The carbamates are esters of carbamic acid. Unlike organophosphates, carbamates are not structurally complex. Presently, the volume of carbamates used exceeds that of organophosphates, because carbamates are considered to be safer than organophosphates.
The oral LD50 in rats, dogs, chickens, ducks, pheasants, quails, and wild birds is 8, 19, 6.3, 0.415, 4.2, 5, and 0.42 mg/kg, respectively. Dogs are commonly poisoned with malicious intent by tainting food. The minimum toxic dose in cattle and sheep is 4.5 mg/kg, becoming lethal at 18 and 9 mg/kg, respectively. Cattle and other domestic animals are often poisoned by accidental exposure. Pigs have been poisoned after drinking water contaminated by this compound. In Africa, wildlife populations (including deer, lions, and birds) are declining because of malicious use of carbofuran. The dermal LD50 in rabbits is 2,550 mg/kg.
The carbamate insecticides act similarly to the organophosphates (see Organophosphates (Toxicity)) in that they inhibit acetylcholinesterase (AChE) at nerve synapses and neuromuscular junctions. This inhibition is reversible because the inhibiting bond is much less durable; thus, the inhibition of blood AChE frequently is not evident at the laboratory. Signs include hypersalivation, GI hypermotility, abdominal cramping, vomiting, diarrhea, sweating, dyspnea, cyanosis, miosis, muscle fasciculations (in extreme cases, tetany followed by weakness and paralysis), and convulsions. In brief, the acronym SLUD (salivation, lacrimation, urination, and diarrhea) describes the overall clinical features of carbamate poisoning. Death usually results from respiratory failure and hypoxia due to bronchoconstriction leading to tracheobronchial secretion and pulmonary edema.
Diagnosis of carbamate poisoning usually depends on history of exposure to a particular carbamate and response to atropine therapy. However, when a history of carbamate poisoning is not provided, but cholinergic signs and a clear positive response to atropine suggest carbamate or organophosphate poisoning, AChE activity levels should be determined in RBCs or whole blood (live animals), or in brain cortex (dead animals). Enzyme activity that is significantly inhibited (>50%) is confirmatory. Signs of hypercholinergic activity are usually seen with AChE inhibition >70%. Screening GI contents for carbamate insecticides by gas chromatography coupled with mass spectrometry is helpful in identification, confirmation, and quantitation of a particular carbamate and aids in differential diagnosis if an organophosphate insecticide is also involved.
Treatment of carbamate poisoning is similar to that of organophosphate poisoning in that atropine sulfate injections readily reverse the effects. Recommended dosages for atropine are as follows: dogs and cats—dosed to effect (repeated as needed), usually 0.2–2 mg/kg, parenterally, one-fourth of the dose given IV and the remainder given SC (cats should be dosed at the lower end of the range); cattle and sheep—0.6–1 mg/kg, one-fourth of the dose IV and the remainder SC, repeated as needed; horses and pigs—0.1–0.2 mg/kg, IV, repeated as needed.
Pralidoxime (2-PAM) should not be used to treat carbamate poisoning. 2-PAM can be beneficial if poisoning is caused by a mixture of organophosphates and carbamates. Signs of excessive cholinergic activity may warrant its use, in case the cause is organophosphate exposure. 2-PAM can be fatal if given too rapidly; it must be administered slowly (ie, in 5% saline over a 10-min period). Also see Organophosphates (Toxicity). Also, 2-PAM solution should be prepared freshly, because old solutions are known to produce cyanide. Use of morphine or barbiturates is contraindicated.