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EC number: 931-515-7 | CAS number: 1334422-18-2
- 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
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Endpoint summary
Administrative data
Link to relevant study record(s)
Description of key information
Olefinic structures related to substances included in this category are metabolised to diols via an epoxide intermediate by hepatic microsomal enzymes. The position of the double bond as well as the degree of substitution influences this metabolism, with alpha olefins with no adjacent branching appearing more biologically reactive relative to internal and/or branched olefins.
Key value for chemical safety assessment
Additional information
Metabolism in vivo
The in vivo absorption and distribution of a number of linear alpha olefins (oct-1-ene, non-1-ene, dec-1-ene) and their corresponding isoalkanes in the rat after inhalation exposure was investigated by Zahlsen et al. (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.
Metabolism in vitro
Montellano and Mico (1980) demonstrated the NADPH-dependent destruction of hepatic microsomal cytochrome P-450 from phenobarbital pre-treated rats by ethylene and other olefins in vitro. The study demonstrated loss of cytochrome P-450 due to alkylation of the haeme function, with mono-oxygenase inactivation occurring to a greater extent with linear and branched alpha olefins relative to that found with internal olefins (with or without branching) where no or minimal loss of cytochrome P-450 was detected. The level of substitution in the region of the olefin double bond appeared to influence the extent of haemoprotein inactivation (2-methyl-1-heptene was inactive while 1-heptene was active).
In an in vitro 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., 1970). 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. While hydrolysis of the oxirane ring by epoxides hydrolase is rapid for alpha-olefins, glycol formation for internal- and branched chain olefins is less efficient due to steric hindrance in the region of the oxirane ring by alkyl groups. This can be illustrated for a series of C8-olefins, where hydrolysis of the epoxide intermediate follows the trend below (Maynert, 1970):
1,2 epoxy-n-C8 > 4,5 epoxy-n-C8 > 2,3 epoxy-iso-C8
Epoxide formation via cytochrome P-450 dependent processes is similarly subject to steric hindrance, with ready accessibility of the alpha double bond in linear olefins contrasting with the relative inaccessibility of the double bond in internal olefins (Maynert et al., 1970).
Similar principles were demonstrated by Leibman and Ortiz (1970), who evaluated the role of epoxides as intermediaries in the microsomal oxidation of olefins to glycols. Hepatic microsomal fractions from phenobarbital induced rabbits were used along with tested compounds xylene, indene, and cyclohexene. Using gas chromatography and thin layer chromatography, the authors demonstrated that epoxides were intermediates in the oxidation of alkenes to glycols.
In another study, two metabolic pathways for oct-1-ene were described by 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.
In a study that investigated the relative importance of electronic and steric factors in determining the suicide substrate activity of terminal alkenes, Luke et al. (1990) used ab initio quantum mechanics coupled with molecular mechanics and the known crystal structure of cytochrome P-450 to assess the relative potency of three prototypical terminal olefins (ethylene and propene, known suicide substrates; 2-methylpropene, known to be inactive as a suicide substrate) towards cytochrome P-450. The observations from this study suggested that while an unsaturated bond appeared necessary for haemoprotein alkylation, only terminal olefins seemed capable of binding irreversibly to cytochrome P-450 with steric hindrance, due to branching, playing a modulating role (e.g. 2-methyl-1-heptene was modelled as inactive with regard to haeme alkylation). The heme alkylation reaction runs in parallel and is independent of epoxide formation. Steric hindrance by substitution at the terminal double bond favours epoxides formation over heme alkylation. Internal olefins (such as cis/trans 3-hexene and cyclohexene) appeared capable of being metabolised to epoxides but were predicted inactive with regard to the haeme alkylation. The authors concluded that a terminal double bond, with no immediate alkyl substitutes, was a likely requirement for haeme alkylation, suggesting that alpha olefins might be biologically more reactive than internal and/or branched olefins.
The relationship between allylic oxidation and epoxidation of alkenes (with increasing alkyl substitution on an olefin promoting allylic oxidation at the expense of epoxidation) was examined by Gorycki and MacDonald (1994) using hexamethyl Dewar benzene (HMDB); 1,2-dimethylcyclohexene (DMCH); and 1,2,4,5-tetramethyl-1,4-cyclohexadiene (TMCH). These chemicals were selected to probe the intermediacy of an alkene radical cation during cytochrome P-450 catalyzed epoxidation. Cytochrome P-450 catalyzed the allylic oxidation of HMDB exclusively; no rearranged products nor epoxide was detected. Additionally, cytochrome P-450 exclusively catalyzed the allylic oxidation of 1,2-dimethylcyclohexene (DMCH) and 1,2,4,5-tetramethyl-1,4-cyclohexadiene (TMCH). The double bonds of HMDB and DMCH were readily epoxidized by (tetrapheny1porphyrinato) iron-(III) chloride with minor production of allylic alcohols. The results appear to indicate that in this model systemt he rates of alkene epoxidation tend to increase with increasing alkene substitution, but it is apparent that cytochrome P-450 has additional mechanistic options or constraints that depress the rate of epoxidation with increasing alkene substitution.
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