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: 252-104-2
CAS number: 34590-94-8
No specific studies for dipropylene glycol methyl ether are available. Two inhalation studies with propylene glycol methyl ether in rats and mice are available for read-across to dipropylene glycol methyl ether. Both studies are reliable without restrictions as they were conducted under GLP and according to OECD guideline 453.
a chronic toxicity/carcinogenicity study, Fischer rats (50/sex/exposure
level) were exposed to vapor concentrations of propylene glycol methyl
ether (PGME) at concentrations of 0, 300, 1000, or 3000 ppm 6 hr/day, 5
days/wk for 2 years. Over
the course of the study, these subjects were evaluated for clinical
signs and body weights. At
the end of two years, survivors were subjected to clinical chemistry and
hematological examinations, urinalyses, determination of body organ
weights, and histopathological examination of a large number of tissues.
In order to evaluate potential toxicity at interim time intervals during
the exposure period, additional subjects were exposed to PGME vapors and
subjected to routine and specialized toxicological tests at the times
shown in the experimental design table below. Specialized
tests at time intervals of 6, 12, 18 and 24 month included evaluation of
1) cell proliferation in liver and kidneys, 2) hepatic mixed function
oxidase (MFO) activity, and 3) a2µ-globulin nephropathy.
A: routine study, Group B: cell proliferation in liver and kidneys,
Group C: Hepatic MFO induction, Group D: a2µ-g nephropathy evaluation.
Atmospheres of PGME were generated by metering the test material into a
glass J-tube assembly through which compressed, heated air was channeled. Evaporated
PGME in the heated air was diluted with room temperature air to the
desired concentration at a flow rate of 2900 liters per minute into
whole-body inhalation chambers. Airflow
in the chambers was maintained at a level that provided approximately 12
changes/hour and normal oxygen concentration. PGME
concentrations were measured from the breathing zone of the animals
inside the chambers two times per hour using a Miran 1A infrared
concentrations were within 0.5% of nominal concentrations throughout the
3000 ppm, rats exhibited decreased activity, incoordination, and
transient sedation during the first week of exposure.
recovered 1-2 hours after removal from the chambers. These
signs disappeared after the second week but returned after 12-18 months
into the study. Mortality
was unaffected until 18 months when males but not females showed higher
mortality rates that were not ascribable to any particular cause.
course of the study, body weights were decreased at the 3000 ppm
exposure level. These decreases were not large but were statistically
significant in female rats. Despite
changes during the study, body weights were not statistically different
from controls at terminal sacrifice.
In the chronic study, no hematology or urinalysis changes were evident. However,
several clinical chemistry parameters in male rats exposed to 3000 ppm
PGME were altered at the 24 month sacrifice: creatinine increased 78%
and urea nitrogen increased 100%. Serum
alkaline phosphatase was increases as well and earlier, at 6 through 24
months at the 3000 ppm level, and at 1000 ppm, at 24 months in male rats.
SGOT (AST) and SGPT (ALT), which could be associated with liver injury,
were mildly and inconsistently increased in male rats during the first
year of exposure at 3000 ppm but not after. No
histological changes accompanied these effects. Liver
and kidney weights were increased at 3000 ppm in both sexes.
Dark foci in the liver were grossly observable in male rats exposed to
1000 and 3000 ppm PGME after 24 months. These subjects also exhibited
eosinophilic hepatocellular foci and cystic degeneration microscopically
that was not reported in female rats. Male
rats showed increased S-phase DNA synthesis when exposed to 3000 ppm
effect was not pronounced (reported in a separate, 2-week study), and
was evident to a lesser extent in female rats. MFO
activity was increased in the livers of rats exposed to 3000 ppm PGME.
In the kidney, histopathology revealed that male rats had a2µ-globulin
nephropathy as is typical for this strain. The
incidence and severity of this condition was increased in males exposed
to 1000 and 3000 ppm PGME compared to controls. No
increase in renal epithelial tumors was observed in rats.
major changes seen in this study were 1) decreased body weights, 2)
liver effects including increased weight, increased MFO activity and
increased cell proliferation primarily in males, 3) kidney effects of
a2µ-globulin nephropathy typical of the Fischer 344 strain, and 4)
slightly increased mortality occurring only after 18 months of exposure
in males. Clinical
chemistry parameters reflected and corroborated these effects.
Rats exhibited a NOAEL of 300 ppm based on altered hepatocellular foci
No carcinogenic effect as evidenced by any increase in tumor incidence,
even in kidneys of the male rats, occurred from exposure to PGME at any
No carcinogenic effect as evidenced by any
increase in tumor incidence occurred from exposure to propylene glycol
methyl ether at any concentration in either species.
Repeated exposure to dipropylene glycol
methyl ether resulted in toxicity only at high exposure levels and
usually consisted of increased organ weights without accompanying
histopathology. In vitro genotoxicty studies are negative, indicating
that dipropylene glycol methyl ether is not genotoxic. No
carcinogenicity studies are available for dipropylene glycol methyl
ether.The sole propylene glycol ether that has been subjected to chronic
toxicity/carcinogenicity testing is propylene glycol methyl ether. Thus,
the propylene glycol methyl ether study is used as a surrogate for
dipropylene glycol methyl ether. Propylene glycol methyl ether, tested
by inhalation in rats and mice at concentrations up to 3,000 ppm, caused
very little chronic toxicity and caused no cancer. Further
justification for the use of read across is contained in the category
document attached at section 13.
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.
På den här webbplatsen används kakor. Syftet är att optimera din upplevelse av den.
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