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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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: 240-841-2 | CAS number: 16812-54-7
- 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
![](https://poisoncentres.echa.europa.eu/o/diss-blank-theme/images/factsheets/A-REACH/factsheet/print_toxicological-information.png)
Repeated dose toxicity: inhalation
Administrative data
- Endpoint:
- sub-chronic toxicity: inhalation
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Reliability:
- 1 (reliable without restriction)
- Rationale for reliability incl. deficiencies:
- other: Comparable to guideline study (OECD 413)
Cross-reference
- Reason / purpose for cross-reference:
- reference to same study
Data source
Referenceopen allclose all
- Reference Type:
- publication
- Title:
- Lung Toxicity after 13-Week Inhalation Exposure to Nickel Oxide, Nickel Subsulfide, or Nickel Sulfate Hexahydrate in F344/N Rats and B6C3F1 Mice
- Author:
- Dunnick JK, Elwell MR, Benson JM, Hobbs CH, Hahn FF, Haly PJ, Cheng YS, Eidson AF
- Year:
- 1 989
- Bibliographic source:
- FUNDAMENTAL AND APPLIED TOXICOLOGY. 12: 584-594
- Reference Type:
- publication
- Title:
- SUBCHRONIC INHALATION TOXICITY OF NICKEL SUBSULFIDE TO RATS AND MICE
- Author:
- Benson JM, Burt DG, Cheng YS, Eidson AF, Gulati DK, Hahn FF, Hobbs CH, Pickrell J
- Year:
- 1 990
- Bibliographic source:
- Inhalation Toxicology. 2:1-19
- Reference Type:
- study report
- Title:
- Unnamed
- Year:
- 1 996
Materials and methods
Test guideline
- Qualifier:
- equivalent or similar to guideline
- Guideline:
- OECD Guideline 413 (Subchronic Inhalation Toxicity: 90-Day Study)
- Deviations:
- not applicable
- Principles of method if other than guideline:
- not applicable
- GLP compliance:
- not specified
- Limit test:
- no
Test material
- Reference substance name:
- Trinickel disulphide
- EC Number:
- 234-829-6
- EC Name:
- Trinickel disulphide
- Cas Number:
- 12035-72-2
- Molecular formula:
- Ni3S2
- IUPAC Name:
- Trinickel disulphide
- Details on test material:
- - Name of test material (as cited in study report): Ni3S2
- Substance type: low temperature form
- Analytical purity: > 97%
Constituent 1
Test animals
- Species:
- mouse
- Strain:
- B6C3F1
- Sex:
- male/female
- Details on test animals or test system and environmental conditions:
- TEST ANIMALS
- Source: Frederick Cancer Research Facility, Frederick, MD
- Age at study initiation: 7-8 wk
- Housing: individual cages in multitiered inhalation chambers throughout the course ofthe studies
- Diet (e.g. ad libitum): ad libitum during non-exposure periods
- Water (e.g. ad libitum): ad libitum
ENVIRONMENTAL CONDITIONS
- Temperature (°C): 23 +/- 2 C
- Humidity (%): 17-45%
- Photoperiod (hrs dark / hrs light): 12 hr dark, 12 hr light
Administration / exposure
- Route of administration:
- inhalation: aerosol
- Type of inhalation exposure:
- not specified
- Vehicle:
- other: no data
- Remarks on MMAD:
- MMAD / GSD: MMAD = 2.4 um
GSD = 2.2 - Details on inhalation exposure:
- GENERATION OF TEST ATMOSPHERE / CHAMBER DESCRIPTION
- Exposure apparatus: Multitiered inhalation chambers, H-1000, Hazleton Systems, Aberdeen, MD
- System of generating particulates/aerosols: Nebulizer. The aerosol was passed through a K-85 discharger to neutralize electrical charge and mixed with diluting air to achieve the desired concentration in the chambers.
- Air change rate: flow through the chamber was 12 ± 2 air changes/h.
- Method of particle size determination: Aerosol size distribution was determined using cascade impactors.
TEST ATMOSPHERE
- Brief description of analytical method used: monitored by taking three 2-h filter samples during the 6-h exposure day and found to be
within ± 10% of target levels.
- Analytical verification of doses or concentrations:
- yes
- Details on analytical verification of doses or concentrations:
- The aerosol concentration in the exposure chambers was monitored by taking three 2-hr filter samples during the 6-hr exposure day that were found to be within ± 10% of target levels. The mean daily concentration in the exposure chambers was calculated from the filter samples.
- Duration of treatment / exposure:
- 6 hr/day
- Frequency of treatment:
- 5 d/wk, 13wk
Doses / concentrationsopen allclose all
- Remarks:
- Doses / Concentrations:
0.11 mg Ni/m3
Basis:
nominal conc.
- Remarks:
- Doses / Concentrations:
0.2 mg Ni/m3
Basis:
nominal conc.
- Remarks:
- Doses / Concentrations:
0.4 mg Ni/m3
Basis:
nominal conc.
- Remarks:
- Doses / Concentrations:
0.9 mg Ni/m3
Basis:
nominal conc.
- Remarks:
- Doses / Concentrations:
1.8 mg Ni/m3
Basis:
nominal conc.
- No. of animals per sex per dose:
- 10 males, 10 females
- Control animals:
- other: yes: filtered air
- Details on study design:
- - Dose selection rationale: based on previous 12-day study
- Positive control:
- Not applicable
Examinations
- Observations and examinations performed and frequency:
- CAGE SIDE OBSERVATIONS: No data
DETAILED CLINICAL OBSERVATIONS: No data
- Time schedule:
BODY WEIGHT: Yes
- Time schedule for examinations: Final
FOOD CONSUMPTION:
- Food consumption for each animal determined and mean daily diet consumption calculated as g food/kg body weight/day: No data
FOOD EFFICIENCY:
- Body weight gain in kg/food consumption in kg per unit time X 100 calculated as time-weighted averages from the consumption and body weight gain data: No data
WATER CONSUMPTION: No data
OPHTHALMOSCOPIC EXAMINATION: No data
HAEMATOLOGY: No data
CLINICAL CHEMISTRY: No data
URINALYSIS: No data
NEUROBEHAVIOURAL EXAMINATION: No data - Sacrifice and pathology:
- GROSS PATHOLOGY: Yes, organ weights
HISTOPATHOLOGY: Yes. Complete histopathology was performed on high-exposure and control groups and to a no-effect level in target tissues. - Other examinations:
- lung Ni concentration
- Statistics:
- The significance of differences between dosed and control group means was assessed using multiple comparison procedures with two-tailed tests.
Results and discussion
Results of examinations
- Clinical signs:
- no effects observed
- Mortality:
- no mortality observed
- Body weight and weight changes:
- no effects observed
- Food consumption and compound intake (if feeding study):
- not examined
- Food efficiency:
- not examined
- Water consumption and compound intake (if drinking water study):
- not examined
- Ophthalmological findings:
- not examined
- Haematological findings:
- not examined
- Clinical biochemistry findings:
- not examined
- Urinalysis findings:
- not examined
- Behaviour (functional findings):
- not examined
- Organ weight findings including organ / body weight ratios:
- effects observed, treatment-related
- Gross pathological findings:
- not specified
- Histopathological findings: non-neoplastic:
- effects observed, treatment-related
- Histopathological findings: neoplastic:
- not examined
- Details on results:
- BODYWEIGHT GAIN: no effect
ORGAN WEIGHTS
lung weight increased in mice exposed to >/= 0.9 mg Ni/m3
HISTOPATHOLOGY: NON-NEOPLASTIC
Inflammatory changes were seen in the lung, nasal cavity, and bronchial lymph node after exposure to NiO.
The lung lesions included alveolar macrophage hyperplasia, inflammation, and fibrosis. Alveolar macrophage hyperplasia consisted of an increase in the number of macrophages within alveolar spaces.
The change in the bronchial lymph nodes consisted of minimal to mild lymphoid hyperplasia.
Effect levels
open allclose all
- Dose descriptor:
- NOEC
- Effect level:
- 1.8 other: mg Ni/m3
- Sex:
- male/female
- Basis for effect level:
- other: no significant change in body weight
- Dose descriptor:
- NOEC
- Effect level:
- 0.4 other: mg Ni/m3
- Sex:
- male/female
- Basis for effect level:
- other: no significant increase in lung weight
- Dose descriptor:
- NOEC
- Effect level:
- 0.1 other: mg Ni/m3
- Sex:
- male/female
- Basis for effect level:
- other: no animals with alveolar macrophage hyperplasia
- Dose descriptor:
- NOEC
- Effect level:
- 0.4 other: mg Ni/m3
- Sex:
- male/female
- Basis for effect level:
- other: no animals with chronic active inflammation
- Dose descriptor:
- NOEC
- Effect level:
- 0.4 other: mg Ni/m3
- Sex:
- male/female
- Basis for effect level:
- other: no animals with fibrosis (8-10 animals)
- Dose descriptor:
- NOEC
- Effect level:
- 0.3 other: mg Ni/m3
- Sex:
- male/female
- Basis for effect level:
- other: no animals with olfactory epthelial atrophy (8-10 animals)
Target system / organ toxicity
- Critical effects observed:
- not specified
Any other information on results incl. tables
Not applicable.
Applicant's summary and conclusion
- Conclusions:
- Toxicity to the lung correlated with solubility of the nickel compound rather than amount of nickel in the lung. Nickel sulfate and nickel subsulfide were more toxic to the lung of rats and mice than was nickel oxide. Rats were more sensitive than mice to the effects of inhaled nickel.
The 3 nickel compounds had similar effects in the respiratory tract in that all produced atrophy of the olfactory epithelium and a chronic inflammation in the lung. - Executive summary:
As part of a study on the toxicity of NiSO4, Ni3S2 and NiO, Dunnick et al. (1989) examined the toxicity of inhaled Ni3S2 in B6C3F1 mice exposed for 6 hr/d, 5 d/wk, for 13 weeks (0.15, 0.3, 0.6, 1.2, and 2.5 mg Ni3S2/m3; 0.11, 0.2, 0.4, 0.9, and 1.8 mg Ni/m3). This dose range was based on results from an earlier 12-day study where 5 mg Ni3S2 /m3 caused lung lesions. Chamber concentrations and aerosol size were determined analytically (MMAD: 2.4 μm; GSD 2.2). Following exposure, mortality, clinical signs of toxicity, body and organ weights, tissue histopathology, reproductive markers, and Ni lung burden were evaluated (see Basic Toxicokinetics section for lung burden data).
No exposure-related mortality or change in bodyweight was observed in mice. Lung weights were significantly increased in the two highest dose groups. No exposure-related changes in thymus, liver, kidney, brain or testis weights were observed. Inflammation was observed in the nasal cavity, bronchial lymph nodes and the lung. Alveolar macrophage hyperplasia was elevated in most of the mice; however, there were no signs at the lowest dose. Chronic active inflammation and lung fibrosis was observed at the two highest doses; olfactory epithelial atrophy was observed in the three highest doses. No reproductive effects were observed (e.g. sperm morphology, estrous cycle). The authors concluded that toxicity to the lung correlated with solubility of the nickel compound rather than amount of nickel in the lung (lung burden is described in Basic Toxicokinetics sections). Nickel sulfate and Ni3S2 were more toxic to the lung of rats and mice than was NiO. Rats were more sensitive than mice to the effects of inhaled nickel. This investigation was part of a comprehensive bioassay conducted by the National Toxicology Program (1996). STUDY RATED BY AN INDEPENDENT REVIEWER
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.
![ECHA](/o/diss-blank-theme/images/factsheets/A-REACH/factsheet/echa_logo.png)