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ACUTE EXPOSURE INFORMATION
- The following are symptoms from carbamate insecticides in general, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for carbofuran, but could potentially occur in individual cases.
- USES: Carbofuran, a carbamate insecticide, is used as a systemic carbamate acaricide, insecticide, and nematicide. It is applied to soil to control insects and nematodes in ornamental plants, trees, and crops.
- TOXICOLOGY: Carbamate insecticides competitively inhibit pseudocholinesterase and acetylcholinesterase, preventing hydrolysis and inactivation of acetylcholine. Acetylcholine accumulates at nerve junctions, causing malfunction of the sympathetic, parasympathetic, and peripheral nervous systems and some of the CNS. Clinical signs of cholinergic excess develop.
- EPIDEMIOLOGY: Exposure to carbamate insecticides is common, but serious toxicity is unusual in the US. Common source of severe poisoning in developing countries. Toxicity generally less severe than with organophosphates.
- WITH POISONING/EXPOSURE
- MILD TO MODERATE POISONING: MUSCARINIC EFFECTS: Can include bradycardia, salivation, lacrimation, diaphoresis, vomiting, diarrhea, urination, and miosis. NICOTINIC EFFECTS: Tachycardia, hypertension, mydriasis, and muscle cramps may develop.
- SEVERE POISONING: MUSCARINIC EFFECTS: Bronchorrhea, bronchospasm, and acute lung injury. NICOTINIC EFFECTS: Muscle fasciculations, weakness, and respiratory failure. CENTRAL EFFECTS: CNS depression, agitation, confusion, delirium, coma, and seizures. Hypotension, ventricular dysrhythmias, metabolic acidosis, pancreatitis, and hyperglycemia can also develop.
- CHILDREN: May have different predominant signs and symptoms than adults (more likely CNS depression, stupor, coma, flaccidity, dyspnea, and seizures). Children may also have fewer muscarinic and nicotinic signs of intoxication (ie, secretions, bradycardia, fasciculations, and miosis) as compared with adults.
- INHALATION EXPOSURE: Vapors rapidly produce mucous membrane and upper airway irritation and bronchospasm, followed by systemic muscarinic, nicotinic, and central effects if exposed to significant concentrations.
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