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The health effects associated with organophosphate poisoning are a result of excess acetylcholine (ACh) present at different nerve synapses and neuromuscular junctions across the body. Specifically, acetylcholinesterase (AChE), the enzyme that normally and constantly breaks down acetylcholine, is inhibited by the organophosphate substance.
Organophosphate-induced delayed neuropathy (OPIDN), also called organophosphate-induced delayed polyneuropathy (OPIDP), is a neuropathy caused by killing of neurons in the central nervous system, especially in the spinal cord, as a result of acute or chronic organophosphate poisoning.
Symptoms of organophosphate poisoning include violent convulsions, vomiting, miosis, lachrymation, sweating, salivation, diarrhea, and potentially death. [ 3 ] Most nerve gases, including sarin , soman , and tabun , are organophosphates, [ 6 ] which are all banned by the Geneva Convention of 1925, as they are deemed a war crime .
Health effects of pesticides may be acute or delayed in those who are exposed. [1] Acute effects can include pesticide poisoning, which may be a medical emergency. [2] Strong evidence exists for other, long-term negative health outcomes from pesticide exposure including birth defects, fetal death, [3] neurodevelopmental disorder, [4] cancer, and neurologic illness including Parkinson's disease ...
As a result of cholinergic crisis, the muscles stop responding to the high synaptic levels of ACh, leading to flaccid paralysis, respiratory failure, and other signs and symptoms reminiscent of organophosphate poisoning. Other symptoms include increased sweating, salivation, bronchial secretions along with miosis (constricted pupils).
Symptoms of a terbufos induced ACC result in muscarinic (diaphoresis, vomiting, miosis, salivation), nicotinic (pallor and muscle weakness with respiratory failure) and CNS poisoning (headache, dizziness, altered level of consciousness) symptoms. [24] The toxic effects can be managed by early recognition of terbufos poisoning, rapid ...
In the treatment of organophosphate toxicity, cholinesterase reactivators such as Pralidoxime reactivate inhibited AChE at peripheral nicotinic receptors.Since AChE mediates effects on both nicotinic and muscarinic receptors, cholinesterase reactivators are co-administered with muscarinic antagonists, primarily atropine.
Exposure to organophosphate pesticides in general has been increasingly associated with changes in children's cognitive, behavioral and motor performance. [54] [55] Infant girls were shown to be more susceptible to harmful effects from organophosphate insecticides than infant boys. [53]