Carbamate pesticide poisoning
Introduction
Introduction to carbamate pesticide poisoning Carbamate pesticide poisoning, also known as acute carbamate insecticide poisoning, is a muscarinic acid caused by a decrease in cholinesterase activity in the body after a short period of intimate contact with the carbamate insecticide. Systemic diseases such as nicotinic and central nervous system symptoms. Carbamate insecticides mainly include naphthyl carbamates (carbaryl), phenyl carbamates (leaf), heterocyclic dimethyl carbamates (isosone), heterocyclic rings. Varieties such as methyl carbamate (carbofuran) have strong selectivity, rapid action and low toxicity. basic knowledge The proportion of the disease: the incidence rate of agricultural workers is about 0.006% - 0.009% Susceptible people: no specific population Mode of infection: non-infectious Complications: pulmonary edema, brain edema, coma
Cause
Carbamate pesticide poisoning cause
Carbamate pesticides can invade the body through the respiratory tract and digestive tract. They can also be slowly absorbed through the skin and mucous membranes. They are mainly distributed in the liver, kidney, fat and muscle tissues. They are rapidly metabolized in the body, and are metabolized by hydrolysis, oxidation and binding. Excretion of urine can generally discharge 70% to 80% of the intake in 24 hours.
The mechanism of action of carbamate pesticides is similar to that of organophosphorus pesticides, mainly inhibiting the activity of cholinesterase, causing the hydroxyl group of serine at the active center of the enzyme to be carbamoylated, thus losing the ability of the enzyme to hydrolyze acetylcholine, carbamate pesticides. A loose complex can be formed directly with cholinesterase without metabolic activation. Since the carbamate pesticide is reversible in combination with cholinesterase, it is rapidly hydrolyzed in the body, and cholinesterase activity It is easier to recover, so its toxicity is lighter than organophosphorus pesticide poisoning.
Prevention
Carbamate pesticide poisoning prevention
No special precautions, early detection, early treatment.
Complication
Carbamate pesticide poisoning complications Complications pulmonary edema cerebral edema coma
Pulmonary edema, cerebral edema, coma and respiratory depression can occur when a large number of oral poisonings occur, and no delayed peripheral neuropathy occurs after poisoning.
Symptom
Symptoms of carbamate pesticide poisoning Common symptoms Nausea drooling Respiratory depression, muscarinic symptoms, coma
Similar to mild organophosphorus pesticide poisoning, but generally mild, with muscarinic symptoms, dizziness, headache, fatigue, nausea, vomiting, salivation, excessive sweating and dilated pupils, blood cholinesterase activity Mildly inhibited, so the general condition is mild, the course of disease is shorter, and the recovery is faster. When a large number of oral poisonings occur, pulmonary edema, cerebral edema, coma and respiratory depression may occur, and delayed peripheral neuropathy does not occur after poisoning.
Examine
Examination of carbamate pesticide poisoning
The cholinesterase activity of whole blood was light and moderately decreased within 12 hours after poisoning, and the corresponding poison was detected in vomit or washing solution.
Diagnosis
Diagnosis and identification of carbamate pesticide poisoning
First, mild poisoning, can appear dizziness, headache, fatigue, blurred vision, numbness, sweating, pale, nausea, vomiting, dilated pupils, muscle tremors, etc., usually return to normal within 24 hours after contact, all The blood choline enzyme activity is often below 70%.
Second, severe poisoning, in addition to the above symptoms aggravated, and one of the following conditions, can be diagnosed as severe poisoning: 1. Pulmonary edema 2 coma brain edema, whole blood cholinesterase is generally below 30%.
