Bisphenol B

Approximate solubility per 100 g: water <0.1 g

Approximate solubility per 100 g: acetone 266 g; benzene 2.3 g; carbon tetrachloride <0.1 g; ether 133 g; methanol 166 g; V.M.P. naphtha <0.1 g

165.8 Ų [M-H]- [CCS Type: DT; Buffer gas: N2; Ionization: ESI-; Dataset: TOXCAST; Source Identifier: DTXSID4022442]

167.17 Ų [M-H]-

Warning

H302 (95.2%): Harmful if swallowed [Warning Acute toxicity, oral]

P264, P264+P265, P270, P273, P280, P301+P317, P305+P351+P338, P330, P337+P317, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 42 reports by companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Hazard Traits - Endocrine Toxicity

Substance: 4,4'-(1-methylpropylidene)bisphenol

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 7.4X10+4(SRC), determined from a structure estimation method(2), indicates that bisphenol B is expected to have to be immobile in soil(SRC). Volatilization of bisphenol B from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.2X10-11 atm-cu m/mole(SRC), using a fragment constant estimation method(2). Bisphenol B is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.5X10-7 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Results of aerobic river die-away tests and anaerobic sediment tests suggest that biodegradation of bisphenol B occurs slowly(3).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 7.4X10+4(SRC), determined from a structure estimation method(2), indicates that bisphenol B is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 1.2X10-11 atm-cu m/mole(SRC), developed using a fragment constant estimation method(2). Bisphenol B is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3). Phenols can undergo sensitized photo-oxidation in surface waters exposed to sunlight via reaction with hydroxyl and peroxy radicals with half-lives on the order of days to weeks at the water surface(4); therefore, photo-oxidation may be an important fate process for bisphenol B in natural water(SRC). According to a classification scheme(5), an estimated BCF of 250(SRC), from an estimated log Kow of 4.13(2) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is high(SRC). Results of aerobic river die-away tests and anaerobic sediment tests suggest that biodegradation of bisphenol B occurs slowly(6).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), bisphenol B, which has an estimated vapor pressure of 2.5X10-7 mm Hg at 25 °C((SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase bisphenol B is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 5 hours(SRC), calculated from its rate constant of 8.2X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2). Particulate-phase bisphenol B may be removed from the air by wet and dry deposition(SRC).

Bisphenol B was detected in 9 of 42 tomato samples, at concentrations of 27.1 to 85.7 ug/kg, in samples of peeled canned tomatoes collected from Italian supermarkets. Of the total of 42 tested tomato samples, BPB was detected in 9 samples (21.4%). BPA and BPB were simultaneously present in 8 of the analyzed samples(1).

IDENTIFICATION AND USE: Bisphenol B is a crystaline or tan granulular substance which is insoluble in water; soluble in acetone; benzene ; ether; methanol; slightly soluble in carbon tetrachloride and naphtha. It is used in the the manufacture of phenolic and polycarbonate resins. HUMAN EXPOSURE AND TOXICITY: Occupational exposure to bisphenol B may occur through dermal contact with this compound at workplaces where it is produced or used. Monitoring and use data indicate that the general population may be exposed to bisphenol B by ingestion of food and dermal contact with this compound or other products containing bisphenol B. ANIMAL STUDIES: In this study, the ability of certain EDCs, bisphenol A (BPA), bisphenol B (BPB), bisphenol F (BPF), 4-n Nonylphenol (NP) and Octylphenol (OP), was investigated to interfere with specific cellular processes, namely, proliferation, by using MCF-7 breast carcinoma cells, and murine bone marrow dendritic cells. The data was correlated on cell growth with the stimulation of cell cycle progression, which could become a step in the development of cancer, and data established a proliferation ranking between the tested EDCs: NP>BPA>OP>BPB>BPF. In addition, the ability of NP, BPA and OP was investigated to induce the differentiation of dendritic cells. The differentiation and activation of these cells could affect a well-regulated immune response and determine an allergic sensitization. It was found that BPA and NP were active in determining differentiation.

Using a structure estimation method based on molecular connectivity indices(1), the Koc of bisphenol B can be estimated to be 7.4X10+4(SRC). According to a classification scheme(2), this estimated Koc value suggests that bisphenol B is expected to be immobile in soil. The estimated pKa of bisphenol B is 10.2(3), indicating that this compound will exist predominately in the non-ionized form in the environment(SRC); the anion form of bisphenol B in not expected to adsorb more strongly to soils containing organic carbon and clay than the neutral counterpart(3).

Bisphenol B's production and use in the manufacture of phenolic and polycarbonate resins(1,2) may result in its release to the environment through various waste streams(SRC). Bisphenol B can be released from resin linings used as corrosion inhibitors to coat cans in the food industry(2).

AEROBIC: In 22-day aerobic river die-away tests using several river water samples in 24 microcosms, bisphenol B showed no degradation in 12 microcosms and incomplete degradation in 12 microcosms. In anaerobic biodegradation tests using pond sediment, bisphenol B showed no degradation over the initial 60 days of incubation; after 84 days, approximately 60% of initial bisphenol B still remained(1).

An estimated BCF of 250 was calculated in fish for bisphenol B(SRC), using an estimated log Kow of 4.13(1) and a regression-derived equation(1). According to a classification scheme(2), this BCF suggests the potential for bioconcentration in aquatic organisms is high(SRC).

The Henry's Law constant for bisphenol B is estimated as 1.2X10-11 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that Bisphenol B is expected to be essentially nonvolatile from water surfaces(2). Bisphenol B's Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to occur(SRC). Bisphenol B is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.5X10-7 mm Hg(SRC), determined from a fragment constant method(1).

/ENDOCRINE MODULATION/ The endocrine-disrupting activities of bisphenol A (BPA) and 19 related compounds were comparatively examined by means of different in vitro and in vivo reporter assays. BPA and some related compounds exhibited estrogenic activity in human breast cancer cell line MCF-7, but there were remarkable differences in activity. Tetrachlorobisphenol A (TCBPA) showed the highest activity, followed by bisphenol B, BPA, and tetramethylbisphenol A (TMBPA); 2,2-bis(4-hydroxyphenyl)-1-propanol, 1,1-bis(4-hydroxyphenyl)propionic acid and 2,2-diphenylpropane showed little or no activity. Anti-estrogenic activity against 17beta-estradiol was observed with TMBPA and tetrabromobisphenol A (TBBPA). TCBPA, TBBPA, and BPA gave positive responses in the in vivo uterotrophic assay using ovariectomized mice. In contrast, BPA and some related compounds showed significant inhibitory effects on the androgenic activity of 5alpha-dihydrotestosterone in mouse fibroblast cell line NIH3T3. TMBPA showed the highest antagonistic activity, followed by bisphenol AF, bisphenol AD, bisphenol B, and BPA. However, TBBPA, TCBPA, and 2,2-diphenylpropane were inactive. TBBPA, TCBPA, TMBPA, and 3,3'-dimethylbisphenol A exhibited significant thyroid hormonal activity towards rat pituitary cell line GH3, which releases growth hormone in a thyroid hormone-dependent manner. However, BPA and other derivatives did not show such activity. The results suggest that the 4-hydroxyl group of the A-phenyl ring and the B-phenyl ring of BPA derivatives are required for these hormonal activities, and substituents at the 3,5-positions of the phenyl rings and the bridging alkyl moiety markedly influence the activities.

/ALTERNATIVE and IN VITRO TESTS/ The estrogenic activities of 13 Bisphenol-A (BPA)-related chemicals for development of new polymers by three in vitro bioassay have been examined in the presence and absence of a post-mitochondrial metabolizing system (S9 mix). BPA, Bisphenol-B (BPB), Bisphenol-F (BPF), Bisphenol-S (BPS), 4,4-ethylidenebisphenol (BP1), 4,4-dihydroxybenzophenone (BP2), 2,2-bis (4-hydroxyphenyl)-hexafluoropropane (BP3), 4,4-(1,4-phenylenediisopropylidene) bisphenol (BP4), 4,4-cyclohexylidenebisphenol (BP5), 4,4-dihydroxydiphenyl ether (BP6), 4-hydroxydiphenylmethane (BP7), 4-cumylphenol (BP8) and 4,4-dihydroxydiphenyl sulfide (BP9) were each diluted with dimethyl sulfoxide to final concentrations ranging from 10(-7) to 10(-3) M in both the yeast two-hybrid system and in a fluorescence polarization system. Dilutions of 10(-9) to 10(-4) M were assayed in the E-screen, respectively. Except for BPS and BP4, the chemicals tested showed estrogenic activity in the absence of cut S9 mix preparation and the activity was enhanced with S9 mix. BPS, which was initially negative, was active with S9 mix in the yeast two-hybrid system. BP2 was weakly estrogenic with or without S9 mix. Chemicals other than BP2 were positive in the competition binding assay. All chemicals tested showed estrogenic activity in the E-screen, the concentration level of which was 10(4) times lower than those of the other two assays.

/ALTERNATIVE and IN VITRO TESTS/ Endocrine disruptor chemicals (EDCs), which are predominantly present in the environment, are able to mimic or antagonise the biological activity of hormones primarily through the interaction with specific receptors. The main consequences are adverse effects on the growth and development of reproductive organs, the induction of cancer and effects on neuronal differentiation. In this study, /the researchers/ investigated the ability of certain EDCs, Bisphenol A (BPA), Bisphenol B (BPB), Bisphenol F (BPF), 4-n Nonylphenol (NP) and Octylphenol (OP), belonging to a homogeneous group of phenol origin, to interfere with specific cellular processes, namely, proliferation, by using MCF-7 breast carcinoma cells, and differentiation, by using murine bone marrow dendritic cells. /The researchers/ correlated the data on cell growth with the stimulation of cell cycle progression, which could become a step in the development of cancer, and /the researchers/ established a proliferation ranking between the tested EDCs: NP>BPA>OP>BPB>BPF. In addition, /the researchers/ investigated the ability of NP, BPA and OP to induce the differentiation of dendritic cells, the powerful antigen-presenting cells of the immune system. The differentiation and activation of these cells could affect a well-regulated immune response and determine an allergic sensitisation. We found that BPA and NP were active in determining differentiation.

The rate constant for the vapor-phase reaction of bisphenol B with photochemically-produced hydroxyl radicals has been estimated as 8.2X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 5 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Bisphenol B is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Phenols can undergo sensitized photo-oxidation in surface waters exposed to sunlight via reaction with hydroxyl and peroxy (RO2) radicals with half-lives on the order of days to weeks at the water surface(3); therefore, photo-oxidation may be an important fate process for bisphenol B in natural water(SRC).

Occupational exposure to bisphenol B may occur through dermal contact with this compound at workplaces where bisphenol B is produced or used. Monitoring and use data indicate that the general population may be exposed to bisphenol B via ingestion of food and dermal contact with this compound or other products containing bisphenol B. (SRC)

Bisphenol B's production and use in the manufacture of phenolic and polycarbonate resins may result in its release to the environment through various waste streams. Bisphenol B can be released from resin linings used as corrosion inhibitors to coat cans in the food industry. If released to air, an estimated vapor pressure of 2.5X10-7 mm Hg at 25 °C indicates bisphenol B will exist in both the vapor and particulate phases in the atmosphere. Vapor-phase bisphenol B will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 5 hours. Particulate-phase bisphenol B will be removed from the atmosphere by wet and dry deposition. If released to soil, Bisphenol B is expected to have no mobility based upon an estimated Koc of 7.4X10+4. Volatilization from moist soil surfaces is not expected to be an important fate process based upon an estimated Henry's Law constant of 1.2X10-11 atm-cu m/mole. Bisphenol B is not expected to volatilize from dry soil surfaces based upon its vapor pressure. Results of aerobic river die-away tests and anaerobic sediment tests suggest that biodegradation of bisphenol B occurs slowly. If released into water, bisphenol B is expected to adsorb to suspended solids and sediment based upon the estimated Koc. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's estimated Henry's Law constant. An estimated BCF of 250 suggests the potential for bioconcentration in aquatic organisms is high. Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions. Sensitized photo-oxidation may be an important fate process for bisphenol B in sunlit natural water. Occupational exposure to bisphenol B may occur through dermal contact with this compound at workplaces where bisphenol B is produced or used. Monitoring and use data indicate that the general population may be exposed to bisphenol B via ingestion of food and dermal contact with this compound in consumer products containing bisphenol B. (SRC)

/The researchers/ previously demonstrated that the estrogenicity of either bisphenol A [BPA; 2,2-bis(4-hydroxyphenyl)propane] or bisphenol B [BPB; 2,2-bis(4-hydroxyphenyl)butane] was increased several times after incubation with rat liver S9 fraction. This metabolic activation, requiring both microsomal and cytosolic fractions, was observed with not only rat liver, but also human, monkey, and mouse liver S9 fractions. To characterize the active metabolites of BPA and BPB, /the researchers/ investigated the structures of the isolated active metabolites by negative mode LC/MS/MS and GC/MS. The active metabolite of BPA gave a negative mass peak at [M-H](-) 267 on LC/MS and a single daughter ion at m/z 133 on MS/MS analysis, suggesting an isopropenylphenol dimer structure. Finally, this active metabolite was confirmed to be identical with authentic 4-methyl-2,4-bis(p-hydroxyphenyl)pent-1-ene (MBP) by means of various instrumental analyses. The corresponding peaks of the BPB metabolite were [M-H](-) 295 and m/z 147, respectively, suggesting an isobutenylphenol dimer structure. Further, coincubation of BPA and BPB with rat liver S9 afforded an additional active metabolite(s), which gave a negative mass peak at [M-H](-) 281 and two daughter ion peaks at m/z 133 and m/z 147 on MS/MS analysis. These results strongly suggest that the active metabolite of either BPA or BPB might be formed by recombination of a radical fragment, a one-electron oxidation product of carbon-phenyl bond cleavage. It is noteworthy that the estrogenic activity of MBP, the active metabolite of BPA, is much more potent than that of the parent BPA in several assays, including two reporter assays using a recombinant yeast expressing human estrogen receptor alpha and an MCF-7-transfected firefly luciferase plasmid.

In the manufacture of phenolic resins.

Manufacture of polycarbonate resin