Registration Dossier
Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 231-887-4 | CAS number: 7775-09-9
- 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
In mice, NOAEL in males is 2000 mg/l in drinking water, whereas for females this is 1000 mg/l, also based on thyroid follicular cell hypertrophy. This corresponds to 60 mg/kg bw/day in females and 80 mg/kg bw/day in males. There was a marginally increased incidence (positive trend) of pancreatic island neoplasms observed in females although the authors considered these results to be equivocal. The effect was only observed in only one sex, the incidences for either adenomas or adenomas and carcinomas (combined) were not statistically significant [the global incidence of hyperplasia plus adenomas remains flat over dose (9/46; 8/47; 6/49; 6/49).] Similar effects were not observed in the rat carcinogenicity study. In the rat the NOAEL for tumourigenic effects on thyroid is 1000 mg/l in drinking water, equivalent to 35 mg/kg bw/day in males and 45 mg/kg bw/day in females. For non-neoplastic effects, the effects on the thyroid are the most critical. The seriousness of the long term TSH stimulation of the follicle cells is relatively limited as only hypertrophy and not hyperplasia were observed even at the two highest doses of sodium chlorate at the end of the 13 week study. In the 2-year study positive trends were observed in the incidences of thyroid gland follicular cell adenoma or carcinoma (combined) in males and females. At 125 mg/l, only at the end of the 2-year study a minimal increase in follicular cell hypertrophy has been observed in males.
The NOAEL for tumorigenic effects on thyroid is 1000 mg/L, equivalent to 35 mg/kg bw/day in males and 45 mg/kg bw/day in females.
For non neoplastic effects, based on thyroid follicular cell hypertrophy, the LOAEL in males is 125 mg/l that corresponds to 5 mg/kg bw/day. As this was the only effect observed, clinically of marginal relevance, and caused by a physiological compensatory mechanism, this could also be the NOAEL.
NOAEL in females is 125 mg/l (equivalent to 5 mg/kg bw/day) based also on thyroid follicular cell hypertrophy.
Key value for chemical safety assessment
Carcinogenicity: via oral route
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed
- Dose descriptor:
- NOAEL
- 5 mg/kg bw/day
Justification for classification or non-classification
Based on results of a 2 -year carcinogenicty study in rats and mice and information on the MoA, the sodium chlorate is not classified.
Additional information
The 2-year chronic NTP studies in mice and rats indicated thyroid effects in rats. There seemed to be a concentration-related increase in percentage of smaller follicles, often showing colloid depletion, which was visible from 5 mg/kg bw/day in males and females.
Although no haematological effects were observed in the chronic NTP study, in particular methaemoglobin forming, the incidence of bone marrow hyperplasia was possibly increased in the male rats and female mice (but lowered in male mice).
In the NTP carcinogenicity study, sodium chlorate resulted in a positive trend in the incidences of pancreatic islet cell adenoma or carcinoma (combined), in female mice although the authors considered these results in mice to be equivocal. The effect was only observed in only one sex, the incidences for either adenomas or adenomas and carcinomas (combined) were not statistically significant [the global incidence of hyperplasia plus adenomas remains flat over dose (9/46; 8/47; 6/49; 6/49).] Similar effects were not observed in the rat carcinogenicity study.
An increase of thyroid neoplasia in male rats (at 75 mg/kg bw/day) was seen. Taking into account the mechanism of action, which is a mechanism that does not directly act on the thyroid but acts via hormone imbalance, strongly suggested from the available data, sodium chlorate should not be considered as a potential human carcinogen. For further details on MoA see Annex I of the CSR: position paper Ledirac and Pontal 2008.
In rodents there is convincing evidence that thyroid hormone imbalance alone leads to tumour formation. Studies have been performed based on the effect of iodine deficiency, partial thyroidectomy and transplantation of TSH-secreting tumours. The weight of the evidence suggests that rodents are more sensitive than human subjects to thyroid tumour induction due to hormonal imbalances that cause elevated TSH levels. It is known for at least 20 different compounds to cause follicular cell neoplasms of the thyroid in rodents, however, none of these compounds is unequivocally associated with thyroid cancer in humans (Capen, 1999 and 2005).
Carcinogenicity: via oral route (target organ): glandular: thyroids
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.

Route: .live1