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Diss Factsheets
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EC number: 203-603-9 | CAS number: 108-65-6
- 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
Link to relevant study record(s)
Description of key information
Key value for chemical safety assessment
- Bioaccumulation potential:
- no bioaccumulation potential
- Absorption rate - oral (%):
- 100
- Absorption rate - dermal (%):
- 30
- Absorption rate - inhalation (%):
- 100
Additional information
Several studies confirm that rapid and extensive hydrolysis of propylene glycol methyl ether acetate (PGMA) to propylene glycol methyl ether (PGME) occurs in vivo when PGMA is administered by the oral, inhalatory or dermal route. Since urinary metabolites and disposition profiles of PGMA were approximately identical to the results obtained with PGME, it is unlikely that there are substantial differences of the systemic toxicity between PGMA and PGME. In fact, toxicity of PGMA is almost the same of PGME. PGMA is readily absorbed via oral and inhalation route. An absortion percentage of 100 % can be taken into account for these routes of exposure. In a study comparing dermal toxicokinetics of PGME and PGMA (ACC 1999), the dermal absorption of PGMA was found to be lower than that of PGME (between 3 and 4 fold less). Dermal absorption of PGME is approximately 30%, therefore since dermal absorption of PGMA was approximately 30% of that of PGME in rats. In conclusion, PGMA is rapidly hydrolysed in vivo in PGME and acetate (blood half life of PGMA is about 2 min for a low dose of PGMA). Hydrolysis can also occur locally (i.e. in the respiratory tract).
Once hydrolysis of PGMA to PGME has occurred, the distribution, further metabolism and excretion is the same as for PGME. The acetic acid released will enter endogenous metabolic processes.
PGME is sufficiently water soluble that it can be excreted unchanged via the urine. However, it is also further metabolised and the main metabolic pathway is O-demethylation, leading to propylene glycol formation. This mechanism is easily saturable. Other pathways are glucurono- and sulfo-conjugation of PGME. Propylene glycol is excreted via urine or enters metabolic pathways to produce CO2 which is exhaled. At high dose, saturation of the metabolic pathways led to urinary elimination of propylene glycol methyl ether as such. Parent and metabolites are rapidly eliminated.
It appears that in rats, there is a sex difference in metabolism of propylene glycol methyl ether, females eliminating faster than males.
Discussion on bioaccumulation potential result:
As a class, the propylene glycol ethers are rapidly absorbed and distributed throughout the body when introduced by inhalation or oral exposure. For detailed information, refer to read-across justification document for P-series glycol ethers. While not tested directly, absorption by inhalation exposure also would be expected to be rapid for PGEs aerosols that are in the respirable range. Dermal absorption is expected to be somewhat slower but, once absorbed, subsequent distribution also should be rapid. Most of the PGE dose would be rapidly excreted. Most excretion for PGEs is via the urine and expired air. A small portion is excreted in the feces.
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