he influence of carbofuran metabolism on acetylcholinesterase inhibition was defined after low dose (50 ug/kg iv and oral) carbonyl-(14)C carbofuran exposures to male Sprague-Dawley rats. Red blood cell acetylcholinesterase (RBC AchE) inhibition (83% at 2 minutes, 37% at 15 minutes for iv and oral, respectively, with recovery by 3 hr), was correlated with carbofuran plasma concentrations (r= 0.97). Eight hour sample collection indicated that ultimate fate 41-47% (14)CO2, 14-15% urine,