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EC number: 810-388-0 | CAS number: 12067-23-1
- 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
![](https://echa.europa.eu/o/diss-blank-theme/images/factsheets/A-REACH/factsheet/print_toxicological-information.png)
Endpoint summary
Administrative data
Key value for chemical safety assessment
Genetic toxicity in vitro
Description of key information
The following in vitro tests for genetic toxicity have been performed on structural analogous read-across substance with a negative result:
Tin sulfide: Ames test, Chromosomal Aberration (key studies)
Tin disulfide: Ames test, Chromosomal Aberration, HPRT (supporting studies).
Link to relevant study records
- Endpoint:
- in vitro gene mutation study in bacteria
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- key study
- Justification for type of information:
- Read-Across Justification_SnS and SnS2 to Sn2S3
- Reason / purpose for cross-reference:
- read-across source
- Species / strain:
- S. typhimurium TA 1535, TA 1537, TA 98, TA 100 and E. coli WP2
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- no cytotoxicity nor precipitates, but tested up to recommended limit concentrations
- Vehicle controls validity:
- valid
- Untreated negative controls validity:
- valid
- Positive controls validity:
- valid
- Additional information on results:
- Tin sulfide was nonmutagenic for all the used bacterial strains with as well as without metabolic activation.
- Remarks on result:
- other: all strains/cell types tested
- Remarks:
- Tin sulfide
- Conclusions:
- Interpretation of results: negative
Read-across substance tin sulfide is non mutagenic for all tested bacterial strains with and without metabolic activation.
Based on this information it is considered that also ditin trisulfide reveals no mutagenic potential under the test conditions. - Executive summary:
Read-across substance tin sulfide was assayed for the mutagenicity by the Bacterial Reverse Mutation Test according to EU method B.13/14 Mutagenicity - Reverse mutation test using bacteria. Four indicators Salmonella typhimurium strains TA 98, TA 100, TA 1535 and TA 1537 and one indicator Escherichia coli WP2 uvrA strain were used. The test substance was suspended in water for injections and assayed in doses of 50-5000 µg which were applied to plates in volume of 0.1 mL. Tin sulfide was nonmutagenic for all the used bacterial strains with as well as without metabolic activation.
Based on this information it is considered that also ditin trisulfide reveals no mutagenic potential under the test conditions.
- Endpoint:
- in vitro gene mutation study in mammalian cells
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- key study
- Justification for type of information:
- Read-Across Justification_SnS and SnS2 to Sn2S3
- Reason / purpose for cross-reference:
- read-across source
- Species / strain:
- Chinese hamster Ovary (CHO)
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- cytotoxicity
- Vehicle controls validity:
- valid
- Untreated negative controls validity:
- not examined
- Positive controls validity:
- valid
- Additional information on results:
- TEST-SPECIFIC CONFOUNDING FACTORS
- Effects of pH: no (tested)
- Effects of osmolality: no (tested)
- Evaporation from medium: no
- Water solubility: no
- Precipitation: slight precipitation of the test item between 7 and 29 mg/mL, and moderate precipitation observed between 57 and 229 mg/mL both in the presence and absence of metabolic activation. At and above 457 mg/mL heavy precipitation of the test item was observed which interfered with the observation of cell monolayer both in the presence and absence of metabolic activation
- Other confounding effects: on
RANGE-FINDING/SCREENING STUDIES: In a preliminary cytotoxicity test Tin disulfide did not cause a significant cell growth inhibition as evaluated by Relative Cloning Efficiency (RCE) up to the highest tested concentration of 1828.42 mg/mL (equivalent to 10 mM) in the presence as well as in the absence of metabolic activation. The test item formed precipitation of the test solution at and above 7 μg/mL but did not cause any appreciable change in the pH and osmolality of the test solutions at the end of the 3-hour exposure to treatment either in the presence or in the absence of metabolic activation.
COMPARISON WITH HISTORICAL CONTROL DATA: In each of these experiments, the respective positive controls produced a statistically significant increase in the frequencies of mutants, under identical conditions and concurrent vehicle control cultures values were within laboratory historical controls.
- Remarks on result:
- other: SnS2
- Conclusions:
- Interpretation of results:
negative with metabolic activation
negative without metabolic activation
It is concluded that read-across substance Tin disulfide does not have the potential to induce gene mutation in CHO cells at the tested concentrations and under the conditions of testing employed. Based on this information it is considered that also ditin trisulfide reveals no mutagenic potential under the test conditions. - Executive summary:
The genotoxic potential of the read-across test item Tin Disulfide (CAS 1315-01-1) to induce gene mutation in mammalian cells was evaluated using Chinese Hamster ovary (CHO) cells.
The study consisted of a preliminary toxicity test, an initial gene mutation assay, and a confirmatory gene mutation assay. Each of these mutation assays comprised of two independent experiments, one each in the presence and absence of metabolic activation system (S-9 fraction prepared from Aroclor 1254 induced rat liver).
Tin disulfide formed a suspension in sterile water at 91421 µg/mL and was found to be homogeneous and stable in water at 1 and 200 mg/mL up to 24 hours while stored at room temperature.
In a preliminary cytotoxicity test Tin disulfide did not cause a significant cell growth inhibition as evaluated by Relative Cloning efficiency (RCE) up to the highest tested concentration of 1828.42 µg/mL (equivalent to 10 mM) in the presence as well as in the absence of metabolic activation. The test item formed precipitation of the test solution at and above 7 µg/mL but did not cause any appreciable change in the pH and osmolality of the test solutions at the end of the 3-hour exposure to treatment either in the presence or in the absence of metabolic activation.
In the initial gene mutation assay, CHO cells were exposed to the test item in duplicate at concentrations of 58, 183, 578 and 1828 µg/mL of the medium for 3 hours in the presence and absence of metabolic activation. In the confirmatory gene mutation assay, CHO cells were exposed to the test item in duplicate at concentrations of 68, 203, 609 and 1828 µg/mL of the medium for 3 hours in the presence and absence of metabolic activation. In a similar way, a concurrent vehicle control and appropriate positive controls i.e., 3-methylcholanthrene in the presence of metabolic activation and ethyl methanesulphonate in the absence of metabolic activation were also tested in duplicate.
The concentration analysis of the dose formulation prepared for the gene mutation assay were found to be well within the acceptance limit of ± 20% of the theoretical concentration and an RSD of less than 15%.
There was no evidence of induction of gene mutations in any of the test material treated cultures either in the presence or absence of metabolic activation. In each of these experiments, the respective positive controls produced a statistically significant increase in the frequencies of mutants, under identical conditions and concurrent vehicle control cultures values were within laboratory historical controls.
The results of the forward gene mutation assay at the hprt locus with read-across substance Tin disulfide indicate that under the conditions of this study, the test item was non-mutagenic when evaluated in the presence or absence of an externally supplied metabolic activation (S9) system.
Based on this information it is considered that also ditin trisulfide reveals no mutagenic potential under the test conditions.
Referenceopen allclose all
Genetic toxicity in vivo
Description of key information
The following in vivo test for genetic toxicity have been performed on structural analogous read-across substance with a negative result:
Tin sulfide: Micronuclues assay (key study).
Link to relevant study records
- Endpoint:
- in vivo mammalian somatic cell study: cytogenicity / erythrocyte micronucleus
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- key study
- Reason / purpose for cross-reference:
- read-across source
- Sex:
- male/female
- Genotoxicity:
- negative
- Toxicity:
- no effects
- Vehicle controls validity:
- valid
- Negative controls validity:
- not valid
- Positive controls validity:
- valid
- Remarks on result:
- other: SnS
- Additional information on results:
- Tin sulphide does not produce micronuclei in the immature erythrocytes in the conditions of the test.
- Conclusions:
- Interpretation of results: negative
Read-across substance tin sulfide does not produce micronuclei in the immature erythrocytes in the conditions of the test. Based on this information it is considered that also ditin trisulfide does not produce micronuclei in vivo. - Executive summary:
The potential of read-across substance tin sulfide to cause cytogenetic damage was assessed in a Mammalian Erythrocyte Micronucleus Test according to OECD guideline 474.
No changes in health status and condition of the animals in any of the groups were recorded during the acclimation and during the study. No significant changes of mean body weight were observed in the animals during the study. All the values of number of NPCE in all dose groups were within the reference range for negative control group. No statistically significant higher values of number of NPCE in any of the dose groups (up to 11 of micronuclei) as compared to negative control group (up to 13 of micronuclei) were noted. Statistically significant differences were observed in the positive control group (NPCE – up to 38 of micronuclei) as compared to control group.
Read-across substance tin sulfide does not induce damage to the chromosomes or the mitotic apparatus of erythroblasts.
Based on this information it is considered that also ditin trisulfide does not produce micronuclei.
Reference
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Additional information
Information from in vitro studies
Read-across substance tin sulfide was assayed for the mutagenicity by the Bacterial Reverse Mutation Test according to EU method B.13/14 Mutagenicity - Reverse mutation test using bacteria. Four indicators Salmonella typhimurium strains TA 98, TA 100, TA 1535 and TA 1537 and one indicator Escherichia coli WP2 uvrA strain were used. The test substance was suspended in water for injections and assayed in doses of 50-5000 µg which were applied to plates in volume of 0.1 mL. Tin sulfide was nonmutagenic for all the used bacterial strains with as well as without metabolic activation.
Based on this information it is considered that also ditin trisulfide reveals no mutagenic potential under the test conditions.
The clastogenicity potential of read-across substance tin sulfide was determined using In Vitro Chromosome Aberration Test according to OECD guideline 473. The test was carried out in human peripheral blood lymphocytes with and without in vitro metabolic activation system in two separate assays. A concentration range of tin sulfide was used in the Preliminary test with and without metabolic activation: 0.05, 0.1, 0.2, 0.5, 1.0, 3.0, and 5.0 mg/mL in 1 mL of culture. There were no cytotoxic effects both with and without metabolic activation. Three concentrations of the Test item: 1.0, 2.5, and 5.0 mg/mL in 1 mL of culture were used in the Main test. At predetermined intervals (4 and 26 hours) after exposure of cell cultures to the Test item, cells were arrested at metaphase with colchicine, harvested, and slides were stained. Metaphase cells were analyzed microscopically for the presence of chromosome aberrations. A total of 200 well-spread metaphases were examined per concentration on coded slides. Concurrent positive (Cyclophosphamide, Thiotepa) and negative (0.5% methylcellulose) controls were included in each experiment. Microscopic slides of the Main test could initially not be evaluated. Therefore a Main test No. 2 was performed with the same conditions as in the Main test. The microscopic slides related to the concentrations of 1.0, 2.5, and 5.0 mg/mL could be properly analyzed in the Main test No. 2 and in the Repeated test. There were no significant increases in the number of cells with chromosome aberrations and no trends of dose-response relationships. The negative results obtained were biologically relevant and reproducible. Under the test conditions used read-across substance tin sulfide did not induce an increase in numerical and structural chromosome aberrations in cultured human peripheral blood lymphocytes.
Based on this information it is considered that also ditin trisulfide does not induce chromosome aberrations.
The read-across test item, Tin disulfide (CAS 1315-01-1) was tested for its mutagenic potential in the bacterial reverse mutation assay. The study was conducted using TA98, TA100, TA1535 and TA1537 strains of Salmonella typhimurium and WP2uvrA (pKM101) strain of Escherichia coli. The study consisted of a preliminary toxicity test and two mutation assays comprising four independent experiments. The bacterial tester strains were exposed to the test item in the presence and absence of metabolic activation system (S-9 fraction prepared from Aroclor 1254 induced rat liver). Tin disulfide formed a suspension in sterile water (SW) at 50 mg/mL and was found to be homogeneous and stable up to 24 hours at 1 and 200 mg/mL when stored at room temperature. In a preliminary toxicity test, the mean number of revertant colonies was more or less comparable to the SW control plates up to the highest tested dose of 5000 µg/plate, both in the presence and absence of metabolic activation. No toxicity of the test item was seen as the intensity of the bacterial background lawn was comparable to that of the SW control plates up to 5000 µg/plate, both in the presence and absence of metabolic activation. There was a slight precipitation of the test item on the basal agar plates at 5000 µg/plate both in the presence and absence of metabolic activation. Based on these observations, it was decided to test up to the maximum dose of 5000 µg/plate in the initial as well as the confirmatory mutation assay. In the initial mutation assay, the read-across test item was exposed in triplicate to 50, 158, 500, 1580 and 5000 µg/plate test doses in the presence and absence of metabolic activation using direct plate incorporation procedure. In the confirmatory assay, the test item was exposed in triplicate to concentrations of 100, 266, 707, 1880 and 5000 µg/plate in the presence and absence of metabolic activation using pre-incubation procedure. The vehicle control (SW) and the appropriate positive controls were tested simultaneously. The mean and standard deviation of numbers of revertant colonies were calculated for each test dose and the controls for all the tester strains. The results from the initial as well as from the confirmatory assays indicate the tested doses showed no positive mutagenic increase in the mean numbers of revertant colonies for all tester strains when compared to the respective vehicle control plates, either in the presence or absence of metabolic activation. The mean numbers of revertant colonies neither doubled for strains TA98, TA100 and WP2uvrA (pKM101) nor tripled for strains TA1535 and TA1537 when compared to the respective vehicle control plates, either in the presence or in the absence of the metabolic activation at any of the tested doses. Under identical test conditions, there was a more than 3-fold increase in the mean numbers of revertant colonies in the positive controls, demonstrating the sensitivity of the assay procedure used. The study indicated that read-across test item Tin disulfide (CAS 1315-01-1) was not mutagenic in this Bacterial Reverse Mutation Assay up to the highest tested dose of 5000 µg/plate.
Based on this information it is considered that also ditin trisulfide reveals no mutagenic potential under the test conditions.
The clastogenic potential of the read-across test item, Tin disulfide to induce chromosome aberrations in mammalian cells was evaluated using cultured Chinese Hamster Ovary (CHO) cells. The study consisted of a preliminary toxicity test and a chromosome aberration assay comprising of three independent experiments: one of each in the presence and absence of metabolic activation and a confirmatory experiment in the absence of metabolic activation (S-P fraction prepared from Aroclor 1254 induced rat liver).
Tin disulfide formed a suspension in sterile water at the required concentration of 91421 µg/mL and was found to be homogeneous and stable up to 24 hours at 1 and 200 mg/mL when stored at room temperature.
In a preliminary cytotoxicity test for the selection of test concentrations, Tin disulfide showed evidence of significant growth inhibition at and above 229 µg/mL and 457 µg/mL in the presence and absence of metabolic activation, respectively, compared to the sterile water control with 3-hour exposure. In the absence of metabolic activation with 21-hour exposure, there was evidence of significant reduction in the growth of CHO cells at and above 229 µg/mL compared to the sterile water control. Exposure of Tin disulfide did not cause any appreciable change in the pH and Osmolality of test solutions.
In the definitive chromosome aberration assay, CHO cells were exposed to the test item in duplicate at concentrations of 23, 73 and 230 µg/mL and 30, 95 and 300 µg/mL of the medium in the presence and absence of metabolic activation, respectively, for 3 hours, and at 23, 73 and 230 µg/mL of the medium in the absence of metabolic activation for 21 hours.
Similarly, concurrent vehicle (sterile water) and positive controls (cyclophosphamide monohydrate in the presence of metabolic activation and ethyl methanesulfonate in the absence of metabolic activation) were also tested in duplicate.
The concentration analysis of the dose formulations prepared for the chromosome aberration assay were found to be well within the acceptance limit of ± 20% of the theoretical concentration and an RSD of less than 15%. In each case, the cells in C-metaphase were harvested at 21 hours after the start of the treatment ( sterile water control, test concentrations or positive controls) and slides were prepared for chromosome analysis.
At the highest concentration tested (300 µg/mL and 230 µg/mL), the reduction in the cell growth was 51% and 52% in the absence and presence of metabolic activation respectively, with 3-hour exposure, whereas in the absence of metabolic activation (230 µg/mL), with the 21-hour exposures, the reduction in cell growth was 53 when compared to the sterile water control.
A total of 200 metaphases per dose level from duplicate cultures from the sterile water control, each treatment group and the positive control were evaluate for chromosome aberrations. The data from the treatment groups and the positive control were statistically compared with the sterile water control.
There was no evidence of induction of chromosome aberrations, including or excluding gaps, either in the presence or in the absence of metabolic activation in any of these experiments. In each of these experiments, under identical conditions, the respective positive control substances produced a large and statistically significant increase in aberrant metaphases.
The study indicated that the read-across test item, Tin disulfide is not clastogenic at the concentrations tested and under the conditions of testing.
Based on this information it is considered that also ditin trisulfide does not induce chromosome aberrations.
The genotoxic potential of the read-across test item Tin Disulfide (CAS 1315-01-1) to induce gene mutation in mammalian cells was evaluated using Chinese Hamster ovary (CHO) cells.
The study consisted of a preliminary toxicity test, an initial gene mutation assay, and a confirmatory gene mutation assay. Each of these mutation assays comprised of two independent experiments, one each in the presence and absence of metabolic activation system (S-9 fraction prepared from Aroclor 1254 induced rat liver).
Tin disulfide formed a suspension in sterile water at 91421 µg/mL and was found to be homogeneous and stable in water at 1 and 200 mg/mL up to 24 hours while stored at room temperature.
In a preliminary cytotoxicity test Tin disulfide did not cause a significant cell growth inhibition as evaluated by Relative Cloning efficiency (RCE) up to the highest tested concentration of 1828.42 µg/mL (equivalent to 10 mM) in the presence as well as in the absence of metabolic activation. The test item formed precipitation of the test solution at and above 7 µg/mL but did not cause any appreciable change in the pH and osmolality of the test solutions at the end of the 3-hour exposure to treatment either in the presence or in the absence of metabolic activation.
In the initial gene mutation assay, CHO cells were exposed to the test item in duplicate at concentrations of 58, 183, 578 and 1828 µg/mL of the medium for 3 hours in the presence and absence of metabolic activation. In the confirmatory gene mutation assay, CHO cells were exposed to the test item in duplicate at concentrations of 68, 203, 609 and 1828 µg/mL of the medium for 3 hours in the presence and absence of metabolic activation. In a similar way, a concurrent vehicle control and appropriate positive controls i.e., 3-methylcholanthrene in the presence of metabolic activation and ethyl methanesulphonate in the absence of metabolic activation were also tested in duplicate.
The concentration analysis of the dose formulation prepared for the gene mutation assay were found to be well within the acceptance limit of ± 20% of the theoretical concentration and an RSD of less than 15%.
There was no evidence of induction of gene mutations in any of the test material treated cultures either in the presence or absence of metabolic activation. In each of these experiments, the respective positive controls produced a statistically significant increase in the frequencies of mutants, under identical conditions and concurrent vehicle control cultures values were within laboratory historical controls.
The results of the forward gene mutation assay at the hprt locus with read-across substance Tin disulfide indicate that under the conditions of this study, the test item was non-mutagenic when evaluated in the presence or absence of an externally supplied metabolic activation (S9) system.
Based on this information it is considered that also ditin trisulfide reveals no mutagenic potential under the test conditions.
Information from in vivo study
The potential of tin sulfide to cause cytogenetic damage was assessed in a Mammalian Erythrocyte Micronucleus Test according to OECD guideline 474.
No changes in health status and condition of the animals in any of the groups were recorded during the acclimation and during the study. No significant changes of mean body weight were observed in the animals during the study. All the values of number of NPCE in all dose groups were within the reference range for negative control group. No statistically significant higher values of number of NPCE in any of the dose groups (up to 11 of micronuclei) as compared to negative control group (up to 13 of micronuclei) were noted. Statistically significant differences were observed in the positive control group (NPCE – up to 38 of micronuclei) as compared to control group.
Tin sulfide does not induce damage to the chromosomes or the mitotic apparatus of erythroblasts.
Based on this information it is considered that also ditin trisulfide does not produce micronuclei.
Justification for selection of genetic toxicity endpoint
GLP and guideline compliant in vitro assays with a structural analogous read-across substances
Justification for selection of genetic toxicity endpoint
GLP and guideline compliant in vivo test with a structural analogous read-across substance
Justification for classification or non-classification
Based on the results obtained in in vitro and in vivo tests on tin sulfide and tin disulfide it is considered that ditin trisulfide is not genotoxic/mutagenic or clastogenic. Therefore ditin trisulfide has not to be classified according to Directive 67/548/EEC and Regulation (EC) No 1272/2008.
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.
Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
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