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EC number: 287-479-1 | CAS number: 85535-87-1
- 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
Key value for chemical safety assessment
Additional information
There were no in vitro or in vivo genetic toxicity identified for alkenes, C10 -13; instead, read-across studies were identified for all genetic toxicity endpoints. Two read-across in vitro gene mutation studies in bacteria were identified from alkenes, C10/C11/C12/C13. In the first study conducted by Brooks et al. (1983), three separate assays were used to determine the mutagenic potential of Olefin 103 PQ/11. Following an initial preliminary toxicity test, the main mutagenicity test was conducted in Salmonella typhimurium strains, TA1537, TA1535, TA100 and TA98 and Escherichia coli WP2 uvrA, both in the presence and absence of rat liver fraction S9, at 31.25, 62.5, 125, 250, 500, I000, 2000 or 4000 µg per plate. The cultures were incubated at 37°C for 48-72 hours before the revertant colonies were counted. Olefin 103 PQ/11 did not cause an increase in the reverse mutation rates in bacteria in the presence or absence of metabolic activation. Positive controls indicated that the test systems were working appropriately.
In the second study that examined test materials pertaining to alkenes, C10/C11/C12/C13, five strains of Salmonella typhimurium and 2 strains of Escherichia coli were exposed to Olefin 11/12 in acetone, Olefin 13/14 in acetone, Olefin HE bleed as an emulsion in acetone at concentrations of 31.25, 62.5, 125, 250, 500, 1000, 2000, or 4000 µg/plate and Olefin intermediate recycle in acetone at concentrations of 31.25, 62.5, 125, 250, 500, 1000, or 2000 µg/plate in the presence or absence of rat liver S9 fraction using a plate incorporation assay and incubated for 48 hours (Brooks, 1982). Although there were occasional increases in the reverse mutation rates in bacteria, the results were slight, were not reproducible, and were not dose dependent. Therefore, the authors concluded that the olefin products did not affect the reverse mutation rates in bacteria in the presence or absence of S9 activation.
Read across within category from alkenes, C10/C11/C12/C13 and alkenes, C11/C13/C14 for cytogenicity assays in mammalian cells. For alkenes, C10/C11/C12/C13, two studies were identified. In the first study,cultures of rat liver cells were exposed to Olefin 103 PQ/11 for 24 hours at concentrations equivalent to 5, 10, 15, 20, 25, 30, 35, or 40 µg/mL for the cytotoxicity assay (Brooks et al., 1983). After 24 hours fresh medium was supplied and cells were plated and cultured for 5 days, then colonies containing at least 50 cells were counted. A concentration of 20 µg/mL caused a reduction of 15% in the cloning efficiency and 25 µg/mL caused a reduction of 59% in cloning efficiency; therefore, concentrations of 5, 10, 20, or 25 µg/mL were used for the chromosomal aberration assay.The rat liver assay using Olefin 103 PQ/11 did not induce chromosomal damage under the experimental conditions of the study.
In the second study, both C10/C11/C12/C13 and alkenes, C11/C13/C14 were examined. In this study,cultures of rat liver cells were exposed to the different olefin products for 24 hours (Brooks, 1982). Since specifics on the study design were not provided, it cannot be determined whether the test conditions complied with OECD 473 guidelines. Preliminary cytotoxicity tests indicated that neither olefin 11/12 nor olefin 13/14 were cytotoxic at any of the concentrations tested (concentrations ranged from 0.1 to 500 µg/mL). Therefore, concentrations of 125, 250, and 500 µg/mL were used to test for mutagenicity. For the olefin HE bleed, concentrations of 12.5, 25, and 50 µg/mL were used in the mutagenicity assay. Although some abnormalities were observed, there were no significant or dose dependent increases observed for any of these olefin compounds. The first sample of olefin intermediate recycle had highly variable results for cytotoxicity. Concentrations of 25, 50, or 100 µg/mL were used in the mutagenicity assay with increases in chromosomal aberrations, as well as cytotoxicity, noted in the two highest concentrations. Retesting the sample a year later led to an increase in cytotoxicity indicating an alteration in the chemical composition. A second fresh sample was tested at the 25, 50 and 100 µg/mL concentrations with no differences between the control group and the treated groups.Based on the results presented above, the study authors concluded that all four test compounds were negative for chromosomal damage in rat liver cells.
Read across from linear alpha olefins was conducted for in vitro gene mutation assays in mammalian cells. For this study, Chinese hamster ovary cells (CHO-K1) were treated to study its potential to induce point mutations in the HGPRT gene in the CHO-K1 cell line in the absence and presence of metabolic activation (±S9) (Papciak et al., 1983). Mutagenicity was evaluated at 4, 16, 128, 512, 1024, and 2048 ug/mL Gulftene 12-16 (±S9); however, results were only provided for concentrations ≥128 ug/mL. In the absence of S9, there were an insufficient number of cells to sub-culture 1 million cells per dish at the 1024 and 2048 ug/mL test concentrations and cell counts for these concentrations were also reduced with metabolic activation (+S9). In addition, the cloning efficiency was depressed at 1024 and 2048 ug/mL, indicating that the immediate toxic effect also delayed growth of surviving cells. There was no increase in the frequency of mutant colonies at any test concentration with or without metabolic activation (±S9). The vehicle control was well within the <90% toxicity level, while the two positive control groups (ethyl methane sulfonate & benzo(a)pyrene) exhibited a positive response indicating that the assay was functional. Based on these results, the study authors concluded that there was no increase in the frequency of mutant colonies in treated cells.
Information is also available to support read across within category from alkenes, C20-24 for in vivo gene mutation assays. In this study, mice dosed intraperitoneally with 500, 1000, or 2000 mg/kg bw of alkenes, C20-24 showed no evidence of increased incidence of micronucleated polychromatic erythrocytes (Durward, 1998).
Based on the lack of observed mutagenic effects in in vitro and in vivo studies withisomerised olefins; alpha, internal, linear and branched – multiple carbon numbersand linear alpha olefins, it is concluded that alkenes, C10-13 are not mutagenic. Based on these findings, alkenes, C10 -13 do not meet the EU criteria for classification and labelling (Dangerous Substances Directive 67/548/EEC and CLP EU Regulation 1272/2008) for mutagenicity.
Justification for Read Across:
Several criteria justify the use of the read across approach to fill data gaps for multiple carbon number isomerised olefin substances using linear alpha olefin substances. Studies indicate that changing the carbon number, the location of the double bond, or adding branching does not measurably alter effects on mammalian health endpoints. There is a consistent toxicity potency pattern for alpha olefins and alpha olefins with range of carbon numbers supported by a low toxicity concern for acute oral, dermal and inhalation exposure. These materials are slightly irritating to skin and mildly irritating to non-irritating to eyes of rabbits. Screening studies indicate that they are not genotoxic. Study results for the aforementioned endpoints indicate a low hazard potential for human health. Since the addition of branching does not measurably alter the results of studies on mammalian health endpoints, there should not be any signficant toxicological differences between substances in multiple carbon number isomerised olefins and linear alpha olefins. Therefore, read across between these categories can be justified.
Short description of key information:
Read-across in vitro gene mutation studies in bacteria (OECD 471) and in vitro cytogenicity studies in mammalian cells (OECD 473) were identified from alkenes, C10/C11/C12/C13 and/or alkenes, C11/C13/C14. A read-across study (OECD 476) from linear alpha olefins for in vitro gene mutation in mammalian cells was identified. One read-across study (OECD 474) for in vivo gene mutation was identified from isomerised olefins; alpha, internal, linear and branched – multiple carbon numbers (alkenes, C20-24).
All genetic toxicity tests, both in vitro and in vivo, were negative.
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
All in vitro genetic toxicity studies (i. e., gene mutation studies in bacteria; cytogenicity studies in mammalian cells; and gene mutation studies in mammalian cells) from linear alpha olefins and multiple carbon number isomerised olefins showed negative results. In vivo mouse micronucleus studies with multiple carbon number isomerised olefins also produced no evidence of mutagenic effects. Based on the weight of evidence approach, alkenes, C10-13 are unlikely to be mutagenic and does not meet the criteria for classification and labelling as described in EU Dangerous Substances Directive 67/548/EEC or CLP EU Regulation 1272/2008.
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