DICHLOROACETYLENE - EFFECTS ON THE RAT TRIGEMINAL NERVE SOMATOSENSORY-EVOKED POTENTIAL

Humans overexposed to trichloroethylene (TCE), under specific conditio ns, were reported to develop trigeminal nerve dysfunction. A degradati on byproduct dichloroacetylene (DCA), however, has been suggested as t he probable neurotoxicant rather than TCE. Studies in mice, rats, and rabbits support the hypothesis of DCA-induced trigeminal neurotoxicity . This study, therefore, was conducted to characterize DCA-induced tri geminal nerve dysfunction in rats using the electrodiagnostic procedur e trigeminal nerve-stimulated somatosensory evoked potential (TSEP). A group of six rats was exposed once to DCA (similar to 300 ppm) or roo m air for 2.25 h and a separate group of six rats was not exposed and served as controls. Trigeminal nerve somatosensory evoked potentials ( TSEPs) were collected before exposure and 2, 4, and 7 days postexposur e. Because DCA was manufactured from TCE with acetylene added as a sta bilizer, another group of rats was exposed to TCE and acetylene withou t generation of DCA. TSEPs from DCA-exposed rats were smaller and slow er compared to their baseline recordings and to the concurrent negativ e controls. TSEPs from the controls and the TCE/acetylene-exposed rats were unchanged. Neuropathology did not reveal treatment-related lesio ns. It was concluded that the rat is mildly to markedly susceptible to DCA-induced trigeminal nerve dysfunction as assessed by TSEP, but tha t the kidney was the likely target organ based on gross observations a nd the DCA literature. (C) 1997 Elsevier Science Inc.