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EC number: 204-812-8 | CAS number: 126-92-1
- 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
Four studies on genetic toxicity are available for C8iso AS Na (CAS 126-92-1).
There is one study addressing genetic toxicity of C8iso AS Na (CAS 126-92-1) in bacteria available.
In the study, performed similar to OECD Guideline 471, Salmonella typhimurium strains TA 1535, TA 1537, TA 98 and TA 100 were treated with C8iso AS Na (CAS 126-92-1, analytical purity 39.6%) in presence and absence of metabolic activation. The tester strains TA 102 or E.coli WP2 were not used during the conduct of the study (Zeiger, 1985). The concentrations tested were 5, 15, 50, 150, 500, and 1500 µg/plate with and without metabolic activation. In the experiment with metabolic activation additionally 5000 µg/plate was tested. Results achieved with vehicle control and positive controls were valid. No cytotoxicity was observed but the limit concentration of 5000 µg/plate was tested. No genotoxicity was observed.
The potential of C8iso AS Na (CAS 126-92-1, analytical purity 39.6%) to induce chromosomal aberration in a mammalian cell line was investigated similar to OECD guideline 473 using Chinese hamster Ovary cells with and without metabolic activation (Loveday, 1990). The test concentrations were 501, 1500 and 5010 µg/mL. Results achieved with the vehicle (water) and positive controls were valid. No cytotoxicity was observed in presence and absence of metabolic activation however the test was conducted up to the limit concentration of 5000 µg/mL. No enhanced chromosome aberration was observed under any conditions of the study.
The potential of C8iso AS Na (CAS 126-92-1, no data on analytical purity) to induce genotoxicity in mammalian cells in vitro was assessed in a study conducted similar to OECD guideline 476 using the mouse lymphoma L5178Y cells with and without metabolic activation (McGregor, 1991). The study comprised of 4 trials with and without metabolic activation. The concentrations tested in the absence of metabolic activation were 156.25, 312.5, 625, 1250, 2500 µg/mL (Trial 1); 200, 1000, 1800, 2600, 3400, 4200 µg/mL (Trial 2); 1000, 1800, 2600, 3400, 4200 µg/mL (Trial 3) and 1000, 1800, 2600, 3400, 4200, 5000 µg/mL (Trial 4). The concentrations tested in the presence of metabolic activation were 200, 1000, 1800, 2600, 3400, 4200 µg/mL (Trial 1), 1000, 1800, 2600, 3400, 4200 µg/mL (Trial 2&3) and 2600, 3000, 3400, 3800, 4200 µg/mL (Trial 4). No treatment related increased mutation frequencies were observed in three of four trials without S9 mix. However, in trial 3, all concentrations showing no marked cytotoxicity were associated with significantly increased mutation frequencies in the absence of metabolic activation. There was no reasonable explanation for this striking result of trial 3. In trial 1 without metabolic activation a statistically significant increased mutation frequency occurred at a single concentration level. At higher concentrations no increased mutation frequencies were observed within this trial. Taken together no increased mutation frequency was evidenced when L5178Y cells were exposed to the test substance without metabolic activation. In the presence of metabolic activation no increased mutation frequencies were observed. In two trials the top dose of 4200 µg/L produced marked cytotoxicity. Therefore also no increased mutation frequency was evidenced when L5178Y cells were exposed to the test substance with metabolic activation.
The potential of C8iso AS Na (CAS 126-92-1, analytical purity 39.6%) to induce sister chromatid exchanges in mammalian cells in vitro was assessed in a study conducted similar to OECD guideline 479 using Chinese hamster Ovary cells with and without metabolic activation (Loveday, 1990). The concentrations tested in the absence of metabolic activation were 149, 498, 1490 µg/mL. The concentrations tested in the presence of metabolic activation were 499, 1490, 4980 µg/mL. Results achieved with the vehicle (water) and positive controls were valid. Cytotoxicity was observed without metabolic activation while no cytotoxicity was observed in presence of metabolic activation. However the test was conducted up to the limit concentration of 5000 µg/mL. No enhanced number of SCEs in the presence or absence of metabolic activation was observed. Therefore, the test substance did not induce sister chromatid exchange.
In conclusion, the substance did not show any genotoxic potential. This is supported by the conclusions of the HERA Draft report “AS are not genotoxic, mutagenic or carcinogenic…” and the conclusions of the SIDS initial assessment profile “Alkyl sulfates of different chain length and with different counter ions were not mutagenic in standard bacterial and mammalian cell systems [...]. There was also no indication for a genotoxic potential of alkyl sulfates in various in vivo studies on mice […].”
Justification for selection of genetic toxicity endpoint
No study selected as all four studies were negative.
Short description of key information:
In vitro gene mutation:
Bacterial reverse mutation assay (Ames test / OECD guideline 471): negative
In vitro mammalian chromosome aberration test (CA / OECD guideline 473): negative
In vitro mammalian cell gene mutation assay (MLA / OECD guideline 476): negative
In vitro sister chromatid exchange in mammalian cells (SCE / OECD 479): negative
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
According to the classification criteria of Directive 67/548/EEC and Regulation (EC) No 1272/2008 the substance does not need to be classified for genotoxicity.
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