nicotinic stimulation include fine-muscle fasciculations and tachycardia. Various CNS manifestations also occur, including headache, respiratory depression, dizziness, anxiety, and mental confusion. Effects can progress to convulsions and coma (Ecobichon, 2001).
The combination of signs and symptoms that are exhibited depends on the specific chemical and the dose, duration, and route of exposure. Mild exposures typically produce only muscarinic and nicotinic signs, but severe exposures evoke CNS signs and pulmonary edema. Adverse effects can occur after dermal, inhalation, or ingestion exposure (Ecobichon, 2001).
The effects of carbamates are typically of shorter duration and milder than those of the organophosphorous compounds. Carbamates are not associated with OPIDN, but death has resulted from intentional administration of high doses of carbaryl (Ecobichon, 2001).
Because of its anticholinesterase activity, the transient effects of carbamates on the nervous system resemble those of cholinergic stimulation. In addition, acute exposures appear to change a variety of neurotransmitter systems in the CNS. Thresholds of such effects have not been determined.
Dietary exposure of swine to carbaryl resulted in a carbamate-induced syndrome that included neurotoxicity (Smalley, 1970; Smalley et al., 1969). Administration at 125–300 mg carbaryl/kg per day administered via the diet for 72–83 days resulted in myasthenia, incoordination, ataxia, tremor, muscle contractions, paraplegia, and prostration. At the higher dosages, those effects had a more rapid onset. The authors observed some recovery after exposure, but the effects recurred with micropathologic findings in the nervous system (Smalley, 1970; Smalley et al., 1969).
Carbamate exposure has behavioral consequences. Few systematic studies have addressed the behavioral effects, however, and they generally have been carried out with end points not considered especially sensitive. For example, acute exposure via various routes appears to decrease locomotor activity as measured in several devices. Decreases in wheel-running activity of rats were noted after acute exposure to carbaryl at only 0.56–2.24 mg/kg administered intraperitoneally. This was less than 4% of the LD50, and the effect was reversed by atropine (Singh, 1973). Acute exposure results in persistent behavioral effects, including reductions in motor activity noted 72 h after oral doses of 20, 75, and 150 mg/kg (Moser, 1995). Those doses represent 9, 33, and 65% of the reported LD50 for oral exposure of rats. Even at the lowest dose studied, autonomic function, motor activity, neuromuscular function, sensorimotor function, and reactivity are altered. An acute dose of only 10 mg/kg increased tolerance to electric shock and thereby attenuated the suppression of operant responding that also resulted in electric shock (Sideroff and Santolucito, 1972). Somewhat longer exposures to carbaryl may have the opposite effect on locomotor activity, reportedly increasing open-field activity and lowering the rate of habituation relative to controls.
An apparently unanswered question with respect to the carbamate insecticides is their effect on cognitive functions, including learning and memory. In a study of acute exposure to carbaryl in monkeys, dose-related decreases in accuracy (increases in errors) were observed in the repeated-learning paradigm after intramuscular injections of 1–10 mg/kg, whereas oral doses up to 50 mg/kg were without effects. Carbaryl was reported to be