Butyrylcholinesterase (BChE) scavenges low doses of organophosphorus (for example,
paraoxon) and
carbamate pesticides (for example,
carbaryl) and in this way protects people from the toxic effects of these
poisons. The protective role of BChE is demonstrated by the finding that
pesticide applicators can have reduced BChE activity with no clinical signs of
poisoning. The question has arisen whether people with genetic variants of BChE are less protected. Seventy-six percent of the population is homozygous for wild-type BChE, while 24% carry at least one genetic variant allele. Most genetic variants of BChE have reduced activity. The clinically most important variant is atypical (D70G) BChE because people with this variant have 2 hours of
apnea after receiving a dose of
succinylcholine that is intended to paralyze muscles for 3-5 minutes. In test tube experiments the atypical variant reacts more slowly with all positively charged compounds (for example
physostigmine, echothiophate). This leaves more toxin available for reaction with
acetylcholinesterase in nerve synapses and predicts that people with atypical BChE will be less protected. Variants with low activity, such as silent BChE, are predicted to be at increased risk from organophosphorus pesticides based on experiments in monkeys and rodents where injection of purified BChE protected animals from the toxic effects of
nerve agents. More studies are needed to strengthen the hypothesis that people with genetic variants of BChE are at higher risk of intoxication from pesticides.