Dichloroacetylene: effects on the rat trigeminal nerve somatosensory evoked potential

Humans overexposed to trichloroethylene (TCE), under specific conditions, were reported to develop trigeminal nerve dysfunction. A degradation byproduct dichloroacetylene (DCA), however, has been suggested as the 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 trigeminal nerve dysfunction in rats using the electrodiagnostic procedure trigeminal nerve-stimulated somatosensory evoked potential (TSEP). A group of six rats was exposed once to DCA (approximately 300 ppm) or room 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 postexposure. Because DCA was manufactured from TCE with acetylene added as a stabilizer, another group of rats was exposed to TCE and acetylene without generation of DCA. TSEPs from DCA-exposed rats were smaller and slower compared to their baseline recordings and to the concurrent negative controls. TSEPs from the controls and the TCE/acetylene-exposed rats were unchanged. Neuropathology did not reveal treatment-related lesions. It was concluded that the rat is mildly to markedly susceptible to DCA-induced trigeminal nerve dysfunction as assessed by TSEP, but that the kidney was the likely target organ based on gross observations and the DCA literature.