MARK D
CURRICULUM FOR THE HEALTH SCIENCES IN SOUTH EASTERN EUROPE
Number (unit, topic): U4-T4
Prior review – Status: D
ECTS (suggested):
Title
Occupational Organophosphate Pesticide Poisoning
Author(s)
Institution
Ass. Prof. Ivan Mikov, MD, PhD,
Specialist in Occupational Medicine
Department of Occupational Medicine,
Medical Faculty, University of Novi Sad, Yugoslavia
Department of Occupational Medicine,
Medical Faculty, University of Novi Sad
Futoska 121,
21000 Novi Sad, FR Yugoslavia
Tel. + 381 21 613 998, 614 277, Fax: + 381 21 624 128
e-mail: driva@eunet.yu
Address for
correspondence
Keywords
Organophosphate
pesticides,
Organophosphorus
compounds, Occupational poisoning, Cholinesterase,
Worker, Health surveillance
Learning objectives
Synopsis (Abstract)
Teaching methods
Most organophosphate pesticides (OP) are used as
insecticides, while a few are used as fungicides,
nematocides or plant regulators. Since the removal of
organochlorine insecticides from use, organophosphate
insecticides have become the most widely used
insecticides available today. All OP share a common
mechanism of toxicity and can cause similar symptoms.
- Introductory lecture with transparencies
- Distribution of guidelines concerning Poison Control
Centres
- Presentation of occupational intoxication with
organophosphate pesticide - clinical case report
Specific recommendations
for teacher
.
Assessment of
students
Written exam: multiple-choice questions
Occupational Organophosphate Pesticide Poisoning
Ivan Mikov, MD, PhD, Department of Occupational Medicine,
Medical Faculty, University of Novi Sad, Novi Sad, Yugoslavia
Chemical structure
Most commercial OP are phosphorothioates since the P=S form is more stable
and more lipid soluble than their oxidised form (P=O) - "oxon" which are much
more toxic. Conversion occurs in the body, chiefly by the action of liver
microsomes.
Mechanism of toxicity
OP exerts their toxic effect through inhibition (phosphorylation) of
acetylcholinesterase enzyme (AChE) activity at nerve endings. AChE inhibition
leads to accumulation of acetylcholine.
Signs and symptoms of acute poisoning by site of acetylcholine neurotransmitter
activity
1. Muscarinic - cholinergic neuroeffector junctions:
nausea, vomiting, diarrhoea, salivation, lachrymation, bronchoconstriction,
bronchorrhoea, bradycardia, miosis, blurred vision, urinary incontinence etc.
2. Nicotinic effects - skeletal nerve-muscle junctions and autonomic ganglia:
muscle fasciculations, loss of reflexes, paralysis
3. Central effects - central nervous system:
Headache, dizziness, behavioural disturbances, confusion, hallucinations,
convulsions, loss of consciousness, respiratory depression etc.
Diagnosis test procedures
- Two types of cholinesterase are clinically significant:
1. Specific or true acetylcholinesterase found principally in the nervous system
and the red blood cells.
2. Non-specific or pseudocholinesterase found principally in the plasma and the
liver.
The organophosphorus compounds inhibit both types, but the level of depression
of specific or the red blood cell cholinesterase (RBC AChE) is a more reliable
indicator of clinically significant reduction of cholinesterase activity. High RBC
AChE inhibition is diagnostic of acute OP poisoning.
- Severity of poisoning:
Mild (RBC AChE > 40%)
Moderate (RBC AChE 20% - 40%)
Severe (RBC AChE < 20%)
- Regeneration of cholinesterase
There is regeneration of cholinesterase primarily by the synthesis of new
enzyme, which takes place at the rate of approximately 1% per day.
Treatment of acute poisoning
- Airway protection
- Skin decontamination
- Atropine - administer i.v. or i.m. until signs of atropinization appear, effective
only against muscarinic manifestations.
- Pralidoxime - administer less than 48 hours after poisoning, reactivator of
AChE. Warning: pralidoxime may actually be hazardous in poisonings by
cholinesterase -inhibiting carbamate compounds
- Seizure control and the other supportive therapy
- Observation - ensure that symptoms do not recur as atropinization is withdrawn
Chronic effects
- Orgnophosphate-induced delayed neuropathy (distal symmetric sensorimotor
neuropathy)
- Central nervous system dysfunction
- Dermatitis
Prevention of poisoning
- Personal protective equipment (respiratory protection, impervious protective
clothing)
- Preventive hygiene activities (consumption of food and smoking must not occur
in work areas potentially contaminated with pesticides, washing of hands, face
and neck prior to breaks, daily showers at the end of shift)
- Health surveillance of workers
Medical aspects of the occupational health program should parallel the hygiene
activities. Preplacement medical examinations should include measurement of
RBC AChE activity for determination of a preexposure baseline because of high
interindividual variability. Periodic medical examination should be made
available on at least an annual basis. But, measurement of RBC AChE activity in
workers exposed to organophosphate pesticides should be available at more
frequent intervals depending on workplace hygienic surveys.
References:
1. Moretto A, Lotti M. Toxicity of pesticides. In: Stacey NH (ed.).
Occupational toxicology. Bristol: Taylor& Francis, 1995:177-204.
2. Reigart RJ, Roberts RJ. Organophosphate insecticides. In: Reigart RJ,
Roberts RJ. Recognition and management of pesticide poisonings.
Washington DC: U.S. Environmental Protection Agency, 1999: 34-47.
3. Mikov M, Jovanovic D, Jokanovic M, Mikov I, Mihajlovic G. Pesticide protection, first aid and management of poisoning. Belgrade: Nova prosveta,
1997, 46pp. (in Serbian)
4. Legaspi JA, Zenc C. Occupational health aspects of pesticides. In: Zenc C
(ed.). Occupational medicine. New York: Mosby, 1994: 617-46.