Pesticide intoxication


 * Pesticides are substances against harmful organisms
 * mainly against insects (insecticides), rodents (rodenticides), molluscs (molluscicides), weeds (herbicides), fungi (fungicides) ...
 * systemic pesticides - penetrate plants, protect more effectively (organophosphates)
 * contact pesticides - kill organisms only in affected areas
 * the most toxic are some insecticides, molluscicides and herbicides
 * The most common intoxication is rodenticides - it is not so severe

Character noxy
Organophosphates are esters of phosphoric acid, either containing sulfur (suffix -thion) and cyp450 metabolizes them to an active derivative containing oxygen (-oxone), or have equal oxygen in the molecule;


 * high acute toxicity ,
 * the spectrum of preparations does not contain highly toxic organophosphates,
 * they do not accumulate in the environment, they are low in adipose tissue, they are not significantly carcinogenic ,
 * representatives - fenitrothion (Sumithion), diazinon, etc.

Professional exposure
The risk of intoxication arises during production, less so during further processing;
 * in addition, they contain solvents and other additives.

Etiopathogenesis
Irreversible acetylcholinesterase (ACHE) inhibition - ACH → ACH degrading enzyme accumulates;
 * the accumulation of ACH can explain most of the symptoms of intoxication, a disorder of cholinergic transmission,
 * the synthesis of the new ACHE takes 60 days ,
 * as a late consequence, neuropathy is due to degeneration of PNS axons.

Toxicity
depends on the ability to inhibit ACHE, on the concentration ...

Clinical picture
First symptoms:
 * with a decrease in ACHE activity below 70% (reduction below 20% - severe poisoning),
 * life-threatening poisoning - activity is immeasurable,
 * depends on the speed of boarding ...
 * acute - accumulating ACH affects two types of receptors (muscarinic - vegetative motor, nicotine - neuromuscular discs), then it is also a mediator in the CNS ,
 * muscarinic symptoms - tearing, salivation, sweating, miosis, vomiting, abdominal pain, diarrhea, bronchial hypersecretion, bronchospasm, bradycardia (as if parasympathetic),
 * the preganglial innervation of the sympathetic nervous system is also affected by ACH → in mild poisoning, the symptoms are expressed differently ( the sympathetic nervous system may antagonize this),
 * nicotine symptoms - fasciculations, tremor, convulsions, paralysis of the respiratory muscles,
 * CNS symptoms - disorientation, headaches, convulsions, respiratory depression, coma.


 * The cause of death is respiratory failure (all systems are comprehensively involved) and cardiac arrhythmias
 * chronic - accumulation may occur rarely, symptoms such as acute,
 * late neuropathy - not due to ACH, about 7-21 days after severe poisoning - calf cramps, numbness, paraesthesia in the legs, weakness.

Investigation methods

 * For monitoring professional exposure - erythrocyte ACHE,
 * we examine neuropathy with EMG.

Differential diagnosis
Heavier exposures may resemble a stroke, a milder infectious disease.

Therapy
Pharmacological antidote is atropine - blocks muscarinic symptoms (not nicotine), before administration of atropine it is necessary to correct respiratory and cardiovascular disorders (give oxygen ) - doses are controlled by mucosal humidity, in severe poisoning - biochemical antidote - oxime - ACHE reactivator (eg obidoxime) ), comprehensive care for vital functions, in case of convulsions - diazepam (in low doses).

Characteristics of noxy
Carbamic acid derivatives, directly inhibiting ACHE (without activation), representatives - pirimicarb (Pirimor®), etc., also include neostigmine (Syntostigmine®) and physostigmine (natural alkaloids, indirectly acting, parasympathomimetic, used in glaucoma ... ).

Professional exposure
In agriculture, due to the lower toxicity they are in preparations for gardeners !; in industry they are used for the production of plastics.

Etiopathogenesis
They enter through all gateways, they inhibit ACHE but reversibly !!!, spontaneous reactivation occurs quite quickly, they do not settle.

Clinical picture
Acute symptoms - as with organophosphates, but they occur earlier, have a milder and shorter course, chronic poisoning - are not known (max. Dermatitis).

Investigation methods
ACHE determination is important only after intoxication (inhalation goes too fast).

Differential diagnosis
It can resemble an infectious disease, it is important to distinguish between organophosphate poisoning, neuropathy does not occur.

Therapy
Atropine is enough, then symptomatically and supportively.

Rodenticides

 * The most commonly used anticoagulants - warfarin (Kumatox), brodifacoum (Volid, Talon) ...,
 * they are small in granules, have a delayed effect, usually potentiated by repeated consumption of poison by rats,
 * delayed toxicity does not deter rats from eating, moreover, it does not vomit rats,
 * low toxicity to humans is also an important condition (they just lie on the ground, they can be ingested by children ...),
 * occupational exposure - does not pose a risk.

Etiopathogenesis
It is well absorbed from the GIT (worse through the skin), they are vit.K antagonists → they block the synthesis of coagulation factors II (prothrombin), VII, IX and X lethal doses contain up to kilograms of the product.

Clinical picture

 * Acute - most often in young children, ingestion of a few grains does not manifest itself, with a larger amount Quick is prolonged, bleeding symptoms are usually only in suicidal attempts (suicide is usually unsuccessful),
 * chronic - very rare.

Investigation methods
Monitoring of INR value.

Therapy
Specific antidote - vitamin K ( Kanavit ) - indicated after ingestion of a large dose.

related articles

 * Intoxication by fungi

Source

 * BENEŠ, Jiří. Study materials  [online]. © 2007. [feeling. 2010]. < http://www.jirben.wz.cz/ >.