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INHALATIONAL EXPOSURE TO CARBONYL SULFIDE (COS) PRODUCES BRAIN LESIONS AND ALTERED BRAINSTEM AUDITORY (BAER) AND SOMATOSENSORY (SEP) EVOKED POTENTIALS IN FISHCER 344N RATS.
Citation:
HERR, D. W., J. GRAFF, V. C. MOSER, K. M. CROFTON, P. B. LITTLE, D. L. MORGAN, AND R. C. SILLS. INHALATIONAL EXPOSURE TO CARBONYL SULFIDE (COS) PRODUCES BRAIN LESIONS AND ALTERED BRAINSTEM AUDITORY (BAER) AND SOMATOSENSORY (SEP) EVOKED POTENTIALS IN FISHCER 344N RATS. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 95(1):118-135, (2007).
Impact/Purpose:
To investigate the neurotoxicity of carbonyl sulfide
Description:
Because of the amount of carbonyl sulfide (COS) emissions and the lack of toxicological data, COS was listed in the Clean Air Act of 1990 as a Hazardous Air Pollutant. In 1999 COS was nominated by the US EPA to the National Toxicology Program for additional toxicological investigation, including neurotoxicity. This manuscript describes the results of an inter-agency investigation into the neurotoxicity of COS. The results show that exposure to 400 ppm COS, for as little as 2 weeks, produces lesions in brainstem regions associated with auditory transmission. These effects were clearly detected using Brainstem Auditory Evoked Responses, in the absence of changes in auditory responsiveness assessed using a Functional Observational Battery or Reflex Modification Audiometry. Cortical lesions were detected using Somatosensory Evoked Potentials. The data produced by this publication may be useful in setting a RfC for COS.