Nonpesticide phosphate esters induce delayed neurotoxicity in cattle. The most common exposures are to complex mixtures of triaryl phosphate used in lubricating oils. Oral ingestion is most common, but dermal exposures have also occurred. Clinical signs of cholinesterase (ChE) inhibition may or may not be seen. Depending on the biochemical targets, the percent reduction in blood ChE is variable and can be < 30% of normal activity. Organophosphate ester-induced delayed neurotoxicity cannot be predicted by inhibition of blood ChEs. Signs of delayed neurotoxicity occur 2 to 25 d after exposure; these signs are neurologic deficiencies of the antigravity muscles and the muscles of the urinary bladder and larynx. Affected cattle may dribble urine and some may be mute. Signs of ChE inhibition generally are not observed in animals with neurological deficiencies. Pathologic findigs are axonopathy and myelin degeneration of nerves with long axons located in both the peripheral and central nervous systems. In the spinal cord, location of the affected nerve tracts is variable. Degenerative changes occur in motor neurons. Calves are less susceptible to organophosphate ester-induced delayed neurotoxicity than cows. A dose of 500 mg triaryl phosphate/kg body weight will produce complete paralysis in a mature cow in 26 d.