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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
Carcinogenicity
Administrative data
Description of key information
It was therefore concluded that long-term treatment of KI per se does not result in thyroid tumor induction in rats. In the salivary gland, KI was suggested to have carcinogenic potential via an epigenetic mechanism, only active at a high dose 1000 ppm in drinking water.
Key value for chemical safety assessment
Carcinogenicity: via oral route
Endpoint conclusion
- Dose descriptor:
- LOAEL
- 100 mg/kg bw/day
Justification for classification or non-classification
Iodide does not induce thyroid tumors in rats. In the salivary gland, KI was suggested to have carcinogenic potential via an epigenetic mechanism, at a high dose. However there is still no data about the possibility of the carcinogenic potential deduction from rat to human. Additionally the potential is only existed at high dose to rat. Therefore, the iodide dose neither meet the carcinogenicity criteria under the Regulation (EC) No. 1272/2008 nor Directive 67/548/EEC.
Additional information
A chronic toxicity and carcinogenicity study, in which male and female F344/DuCrj rats were administrated potassium iodide (KI) in the drinking water at concentrations of 0, 10, 100 or 1000 ppm for 104 weeks was conducted. In the test, neither focal hyperplasias, adenomas nor carcinomas derived from the follicular epithelium were increased, despite the fact that KI was administered for 2 yr. It was therefore concluded that long-term treatment of KI per se does not result in thyroid tumor induction in rats. In contrast, SCCs were observed in the submandibular gland in the 1000 ppm groups of both sexes, along with focal acinar atrophy and/or ductular proliferation, frequently accompanied by squamous metaplasia. Based on the fact that the cell proliferation of these proliferating ductules was higher in cases with metaplasia, and the evidence of a morphological continuum from meta-plasias to squamous cell carcinomas, a histogenetic relationship is suspected, which was also described in previous investigation (Takegawa et al., 1998).
Based on these findings, it suggests that excess KI has a thyroid tumor-promoting effect, but KI per se does not induce thyroid tumors in rats. In the salivary gland, KI was suggested to have carcinogenic potential via an epigenetic mechanism, only active at a high dose (1000 ppm in drinking water).
The default value of volume of drinking water for rat is well accepted of 10 ml/100g bw·day, and the average body weight for rat is 250g. Based on these the LOAEL for salivary glands for carcinogenicity is proposed to be 100 mg/kg bw·day of iodide by drinking water.
Carcinogenicity: via oral route (target organ): digestive: salivary glands
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