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EC number: 234-853-7 | CAS number: 12036-76-9
- 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
Genetic toxicity: in vivo
Administrative data
- Endpoint:
- in vivo mammalian germ cell study: cytogenicity / chromosome aberration
- Remarks:
- Type of genotoxicity: chromosome aberration
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Reliability:
- 2 (reliable with restrictions)
Data source
Reference
- Reference Type:
- publication
- Title:
- Unnamed
- Year:
- 1 977
Materials and methods
Test guideline
- Qualifier:
- no guideline followed
- Principles of method if other than guideline:
- Female mice (10 per group) were fed diets containing 0, 0.25, 0.5, or 1% lead acetate for one month, and another group of 5 mice received 0.25% lead acetate for three months. Bone marrow was collected and examined for chromosome or chromatid aberrations. Additional female mice (n=10) received two intraperitoneal injections of 25 mg/kg lead at 24-hour intervals and were sacrificed 30 hours after the second injection for the micronucleus test. The micronucleus test was also performed on mice that received 0.25% lead in the diet for one month.
- GLP compliance:
- not specified
- Type of assay:
- other: chromosome aberration assay; micronucleus assay
Test material
- Reference substance name:
- Lead di(acetate)
- EC Number:
- 206-104-4
- EC Name:
- Lead di(acetate)
- Cas Number:
- 301-04-2
- IUPAC Name:
- lead (II) acetate trihydrate
- Test material form:
- not specified
Constituent 1
Test animals
- Species:
- mouse
- Strain:
- C57BL
- Sex:
- female
- Details on test animals or test system and environmental conditions:
- TEST ANIMALS
- Age at study initiation: 8 weeks.
- No other details reported.
Administration / exposure
- Route of administration:
- oral: feed
- Vehicle:
- Not reported.
- Details on exposure:
- Lead acetate was provided in the diet at 0, 0.25, 0.5, or 1%.
The micronucleus test used two intraperitoneal injections of 25 mg/kg lead in 0.1 mL water. - Duration of treatment / exposure:
- Diet: one month (an additional group received 0.25% lead in the diet for three months).
Micronucleus test: two injections at 24-hour intervals. - Frequency of treatment:
- Diet: animals ate lead-containing food ad libitum.
- Post exposure period:
- 30 hours for the injection studies.
Doses / concentrations
- Remarks:
- 0, 0.25, 0.5, or 1% lead acetate
Basis: nominal in diet
- No. of animals per sex per dose:
- 10 females per group.
- Control animals:
- yes, concurrent no treatment
- Positive control(s):
- Micronucleus test: Myleran, 50 mg/kg in 0.01 mL dimethyl sulfoxide, or Mitomycine C, 5 mg/kg in 0.1 mL water.
Examinations
- Tissues and cell types examined:
- Bone marrow
- Details of tissue and slide preparation:
- Diet: bone marrow was exposed to hypotonic treatment (sodium citrate), fixed in methanol:acetic acid (3:1), spread on defatted slides, and stained with toluidine blue.
Micronucleus test: bone marrow was centrifuged with fetal calf serum and sedimented cells were spread on a slide. Slides were air-dried and stained by the May-Grunwald-Giemsa method. - Evaluation criteria:
- Diet: 100 metaphases per mouse were examined for chromatid or chromosome aberrations.
Micronucleus test: 1,000 polychromatic erythrocytes per mouse were examined for the presence of micronuclei. - Statistics:
- Chi-square test.
Results and discussion
Test results
- Sex:
- female
- Genotoxicity:
- ambiguous
- Toxicity:
- not examined
- Vehicle controls validity:
- not examined
- Negative controls validity:
- valid
- Positive controls validity:
- valid
Any other information on results incl. tables
The number of chromatid or chromosome aberrations did not increase with lead treatment except for chromatid gaps at 0.5 or 1% lead acetate. No change in the frequency of micronuclei was observed in mice treated with lead in the diet or by intraperitoneal injection.
Applicant's summary and conclusion
- Conclusions:
- Interpretation of results (migrated information): ambiguous
The authors suggest that lead appears to have no genetic action, except for the increase in chromatid gaps, which, in their opinion, does not have any genetic consequence. - Executive summary:
Female mice (10 per group) were fed diets containing 0, 0.25, 0.5, or 1% lead acetate for one month, and another group of 5 mice received 0.25% lead acetate for three months. Bone marrow was collected and examined for chromosome or chromatid aberrations. Additional female mice (n=10) received two intraperitoneal injections of 25 mg/kg lead at 24-hour intervals and were sacrificed 30 hours after the second injection for the micronucleus test. The micronucleus test was also performed on mice that received 0.25% lead in the diet for one month. The number of chromatid or chromosome aberrations did not increase with lead treatment except for chromatid gaps at 0.5 or 1% lead acetate. No change in the frequency of micronuclei was observed in mice treated with lead in the diet or by intraperitoneal injection. The authors suggest that lead appears to have no genetic action, except for the increase in chromatid gaps, which, in their opinion, does not have any genetic consequence.
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