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EC number: 222-374-6 | CAS number: 3452-07-1
- 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
Key value for chemical safety assessment
Additional information
There was one key toxicokinetic study identified which evaluated the absorption and distribution of linear alpha olefins, oct-1-ene, non-1-ene, and dec-1-ene, and the corresponding C8, C9, and C10 isoalkanes in rats (Zahlsen, 1993). Male Sprague-Dawley rats (16/dose) were exposed via whole body inhalation to 100 ppm vapour of the individual test substances for 12 hours/day for 3 consecutive days. Concentrations of the hydrocarbons were measured in blood, brain, liver, kidney and perirenal fat immediately following each 12 hour exposure and 12 hours following the last exposure. Higher concentrations of linear alpha olefins were measured in each of the respective organs compared with measured concentrations of the corresponding isoalkanes, with the highest concentrations measured in fat. All measured concentrations of linear alpha olefins and isoalkenes were significantly decreased following the 12 hour recovery period; however the largest residual accumulations were measured in the fat. With the exception of the kidney, accumulation of the respective test substances in all organs was shown to increase with increasing carbon number.
There were two supporting studies available which identified metabolic pathways of linear alpha olefins. In an in vitro toxicokinetic study designed to determine if carbon-carbon double bonds are metabolized to glycols via direct dihydroxylation of the olefinic bond or via epoxide intermediates, complete metabolic conversion of oct-1-ene to glycolic products was accomplished using an NADPH generating system and rat liver microsomes (Maynert et al., 1969). When competitive inhibitors of epoxide hydrolase were used in the experiment, both epoxides and glycols were formed. In the absence of the inhibitor, only glycols were formed confirming that the metabolism of olefins proceeds via epoxide intermediates.
In the second study, two metabolic pathways for oct-1-ene are described (White et al., 1986). Oct-1-ene was converted to octane-1,2-oxide which was rapidly hydrolyzed to octane-1,2-diol using an in vitro NADPH generating system (pathway 1). An alternative metabolic route was described in which oct-1-ene was converted to a reactive intermediate, octen-3-one, which formed S-3-oxo-octyl-acetylcysteine in in vitro systems using NADPH, cytochrome P450, NAD(P), and N-acetylcysteine (pathway 2). Metabolism of oct-1-ene via pathway 1 was significantly more rapid (40 times) that metabolism via pathway 2.
There were no studies identified which assessed or described the excretion profile for linear alpha olefins or single or multiple carbon number isomerised olefins.
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