For some time, compounds known as triaryl phosphates (eg,
triorthocresyl phosphate) have been used as flame retardants, plasticizers,
lubricating oils, and hydraulic fluids. They are weak cholinesterase inhibitors but
do inhibit “neurotoxic esterase” (NTE) present in the brain and spinal cord. A form
of delayed neurotoxicity results from the inhibition and ageing of NTE, often
referred to as OP-induced delayed neuropathy (OPIDN). Triaryl phosphates have caused
accidental poisonings in people and other species (mostly cattle). Some other OPs,
including EPN, leptophos, parathion, haloxon, diisopropylphosphorofluoridate, and
tetraethyl pyrophosphate, are known to cause OPIDN, and field cases have been seen.
The lesions associated with delayed neurotoxicity include demyelination of
peripheral and spinal motor tracts due to loss of neurotoxic esterase function.
Clinical signs associated with delayed neurotoxicity include muscle weakness and
ataxia that progresses to flaccid paralysis. Signs are usually not manifest until
10–14 days after exposure to a neurotoxic triaryl phosphate. There are no specific
Last full review/revision August 2014 by Ramesh C. Gupta, DVM, MVSc, PhD, DABT, FACT, FACN, FATS