic effects. Cholinesterase-inhibiting pesticides are the exception, and most clinical laboratories perform at least one type of test (most commonly the blood test). Tests on leaves, clothing, and other surfaces are usually performed by regulatory, public health, or research agencies and generally not by clinical laboratories. These tests are often comprise a crucial part of these agencies’ case confirmation procedures. Measurement of pesticide residues is not restricted to cholinesterase inhibiting pesticides. Results should supplement clinical information and may be used to aid diagnosis. It is important to remember that tests are confirmatory and that a diagnosis of pesticide poisoning is primarily clinical. We will discuss these tests in a bit more detail.
  13. If the exposure dose is sufficient to produce cholinesterase depression, blood tests will detect this within minutes to an hour. Cholinesterase measured in clinical laboratories is an indicator for acetylcholinesterase activity occurring at cholinergic nerve terminals. The term cholinesterase refers to two different enzymes that are measured clinically. Cholinesterase on the RBC surface is structurally identical to acetylcholinesterase and is also known as “true cholinesterase”. It is present in RBCs and at neuromuscular junctions and is involved in synaptic transmission. It is a marker of acute toxic effects and more accurately reflects actual activity at cholinergic nerve terminals. Depression of RBC cholinesterase is more commonly associated with toxic effects. Plasma cholinesterase is accurately termed butyrylcholinesterase, not acetylcholinesterase, and is sometimes called “pseudo” cholinesterase. Its function is unknown. It is a marker of exposure, but its activity does not necessarily mirror that at cholinergic nerve terminals. It is important to obtain both plasma and RBC cholinesterase tests, since pesticides may preferentially inhibit one enzyme over the other. For example, the organophosphate dichlorvos causes preferential inhibition of plasma cholinesterase. Depression in plasma cholinesterase may be observed at lower exposure doses than those causing depression in RBC cholinesterase. See: Lotti M. Cholinesterase inhibition: complexities in interpretation. Clin Chem. 1995;41:1814-8. Mason HJ. The recovery of plasma cholinesterase and erythrocyte acetylcholinesterase activity in workers after over-exposure to dichlorvos.Occup Med. 2000; 50:343-7.
  14. Cholinesterase tests should be interpreted with caution, as an individual’s normal cholinesterase activity (prior to exposure to cholinesterase inhibitors) is termed the “baseline”. The baseline cholinesterase activity in a typical unexposed population varies by 20%. Consequently, cholinesterase tests can be accurately interpreted only if an individual baseline is available. Cholinesterase-inhibiting pesticides cause lower enzyme levels compared to the baseline. In the absence of a baseline, a diagnosis of cholinesterase inhibition may still be made if the value is significantly low compared to the lab lower limit of normal. It should be noted that normal values at different labs may vary by as much as 4-fold. Comparing to lab normal may lead to false negatives. There is no accurate correlation of cholinesterase levels with signs and symptoms of cholinesterase inhibition. The manifestation of health effects depends on rate of decline of cholinesterase activity as well as the absolute level of activity. Chronically exposed persons may tolerate greater depression without symptoms than those who are acutely poisoned. Although it is said that acute symptoms may be observed when RBC cholinesterase is depressed 80% of baseline or greater, there is little data to support this information. As with cholinergic nerve terminals, inhibitor pesticides may reversibly bind to cholinesterase in vitro. Reversal of inhibition in a drawn blood sample will cause a false negative result. Reversal of inhibition is most likely to occur with carbamates, at higher storage temperatures, and with prolonged storage times. To decrease the rate of reversal, it is extremely important that blood samples be stored and transported on ice and analyzed as soon as possible.
  15. After removal of contaminated clothing, decontamination, specific steps should be followed if cholinesterase inhibitor poisoning is suspected. Samples of serum for cholinesterase and urine for metabolites should be collected before administering any specific antidotes or medications, as these can affect cholinesterase results. Clothing should be double bagged and stored away from patient care and staff areas. If symptoms are severe enough to require intravenous medication, the patient should be hospitalized. Atropine and pralidoxime (2-PAM) are specifically used to treat poisoning due to cholinesterase inhibitors. These will be discussed in the next few slides. To prevent re-exposure at the workplace, work practices may need to change, restrictions may have to be placed on job duties, or the worker may have to be medically removed. Medical removal or reassignment to a different job should be considered for workers in a biologic monitoring program with cholinesterase depression below a predetermined threshold even if they are asymptomatic.
  16. Atropine and 2-PAM (pralidoxime) are the 2 drugs used specifically to treat cholinesterase inhibitor poisoning. This slide describes the differences between and the uses of the two drugs. Atropine is a belladonna alkaloid and an antagonist and temporarily blocks the binding of acetylcholine to the end organ receptor by competing for binding sites. Indications for atropine administration are excess secretions (for example bronchorrhea, pulmonary edema) and bradycardia. It can be used to treat poisoning by both organophosphates and carbamates. 2-PAM is a type of oxime used in the US. Different oximes are used in other countries. Unlike atropine, 2-PAM regenerates cholinesterase and permanently reverses cholinesterase inhibition, thereby affecting cholinesterase levels. 2-PAM should be used only to treat organophosphate poisoning, as there have been case reports of paradoxical worsening of symptoms when used to treat poisoning with certain carbamates. 2-PAM should be used if muscle paralysis, especially respiratory failure, is observed.
  17. Atropine temporarily reverses the muscarinic effects of cholinesterase inhibitors; these are the symptoms described by the acronyms SLUD and DUMBELS. Atropine does not affect cholinesterase levels. A diagnostic dose should be first administered; a temporary reversal of symptoms provides evidence of cholinesterase-inhibitor involvement. Therapeutic doses may be repeated every 10-30 minutes. Frequent administration over several days may be required to control secretions.
  18. Nerve agents work by inhibiting the enzyme AChE, thus allowing the neurotransmitter ACh to accumulate.
  19. The classic anticholinergic syndrome is described as below:- Hot as hell Blind as a bat Red as a beet Dry as a bone Mad as a hatter Patients may have:- Elevated BP, red dry skin, dilated pupils, bowel sounds, urinary retention, delirium and convulsion It can occur with any anticholinergic drugs e.g. cogentin, anticholinergic plants e.g. datura, as well as antihistamines, antidepressant drugs and antipsychotic drugs.
  20. If organophosphate poisoning is not treated, “aging” of the organophosphate-enzyme complex occurs. After aging has occurred, the bond between acetylcholinesterase and the organophosphate becomes permanent and normal cholinesterase activity will return only following regeneration of new enzyme. This can take up to 3 months for RBC and several weeks for plasma cholinesterase. The time it takes for aging to occur varies according to the specific pesticide, but takes no longer than 48 hours. For some pesticides, such as sarin, used in the Tokyo subway attacks, aging can occur in a matter of minutes. 2-PAM slows down “aging” of the phosphorylated cholinesterase and binds to the organophosphate pesticide, making it nonreactive. This results in cholinesterase regeneration and a rise in serum levels of RBC and plasma cholinesterase. To accurately measure cholinesterase depression, it is crucial that cholinesterase tests are drawn before 2-PAM administration. Treatment with 2-PAM may be partially effective after 48 hours if large amounts are ingested or if transfer of highly lipophilic organophosphates from fat to blood occurs over a long time period. 2-PAM relieves both muscarinic symptoms (in smooth muscle) as well as nicotinic symptoms (skeletal muscle).
  21. 2-PAM is administered by slow IV infusion. The doses for adult and pediatric administration are indicated here. Repeat doses are usually required. In the presence of hypoxemia, 2-PAM can cause arrhythmias. Oxygen should be administered to prevent this from occurring. Continuous blood pressure monitoring is required to prevent another potential side effect, hypertension.
  22. The next group of insecticides we will focus on are the pyrethrins and pyrethroids.
  23. Pyrethrins are the insecticidal extract of a particular type of chrysanthemum flower. They are broken down easily in the presence of light and water, limiting their outdoor use. The pyrethroid pesticides are synthetically derived, light-stable relatives of pyrethrin. Light stability allows pyrethroids to be used outdoors. They are often used with the synergist piperonyl butoxide. Because piperonyl butoxide is not used alone, there are no reports of human toxicity due to this synergist. It is possible, however, that it may contribute to health effects.
  24. The natural pyrethrin pesticides have low systemic toxicity, but can cause respiratory sensitization, including exacerbation of pre-existing asthma. Fatal asthma attacks have been described following exposure to pyrethrin-containing pet flea shampoos. The respiratory effects may be due to lactone impurities in the crude pyrethrin extract. Skin reactions to pyrethrin pesticides are common. Paresthesia, described as numbness, tingling, and the sensation of insects crawling on the skin, are typical for both pyrethrin and pyrethroid pesticides. In addition, burning, itching, and numbness has been described, and erythema may be observed following exposure. Dermal sensitization to pyrethrins may result in allergic dermatitis. See: Wax PM and Hoffman RS. Fatality associated with inhalation of a pyrethrin shampoo. Clin Toxicol. 1994; 32:457-460
  25. Pyrethroid pesticide use is increasing, both for residential and agricultural use. Because of their low acute systemic toxicity, these pesticides are replacing organophosphates, which continue to be restricted by US EPA for both structural and agricultural uses. They are commonly found in pet flea and tick products, and are widely used as over the counter remedies for head lice and scabies. They are used for malaria vector control in developing countries, replacing DDT for this use. In the US, they are used to control the West Nile virus. The World Health Organization recommends their use to “disinsect” aircraft for purposed of vector control, as required by several countries. The practice of disinsection is not allowed in the US because of concerns about resulting adverse health effects among passengers and crew. A flight attendant is shown “disinsecting” aircraft. The pesticide in this old photo is unlikely to have been a pyrethroid, but might be an organochlorine insecticide.
  26. The health effects of pyrethrins are similar to those of pyrethroids. The most common symptoms are paresthesia, burning, itching, and numbness; erythema may be observed in the areas of contact. Both irritant and allergic contact dermatitis may be observed following pyrethroid exposure. Rhinitis is common, as the respiratory nerve endings may be affected directly. Unlike the natural pyrethrins, respiratory sensitization and exacerbation of asthma has not been observed with the synthetic pyrethroids. However, under experimental conditions, certain formulations of pyrethroids have been found to result in increased airway responsiveness and respiratory irritant symptoms among asthmatics. Pyrethroids are slowly absorbed through skin, but prolonged or high level exposure may result in systemic effects. These range from dizziness, headache, and fatigue following mild exposures to vomiting, diarrhea, altered consciousness, fasciculations, seizures, and pulmonary edema with high level exposures. In vitro, certain pyrethroids (fenvalerate, sumithrin, d-trans allethrin) demonstrate estrogenic and antiprogestagenic activities and concern has been raised about their potential to act as endocrine disruptors. The photo at right shows pyrethroid application for control of West Nile Virus. References: Salome CM et al. The effect of insecticide aerosols on lung function, airway responsiveness and symptoms in asthmatic subjects. Eur Respir J. 2000; 16:38-43. Garey J and Wolff MS. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Biochem Biophys Res Comm. 1998; 251:855-859. He F et al. Clinical manifestations and diagnosis of acute pyrethroid poisoning. Arch Toxicol. 1989; 63:54-58.
  27. Both the natural pyrethrins and the synthetic pyrethroids share the same mechanism of toxicity. Both compounds prolong the inactivation of sodium channels on nerve membranes, prolonging neuronal excitation. Symptoms reported after exposure to these compounds are caused by these nerve membrane effects: paresthesia is due to effects on the sodium channels of nerves supplying the skin; rhinitis is due to effects on nerves in the nasal mucous membranes; and gastrointestinal irritation following ingestion is due to effects on GI mucosal nerves. The structure of pyrethroid pesticides (but not pyrethrins) affects the duration of sodium channel inactivation, and consequently the duration of symptoms. Pyrethroid pesticides may be roughly categorized into Type I &amp; II. Type I pyrethroids inactivate sodium channels for a shorter period of time than Type II. Examples of Type I pyrethroids are permethrin and resmethrin. In animals, severe systemic poisoning by Type I pyrethroids results in reflex hyperexcitability and fine tremor. Type II pyrethroids have an attached alpha-cyano group, which prolongs the time the sodium channel remains inactivated; this results in longer-lasting symptoms. Examples are cypermethrin and esfenvalerate. In animals, severe systemic poisoning by Type II pyrethroids results in salivation, hyperexcitability, choreoathetosis, and seizures. Although the mechanism is unclear, pyrethroid toxicity may be enhanced by simultaneous exposure to organophosphates. Reference: Coats JR. Mechanisms of toxic action and structure-activity relationships for organochlorine and synthetic pyrethroid insecticides. Environ Health Perspect. 1990; 87:255-262
  28. Following dermal exposure, immediate decontamination of the skin with soap and water or saline is an important first aid measure, since the dermal symptoms are prevalent. If a large amount has been ingested, and the patient is seen within one hour or ingestion, gastric contents should be emptied. Vitamin E cream may be effective for controlling paresthesia if used promptly after exposure and decontamination. Vitamin E may work by either sequestering pyrethroid into the vitamin or by a membrane interaction. Antihistamines may be effective for allergic reactions. There are no proven effective therapeutic measures for systemic poisoning, although many experimental therapies have been tried in animals. For non-dermal effects, symptomatic therapy should be administered. For example, anticonvulsants should be administered for seizures; case reports suggest that pyrethroid-induced seizures may require prolonged treatment with multiple anticonvulsants. If signs and symptoms are suggestive of sensitization or allergic reaction, workers should be removed from further exposure and residential use should be advised against. Reference: Ray DE, Forshaw PJ. Pyrethroid insecticides: poisoning syndromes, synergies, and therapy. Clin Toxicol. 2000; 38:95-101.
  29. A 35 year-old non-pregnant female complained of burning and itching on her arms and face and chest tightness that began immediately after putting on clothes she had taken out of her closet. She had just entered her house 2 hours after setting off a flea bomb. Physical exam was remarkable for redness on the skin of her face and arms. Her chest tightness had resolved shortly after leaving her house and on exam her lungs were clear.
  30. The woman brought in the flea bomb package– a drug store brand household insect fogger with the following ingredients listed on the label: 0.435% permethrin 0.05% pyrethrins 0.4% piperonyl butoxide 99.115% inert ingredients The label also recommended that 4 hours elapse between the start of fogging and entry into the structure being treated. In this case, exposure to both pyrethrins and a pyrethroid occurred as a result of premature entry into a treated structure. The exposure was limited and treatment should consist of removal of the contaminated clothing, decontamination and consideration of topical vitamin E cream.
  31. The last group of insecticides covered will be the organochlorines.
  32. US EPA has banned the use of many organochlorines and these products are now primarily of historical interest in the US. DDT and chlordane are examples of organochlorines no longer used in the US. DDT was banned from US use in the 1970s due to its long environmental half-life and toxicity to avian wildlife. However, the US manufacture of DDT for export to other countries continued for some time following the ban on its use. One of the continuing uses for DDT is malaria control. Although pyrethroid pesticides have been used for malaria control in endemic areas, insect resistance has led to a growing debate regarding the advisability of renewing the active use of DDT for this purpose. Lindane is the active ingredient of Kwell, used as a human scabicide. This sale of lindane for this purpose was banned in California in January 2000 (although existing stock could continue to be sold). Hexachlorobenzene is a fungicide used as a seed protectant. It will be discussed in a later section.
  33. Organochlorines are absorbed through the skin, lungs, and the GI tract. A significant part of the absorbed dose is stored in adipose tissue. The CNS is the site of acute toxic effects. Specific effects vary by compound, but include headache, dizziness, irritability, incoordination, tremor, and seizures. Paresthesia is associated with DDT exposure. Acute toxic effects should be treated with anticonvulsants. Because high tissue levels of organochlorines increase myocardial irritability, oxygen should be administered ( hypoxemia may exacerbate arrhythmias) and cardiac monitoring should be performed. Animal studies suggest that several organochlorines may be carcinogenic. For example, dieldrin induces liver tumors only in mice; DDT induces hepatic and other tumors in non-human primates. Evidence of association between organochlorine exposure and risk for human hepatic cancer risk is equivocal, based on worker studies. The association between organochlorine exposure and breast cancer has been the subject of numerous studies. Although these studies have yielded both positive and negative results, overall the data do not support an association. In vitro studies suggest that organochlorines may cause endocrine disruption by interacting with estrogen and androgen receptors. See: Calle EE et al. Organochlorines and breast cancer risk. CA Cancer J Clin. 2002 Sep-Oct;52(5):301-9. Sielken RL et al. Cancer dose-response modeling of epidemiological data on worker exposures to aldrin and dieldrin. Risk Anal. 1999 Dec;19(6):1101-11. Takayama S et al. Effects of long-term oral administration of DDT on nonhuman primates.J Cancer Res Clin Oncol 1999;125(3-4):219-25.
  34. In addition to systemic effects, organochlorines have dermal effects. There are historical reports of chloracne due to DDT among workers. The photo at right shows chloracne in a DDT production worker. Occasional reports exist of skin irritation due to lindane’s use as a scabicide, although this was not reproduced in a patch test series. From: Bowen and Moursund. 1956 Arch Dermatol
  35. In summary, insecticides are widely used. Exposure can occur in a variety of settings, at work and at home. Specific toxic effects are determined by the chemical category of the insecticide, although non-specific and solvent-related symptoms may be common to all. Decontamination and symptomatic therapy remain the mainstays for treatment of all pesticides. Specific therapy is limited to the cholinesterase inhibitors (2-PAM and atropine) and pyrethroids (vitamin E cream). Primary prevention of insecticide illness involves use reduction. Physicians should counsel patients to reduce or eliminate use of insecticides where possible. Use in homes, especially where children are present, should be actively discouraged to prevent accidental exposure. Caution should also be exercised in prescribing therapeutic pesticides such as lindane for scabies, as significant adverse effects may result from inappropriate administration.