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EC number: 205-581-6 | CAS number: 143-06-6
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
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- Density
- Particle size distribution (Granulometry)
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- 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
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- Toxicological Summary
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Endpoint summary
Administrative data
Key value for chemical safety assessment
Genetic toxicity in vitro
Description of key information
In Vitro bacterial reverse mutation assay: The test material was not mutagenic to strains TA 98, 100, 1535, 1537, and 1538 of Salmonella typhimurium in the absence or presence of metabolic activation.
In vitro micronucleus test: The test material did not induce micronuclei in human lymphocytes after in vitro treatment.
In Vitro Mouse Lymphoma assay: The test material did not induce mutation at the TK locus of L5178Y mouse lymphoma cells in vitro 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
Genetic Toxicity In Vitro
In a key pre-GLP in vitro bacterial reverse mutation test, the ability of the test material to revert five strains of Salmonella typhimurium (TA 98, 100, 1535, 1537, and 1538) from histidine dependence to histidine independence was determined in the absence and presence of a Aroclor induced rat liver homogenate activation system (±S9).
An initial cytotoxicity test in the presence and absence of metabolic activation was conducted using strain TA 1535. Based on the results observed in this cytotoxicity determination, concentrations of the test material that were non toxic and slightly toxic were selected for the mutagenesis assay.
The test material was tested at concentrations of 2000, 4000, 6000, 8000, 10000 µg/plate in the absence of metabolic activation (-S9) and at concentrations of 2000, 4000, 6000, 8000, 10000 µg/plate in the presence of metabolic activation (+S9). In the presence of metabolic activation an additional test plate without glucose-6-phosphate and NADP (negative control)) at a concentration of 10000 µg/plate was used in Trial 1 and at a concentration of 6000 µg/plate in Trial 2.
Dimethylsulfoxide (DMSO) was used as the solvent control while N-methyl-N’-nitro-N-nitrosoguanidine (MNNG – 2 µg/plate); 9-Aminoacridine (9AAc – 50 µg/plate); 2-Nitrofluorene (2NF – 25 µg/plate) were used as positive controls in the absence of metabolic activation. 2-Aminoanthracene (2AA) at concentrations of 5, 10, and 100 µg/plate was used as the positive control in the presence of metabolic activation.
Based on the results observed in this bacterial reverse mutation assay, the test material was not considered to be mutagenic to strains TA 98, 100, 1535, 1537, and 1538 ofSalmonella typhimuriumin the absence or presence of metabolic activation.
In a key Guideline (OECD 487) in vitro micronucleus test, the test material was assayed to evaluate its ability to induce micronuclei in human lymphocytes, following in vitro treatment in the presence and absence of S9 metabolic activation.
Two main experiments were performed in this study. In the first experiment, the cells were treated for 3 hours in the presence and absence of S9 metabolism, respectively. The harvest time of 32 hours corresponding to approximately 2.0 cell cycles was used. As negative results were obtained, a second experiment was performed in the absence of S9 metabolism using a continuous treatment until harvest at 31 hours. Solutions of the test material were prepared in culture medium. For both experiments, the highest dose level of 1600 μg/mL was used (corresponding to10 mM), the upper limit to testing indicated in the Study Protocol. The following lower concentrations were assayed: 1070, 711, 474, 316, 211, 140, 93.6, 62.4 and 41.6 μg/mL. Each experiment included appropriate negative and positive controls and two cell cultures were prepared at each test point. The actin polymerisation inhibitor cytochalasin B was added prior to the targeted mitosis to allow the selective analysis of micronucleus frequency in binucleated cells. Dose levels were selected for the scoring of micronuclei on the basis of the cytotoxicity of the test material treatments calculated by the cytokinesis-block proliferation index (CBPI). For both experiments, the following dose levels were selected for scoring: 1600, 1070 and711 μg/mL. One thousand binucleated cells per culture were scored to assess the frequency of micronucleated cells.
Following treatment with the test material, no statistically significant increase in the incidence of micronucleated cells over the control value was observed at any dose level, in any treatment series. Statistically significant increases in the incidence of micronucleated cells were observed following treatments with the positive controls Cyclophosphamide and Colchicin and all results were within the distribution of historical negative control data.
Based on the results observed, the test material did not induce micronuclei in human lymphocytes after in vitro treatment.
In a key Guideline (OECD 490) in vitro gene mutation study in mammalian cells, the test material was examined for mutagenic activity by assaying for theinduction of 5 trifluorothymidine resistant mutants in mouse lymphoma L5178Y cells after in vitro treatment, in the absence and presence of S9 metabolic activation, using a fluctuation method.
A preliminary solubility trial indicated that the maximum practicable concentration of the test material in the final treatment medium was 1600 µg/mL corresponding to 10 mM using RPMI minimal medium as solvent. A cytotoxicity assay was performed both in the absence and presence of S9 metabolic activation. Due to a technical oversight, the test material was assayed at a maximum dose level of 1470 µg/mL and at a wide range of lower dose levels: 734,367, 183, 91.7, 45.9, 22.9, 11.5 and 5.73 µg/mL.
In the absence of S9 metabolic activation, using the 3 hour treatment time, no cells survived treatment at the highest dose level. A severe toxicity reducing relative survival (RS) to 3% of the concurrent negative control value was observed at 734 µg/mL, while no relevant toxicity was noted over the remaining concentrations tested. Using the 24 hour treatment time, no cells survived treatment at the two highest dose levels, mild toxicity was noted at the next lower concentration (RS=62%), while no relevant toxicity was observed over the remaining dose levels tested. Following treatment in the presence of S9 metabolic activation, using the short treatment time (3 hours), no cells survived treatment at the highest dose level. Test material treatment at 734 µg/mL yielded moderate toxicity reducing RS to 28%, while no relevant toxicity was observed over the remaining dose levels tested.
On the basis of the results observed in the preliminary cytotoxicity test, two independent assays (Main Assay I and Main Assay II) for mutation at the TK locus were performed.
In Main Assay I, using the short treatment time, the test material was assayed at the dose levels of 236, 295, 369, 461, 576, and 720 µg/mL (3 hour treatment) in the absence of metabolic activation (-S9) and at dose levels of 295, 369, 461, 576, 720, and 900 µg/mL (3 hour treatment) in the presence of metabolic activation (+S9). Adequate levels of cytotoxicity, covering a range from the maximum to slight or no toxicity, were observed in the treatment series in the presence of S9 metabolic activation, while test item treatment in the absence of S9 metabolism yielded a steep decline in relative total growth (RTG) and no concentration tested showed an adequate level of cytotoxicity (RTG value between 10-20%). No relevant increases in mutant frequencies were observed at any concentration in the absence or presence of S9 metabolism.
Main Assay II was performed in the absence of metabolic activation (-S9), using a long treatment time and by repeating the 3 hour treatment series. A different concentration spacing was used to attain data points within approximately 10-20% RTG range. The test material was assayed at dose levels of 356, 389, 430, 471, 521, 570, and 630 µg/mL for the 3 hour treatment and at dose levels of 322, 356, 389, 430, 471, 521, and 570 µg/mL for the 24 hour treatment.
No relevant increases in mutant frequencies were observed following treatment with the test material, in the absence or presence of S9 metabolism. Negative and positive control treatments were included in each mutation experiment both in the absence (methylmethanesulphonate (MMS)) and presence (benzo(a)pyrene (B(a)P) of S9 metabolism. The mutant frequencies in the solvent control cultures fell within the normal range. Marked increases were obtained with the positive control treatments indicating the correct functioning of the assay system.
Based on the results observed, it was concluded that the test material does not induce mutation at the TK locus of L5178Y mouse lymphoma cells in vitro in the absence or presence of S9 metabolic activation.
Genetic Toxicity In Vivo
No data available
Justification for classification or non-classification
Not classified for germ cell mutagenicity according to the CLP Regulation (EC 1272/2008), section 3.5.
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