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Delayed Neurotoxicity from Triaryl Phosphates and Other Organophosphates and Carbamates in Animals


Ramesh C. Gupta

, DVM, PhD, DABT, FACT, FACN, Toxicology Department, Breathitt Veterinary Center, Murray State University;

Robin B. Doss

, Breathitt Veterinary Center, Murray State University

Reviewed/Revised Aug 2022 | Modified Nov 2022

Compounds known as triaryl phosphates (eg, triorthocresyl phosphate and related compounds) have been used as flame retardants, plasticizers, lubricating oils, and hydraulic fluids. They are weak cholinesterase (ChE) inhibitors but do inhibit neurotoxic esterase (NTE) present in the brain and spinal cord.

A form of delayed neurotoxicity results from the inhibition and aging of NTE, often referred to as OP-induced delayed neuropathy (OPIDN). Triaryl phosphates have caused accidental poisonings in humans and other species (mostly cattle). Some other OPs are known to cause OPIDN, including the following:

  • Chlorpyrifos

  • Dichlorvos

  • Ethyl 4-nitrophenyl phenylphosphonothioate (EPN)

  • Haloxon

  • Isofenphos

  • Leptophos

  • Methamidophos

  • Mevinphos

  • Mipafox

  • Parathion

  • Diisopropylphosphorofluoridate

  • Tetraethyl pyrophosphate

  • Ttrichlorfon

  • Trichloronat

Field cases have been seen with some of these OPs.

Delayed peripheral neuropathy can also be caused by carbamate pesticides, such as carbaryl, carbofuran, and metolacarb. The lesions associated with delayed neurotoxicity include demyelination of peripheral and spinal motor tracts due to loss of NTE function.

Clinical signs associated with delayed neurotoxicity include muscle weakness and ataxia that progresses to flaccid paralysis. Signs do not usually manifest until 10–14 days after exposure to a neurotoxic triaryl phosphate or any other OP compound.

There are no specific antidotes.

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