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EC number: 202-708-7 | CAS number: 98-86-2
- 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
Key value for chemical safety assessment
Additional information
Information on the toxicokinetics of acetophenone is limited to the identification of metabolites excreted in urine without a comprehensive quantitative investigation of excretion. There are no further data available, e.g. on dermal absorption, or data from human experience, or to make conclusionson the potential for bioaccumulation.
Products of the biotransformation of acetophenone were identified in urine of rabbits and rats after i.p. injection of acetophenone or ethylbenzene, which is metabolised to acetophenone. Main products in urine are mandelic acid and benzoic acid (together ca. 50% of the metabolites of ethylbenzene in urine) followed by phenylglyoxalic acid and omega-hydroxyacetophenone (together 15% of the metabolites of ethylbenzene in urine) (Engström, 1984). In the course of the formation of benzoic acid, the14C-labeled methyl group of acetophenone is oxidized and eliminated via exhalation of CO2 reaching an amount of 30 % of the available14C within 13 hrs p.a.(Sullivan et al., 1976). 1-Phenylethanol, phenylglyoxal, 1-phenyl-1,2-ethanediol, p-hydroxyacetophenone, and m-hydroxyacetophenone were identified as minor metabolites amounting in total to less than 10 % of the metabolites of ethylbenzene in urine (Engström, 1984; Kiese and Lenk, 1974). These metabolites are partly excreted as conjugates, as e.g. the glucuronic acid conjugate of 1-phenylethanol, the glycine conjugate yielding hippuric acid, and as sulfate conjugates. Unchanged acetophenone in urine amounted to ca. 0.01 % (Kiese and Lenk, 1974). In vitro, cytosol from liver, kidney, heart and lungs was involved in the reduction of acetophenone to 1-phenylethanol. The rate of reduction in liver microsomes reached 10% of the rate in liver cytosol, only (Leibman, 1971).
A diagram of the suggested metabolism pathways is included in the following endpoint study record (see: WoE.Basic toxicokinetics: metabolites in urine.Engström_1984).
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