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EC number: 215-609-9 | CAS number: 1333-86-4
- 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

Respiratory sensitisation
Administrative data
- Endpoint:
- respiratory sensitisation: in vivo
- Type of information:
- experimental study
- Adequacy of study:
- other information
- Reliability:
- 3 (not reliable)
- Rationale for reliability incl. deficiencies:
- unsuitable test system
- Remarks:
- intranasal application
Data source
Reference
- Reference Type:
- publication
- Title:
- Unnamed
- Year:
- 2 006
Materials and methods
Test guideline
- Qualifier:
- no guideline available
- Principles of method if other than guideline:
- Mice were intranasally exposed to ovalbumin (OVA) alone or in combination with ultrafine carbon black particles. The induction of airway inflammation and the immune adjuvant activity were studied in the lungs and lung-draining peribronchial lymph nodes (PBLN) at day 8. OVA-specific antibodies were measured at day 21, and the development of allergic airway inflammation was studied after OVA challenges (day 28)
- GLP compliance:
- not specified
Test material
- Reference substance name:
- Carbon black
- EC Number:
- 215-609-9
- EC Name:
- Carbon black
- Cas Number:
- 1333-86-4
- Molecular formula:
- C
- IUPAC Name:
- carbon
Constituent 1
Test animals
- Species:
- mouse
- Strain:
- Balb/c
- Sex:
- female
Test system
- Route of induction exposure:
- other:
- Route of challenge exposure:
- intranasal
- No. of animals per dose:
- 6 / group
- Details on study design:
- Mice were anaesthetized by an intramuscular injection of ketamine and exposed to 20 µL of OVA (0.5 mg/mL or particle + OVA (3.3 and 0.5 mg/mL, respectively) in PBS by intranasal droplet application on days 0, 1 and 2 (total dose of 200 µg particles and 30 µg OVA). Mice were killed on day 8, or challenged to study asthma-like allergic airway inflammation. For the latter, mice were anaesthetized by an intramuscular ketamine injection and challenged by intranasal droplet application of 20 µL OVA (0.5 mg/mL) in PBS on days 25, 26 and 27. Mice were killed on day 28 by an overdose of pentobarbital.
Results and discussion
- Results:
- Ultrafine (below 30 nm in diameter) but not fine (over 200 nm in diameter) carbon black particles (200 µg) induced airway inflammation and displayed adjuvant activity. The latter was evidenced by the induction of immune sensitisation to co-administered ovalbumin and demonstrated by increased levels of cytokines associated with a Th2 immune response and by the occurrene of allergic airway inflammation after an intranasal OVA challenge.
Ultrafine carbon black bound 100% of the OVA, whereas fine carbon black only bound around 10% of the OVA.
Allergic airway inflammation as well as a stimulation of local immune responses (changes in cellular composition of BAL and PBLN, and production of a number of type 2 cytokines in PBLN) were found after intranasal challenges with antigen.
Applicant's summary and conclusion
- Interpretation of results:
- study cannot be used for classification
- Conclusions:
- Ultrafine (below 30 nm in diameter) but not fine (over 200 nm in diameter) carbon black particles (200 µg) induced airway inflammation and displayed adjuvant activity. The latter was evidenced by the induction of immune sensitisation to co-administered ovalbumin and demonstrated by increased levels of cytokines associated with a Th2 immune response and by the occurrene of allergic airway inflammation after an intranasal OVA challenge. A systemic antibody response was not detected. The study is not suitable to derive any conclusions about the respiratory sensitisation of carbon black per se.
- Executive summary:
In a non-validated mouse allergic airway sensitisation model, mice were intranasally exposed to ovalbumin alone or in combination with carbon black particles. The induction of airway inflammation and the immune response were studied in the lungs and lung-draining peribronchial lymph nodes at day 8. Ovalbumin specific antibodies were measured at day 21, and the development of allergic airway inflammation was studied after ovalbumin challenge at day 28. “Ultrafine” (primary structure below 30 nm in diameter) but not fine (particle size >200 nm in diameter) carbon black particles were shown to induce airway inflammation and displayed adjuvant activity.
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