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Diss Factsheets
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EC number: 926-571-4 | CAS number: 1187203-96-8
- 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:
- weight of evidence
- Reliability:
- 4 (not assignable)
- Rationale for reliability incl. deficiencies:
- other: Secondary literature: EU Risk Assessment Report Bisphenol A (review)
Data source
Referenceopen allclose all
- Reference Type:
- publication
- Title:
- 4,4'-Isopropylidenediphenol (Bisphenol A) (CAS-No. 108-95-2)
- Author:
- European Chemicals Bureau (ECB)
- Year:
- 2 003
- Bibliographic source:
- EU Risk Assessment Report, 3rd Priority List, Volume 37
- Reference Type:
- publication
- Title:
- 4,4´-Isopropylidenediphenol (bisphenol-A)
- Author:
- European Chemicals Bureau (ECB)
- Year:
- 2 008
- Bibliographic source:
- EU Risk Assessment Report, Human Health Addendum of April 2008 (to be read in conjunction with published EU RAR of BPA, 2003)
- Reference Type:
- other company data
- Title:
- Unnamed
- Year:
- 2 010
- Report date:
- 2010
Materials and methods
Test material
- Reference substance name:
- 4,4'-isopropylidenediphenol
- EC Number:
- 201-245-8
- EC Name:
- 4,4'-isopropylidenediphenol
- Cas Number:
- 80-05-7
- Molecular formula:
- C15H16O2
- IUPAC Name:
- 2,2-bis(4-hydroxyphenyl)propane
Constituent 1
Results and discussion
Applicant's summary and conclusion
- Executive summary:
The 2003 EU RAR concluded:
"Animal data indicates that absorption of BPA from the gastrointestinal tract is rapid and extensive following oral administration, although it is not possible to reliably quantify the extent of absorption. Following dermal exposure, available data suggest limited absorption of about 10% of the applied dose. BPA is removed rapidly from the blood and the data indicate extensive first pass metabolism following absorption from the gastrointestinal tract. In view of this first pass metabolism, the bioavailability of unconjugated BPA is probably limited following oral exposure to no more than 10 to 20% of the administered dose. The major metabolic pathway in rats involves glucuronide conjugation, with approximately 10% and 20% of the administered dose recovered in urine as the glucuronide metabolite in males and females, respectively. The major route of excretion is via the faeces with the urinary route being of secondary importance. Over seven days post dosing, approximately 80% and 70% of the administered dose was eliminated in the faeces in male and female rats, respectively. The first pass metabolism and extensive and rapid elimination of BPA suggest that the potential for transfer to the foetus and bioaccumulation may be limited. There are no data on the toxicokinetics of BPA following inhalation exposure."
The 2008 updated EU RAR concluded:
"New information on the toxicokinetics of BPA in humans and in pregnant and non-pregnant rodents of different ages provides an important contribution to the knowledge of kinetic properties of BPA. Human studies have demonstrated that at comparable exposure levels the blood concentrations of free BPA in humans are much lower than those in rodents. In rats, mice, monkeys, and humans, the available evidence suggests that following oral administration, BPA is rapidly and extensively absorbed from the gastrointestinal tract. For the purposes of risk characterisation, absorption via the oral and inhalation routes will be assumed to be 100%; dermal absorption will be taken to be 10%. A number of studies in rats suggest that BPA metabolites and free BPA have a limited distribution to the embryo/foetal or placental compartments following oral administration. Maternal and embryo/foetal exposure to free BPA did occur, but systemic levels were found to be low due to extensive first-pass metabolism. There are differences between humans and rodents in the distribution of BPA. After oral administration, BPA is rapidly metabolised in the gut wall and the liver to BPA glucuronide. In humans, the glucuronide is released from the liver into the systemic circulation and cleared by urinary excretion. In contrast, BPA glucuronide is eliminated in bile in rodents and undergoes enterohepatic recirculation after cleavage to BPA and glucuronic acid by glucuronidase in the intestinal tract."
There is no reliable and significant new information on the toxicokinetics of Bisphenol A.
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