Genetic polymorphisms and susceptibility have not been systematically explored with respect to carbamates. Two reports in humans might be pertinent. A pilot case-control study looked at the association between environmental exposure and acute leukemia in infants who were either positive or negative for a translocation involving chromosome band llq231 (that is, MLL+ve and MLL−ve infant acute leukemia). The data from that study indicate that fetal exposure to carbamate-based insecticides in some settings increased the odds ratio for infant acute leukemia but only in the presence of MLL+ve rearrangements (Alexander et al., 2001). Those data suggest that MLL+ve people might be more susceptible to carbamates. However, other mosquitocides might have been present, and the authors note limitations of the study, including the small number of cases and the potential nonrepresentativeness of controls. In addition, Loewenstein-Lichenstein and colleagues (1995) reported a soldier homozygous for “atypical” butyrylcholinesterase who experienced severe symptoms after pyridostigmine prophylaxis during the Gulf War.
In a rodent study, females exhibited greater sensitivity to carbaryl than males (Gaines, 1969).
As with the organophosphorous insecticides, carbamate insecticides act by inhibiting acetylcholinesterase, the enzyme responsible for the breakdown and therefore the termination of the activity of acetylcholine. Failure to break down acetylcholine results in sustained effects of this neurotransmitter and consequent overstimulation of cholinergically mediated synapses, particularly nicotinic neuromuscular synapses, muscarinic parasympathetic synapses, and cholinergic synapses of the CNS (Ecobichon, 2001).
In contrast with the phosphorylation that occurs with organophosphorous insecticides, carbamylation of cholinesterase is reversible. Regeneration of the enzyme activity occurs within a few hours: the carbamate is cleaved and loses its ability to inhibit anticholinesterase.
As would be anticipated from its mechanism of action, the symptoms of carbamate-insecticide poisoning are similar to those of organophosphorous-insecticide poisoning. The clinical symptoms of acute exposure to carbaryl are derived from its effects on acetylcholine synapses, including actions at the synapses of the CNS and neuromuscular junctions, sensory nerve endings, ganglionic synapses of the parasympathetic and sympathetic nervous system, postganglionic sympathetic nerve terminals innervating sweat glands and blood vessels, sympathetic nerve terminals in the adrenal medulla, and postganglionic parasympathetic nerve terminals. Specifically, the effects stem from the accumulation of acetylcholine at those synapses. Carbamate toxicity typically involves the nervous and respiratory systems. Effects of peripheral muscarinic stimulation include increases in bronchial secretions and bronchoconstriction; excessive sweating, salivation, and lacrimation; pinpoint pupils; bradycardia; and vomiting and diarrhea. Effects of peripheral