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EC number: 231-635-3 | CAS number: 7664-41-7
- 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
No evidence of carcinogenicity was seen in a study with ammonium sulphate. An investigative study suggests that long-term exposure to drinking water containing ammonia (aqueous ammonia) may cause irritant gastritis which in turn may promote gastric carcinogenesis initiated by MNNG. However there is no evidence that ammonia is carcinogenic.
Key value for chemical safety assessment
Carcinogenicity: via oral route
Endpoint conclusion
- Dose descriptor:
- NOAEL
- 67 mg/kg bw/day
Justification for classification or non-classification
No classification for carcinogenicity is proposed. there is no evidence that the substance is carcinogenic.
Additional information
No evidence of carcinogenicity was seen in a rat dietary study with ammonium sulphate (Ota et al, 2006). The NOAEL for this study was 0.6% (dietary level) equivalent to 256 and 284 mg/kg bw/day in males and females respectively [67 and 74 mg/kg bw/d ammonia equivalents].
In a non-standard mechanistic assay, Tsuji et al (1992) exposed MNNG-initiated rats to 0.01% ammonia solution via drinking water. Gastritis was seen in all animals, indicating a local irritnat effect. The incidence of gastric tumours was increased in treated animals, suggesting that ammonia may be acting as a promoter of carcinogenesis.
Solutions of hydrazine as 0.001%, methylhydrazine as 0.01%, methylhydrazine sulfate as 0.001%, and ammonium hydroxide as 0.3, 0.2 and 0.1% were administered continuously in the drinking water of 5- and 6-week-old randomly bred Swiss mice for their entire lifetime. Similarly ammonium hydroxide as a 0.1% solution was given to 7-week-old inbred C3H mice. Hydrazine and methylhydrazine sulfate significantly increased the incidence of lung tumors in Swiss mice, while methylhydrazine enhanced the development of this neoplasm by shortening its latent period. The ammonium hydroxide treatments in Swiss and C3H mice were, however, without carcinogenic effect, and did not inhibit the development of breast adenocarcinomas in C3H females, which are characteristic of these animals. The present study thus proves for the first time the carcinogenicity of methylhydrazine, provides further evidence of the tumor-inducing capability of hydrazine by itself and negates the possibility that the metabolite of hydrazine, ammonium hydroxide, could interfere in the development of neoplasia (Toth, 1972).
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