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EC number: 231-778-1 | CAS number: 7726-95-6
- 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
Developmental toxicity / teratogenicity
Administrative data
- Endpoint:
- developmental toxicity
- Type of information:
- experimental study
- Adequacy of study:
- supporting study
- Study period:
- 1996
- Reliability:
- 2 (reliable with restrictions)
Data source
Reference
- Reference Type:
- publication
- Title:
- Prenatal Exposure to Sodium Bromide Affects the Postnatal Growth and Brain Development
- Author:
- Disse M., Joó F., Schulz H. and Wolff J.R.
- Year:
- 1 996
- Bibliographic source:
- J. Brain Res., 37, 1, 127-134.
Materials and methods
Test guideline
- Qualifier:
- no guideline available
- Principles of method if other than guideline:
- Method: other
- GLP compliance:
- no
Test material
- Reference substance name:
- Sodium bromide
- EC Number:
- 231-599-9
- EC Name:
- Sodium bromide
- Cas Number:
- 7647-15-6
- IUPAC Name:
- sodium bromide
- Details on test material:
- Sodium bromide
Constituent 1
Test animals
- Species:
- rat
- Strain:
- Sprague-Dawley
- Details on test animals or test system and environmental conditions:
- no further details
Administration / exposure
- Route of administration:
- oral: drinking water
- Vehicle:
- water
- Details on exposure:
- 18 rats were dosed with NaBr
14 rats were given tap water
4 rats were given NaCl solution
250 mg% in drinking water
Drinking water supplied ad libitum - Analytical verification of doses or concentrations:
- no
- Details on analytical verification of doses or concentrations:
- no further details
- Duration of treatment / exposure:
- days 5 to 15 post mating
- Frequency of treatment:
- Daily
- Duration of test:
- 90 days
Doses / concentrations
- Remarks:
- Doses / Concentrations:
250 mg% in drinking water
Basis:
nominal in water
- No. of animals per sex per dose:
- 250 mg% in drinking water (250 mg NaBr / 100 mL water)
- Control animals:
- yes, concurrent no treatment
- Details on study design:
- Sex: female
Duration of test: 100 days
Results and discussion
Results: maternal animals
Effect levels (maternal animals)
- Basis for effect level:
- other: effect type not specified
Results (fetuses)
- Details on embryotoxic / teratogenic effects:
- Embryotoxic / teratogenic effects:no effects
Fetal abnormalities
- Abnormalities:
- not specified
Overall developmental toxicity
- Developmental effects observed:
- not specified
Any other information on results incl. tables
Bromide levels measured in the blood of dams and blood and brain homogenates of pups prior to and immediately after birth were higher than controls but dropped to control levels by PD 19. Compared to controls, a smaller body weight was observed in all bromide-treated rats from birth onwards. Similarly brain weights were consistently smaller in the bromide treated group than in controls remaining about 10% lower than normal brain weight in adults from PD 8. The protein content was also consistently lower in brains of bromide treated rats than in controls from birth onwards. Differences were still apparent at PD 90.
Applicant's summary and conclusion
- Conclusions:
- Bromide levels measured in the blood of dams and blood and brain homogenates of pups prior to and immediately after birth were higher than controls but dropped to control levels by PD 19. Compared to controls, a smaller body weight was observed in all bromide-treated rats from birth onwards. Similarly brain weights were consistently smaller in the bromide treated group than in controls remaining about 10% lower than normal brain weight in adults from PD 8. The protein content was also consistently lower in brains of bromide treated rats than in controls from birth onwards. Differences were still apparent at PD 90.
Bromide was shown to have little or no effect on development during PD 1 – 10. During PD 10-40 the differences between the treated and control brain weight and protein content peaked and the fell significantly. From PD 40 onwards, deficits in body and brain weights and brain protein content asymptotically reached maximal values.
18 female rats were treated with the test material between days 5 and 15 of gestation and tap water thereafter. A further 18 dams were treated with either tap water or saline solution over the same time period. Postnatal growth was followed by measuring the body weights of the pups. Blood and whole brain homogenates were obtained from pups sacrificed on various days throughout the course of the study until postnatal day 90. Bromide levels in the blood and brain were determined along with body weight, brain weight and brain protein content. - Executive summary:
18 female rats were treated with the test material between days 5 and 15 of gestation and tap water thereafter. A further 18 dams were treated with either tap water or saline solution over the same time period. Postnatal growth was followed by measuring the body weights of the pups. Blood and whole brain homogenates were obtained from pups sacrificed on various days throughout the course of the study until postnatal day 90. Bromide levels in the blood and brain were determined along with body weight, brain weight and brain protein content.
Bromide levels measured in the blood of dams and blood and brain homogenates of pups prior to and immediately after birth were higher than controls but dropped to control levels by PD 19. Compared to controls, a smaller body weight was observed in all bromide-treated rats from birth onwards. Similarly brain weights were consistently smaller in the bromide treated group than in controls remaining about 10% lower than normal brain weight in adults from PD 8. The protein content was also consistently lower in brains of bromide treated rats than in controls from birth onwards. Differences were still apparent at PD 90.
Bromide was shown to have little or no effect on development during PD 1 – 10. During PD 10-40 the differences between the treated and control brain weight and protein content peaked and the fell significantly. From PD 40 onwards, deficits in body and brain weights and brain protein content asymptotically reached maximal values.
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