Record Display for the EPA National Library Catalog

RECORD NUMBER: 598 OF 1325

Main Title Initial Submission: Subchronic Inhalation Toxicity of Isooctanol in Male CRL CD Rats with Cover Letter dated 08/10/1992.
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-0992-10553
Stock Number OTS0570889
Additional Subjects Toxicology ; Health effects ; Toxic substances ; Isooctanol ; Subchronic toxicity ; Mammals ; Rats ; Inhalation ; CAS No 26952-21-6
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NTIS  OTS0570889 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 52p
Abstract
Groups of 10 male CelacD(SD)BR rate were exposed to either 0.11, 0.60 or 3.1 mg/L of isooctanol in air. Exposures were 6 hours/day, 5 daya/week for 2 weeks. A control group was simultaneously exposed to air. At the end of the exposure period and after a 14-day recovery period, blood and urine samples were collected for clinical analysis and rate wer6 sacrificed for pathological examination. Clinical signs of toxicity observed during the exposure phase included lung noise in a few rats exposed to 0.11 or 0.60 mg/L. Rats exposed to 3.1 mg/L exhibited lung no1ae, neeal and ocular discharges, red-stained perineum, inactivity, impaired balance, ruffled fur, and alopecia. High level rats also had a significantly lower group mean body weight compared to controls from test day 2 throughout the study. Clinical pathology measurements made at the end of the exposure and recovery periods showed no compound-related differences between control rats and rats exposed to 0.11 ag/L. Rata exposed to 0.60 or 3.1 ag/L showed significant increases in red blood cell-parameters which were interpreted to be evidence of treatment-related polycythemia. Rats from the 3.1 ag/L.group also showed significant decreases in white blood cell counts and absolute numbers of lymphocytes which were interpreted to be evidence of physiologic stress with endogenous steroid release. Other homatologic and clinical chemical differences were interpreted to be within the range of expected biological variation. None of these treatment-related effects were present after a 14-day recovery.