Record Display for the EPA National Library Catalog

RECORD NUMBER: 5 OF 6

Main Title Initial Submission: Thirteen-Week Inhalation Exposure of Rats and Dogs to Hexafluoroacetone (HFA) with Cover Letter dated 10/16/1992.
CORP Author Du Pont de Nemours (E.I.) and Co., Newark, DE. Haskell Lab. for Toxicology and Industrial Medicine.; Environmental Protection Agency, Washington, DC. Office of Toxic Substances.
Year Published 1992
Report Number 8EHQ-1092-11696
Stock Number OTS0571624
Additional Subjects Toxicology ; Health effects ; Hexafluoroacetone ; Subchronic toxicity ; Mammals ; Rats ; Inhalation ; Dogs ; CAS No 13098-39-0
Holdings
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Status
NTIS  OTS0571624 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 80p
Abstract
Previous studies have indicated damage to a number of specific organs in rats following exposure to HFA. In order to determine a toxicologically acceptable level for the compound in industrial atmospheres, young, growing, male and female ChR-CD rats and mature, male, beagle dogs were exposed to atmospheres containing 0, 0.1, 1 and 12 parts per million (ppm, v/v ratio) of HFA. The exposures lasted six hours per day, five days per week for thirteen weeks. The suitability of common biochemical and hematological tests as indicators of RFA exposure was also evaluated. At the 12 ppm level, HFA had a significant (p < 0.05) effect on the total body, adrenal, testes, and pituitary weights of rats. There was a tendency toward increased weight of the heart, stomach, liver and lungs as well as lymphocytosis and kidney dysfunction. Histopathologically there was reversible damage to the testes, spleen, thymus, lymph nodes, and bone marrow. Similar effects were onserved in dogs exposed to this same concentration. In both species, the testis was the most susceptible organ. An indication of reversible kidney dysfunction in the rats and increased lung weight in the dogs was observed at the 1 ppm level. There were no gross, biochemical, hematological or histopathologic changes in either species attributable to RFA at the 0.1 ppm exposure level. The average lung weight in dogs exposed to this level, however, was greater than that of the controls. There was no consistent dose-response relationship between average dog-lung weight and HFA concentration.