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EC number: 210-817-6 | CAS number: 623-84-7
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Endpoint summary
Administrative data
Key value for chemical safety assessment
Additional information
PGDA was tested in the Ames test up to the limit of toxicity (5 mg/plate). The test substance induced no statistically significant dose related increase in the numbers of revertant (His+) colonies in any of the five tester strains (TA 1535; TA 1537; TA 1538; TA 98; TA 100). The test substance can therefore be considered as non mutagenic in this test system.
PGDA was evaluated in an in-vitro chromosomal aberration-assay utilizing Chinese Hamster Ovary (CHO) cells in the presence and absence of a metabolic activation system. The substance was tested up to cytotoxic concentrations (5000 µg/ml in the absence of S9 -mix and 1000 µg/ml in the presence of S-9 mix). None of the tested concentrations produced a statistically significant increase in the frequencies of chromosome aberrations at the second (9 hours post-treatment) and third (13 hours post-treatment) fixation times both in the presence and absence of a metabolic system and at the first (4 hours post-treatment) fixation time in the presence of S-9 mix. However, at the first fixation time in the absence of S9 -mix; the test substance induced a statistically significant increase in the number of chromosome aberrations at all three doses tested without a clear dose response relationship. In a repeat experiment the two lowest test substance concentrations induced a statistically significant increase. However, still no positive dose-response relationship could be demonstrated. Furthermore, as in the first experiment, statistical significance is obtained only as a result of the incidental low number of aberrations in the solvent control group compared to solvent control groups at the second and third fixation time. Moreover there appeared to be a large variation between the number of spontaneous aberrations in all solvent control groups. Therefore, the observed increase in the number of chromosome aberrations is not considered to be due to a clastogenic effect of the test substance. Positive control chemicals, ethyl methanesulfonate and cyclophosphamide produced statistically significantly increased incidence of chromosome aberrations. It is concluded that PGDA is not clastogenic in CHO cells under the experimental conditions described.
The genotoxic potential of the test article propylene glycol diacetate to induce gene mutation in mammalian cells was evaluated using Chinese Hamster ovary (CHO) cells. In the initial gene mutation assay, CHO cells were exposed to the test article in duplicate at concentrations of 16, 51, 160, 507, and 1602 μg/mL of the medium for 4 hours in the presence and absence of metabolic activation. In the confirmatory gene mutation assay, CHO cells were exposed to the test article in duplicate at concentrations of 20, 59, 178, 534, and 1602 μg/mL of the medium for 4 hours in the presence and absence of metabolic activation. There was no evidence of induction of gene mutations in any of the test material treated cultures either in the presence or absence of metabolic activation. In each of these experiments, the respective positive controls produced a statistically significant increase in the frequencies of mutants, under identical conditions and concurrent solvent control cultures values were within laboratory historical controls. The results of the forward gene mutation assay at the hprt locus with propylene glycol diacetate indicate that under the conditions of this study, the test article was non-mutagenic when evaluated in the presence or absence of an externally supplied metabolic activation (S9) system.
Short description of key information:
GLP studies according to OECD guidelines 471, 473 and 476 are available for PGDA.
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
PGDA was not mutagenic in bacteria (Salmonella typhimurium TA 1535, TA 1537, TA 1538, TA 98, and TA 100) and in mammalian cells in vitro. PGDA was also not considered to be clastogenic in vitro. Hence, the data available indicates that PGDA is not genotoxic and no classification is required according to EU criteria.
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