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EC number: 203-539-1 | CAS number: 107-98-2
- 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
Short description of key information on bioaccumulation potential result:
Several in vitro and in vivo toxicokinetics studies are available for propylene glycol methyl ether.
Short description of key information on absorption rate:
An in vitro dermal absorption using human skin s available for propylene glycol methyl ether.
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
Propylene glycol methyl ether is readily absorbed via oral and inhalation route. An absorption percentage of 100 % can be taken into account for these routes. Human data have shown that dermal absorption of vapour via the skin is limited. When exposed whole-body (normal clothing), vapour provided contribution of approximately 4-8 % to the total body burden. An in vitro absorption rate of 1.17 mg/cm2/h was estimated for pure propylene glycol methyl ether on human skin. If the dermal absorption of liquid propylene glycol methyl ether is compared to other glycol ethers, the available data shows that propylene glycol methyl ether is less absorbed than ethylene glycol butyl ether (it is estimated that propylene glycol methyl ether is twice less absorbed that ethylene glycol butyl ether). According to this data, a dermal absorption factor of 30 % for liquid propylene glycol methyl ether should be considered as a worst case value for the risk assessment.
According to the PBPK model, vapour of propylene glycol methyl ether absorbed through the skin in humans contributed to about 5 to 10 % to the total body burden of propylene glycol methyl ether. Also according to this model, maximum concentration in blood are about 2.5 fold more higher in rats than in humans after a 6h inhalation exposure at the same level (for exposure levels above 100 ppm). For exposure concentrations below 100 ppm, the rat and human blood levels of propylene glycol methyl ether are similar which leads to the use of a factor of 1 instead of 0.4 in this range of concentrations. Main target organs were liver, thymus and spleen (concentration > blood levels after oral dosing). Little amount of the parent molecule or metabolites were found in fat or testes. According to the data available, propylene glycol methyl ether does not seem to accumulate in the body.
The main metabolic pathway is O-demethylation leading to propylene glycol formation. This mechanism is easily saturable. Other paths are glucurono- and sulfo-conjugation. Propylene glycol is excreted via urine or enter metabolic pathways to produce CO2. 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:
According to the PBPK model, vapour of propylene glycol methyl ether absorbed through the skin in humans contributed to about 5 to 10 % to the total body burden of propylene glycol methyl ether. Also according to this model, maximum concentration in blood are about 2.5 fold more higher in rats than in humans after a 6h inhalation exposure at the same level (for exposure levels above 100 ppm). For exposure concentrations below 100 ppm, the rat and human blood levels of propylene glycol methyl ether are similar which leads to the use of a factor of 1 instead of 0.4 in this range of concentrations. Main target organs were liver, thymus and spleen (concentration > blood levels after oral dosing). Little amount of the parent molecule or metabolites were found in fat or testes. According to the data available, propylene glycol methyl ether does not seem to accumulate in the body.
The main metabolic pathway is O-demethylation leading to propylene glycol formation. This mechanism is easily saturable. Other paths are glucurono- and sulfo-conjugation. Propylene glycol is excreted via urine or enter metabolic pathways to produce CO2. At high dose, saturationof 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 absorption rate:
Propylene glycol methyl ether is readily absorbed via oral and inhalation route. An absorption percentage of 100 % can be taken into account for these routes. Human data have shown that dermal absorption of vapour via the skin is limited. When exposed whole-body (normal clothing), vapour provided contribution of approximately 4-8 % to the total body burden. An in vitro absorption rate of 1.17 mg/cm2/h was estimated for pure propylene glycol methyl ether on human skin. If the dermal absorption of liquid propylene glycol methyl ether is compared to other glycol ethers, the available data shows that propylene glycol methyl ether is less absorbed than ethylene glycol butyl ether (it is estimated that propylene glycol methyl ether is twice less absorbed that ethylene glycol butyl ether). According to this data, a dermal absorption factor of 30 % for liquid propylene glycol methyl ether should be considered as a worst case value for the risk assessment. For detailed information on rates also refer to read-across justification document for P-series glycol ethers.
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