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Delayed Neurotoxicity from Triaryl Phosphates

By

Ramesh C. Gupta

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

Last full review/revision Aug 2014 | Content last modified Aug 2014

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 aging 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 antidotes.

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The acronym SLUD stands for salivation, lacrimation, urination, and defecation, which are the clinical signs associated with muscarinic cholinergic overstimulation caused by certain toxins. Signs of SLUD are most consistent with exposure to which of the following classes of chemicals?
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