Bisphenol AF

336.23

336.23

1891568

216-036-7

OH7IX8A37J

152522

DTXSID7037717

White to light gray powder

2908199090

40.5

4.5

DryPowder; OtherSolid; PelletsLargeCrystals

1.4±0.1 g/cm3

160-162 °C

400°C

>100°C

1.506

Insoluble in water.

Store in a tightly closed container. Store in a cool, dry, well-ventilated area away from incompatible substances.

5.4X10-7 mm Hg at 25 deg C (est)

Henry's Law constant = 5.7X10-10 atm-cu m/mol at 25 °C (est)

pka = 9.2 at 25 °C (est)

166.06 Ų [M-H]-

Hydroxyl radical reaction rate constant = 8.0X10-11 cu cm/molecule-sec at 25 °C (est)

NONH for all modes of transport

2

36/37/38

26-36-37/39

SN2780000

Xi

Corrosive

Stable at room temperature in closed containers under normal storage and handling conditions.

P261-P305 + P351 + P338

H315-H319-H335

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.

|Danger|H315 (63.55%): Causes skin irritation [Warning Skin corrosion/irritation]|P201, P202, P260, P261, P264, P271, P273, P280, P281, P302+P352, P304+P340, P305+P351+P338, P308+P313, P310, P312, P314, P321, P332+P313, P337+P313, P362, P391, P403+P233, P405, and P501|Aggregated GHS information provided by 214 companies from 18 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

The presence of bisphenol AF in dust samples from New York (Albany, n = 38), China (n = 55), Japan (n = 22), and Korea (n = 41) was monitored in 2006 and 2010. Bisphenol AF was not detected in dust samples from New York or China(1); bisphenol AF was detected in 76% of dust samples from Korea, with a maximum level of 0.091 ug/g, and 9% of dust samples from Japan, with a maximum level of 0.011 ug/g(1).

Exposure to xenoestrogens occurs against a backdrop to physiological levels of endogenous estrogens. Endogenous estrogen levels vary from low levels in early childhood to high levels during pregnancy and in young women. However, few studies have addressed how xenoestrogens interact with endogenous estrogens. The current study was designed to characterize the individual dose-response curves of estradiol-17beta (E(2)), bisphenol A (BPA), tetrabromo-bisphenol A (TBBPA), and bisphenol AF (BPAF, 4,4'-hexafluoroisopropylidene diphenol) on estrogen-dependent luciferase expression in T47D-KBluc cells and to determine how binary (8 x 8 factorial) and ternary (4 x 4 x 4 factorial) mixtures of an endogenous estrogen (E(2)) interact with BPA and/or BPAF. Log EC(50) and hillslope values with SEs, respectively, for individual compounds were as follows: E(2), -12.10M +/- 0.06071, 0.7702 +/- 0.1739; BPA, -6.679M +/- 0.08505, 1.194 +/- 0.2137; and BPAF, -7.648M +/- 0.05527, 1.273 +/- 0.1739. TBBPA was not evaluated in mixture studies because of its minimally estrogenic response at 3 x10(-5)M and elicited cytotoxicity at higher concentrations. Both the binary mixtures of E(2) with BPA and BPAF and the ternary mixture of E(2), BPA, and BPAF behaved in an additive manner. For binary mixtures, as E(2) concentration increased, higher concentrations of BPA and BPAF were necessary to induce a significant increase in the estrogenic response. Understanding the behavior of mixture interactions of xenoestrogens, like BPA and BPAF, with endogenous estrogens will allow a better assessment of the potential risk associated with exposure to these chemicals, individually or as mixtures.|The estrogenic activities of BPA, BPAF, BPAP, BPF were tested based on recombinant gene yeast assay. Six mixtures were designed based on the result of the test,each of which had an equitoxic ratio ray (EC10 or EC50). The EC50 values are 6.81 x 10(-6) mol x L(-1), 7.44 x 10(-7) mol x L(-1), 1.43 x 10(-5) mol x L(-1), 7.52 x 10(-6) mol x L(-1) for BPA, BPAF, BPAP and BPF respectively,which reveals that the estrogenic activities order among the four bisphenols was BPAF> BPA> BPF> BPAP. The experiment shows that when BPA mixes with BPAF, BPAP and BPF in different ratios individually, different combination effects are produced. It reveals that the combined ratios of the components may affect the combined effect. The dose addition model and the independent action model are used to identify the combined effect. They are testified to be more intuitionistic and more comprehensive than other joint effect indices.

LD50 Rat oral 3400 mg/kg

Bisphenol AF's production and use as a cross-linking agent in fluorocarbon elastomers and specialty polymers(1,2) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 7.6X10+5(SRC), determined from a structure estimation method(2), indicates that bisphenol AF is expected to be immobile in soil(SRC). The estimated pKa of bisphenol AF is 9.2(3), indicating that this compound will exist partially in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of bisphenol AF from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 5.7X10-10 atm-cu m/mole(SRC), using a fragment constant estimation method(2). Bisphenol AF is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 5.4X10-7 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Biodegradation data in soil were not available(SRC, 2012).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 7.6X10+5(SRC), determined from a structure estimation method(2), indicates that bisphenol AF 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 5.7X10-10 atm-cu m/mole(SRC), developed using a fragment constant estimation method(2). According to a classification scheme(4), an estimated BCF of 420(SRC), from an estimated log Kow of 4.47(2) and a regression-derived equation(2). 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(5); therefore, photo-oxidation may have some importance as a fate process for bisphenol AF in natural water(SRC). Bisphenol AF is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3). Biodegradation data in water were not available(SRC, 2012).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), bisphenol AF, which has an estimated vapor pressure of 5.4X10-7 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 AF 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 1.6 hours(SRC), calculated from its rate constant of 8.0X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2). Particulate-phase bisphenol AF may be removed from the air by wet and dry deposition(SRC).

The rate constant for the vapor-phase reaction of bisphenol AF with photochemically-produced hydroxyl radicals has been estimated as 8.0X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 1.6 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Bisphenol AF 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 have some importance as a fate process for bisphenol AF in natural water(SRC).

An estimated BCF of 420 was calculated in fish for bisphenol AF(SRC), using an estimated log Kow of 4.47(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).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of bisphenol AF can be estimated to be 7.6X10+5(SRC). According to a classification scheme(2), this estimated Koc value suggests that bisphenol AF is expected to be immobile in soil. The estimated pKa of bisphenol AF is 9.2(3), indicating that this compound will exist partially in anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4).

The Henry's Law constant for bisphenol AF is estimated as 5.7X10-10 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that bisphenol AF is expected to be essentially nonvolatile from water surfaces(2). Bisphenol AF's Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to occur(SRC). Bisphenol AF is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 5.4X10-7 mm Hg(SRC), determined from a fragment constant method(1).

According to the 2006 TSCA Inventory Update Reporting data, the number of persons reasonably likely to be exposed in the industrial manufacturing, processing, and use of bisphenol AF is 1000 or greater; the data may be greatly underestimated(1).|NIOSH (NOES Survey 1981-1983) has statistically estimated that 4388 workers (1460 of these were female) were potentially exposed to bisphenol AF in the US(1). Occupational exposure to bisphenol AF may occur through inhalation and dermal contact with this compound at workplaces where bisphenol AF is produced or used(2). The general population may be exposed to bisphenol AF via dermal contact with this compound from consumer products containing polymers made from bisphenol AF(2). Contact via food and cosmetics may be possible since the tubing and seals in the food and pharmaceutical industry are made from bisphenol AF polymers(2). Monitoring data indicate that the general population may be exposed to bisphenol AF via inhalation of indoor dust(3).[(1) NIOSH; NOES. National Occupational Exposure Survey conducted from 1981-1983. Estimated numbers of employees potentially exposed to specific agents by 2-digit standard industrial classification (SIC). Available from, as of Nov 5, 2012: http://www.cdc.gov/noes/ (2) NTP; Chemical Information Profile for Bisphenol AF

Exogenous agents, synthetic and naturally occurring, which are capable of disrupting the functions of the ENDOCRINE SYSTEM including the maintenance of HOMEOSTASIS and the regulation of developmental processes. Endocrine disruptors are compounds that can mimic HORMONES, or enhance or block the binding of hormones to their receptors, or otherwise lead to activating or inhibiting the endocrine signaling pathways and hormone metabolism. (See all compounds classified as Endocrine Disruptors.)

Endocrine-disrupting chemicals (EDCs) are widely found in the environment. Estrogen-like activity is attributed to EDCs, such as bisphenol A (BPA), bisphenol AF (BPAF), and zearalenone (Zea), but mechanisms of action and diversity of effects are poorly understood. /The researchers/ used in vitro models to evaluate the mechanistic actions of BPA, BPAF, and Zea on estrogen receptor (ER) alpha and ERbeta. /The researchers/ used three human cell lines (Ishikawa, HeLa, and HepG2) representing three cell types to evaluate the estrogen promoter activity of BPA, BPAF, and Zea on ERalpha and ERbeta. Ishikawa/ERa stable cells were used to determine changes in estrogen response element (ERE)-mediated target gene expression or rapid action-mediated effects. The three EDCs showed strong estrogenic activity as agonists for ERalpha in a dose-dependent manner. At lower concentrations, BPA acted as an antagonist for ERalpha in Ishikawa cells and BPAF acted as an antagonist for ERbeta in HeLa cells, whereas Zea was only a partial antagonist for ERalpha. ERE-mediated activation by BPA and BPAF was via the AF-2 function of ERalpha, but Zea activated via both the AF-1 and AF-2 functions. Endogenous ERalpha target genes and rapid signaling via the p44/42 MAPK pathway were activated by BPA, BPAF, and Zea. BPA and BPAF can function as EDCs by acting as cell type-specific agonists (= 10 nM) or antagonists (= 10 nM) for ERalpha and ERbeta. Zea had strong estrogenic activity and activated both the AF-1 and AF-2 functions of ERalpha. In addition, all three compounds induced the rapid action-mediated response for ERalpha.|/The researchers/ report that the mechanisms by which biphenol A (BPA) and two congeners, bisphenol AF and bisphenol C (BPC), bind to and activate estrogen receptors (ER) alpha and beta differ from that used by 17beta-estradiol. /The researchers/ show that bisphenols act as partial agonists of ERs by activating the N-terminal activation function 1 regardless of their effect on the C-terminal activation function 2, which ranges from weak agonism (with BPA) to antagonism (with BPC). Crystallographic analysis of the interaction between bisphenols and ERs reveals two discrete binding modes, reflecting the different activities of compounds on ERs. BPA and 17beta-estradiol bind to ERs in a similar fashion, whereas, with a phenol ring pointing toward the activation helix H12, the orientation of BPC accounts for the marked antagonist character of this compound. Based on structural data, we developed a protocol for in silico evaluation of the interaction between bisphenols and ERs or other members of the nuclear hormone receptor family, such as estrogen-related receptor gamma and androgen receptor, which are two known main targets of bisphenols. ...

Impurities in Commercial Products: o,p-monoadducts, o,p-bisphenol AF, bis-hexafluoroacetone, trimer, phenol, hydrofluoric acid, and water (technical grade); fluoride, color (APHA), methanol insolubles (at 105 °C), phenol, and water.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/ENDOCRINE MODULATION/ /The researchers/ aimed to determine the relative preference of bisphenol AF for the human nuclear estrogenic receptors ERalpha and ERbeta and the bisphenol A-specific estrogen-related receptor ERRgamma, and to clarify structural characteristics of receptors that influence bisphenol AF binding. /The researchers/ examined receptor-binding activities of bisphenol AF relative to [(3)H]17beta-estradiol (for ERalpha and ERbeta) and [(3)H]bisphenol A (for ERRgamma). Functional luciferase reporter gene assays were performed to assess receptor activation in HeLa cells. /The researchers/ found that bisphenol AF strongly and selectively binds to ERs over ERRgamma. Furthermore, bisphenol AF receptor-binding activity was three times stronger for ERbeta [IC50 (median inhibitory concentration) = 18.9 nM] than for ERalpha. When examined using a reporter gene assay, bisphenol AF was a full agonist for ERalpha. In contrast, it was almost completely inactive in stimulating the basal constitutive activity of ERbeta. Surprisingly, bisphenol AF acted as a distinct and strong antagonist against the activity of the endogenous ERbeta agonist 17beta-estradiol. ... Results suggest that bisphenol AF could function as an endocrine-disrupting chemical by acting as an agonist or antagonist to perturb physiological processes mediated through ERalpha and/or ERbeta.

2,2-bis(4-hydroxyphenyl)hexafluoropropane

Custom compounding of purchased resin|Phenol, 4,4'-[2,2,2-trifluoro-1-(trifluoromethyl)ethylidene]bis-: ACTIVE

In this study, a simple and universal analytical method was developed for the determination of trace BPAF in various tissues and excreta of rats after they were orally dosed. The samples were hydrolyzed with glucuronidase/arylsulfatase followed by ultrasonic extraction with acetonitrile. The crude extract was purified with a mixed-mode anion exchange (Oasis MAX) solid-phase extraction (SPE) cartridge. Separation and quantification was then conducted by ultra-high-pressure liquid chromatography/electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS) in negative ionization mode. The recoveries at three fortification levels in different biological samples were from 71.0% to 102.3% with relative standard deviations no more than 13.2% (n=6). The quantification limits of the method were from 0.5 ug/kg to 3 ug/kg depending on the matrix. This method was successfully applied to the determination of BPAF in tissues, serum, urine and feces of orally dosed rats.