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EC number: 231-659-4 | CAS number: 7681-11-0
- 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
According to “Guidance on information requirements and chemical safety assessment Chapter R.7a: Endpoint specific guidance”, the bacterial reverse mutation test is just the screening test to genotoxicity. At the tonnage band of 100-1000 tones per year, the genotoxicity assessment for the substance should based on in vitro and in vivo mutagenicity test on mammalian. Existing both of the in vitro and in vivo mutagenicity test on mammalian gave negative results. Thus screening test of Ames test is unnecessary.
The mutagenic potentiatial for iodide (in potassium iodide ) was studied using the L5178Y mouse (TK+/-) lymphoma assay (Kessler et al., 1980), The established mutagens ethylmethanesulphonate (EMS) and dimethylnitrosamine (DMN)were highly active in this assay, whereas iodide (KI) was inactive. Using the BALB/c 3T3transformation assay well assessed the transformational capacities of these same agents and the positive mutagen N-ethyl-N-nitro-N-nitrosoguanidine(MNNG). All concentrations of the iodide tested were inactive in this assay it can be concluded that KI did not possess any biologically significant mutagenic cell transforming ability.
Another study (J.M. Poul,, and P. Sanders, 2004) on genotoxic effects of potassium iodide was conducted in vitro using the alkaline comet assay at concentration of 0.625, 1.25, 2.5, 5 and 10 mM. Additionally in the test cell viability was also measured using the Trypan blue exclusion method and expressed as proportion of total cells. The test results showed that potassium iodide did not induced DNA damage or cytotoxicity in the alkaline comet assay for doses up to 10 mM.
In the same study, the chromosome damage effects of potassium iodide were evaluated in vitro using cytokinesis-block micronucleus test at concentration of 0.625, 1.25, 2.5, 5 and 10 mM. Additionally in the test cytotoxicity was also measured by the binucleated (BN) cell ratio between treated and control slides. The test results showed that potassium iodide did not induce chromosome damage or cytotoxicity in the alkaline comet assay for doses up to 10 mM.
In an in vivo chromosome aberration test on embryonic hepatocytes, Stable iodine of 10 mg/kg is administered to the rats 7 days after fertilization. Then the embryonic liver was homogenated and the cells in metaphase were stained and checked under metaphase. The chromosome aberration cells were counted respectively for the concentration group and control group. The chromosome aberration rate in the concentration group was compared with that in the control group. The result showed there was no singnificant difference between iodide dosed group with the control group.
Therefore, it can be concluded that the iodide has neither genetic toxicity nor cytotoxicity to mamaliam cells.Short description of key information:
Ames test: Waived due to all negative results in existing mutagenic and cytogenic test on mammalian cells.
In vitro mutagenic and DNA damage test on mammalian cell: 1) L5178Y mouse (TK+/-) lymphoma assay: negative; 2) alkaline comet assay: negative
In vitro chromosomal aberration/micronucleus test: cytokinesis-block micronucleus test: negative
In vitro chromosomal aberration test: Negative
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
Based on this information, the iodide can not meet the classification criteria of geneticmutation under the Regulation (EC) No. 1272/2008 nor Directive 67/548/EEC.
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