How do organophosphates and carbamates poison humans?

• A. They depress levels of the cholinesterase enzyme
• B. They cause dehydration
• C. They affect only the skin
• D. They block vitamin absorption

Answer: (A)

They poison humans by inhibiting acetylcholinesterase, the enzyme that normally breaks down acetylcholine after a nerve signal. When this enzyme is inhibited, acetylcholine accumulates at nerve endings and neuromuscular junctions, causing excessive stimulation of both muscarinic (parasympathetic) and nicotinic receptors. That leads to a range of symptoms such as increased secretions, sweating, urination, diarrhea, vomiting, bronchoconstriction, slowed heart rate, pupil constriction, muscle twitching, weakness, and potentially respiratory failure. Organophosphates and carbamates differ in how long they keep the enzyme inhibited—organophosphates can cause longer-lasting, sometimes irreversible inhibition through aging, while carbamates are typically reversible. Treatments focus on blocking muscarinic effects with atropine and reactivating the enzyme with pralidoxime for organophosphate poisoning, along with supportive care. The reason this option is correct is that it identifies the key mechanism: inhibition of cholinesterase, which prevents breakdown of acetylcholine and leads to widespread cholinergic overactivity. Dehydration, skin-only effects, or vitamin absorption interference are not how these pesticides exert their primary toxic effect.