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EC number: 221-218-4 | CAS number: 3033-29-2
- 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
Endpoint summary
Administrative data
Key value for chemical safety assessment
Genetic toxicity in vitro
Description of key information
In vitro genemutation in bacteria
Under the conditions of an OECD 471, EEC 92/69, Part B and TSCA 798.5265 guideline study, Dioctyltin mercaptopropionate does not induce reverse gene mutations in Salmonella typhimurium with or without metabolic activation.
In vitro cyytogenicity (Chromosome Aberration Assay)
Under the conditions of an OECD 473, EEC Council Directive 92/69, Part B and TSCA 798.5375 guideline study, Dioctyltin mercaptopropionate does not induce chromosomal aberrations in Chinese hamster ovary cells, in the presence or absence of metabolic activation.
In vitro genemutation in mammalian cells
Under the conditions of and OECD 476 and EEC Council Directive 87/302 Part B guideline study, Dioctyltin mercaptopropionate does not induce gene mutations in Chinese hamster V79 cells after in vitro treatment, either in the absence or presence of S9 metabolic activation.
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Genetic toxicity in vivo
Endpoint conclusion
- Endpoint conclusion:
- no study available
Additional information
In vitro gene mutation in bacteria
The genetic toxicity of the test material was investigated in accordance with the standardised guidelines OECD 471, EEC 92/69, Part B and TSCA 798.5265, under GLP conditions using the reverse mutation assay. The study was awarded a reliability score of 1 in accordance with the criteria set forth by Klimisch et al. (1997).
The test material was examined for mutagenic activity by assaying for reverse mutation to histidine prototrophy in the prokaryotic organism Salmonella typhimurium. The five tester strains TA1535, TA1537, TA98, TA100 and TA102 were used. Experiments were performed both in the absence and presence of metabolic activation, using liver S9 fraction from rats pre-treated with phenobarbitone and betanaphthoflavone. Test material solutions for the main assays were prepared using acetic acid/ethanol (1:1) in sterile distilled water at a concentration of 2 % v/v.
In the preliminary toxicity test, the test material was assayed (using the solvent acetic acid 1 % v/v in sterile distilled water) at a maximum dose-level of 100 µg/plate and at nine lower dose-levels spaced at approximately half-log intervals: 31.6, 10.0, 3.16, 1.00, 0.316, 0.100, 0.0316, 0.0100 and 0.00316 µg/plate. No signs of toxicity were observed at any dose-level with any tester strain, in the absence or presence of S9 metabolic activation.
Two main experiments were performed, one using a plate incorporation method, the other using a pre-incubation method. In Main Assay I, using a plate incorporation method, and in Main Assay II, using a pre-incubation method, the test material was assayed at a maximum dose-level of 200 µg/plate and four lower dose-levels separated by two-fold dilutions: 100, 50.0, 25.0, and 12.5 µg/plate. No signs of toxicity were observed up to the highest dose-level tested with any tester strain in the absence or presence of S9 metabolism.
The test material did not induce two-fold increases in the number of revertant colonies in the plate incorporation or pre-incubation assay, at any dose-level, in any tester strain, in the absence or presence of S9 metabolism.
Under the conditions of the study the test material does not induce reverse mutation in Salmonella typhimurium with or without metabolic activation.
In vitro cytogenetic (Chromosome Aberration Assay)
The potential of the test material to cause chromosomal damage in Chinese hamster ovary cells, following in vitro treatment both in the presence and absence of S9 metabolic activation was investigated in accordance with the standardised guidelines OECD473, EEC Council Directive 92/69, Part B and TSCA 798.5375 under GLP conditions. The study was awarded a reliability score of 1 in accordance with the criteria set forth by Klimisch et al. (1997).
Solutions of the test material were prepared in acetic acid:ethanol (1:1 v/v) in sterile distilled water at a concentration of 10 %.
Two independent assays for chromosomal damage were performed. Treatments were performed in the presence and absence of S9 metabolism.
In the first experiment, both in the presence and absence of S9, the treatment time was 3 hours and a single harvest time at 20 hours was employed. Dose-levels of 100, 50.0, 25.0, 12.5, 6.25, 3.13, 1.56, 0.781 and 0.391 µg/mL were used both in the presence and absence of S9 metabolism. As negative results were obtained in the first experiment, a second experiment was performed using continuous treatment in the absence of metabolic activation. Dose-levels of 100, 40.0, 16.0, 6.40, 2.56, 1.02, 0.410, 0.164 and 0.0655 µg/mL were used. Two cell cultures were prepared at each test point.
Dose-levels were selected for the scoring of chromosomal aberrations on the basis of the cytotoxicity of the test material treatments as determined by the reduction of cell counts. Additional information on the cytotoxicity of treatments was obtained from mitotic index evaluation.
For the first experiment, the treatment-levels selected for scoring were 50.0, 25.0 and 12.5 µg/mL in the presence of S9 metabolism and 100, 50.0 and 25.0 µg/mL in the absence of S9 metabolism. For the second experiment, the treatment-levels selected for scoring were 2.56, 1.02 and 0.410 µg/mL.
One hundred metaphase spreads were scored for chromosomal aberrations from each culture, except for replicate cultures treated with the positive controls Cyclophosphamide and Mitomycin-C since in the first experiment, due to the high number of chromosomal aberrations, scoring was terminated at 50 metaphases.
Following treatment with the test material no statistically significant increases in the number of cells bearing aberrations (including and excluding gaps) were observed at any dose-level selected for scoring. Statistically significant increases in the number of cells bearing aberrations (including and excluding gaps) were observed following treatments with the positive controls Cyclophosphamide and Mitomycin-C, indicating the correct functioning of the test system.
Under the conditions of the study the test material does not induce chromosomal aberrations in Chinese hamster ovary cells, in the presence or absence of metabolic activation.
In vitro gene mutation in mammalian cells
The mutagenic activity of the test material was investigated in accordance with the standardised guidelines OECD 476 and EEC Council Directive 87/302 Part B, under GLP conditions, by assaying for the induction of 6-thioguanine resistant mutants in Chinese hamster V79 cells afterin vitrotreatment. The study was awarded a reliability score of 1 in accordance with the criteria set forth by Klimisch et al. (1997).
Experiments were performed both in the absence and presence of metabolic activation, using liver S9 fraction from rats pre-treated with phenobarbitone and betanaphthoflavone. Test material solutions were prepared using acetic acid:ethanol (1 : 1) in sterile distilled water at a concentration of 15 % v/v.
A preliminary cytotoxicity assay was performed. The test material was assayed at a maximum dose-level of 150 µg/mL and a wide range of lower dose-levels: 75.0, 37.5, 18.8, 9.38, 4.69, 2.34, 1.17 and 0.586 µg/mL. Treatment with the test material in the absence of S9 metabolic activation resulted in severe toxicity at higher dose-level tested reaching 8 % of the negative control value at 18.8 µg/mL. In the presence of S9 metabolic activation no toxicity was observed at any dose-level. On the basis of the survival data obtained, the maximum dose-levels for the first mutation assay were selected as 14.1 µg/mL for treatment in the absence of S9 metabolism, and 150 µg/mL in its presence.
Two assays for mutation to 6-thioguanine resistance were performed. In the absence of S9 metabolism the first experiment was performed using dose-levels of 14.1, 9.38, 4.69, 2.34, 1.17 and 0.586 µg/mL. In the second experiment the dose range was modified to take account of toxicity results obtained in the first experiment and the following dose-levels were used: 18.0, 15.0, 12.0, 8.00, 5.33 and 3.55 µg/mL. In the presence of S9 metabolism the first experiment was performed using dose-levels of 150, 75.0, 37.5, 18.8 and 9.38 µg/mL. In the second experiment the dose-range was modified to focus on the highest concentration that could be tested (150, 100, 66.7, 44.4 and 29.6 µg/mL).
No significant increases in mutant numbers or mutant frequency were observed following treatment with the test substance at any dose-level, in the absence or presence of S9 metabolism. In both mutation assays dose-related toxicity was observed only in the absence of S9 metabolism.
Negative and positive control treatments were included in each mutation experiment in the absence and presence of S 9 metabolism. Marked increases were obtained with the positive control treatments indicating the correct functioning of the assay system.
Under the conditions of this study the test material does not induce mutation in Chinese hamster V79 cells after in vitro treatment, either in the absence or presence of S9 metabolic activation.
Justification for classification or non-classification
Dioctyltin mercaptopropionate is non genotoxic, which was proved in gene mutation tests in bacteria and mammalian cells and a cytogenicity study in mammalian cells.
In accordance with the criteria for classification as defined in Annex I, Regulation (EC) No 1272/2008, Dioctyltin mercaptopropionate does not require classification with respect to genetic toxicity.
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