Registration Dossier
Registration Dossier
Data platform availability banner - registered substances factsheets
Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.
The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.
Diss Factsheets
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: 200-662-2 | CAS number: 67-64-1
- 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
Specific investigations: other studies
Administrative data
Link to relevant study record(s)
Description of key information
Additional information
Acetone treatment of rats (1 or 5% in drinking water for 7-12 days) was shown to induce oxidative stress and lipid peroxidation in liver, plasma and erythrocytes (weight of evidence approach: Armutcu et al., 2005; Orellana et al., 2001; Puntarolo and Cederbaum, 1988).
Sensory irritation
Studies using objective measures of sensory irritation tended to show that acetone is an extremely weak sensory irritant for humans with a sensory irritation threshold (nasal pungency) between 10,000 to 40,000 ppm. The odor detection threshold of acetone is much lower ranging from about 20 - 400 ppm based on reliable studies. Loss of sensitivity due to adaptation and/or habituation to the odor of acetone may occur, as was shown in studies comparing occupationally exposed workers with unexposed subjects. An evaluation of studies on subjectively reported irritation symptoms at acetone concentrations below 1000 ppm showed that perception of odor intensity, information bias, and habituation by exposure to acetone are confounding factors in the reporting of irritation thresholds and health symptoms (Arts et al., 2002; Cometto-Muniz and Cain, 1993, 1995; Dalton et al., 1997a, b; Morgott, 2001; Wysocki et al., 1997).
In the Alarie test with Swiss-Webster mice (N = 4/group) sensory irritation was observed with RD50 values of 77,516 ppm acetone ( 95% confidence interval: 59,004-115,366 ppm) for a 10 min-exposure (Alarie and Luo, 1986; Kane et al., 1980), and 23,480 ppm acetone for a 5 min-exposure (De Ceaurizz et al., 1981).
Local dermal effects
Acetone was shown to be a defatting agent at contact with mouse skin. Defatting of the epidermis lead to a substantial reduction in residual stratum corneum lipids and subsequently to disturbation of the epidermal permeability barrier and to transepidermal water loss. These effects were reversible within 48 hours by de novo lipid biosynthesis. Restoration of the permeability barrier was retarded as long as an occlusive impermeable membrane was present. After removal, the permeability barrier function of the epidermis was fully restored within 24 hours (Weight of evidence approach: Grubauer et al., 1989a, b).
The sequelae of the fat solubilizing property of acetone was also investigated in the skin of human volunteers after permanent contact with a glass reservoir filled with acetone for 30 or 90 min. Acetone induced local cellular changes, mainly in the stratum corneum and the stratum spinosum. Microscopic and ultrastructural examination indicated intracellular edematous lesions with e.g. vacuolation and swollen mitochondria, and rupture of cell membranes and desmosomes. After the 90 min-exposure, a significant reduction of protein synthesis was measured while collagen synthesis was unaffected. DNA synthesis was moderately but significantly increased. Within 72 hrs after discontinuation of exposure, a high degree of restoring activity was demonstrated. The application of a protective gel (composition: 50% water, 25% glycerin, 10-15% cellulose methasol gum, 2-3% preservative) prior to acetone exposure substantially reduced the ultrastructural changes of the epidermal cells. This protection presumably resulted from blocking the absorption and migration of the lipid solvent acetone through the epidermis (Weight of evidence approach: Lupulescu and Birmingham, 1972, 1973, 1975, 1976). Wearing appropriate gloves will avoid this effect.
A local, short-lasting proliferative response in epidermal cells of mouse skin was induced up to 12 hrs after a single dermal application of 0.2 mL. The mechanism is not known. The authors discussed a very weak skin irritating activity of acetone as a possible trigger (Weight of evidence approach: Iversen et al., 1988).
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.