Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 204-826-4
CAS number: 127-19-5
- Clinical pathology was evaluated at 3,6,12,18,24 months; interim sacrifice was carried out at 12 months; hepatic cells proliferation was examined at two weeks and three and twelve months.- No compound-related effects on survival were observed. - Rats exposed to 350 ppm had lower body weight and/or body weight gain. - There were no compound-related adverse effects on the incidence of clinical signs of toxicity. No hematologic changes were observed.- SERUM SORBITOL DEHYDROGENASE ACTIVITY was increased in rats exposed to 350 ppm. - SERUM CHOLESTEROL and GLUCOSE CONCENTRATIONS WERE SIGNIFICANTLY HIGHER IN 100 AND 350 PPM FEMALE RATS. - Compound-related morphological changes were observed in the liver. Exposure to 100 or 350 ppm produced increased absolute and/or relative LIVER WEIGHT, HEPATIC FOCAL CYSTICDEGENERATION, HEPATIC PELIOSIS, BILIARY HYPERPLASIA (350 ppm only), and LIPOFUCSIN/HEMOSIDERIN accumulation in KUPFFERCELLS. Male rats exposed to 350 ppm had higher KIDNEY WEIGHT correlated with the gross and microscopy changes resulting from a compound-related increase in severity of CHRONICPROGRESSIVE NEPHROPATHY.- No increase in hepatic cells proliferation was seen at any exposure concentration.
purpose of the study was to evaluate the oncogenic potential of the test
substance in rats when administered by inhalation. Groups of 87 male and
87 female Crl:CD®BR rats were exposed to either 0, 25, 100, or 350 ppm
test substance for six hours per day, five days per week, for up to two
years. Chamber atmospheres were analysed during the exposure period for
test substance concentration, temperature, humidity, and airflow rate.
Body weights were obtained weekly during the first three months of the
study and every other week for the remainder of the study. Clinical
signs of toxicity were monitored throughout the study. An
ophthalmological examination was performed on all animals prior to study
start. All surviving rats were examined prior to their respective final
sacrifices. At 3, 6, 12, 18, and 24 months, haematology, clinical
chemistry, and urinalysis parameters were measured for ten rats per sex
per concentration (females were not evaluated at 24 months). Interim
sacrifices to determine the rate of hepatic cell proliferation were
conducted on approximately five rats per sex per concentration and
occurred on test days 28, 89, and 384. Ten rats per sex per
concentration also underwent a 12-month interim sacrifice. All surviving
rats underwent gross necropsy after approximately 24 months of exposure.
Selected tissues were weighed and tissues were collected for microscopic
overall mean concentrations of test substance in the exposure chambers
for the two-year test period were 0.0, 25.2, 101.0, and 350.5 ppm. Mean
chamber temperatures generally ranged between 16-29°C. Mean chamber
relative humidity generally ranged between 20-65%. Mean chamber air flow
ranged between 738-1046 L/min.
were several compound-related effects observed in rats exposed to the
test substance. Male and female rats exposed to 350 ppm had lower body
weight and/or body weight gain. There were no adverse, compound-related
effects on the incidence of clinical signs of toxicity, on the incidence
of ophthalmoscopically observable ocular lesions, or on survival in rats
of either sex at any exposure concentration.
effects on haematology parameters on urinalysis parameters in rats were
not observed. However, male and female rats exposed to 350 ppm test
substance had compound-related increases in sorbitol dehydrogenase
activity that were indicative of minimal to mild hepatocellular injury.
In addition, serum cholesterol and serum glucose concentrations were
significantly higher in 10 and 350 ppm females, and were considered to
be compound related.
were several compound-related effects observed in the livers of rats
exposed to the test substance. Male and female rats exposed to 100 or
350 ppm test substance had higher absolute and/or relative liver weight
at either the 12-month or the 24-month sacrifice. The changes in liver
weight most likely represent enzyme induction associated with metabolism
of the test substance. Male rats exposed to 100 or 350 ppm had an
increased incidence of hepatic focal cystic degeneration and hepatic
peliosis, and the incidence of biliary hyperplasia was also elevated in
350 ppm males. In addition, male and female rats exposed to 350 ppm of
the test substance, and 100 ppm females had an increased incidence of
hemosiderin and lipofuscin pigment accumulation in the hepatic Kupffer
addition to the compound-related changes on the liver, 350 ppm male rats
exhibited significantly higher absolute and relative kidney weights
which correlated with the gross and microscopic changes resulting from a
compound-related increase in severity of chronic progressive nephropathy.
rats, exposure to the test substance for 2 years did not produce an
oncogenic response in the liver or any other tissue of either sex at any
exposure concentration. In addition, there were no compound-related
effects on hepatic cell turnover in rats of either sex at any exposure
concentration. Therefore, the no-observable-adverse-effect level (NOAEL)
for oncogenicity was 350 ppm in rats.
NOAEL for toxicity for male and female rats is 25 ppm based on effects
on body weight, clinical chemistry parameters, organ weight parameters,
and/or morphological changes at 100 and 350 ppm.
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
Damit Sie die Website optimal nutzen können, verwenden wir Cookies.
Welcome to the ECHA website. This site is not fully supported in Internet Explorer 7 (and earlier versions). Please upgrade your Internet Explorer to a newer version.
Do not show this message again