Quick Search

PRODUCTS

TETRABROMOBİSFENOL A (TETRABROMOBISPHENOL A)

TETRABROMOBISPHENOL A

Cs no: CAS No: 79-94-7

SYNONYMS: CARBONATE OLIGOMER;3,5,3',5'-Tetrabromobisphenol A;3,5,3',5'-tetrabromobisphenola;4,4'-(1- methylethylidene)bis(2,6-dibromo-pheno;4,4'-(1-methylethylidene)bis(2,6-dibromophenol);4,4'-(1-methylethylidene)bis[2,6-dib (1-methylethylidene)bis[2,6-dibromo-Phenol;Great lakes BA-59P; Tetrabromobisphenol A; 79-94-7; 3,3',5,5'-Tetrabromobisphe bromdiyan; 4,4'-(propane-2,2-diyl)bis(2,6-dibromophenol); 2,2-Bis(3,5-dibromo-4-hydroxyphenyl)propane; 4,4'-Isopropylidene dibromophenol); Firemaster BP 4A; Tetrabromodian; tetrabromodiyan; TBBPA; Fire Guard 2000; TETRABROMOBISPHENOL A; Saytex RB 100PC; Phenol, 4,4'-(1-methylethylidene)bis[2,6-dibromo-; Tetrabromodiphenylopropa BP4A; tetrabromodifenilopropan; difenil propan; FG 2000; 4,4'-propane-2,2-diylbis(2,6-dibromophenol); UNII-FQI02RFC3A; 4,4 Methylethylidene)bis(2,6-dibromophenol); BA 59; dibromofenol, tetra bromo bisfenol A; bis fenol A; 3,5,3',5'-Tetrabromobisph 59775; CCRIS 6274; HSDB 5232; Saytex RB-100; 4,4'-Isopropylylidenebis(2,6-dibromophenol); 2,2-Bis(4-hydroxy-3,5-dibromoph EINECS 201-236-9; FQI02RFC3A; 2,2',6,6'-Tetrabromo-4,4'-isopropylidenediphenol;2,6-dibromo-4-[2-(3,5-dibromo-4-hydroxyph yl]phenol; 4,4'-(2,2-PROPANEDIYL)BIS(2,6-DIBROMOPHENOL); CHEMBL184450; DTXSID1026081; CHEBI:33217; Phenol, 4,4'- isopropylidenebis(2,6-dibromo-; Phenol, 4,4'-isopropylidenebis[2,6-dibromo-; 4,4'-(2,2-propanediyl) bis[2,6-dibromo]phenol; M Phenol, 4,4'-(1-methylethylidene)bis(2,6-dibromo-; FR-1524; DSSTox_CID_6081; 4,4'-(1-Methylethylidene)bis(2,6-dibromopheno dibromo-4-hydroxyphenyl)propane; DSSTox_RID_78008; DSSTox_GSID_26081; W-104257; 2,6-dibromo-4-[1-(3,5-dibromo-4-hy methylethyl]phenol; CAS-79-94-7; TetrabromobisphenolA; 25639-54-7; Tetrabromo bisphenol A; 4,4'-(1-methylethylidene)bis[2 dibromophenol]; 3,3',5,5'-Tetrabromo bisphenol A; FLAME CUT 120G; 33'55'-Tetrabromobisphenol A; 3osw; XDI; 4,6-dibromop 100 ABS; 2,5-dibromophenyl)propane; TETRABROMO-4,4'-ISOPROPYLIDENEDIPHENOL; bmse000567; Tetrabromobisphenol ''A Oprea1_822733; SCHEMBL18647; MLS002152878; BIDD:ER0631; C15H12Br4O2; 330396_ALDRICH; ARONIS002155; 2,6,6'-Tetra A; CTK4F6165; KS-00003VGG; 3,3',5'-Tetrabromobisphenol A; BBC/271; 2,5-dibromo-4-hydroxyphenyl)propane; BDBM5015079 59775; SBB080626; STK048486; ZINC01689786; 2,6-dibromo-4-[1-(3,5-dibromo-4-hydroxy-phenyl)-1-methyl-ethyl]phenol; AKO 2,2'',6,6''-Tetrabromobisphenol A; 3,3'',5,5''-tetrabromobisphenol A; 3,3',5,5'-tetrabromobisphenol A; LS-1786; MCULE-85784 NCGC00091463-01; NCGC00091463-02; NCGC00091463-03; NCGC00091463-04; NCGC00091463-05; NCGC00091463-06; NCGC NCGC00258734-01; NCGC00259530-01; 30496-13-0; AC-11719; AK113742; AS-12834; SMR001224492; Phenol,4'-isopropyliden 3,3',5,5'-Tetrabromobisphenol A, 97%; AX8153220; phenol, 4,4'-isopropylidenebis (dibromo-); 2,2-bis(3,5dibromo-4-hydroxyph 4,4''-Isopropylidenebis(2,6-dibromophenol); 4,4'-isopropylidene-bis(2,6-dibromophenol); FT-0617111; FT-0682679; 2,2-bis(3,5- hydroxyphenyl)-propane; 2,2-bis-(3,5-dibromo-4-hydroxyphenyl)propane; C13620; Z-0813; 2,2-bis-(3,5-dibromo-4-hydroxyphe tetrabromobisphenol A 100 microg/mL in Methanol; Phenol,4'-(1-methylethylidene)bis[2,6-dibromo-; Q425246; SR-010005969 Tetrabromodian: tetrabromodihydroxy diphenylpropane; 4,4''-(1-Methylethylidene)bis(2,6-dibromophenol); 4,4''-(2,2-propane dibromo]phenol; 4,4''-(propane-2,2-diyl)bis(2,6-dibromophenol); SR-01000596914-1; 2,2',6,6'-Tetrabromo-4,4'-isopropylidene b (4'-hydroxy-3',5'-dibromophenyl)-propane; 3,3',5,5'-Tetrabromobisphenol A,

TBBPA is produced by the reaction of bromine with bisphenol A.

Most commercial TBBPA products consist of a mixture that d of bromination with the formula C15H16-xBrxO2 where x = 1 to 4. Its re-retarding properties correlate with %Br.

The annual Europe has been estimated as 6.200 tons in 2004.TBBPA is mainly used as a reactive component of polymers, meaning that it is incorporated into the polymer backbone.

It is u re-resistant polycarbonates by replacing some bisphenol A. A lower grade of TBBPA is used to prepare epoxy resins, used in boards. Toxicity A study was published by the European Food Safety Authority (EFSA) in December 2011 on the exposure of TBBPA and its der The study, which examined at 344 food samples from the sh and other seafood food group, concluded that "current dietary TBBPA in the European Union does not raise a health concern." EFSA also determined that "additional exposure, particularly o to TBBPA from house dust is unlikely to raise a health concern".Some studies suggest that TBBPA may be an endocrine disruptor and immunotoxicant.

As an endocrine disruptor, TBBPA ma both estrogens and androgens. Further, TBBPA structurally mimics the thyroid hormone thyroxin (T4) and can bind more s transport protein transthyretin than T4 does, likely interfering with normal T4 activity. TBBPA likely also suppresses immune r inhibiting expression of CD25 receptors on T cells, preventing their activation, and by reducing natural killer cell activity.A 2013 literature review on TBBPA concludes that TBBPA does not produce "adverse eects that might be considered to be re disturbances in the endocrine system".

Therefore, in accordance with internationally accepted denitions, TBBPA should no an "endocrine disruptor". Furthermore, TBBPA is rapidly excreted in mammals and therefore does not have a potential for bio Measured concentrations of TBBPA in house dust, human diet and human serum samples are very low.

 

Daily intakes of TBBP estimated to not exceed a few ng/kg bw/day. Exposures of the general population are also well below the derived-no-eect-le derived for endpoints of potential concern in REACH. TBBPA degrades to bisphenol A and to TBBPA dimethyl ether, and experiments in zebrash (Danio rerio) suggest that during TBBPA may be more toxic than either BPA or TBBPA dimethyl ether.[S-phrases (outdated) S60 S61[ Application: EcoFlameRetardant B-51 is an aromatic brominated ame retardant that is especially ecient as an additive am EPS and in foam polystyrene. The unsaturated end groups provide the unique function of initiating FR performance. EcoFlame also used at low levels with other ame retardants, such as EcoFlameRetardant 8-641 to provide a synergistic response to re EcoFlameRetardant 8- 51 has excellent UV stability and styrene solubility for a broad range of uses.Natural occurrence Tetrabromobisphenol A does not occur naturally (ECHA, 2006). 1.4.2

 

Environmental occurrence Tetrabrom rst detected in the environment in 1983 at a level of 20 ng/g in sediment from the Neya River in Japan (Watanabe et al., 1983 have detected tetrabromobisphenol A in various biotic and abiotic matrices from dierent parts of the world over the past few and Table 1.3). This chemical was detected in air, dust, water, soil, sediment, and sewage sludge from various areas across the al., 2009), including the Arctic, which indicates its ability to undergo long-range transport (Xie et al., 2007; de Wit et al., 2010). T detection of tetrabromobisphenol A and the ubiquitous nature of this contaminant indicates that it is continuously released in environment due to its reported half-life in the soil (t0.5 = 48-84 days) (NTP, 2014). Moreover, tetrabromobisphenol A is frequ biotic samples, including sh, birds, and human tissue (Covaci et al., 2009; Table 1.3). A recent review reported that China was aected by pollution with tetrabromobisphenol A.

 

The most serious cases of tetrabromobisphenol A pollution were found in (a primitive e-waste dismantling site), with concentrations reaching 66 010-95 040 pg/m3 in the air (mean, 82 850 pg/m3), in S Shandong (a tetrabromobisphenol A-manufacturing site) with concentrations ranging from 1.64 to 7758 ng/g dry weight in th ng/g) and in Chaohu Lake, Anhui (industrial concentration site), with concentrations reaching 850-4870 ng/L in water (Liu et al Occupational exposure Occupational exposures to tetrabromobisphenol A have been measured in facilities manufacturing el and, at higher concentrations, in recycling facilities.

Mean concentrations of tetrabromobisphenol A in the air were reported t the dismantling hall and 140 ng/m3 in the shredder at an electronic products recycling plant, and to be several orders of mag those found in the other indoor microenvironments investigated (e.g. 0.036 ng/m3 in the oces) (Sjödin et al., 2001). A low co tetrabromobisphenol A (0.011 ng/m3) was measured in the particulate matter collected from a medical equipment-manufact (Batterman et al., 2010). Occupational exposure of workers to tetrabromobisphenol A at a Chinese printed circuit-board plant dermal absorption, and inhalation of dust varied widely by process, with the greatest estimated exposures being 1930, 431, a body weight (bw) per day, respectively.

 

Raw-material warehouse workers were the most highly exposed, with an average over 2413 pg/kg bw per day. Dust ingestion was the predominant pathway of exposure (Zhou et al., 2014). Low levels.

Exposure of the general population As a reactive ame retardant, the only potential for exposure is from unreacted tetrabrom which may exist where an excess has been added during the production process. When used as an additive (up to 22% by we for the migration of tetrabromobisphenol A out of the matrix is greater, due to abrasion, weathering and high temperatures ( Exposure of the general population predominantly occurs through the diet and through ingestion of indoor dust. While intake children is predominantly via ingestion of indoor dust, intake by adults occurs mainly via the diet. Very young children are est higher daily intake than adults.

 

Exposure may occur prenatally, and tetrabromobisphenol A has been measured in breast milk Average estimated exposures of the population in the United Kingdom to tetrabromobisphenol A via inhalation of outdoor an dierent microenvironments were 100-300 pg per day (Abdallah et al., 2008). 

In Japan, adults were reported to inhale tetrabro 67-210 pg per day, while the exposure of children was 37-114 pg per day (Takigami et al., 2009). The daily intake of tetrabrom Chinese population via inhalation and ingestion of indoor dust particles of dierent particle sizes accumulated in air-condition estimated.

The results revealed that approximately 28.7 pg/kg bw per day particulate matter (PM)2.5- bound tetrabromobisph inhaled deep into the lungs, while 14.5 pg/kg bw per day PM10-bound tetrabromobisphenol A tends to be Species (No. of sam tissue Location Concentration Mean (range) or range (ng/g lipid weight)a Reference Bull shark (13) Muscle Florida, USA 0.03-35 Restrepo et al.The studies reviewed below indicated neither enhanced cell proliferation nor suppression of apoptosis tetrabromobisphenol A, which was associated with an increase in apoptosis in several experimental systems. (a) Humans No humans were available to the Working Group. In human A549 epithelial alveolar lung cells and the human thyroid cell line Cal tetrabromobisphenol A decreased the rates of DNA synthesis. A549 cells tended to arrest in the G1 phase, while Cal-62 cells t the G2 phase. MAPK cascades were also aected, but not in association with an increase in cell proliferation (Strack et al., 200 & Chambard, 2010). (b) Experimental systems (i) Non-human mammalian systems in vivo Apoptosis was induced in the testes exposed to drinking-water containing tetrabromobisphenol A at a concentration of 200 µg/L during gestation, lactation, and u Tetrabromobisphenol A 275 age 70 days. In addition, expression of the proapoptotic Bax gene was increased, while expressio apoptotic Bcl-2 gene was decreased in tetrabromobisphenol A-exposed mice compared with controls (Zatecka et al., 2013). Al incidences of atypical endometrial hyperplasia were observed in the uterus of female Wistar Han rats exposed to tetrabromo mg/kg bw per day) in a 2-year study of carcinogenicity (NTP, 2014; Dunnick et al., 2015), this eect was considered to be a pre rather than an early event in the development of uterine cancer. [The Working Group noted that, in the 3-month study at dos week) of up to 1000 mg/kg bw (NTP, 2014), no treatment-related lesions were observed in the uterus of Wistar Han rats, Fisch or B6C3F1/N mice treated with tetrabromobisphenol A.] (ii) Non-human mammalian systems in vitro In a non-transformed ra line, tetrabromobisphenol A decreased rates of DNA synthesis. NRK cells tended to arrest in the G1 phase. MAPK cascades we but not in association with an increase in cell proliferation (Strack et al., 2007; see also Cagnol & Chambard, 2010).

 

Tetrabrom induced cell death in mouse TM4 cells, a cell line derived from mouse testicular Sertoli cells, via apoptosis involving mitochond depolarization due to increases in cytosolic Ca2+ levels. Intracellular levels of Ca2+ were elevated in TM4 cells within 1-3 minu with tetrabromobisphenol A at 30 µM; after 18 hours, cell viability was < 50%. Tetrabromobisphenol A also caused rapid mitoc membrane depolarization. The loss of cell viability by tetrabromobisphenol A was suppressed by the caspase inhibitor Ac-DEV that this loss was due in part to apoptosis.

 

Tetrabromobisphenol A also inhibited Ca2+-adenosine triphosphatase activity in ra sarcoplasmic reticulum vesicles and in pig cerebellar microsomes at concentrations as low as 0.5 µM (Ogunbayo et al., 2008). primary cultured neurons from rat cerebellum with tetrabromobisphenol A at 5 µM for 24 hours induced apoptosis-like nucle characterized by condensed chromatin and DNA fragmentation; however, other hallmarks of apoptosis, including activation o not observed.

  • Share !
E-NEWSLETTER