EMmedonline

Pesticides are classified into

• Insecticides

  • Organophosphate

  • Carbamate

  • Organochlorines

  • Pyrethrins/pyrethroids

  • Neonicotinoids

  • N,N-diethyl-3-methylbenzamide (DEET)

• Herbicides

• Chlorophenoxy herbicides

• Bipyridyl herbicides

• Urea substituted herbicides

• Glyphosate

• Organophosphate herbicide

• Rodenticides

• Nonanticoagulants

• Anticoagulants

CARBAMATES

• N-methyl carbamates are cholinesterase inhibitors that are structurally related to organophosphate compounds.

• It includes carbaryl, primicarb, propoxur, trimethacarb.

• Carbamates can be toxic after dermal, inhalation and GI exposure.

• Carbamates transiently and reversibly bind to and inhibit cholinesterase enzyme through carbamylation. Therefore aging doesn't occur .

Clinical Feature : Similar to cholinergic crisis as in OP poisoning.

Diagnosis : Measurement of cholinesterase is generally not useful. Cholinesterase levels may return spontaneously to normal level by 4-8 hrs after exposure.

Treatment

• Atropine is the antidote of choice. The therapy is not usually required for more than 6 -12hrs until the carbamylated cholinesterase enzyme recovers spontaneously

• Pralidoxome is not recommended to be used as the binding is reversible spontaneously.

NEONICOTINOIDS

• Nicontine was first used as pesticide in 1960. Nicotine poisoning is severe and fatal. It was stopped due to resistance.

• Neonicotinoid group includes acetamipid, clothianidin, dinotefuran, imidacloprid. Impidacloprid is now widely used.

Mechanism of action

• It acts by binding irreversibly to the acetylcholine receptors leading to spontaneous discharge of nerve impulse and followed by failure of the neuron to propagate any signal.

• In insects ach receptors are present only within CNS.

• Mammalian nicotinic receptors are of different subtypes and are present at NMJ of CNS as well; but the binding affinity of the imidacloprid at nicotinic receptors in mammals is much less than that of insects. Therefore it is considered less toxic to humans.

Symptoms

• Drowsiness,dizziness

• Vomiting, disorientation

• Fever

• Sweating

• Tachycardia, tachypnea

Management

• There is no specific antitode.

• Symptomatic and supportive care

PYRETHRINS & PYRETHROIDS

• Pyrethrins are naturally occurring active extract derived form the chrysanthemum plant.

• Pyrethroids are synthatetic analog of pyrethrin and are considered safer than organochlorine and organophosphate insecticide.

• They are commonly used as aerosol in automated insect spray in public places.

• They are rapidly metabolised in liver and therefore are of low toxicity in humans.

Pathophysiology

• Pyrethroids block the sodium channel at the neuronal cell membrane, causing repetitive neuronal discharge.

• There is additional effect on gamma aminobutyric acid receptors.

• It also cause increased nicotininic cholinergic transmission, norepinephrine release and interference with sodium calcium exchange across membranes.

Clinical Feature

• These compounds can cause dermal, pulmonary, GI and neurologic illness.

• Allergic hypersensitivity reaction is the commonest manifestation.

• Contact dermatitis, allergic rhinitis.

• Parasthesia, hyperexcitiability, tremors, seizures, incordination, muscle weakness, respiratory failure, dizziness, headache and non specific nausea, vomiting, diarrhea.

• Alteration of consciousness, muscle fasciculation, pulmonary edema and seizure can occur.

Treatment

• Removal of source

• Dermal, ocular or GI decontamination.

• Supportive care

Availability

• All out : Prallatherin

• Good Knight

ORGANOCHLORINES

• Dichlorodiphenyltrichloroethane (DDT) is the prototype insecticide of these chlorinated hydrocarbon.

• Chlordane, heptachlor, dieldrin and aldrin are compounds used for termite and roach control.

• These compounds are banned in US due to its environmental toxicity.

• Hexachlorocyclohexane (Lindane) is a general garden organochlorine insecticide . It is well absorbed by ingestion and inhalation. Dermal absorption occurs, particularly if the skin is abraded or repeated application is used.

Pathophysiology

• Organochlorines are central neurologic stimulants that can be toxic after dermal, inhalation and GI exposure.

• They antagonise GABA mediated inhibition of central neurons, leading to hyperexcitability.

• They are also capable of inducing hepatic microsomal enzyme system.

Clinical Feature

• Mild poisoning presents with dizziness, ataxia, fatigue, malaise, headache, neurologic stimulation with hyperexcitability, irritability, delirium, apprehension, tremulousness, myoclonus and facial parasthesia.

• More severe exposure may result in seizure, coma, respiratory failure and death.

• Aspiration pneumonitis.

• Cardiac dysarrythmia due to sensitisation of myocardium to endogenous catecholamine .

Treatment

• Removal of clothing and skin decontamination with mild detergent and water.

• Activated charcoal and gastric lavage are probably useful

• Administration of oxygen

• Intubation to protect airway from aspiration, seizures and to correct hypoxia.

• Seizures are controlled using benzodiazipines.

• Epinephrine must be avoided as organochlorines can sensitise the myocardium to endogenous catecholamines.

• Exchange resin cholestyramine is potentially useful for symptomatic patients exposed to chlordecone.

N,N Diethyl-3-Methylbenzamide (DEET)

• DEET are used as over the counter insect repellent.

• DEET is absorbed through skin and is a neurotoxin that causes seizures in large ingestion.

• Sytemic toxicity is rare but manifest as restlesness, insomnia, altered behaviour, confusion, neurologic depression, slurred speech, ataxia, tremors, muscle cramps, hypertonia and seizures.

• DEET induced hypotension and bradycardia has been reported.

• Treatment

  • Decontamination with mild detergent and water

  • Activated charcoal.

  • Benzodiazipines for seizure control.