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Diss Factsheets
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EC number: 202-874-0 | CAS number: 100-64-1
- 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
Endpoint summary
Administrative data
Link to relevant study record(s)
Description of key information
Cyclohexanone oxime (CHO) is almost completely absorbed via the oral route. The absorption after dermal exposure is in the range of 5%. Metabolism of the main metabolite hydroxylamine leads to the formation of nitric oxide and a nitrosylhemoglobin complex, the latter being the probable causative reactive intermediate for the observed haematotoxicity. Within 24 h most of the administered compound is eliminated.
Key value for chemical safety assessment
- Bioaccumulation potential:
- no bioaccumulation potential
- Absorption rate - oral (%):
- 100
- Absorption rate - dermal (%):
- 5
Additional information
After oral exposure of rats to CHO, 68 -87% of the administered dose was excreted in the urine, elimination in the feces accounted for 5-9% of the dose, 2% were expired as CO2 and very low levels of radioactivity (2-3%) were retained in the tissues 24 hours after exposure.
No information is available for inhalation exposure.
Within 24 h after dermal application, 3.9% of the administered dose was excreted in urine and 0.1% in feces, 4.5% remained at the application site and 23% had volatilised within 3-5 min after application. Therefore the systemic uptake after dermal exposure is in the range of 5% of the administered dose. The substance is cleaved to cyclohexanone and hydroxylamine. Cyclohexanone is further oxidised to cyclohexanol and cis- and trans-cyclohexane-1,2-diol, which are then conjugated by glucuronic acid. Metabolism of the main metabolite hydroxylamine: electron paramagnetic resonance analysis showed the in vivo formation of nitric oxide and a nitrosylhemoglobin complex (considered to be generated from hydroxylamine), the latter being the probable causative reactive intermediate for the observed haematotoxicity of cyclohexanone oxime. Nitric oxide is a more potent haematotoxin compared to cyclohexanone oxime.
The main metabolites in urine after oral exposure of rats were monoglucuronides of cis- and trans-cyclohexane-1,2-diol, and the glucuronide of cyclohexanol. It can be assumed that absorption after oral exposure is nearly complete.
Distribution and elimination after dermal application were not different from those observed after oral administration.
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