D-Glucopyranose, oligomeric, butyl glycoside

Endpoint summary

Additional information

There is only limited data available on the genetic toxicity of D-Glucopyranose, oligomeric, butyl glycoside. In order to fulfil the standard information requirements set out in Annex VII and VIII, 8.4, in accordance with Annex XI, 1.5, of Regulation (EC) No 1907/2006, read-across from structurally related substances is conducted.

A detailed justification for the grouping of chemicals and read-across is provided in the technical dossier (see IUCLID Sections 7.1 and 13).

In vitro

For genetic toxicity, data on D-Glucopyranose, oligomeric, butyl glycoside (Mouse lymphoma assay) and on substances which share a strong structural relationship with D-Glucopyranose, oligomeric, butyl glycoside exist. Based on the category approach, the results of three studies on genetic toxicity in vitro of the category members D-Glucopyranose, oligomers, hexyl glycosides, D-Glucopyranose, oligomers, decyl octyl glycosides and D-Glucopyranose, oligomeric, C10-16-alkyl glycosides were used (Microbiological Associates, 1991).

- Gene mutation in bacteria

A bacterial gene mutation assay (Ames test) was conducted with D-Glucopyranose, oligomers, hexyl glycosides in compliance with OECD guideline 471 and under GLP conditions (SafePharm, 1998). In two series of experiments, the test substance at concentrations ranging from 50 to 5000 µg/plate did not induce mutations in Ames test in the absence and presence of metabolic activation in the selected strains of Salmonella typhimurium (TA 98, TA 100, TA 1535 and TA 1537) and Escherichia coli (WP2 uvrA).

- Gene mutation in mammalian cells

The genotoxic potential of D-Glucopyranose, oligomeric, butyl glycoside was assessed using a gene mutation assay in cultured mammalian cells (mouse lymphoma L5178Y cells) according to OECD guideline 476 (WIL Research Europe B.V., 2012). Based on a preliminary toxicity study, concentrations ranging from 1 to 2360 µg/mL were used for the treatment of cells in two independent experiments. Incubation times of 24 hours and 3 hours were used in the absence and presence of S9-mix, respectively. No increase in mutant frequency was observed at any of the concentration tested in both experiments. Therefore, it was concluded that under the conditions used in the study, the test material was not mutagenic at the TK-locus of mouse lymphoma L5178Y cells in the absence and presence of metabolic activation. An analogous Mouse lymphoma assay conducted with the structurally related category member D-Glucopyranose, oligomers, decyl octyl glycosides (CAS 68515-73-1) demonstrated no genetic toxicity in mammalian cells, either, and, therefore, supports the toxicological comparability of the substances in the category.

- Chromosome aberrations

D-Glucopyranose, oligomeric, C10-16-alkyl glycosides was assayed in an in vitro mammalian chromosome aberration test conducted according to OECD guideline 473 and in compliance with GLP (Henkel, 1995). In this experiment, Chinese hamster lung fibroblasts (V79) were treated with the test substance at concentrations up to 160 µg/mL. Continuous treatment for 4 h was performed with and without S9-mix followed by culture periods of 7, 20 and 28 h, respectively. For chromosome analysis, concentrations ranging from 2 to 80 µg/mL were selected. The test substance did not induce chromosomal aberrations at any of the concentrations tested, both in the presence or absence of metabolic activation. Under the conditions of this assay, the test substance did not show clastogenic activity in vitro.

Justification for selection of genetic toxicity endpoint
Hazard assessment is conducted based on a Mouse lymphoma assay with the substance itself and by means of read-across based on a category approach with structurally related substances according to the criteria laid down in Annex XI, 1.5 of Regulation (EC) No 1907/2006. The substances of the Category are generated by the reaction of D-glucose with alcohols of varying chain length and share identical structural characteristics only differing by the alkyl chain length of the respective alcohol and varying degree of oligomerisation. Upon hydrolysis they are degraded into glucose and fatty alcohols again which can be further metabolised by common endogenous pathways like glycolysis and, in case of the alcohols, degraded in the endogenous pathway of beta-oxidation subsequently to their oxidation into fatty acids. No specific study was selected, since three different endpoints are addressed by genetic toxicity in vitro: mutagenicity in bacteria, chromosomal aberration in mammalian cells and mutagenicity in mammalian cells; genetic toxicity in vivo is no mandatory endpoint according to Regulation (EC) No 1907/2006. However, all available in vitro and in vivo genetic toxicity studies were negative. All available studies are adequate and reliable based on the identified similarities in structure and intrinsic properties between source and target substance and overall quality assessment (refer to the endpoint discussion for further details).

Short description of key information:
In vitro:
RA-C, OECD 471 (Ames): negative
OECD 476 (Mouse lymphoma assay): negative
RA-C, OECD 473 (Chromosome aberration): negative

Endpoint Conclusion: No adverse effect observed (negative)

Justification for classification or non-classification

The available data on genetic toxicity of D-Glucopyranose, oligomeric, butyl glycoside and substances structurally related to D-Glucopyranose, oligomeric, butyl glycoside according to the criteria laid down in Regulation (EC) No 1907/2006, Annex XI, 1.5, do not meet the criteria for classification according to Regulation (EC) 1272/2008 or Directive 67/548/EEC; therefore, D-Glucopyranose, oligomeric, butyl glycoside is not considered to exert genetic toxicity, either, and the data are thus conclusive but not sufficient for classification.