Registration Dossier
Registration Dossier
Data platform availability banner - registered substances factsheets
Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.
The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.
Diss Factsheets
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: 235-185-9 | CAS number: 12125-01-8
- 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
Basic toxicokinetics
Administrative data
- Endpoint:
- basic toxicokinetics
- Type of information:
- migrated information: read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- key study
- Study period:
- No data
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: Collection of data. Sources: data from toxicological databases and experimental data of unpublished toxicological tests.
Cross-reference
- Reason / purpose for cross-reference:
- reference to same study
Data source
Reference
- Reference Type:
- review article or handbook
- Title:
- Unnamed
- Year:
- 2 010
- Report date:
- 2010
Materials and methods
- Objective of study:
- absorption
- distribution
- excretion
- metabolism
- toxicokinetics
Test guideline
- Qualifier:
- no guideline available
- Principles of method if other than guideline:
- No data
- GLP compliance:
- not specified
Test material
- Reference substance name:
- Ammonium chloride
- EC Number:
- 235-186-4
- EC Name:
- Ammonium chloride
- Cas Number:
- 12125-02-9
- IUPAC Name:
- ammonium chloride
- Test material form:
- not specified
- Details on test material:
- No data
Constituent 1
- Radiolabelling:
- not specified
Test animals
- Species:
- other: No data
- Strain:
- not specified
- Sex:
- not specified
Administration / exposure
- Route of administration:
- oral: unspecified
- Vehicle:
- not specified
- Duration and frequency of treatment / exposure:
- No data
Doses / concentrations
- Remarks:
- Doses / Concentrations:
No data
- No. of animals per sex per dose / concentration:
- No data
- Control animals:
- not specified
Results and discussion
- Preliminary studies:
- No data
Main ADME resultsopen allclose all
- Type:
- absorption
- Results:
- After repeated oral application ammonium chloride enters readily the body as a result of absorption by the gastrointestinal tract and the main target for toxicity are the kidneys.
- Type:
- distribution
- Results:
- Repeated toxicity study on rats by oral exposure caused significant changes with metabolic effect.
- Type:
- metabolism
- Results:
- After absorption by the gastrointestinal tract, the test substance is utlized in the liver to form amino acids and proteins.
- Type:
- excretion
- Results:
- Increased excretion of electrolytes and water causes loss of extracellular fluid and promotes the mobilisation of edema fluid.
Toxicokinetic / pharmacokinetic studies
- Details on absorption:
- No more data
- Details on distribution in tissues:
- Test substance induces metabolic acidosis (shown by decreased plasma- and urinary-pH)
Feeding of high level of the test substance caused decreased appetite, growth retardation, increased water consumption and increased urinary volume.
Several studies with rats recorded increased kidney weight, renal hypertrophy with new cell formation (increase in total DNA and total RNA) and enlargement of existing cells.
Increase in urinary ammonium, urea, sodium, chloride and calcium were also recorded.
Chronic stimulation of adrenal cortex by NH4+ induced acidosis caused hypertrophy of adrenal zona glomerulosa.
Biochemistry showed:
- increased plasma chloride, BUN and plasma proteins
- increased urinary calcium and phosphate excretion
Haematology revealed:
- increase in total erythrocytes, haemoglobin and haematocrit concentration
- Details on excretion:
- No more data
Metabolite characterisation studies
- Metabolites identified:
- not specified
Bioaccessibility (or Bioavailability)
- Bioaccessibility (or Bioavailability) testing results:
- No data
Any other information on results incl. tables
Metabolism
When ammonium ions are converted to urea, liberated hydrogen ion reacts with bicarbonate ion to form water and carbon dioxide. The chloride ion displaces the bicarbonate ion. Chloride is loaded into the kidneys. The increased chloride concentration in the extracellular fluid produces an increased load to the renal tubules.
Human data
Human incidental exposure following oral administration showed that ammonium chloride is rapidly absorbed from the gastrointestinal tract and complete absorption occurs within 3 to 6 hours. In healthy persons absorption of ammonium chloride given by mouth was practically complete. Only 1 to 3% of the dose was recovered in the faeces. Substantial first pass metabolism occurs in the liver.
Applicant's summary and conclusion
- Conclusions:
- Interpretation of results (migrated information): no data
The test substance ammonium chloride enters readily the body after oral application as a result of absorption by the gastrointestinal (GI) tract. After absorption by the GI tract, the test substance is utlized in the liver to form amino acids and proteins.
The main target for toxicity are the kidneys. - Executive summary:
After oral application ammonium chloride enters readily the body as a result of absorption by the gastrointestinal (GI) tract. After absorption by the GI tract, the test substance is utlized in the liver to form amino acids and proteins. The main target for toxicity are the kidneys.
When ammonium ions are converted to urea, liberated hydrogen ion reacts with bicarbonate ion to form water and carbon dioxide. The chloride ion displaces the bicarbonate ion. Chloride is loaded into the kidneys. The increased chloride concentration in the extracellular fluid produces an increased load to the renal tubules.
Increased excretion of electrolytes and water causes loss of extracellular fluid and promotes the mobilisation of edema fluid.
Furthermore, the test substance induces metabolic acidosis (shown by decreased plasma- and urinary-pH) and feeding of high level of the test substance causes decreased appetite, growth retardation, increased water consumption and increased urinary volume. Several studies with rats recorded increased kidney weight, renal hypertrophy with new cell formation (increase in total DNA and total RNA) and enlargement of existing cells.
For the following parameters an increase was also recorded: urinary ammonium, urea, sodium, plasma chloride, BUN, plasma proteins, urinary calcium, phosphate excretion, total erythrocytes and haemoglobin and haematocrit concentration.
Chronic stimulation of adrenal cortex by NH4+ induced acidosis caused hypertrophy of adrenal zona glomerulosa.
Human incidental exposure following oral administration showed that ammonium chloride is rapidly absorbed from the gastrointestinal tract and complete absorption occurs within 3 to 6 hours. In healthy persons absorption of ammonium chloride given by mouth was practically complete. Only 1 to 3% of the dose was recovered in the faeces. Substantial first pass metabolism occurs in the liver.
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.