ペンタブロモ（フェノキシベンゼン）

Pesticide -> EPA IRIS

Pesticide -> EPA IRIS

log Kow = 6.84

6.84

7.32

Methanol, 1g/100g; dioctylphthalate, >100g/100g; completely miscible in methylene chloride, toluene, freon 11, polyol, styrene, and methyl ethyl ketone

In water, 0.0133 mg/L (commercial product)

In water, 9.0X10-7 mg/L at 20 °C

9e-10 mg/mL at 20 °C

-5 °C

MP: -7 to -3 °C (commercial)

-5 °C

This chemical does not meet GHS hazard criteria for 100% (3 of 3) of all reports.

Not Classified

Aggregated GHS information provided per 3 reports by companies from 1 notifications to the ECHA C&L Inventory.

Hazard Traits - Developmental Toxicity; Endocrine Toxicity; Hepatotoxicity and Digestive System Toxicity; Neurotoxicity; Reproductive Toxicity

Hazard Traits - Bioaccumulation; Environmental Persistence

Regulation (EC) No 178/2002 (amended)

S - indicates a substance that is identified in a final Significant New Use Rule.

Substance: Diphenyl ether, pentabromo derivative

Moderately irritating to skin; [Hawley] May cause liver injury; Can be absorbed through skin; The technical product is a mixture of tetra-, penta-, and hexabromodiphenyl ethers; [ICSC] A mild skin and moderate eye irritant, based on animal studies; [CHEMINFO] See Decabromodiphenyl ether.

European Union; Diphenyl ether, pentabromo derivative (pentabromodiphenyl ether). European Union Risk Assessment Report. Luxembourg: Office for Official Publications of the European Committees, (2001).[Available from, as of October 28, 2010: http://ecb.jrc.ec.europa.eu/DOCUMENTS/Existing-Chemicals/RISK_ASSESSMENT/REPORT/penta_bdpereport015.pdf]

USEPA, Office of Research and Development, National Center for Environmental Assessment: An Exposure Assessment of Polybrominated Diphenyl Ethers, EPA/600/R-08/086F (May 2010).[Available from, as of September 23, 2010: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=210404#Download]

WHO; Environ Health Criteria 162: Brominated Diphenyl Ethers (1994). EHC are designed for scientists and administrators responsible for the establishment of safety standards and regulations and provide basic scientific risk evaluations of a wide range of chemicals and groups of chemicals.[Available from, as of October 26, 2010: http://www.inchem.org/documents/ehc/ehc/ehc162.htm]

(a) Chemical substances and significant new uses subject to reporting. (1) The chemical substances identified as tetrabromodiphenyl ether, pentabromodiphenyl ether, hexabromodiphenyl ether, heptabromodiphenyl ether, octabromodiphenyl ether, and nonabromodiphenyl ether, or any combination of these substances resulting from a chemical reaction are subject to reporting under this section for the significant new uses described in paragraph (a)(2) of this section. (2) The significant new use is manufacture or import for any use on or after January 1, 2005. (b) Specific requirements. The provisions of subpart A of this part apply to this section except as modified by this paragraph. (1) Persons who must report. Section 721.5 applies to this section except for section 721.5(a)(2). A person who intends to manufacture or import for commercial purposes a substance identified in paragraph (a)(1) of this section and intends to distribute the substance in commerce must submit a significant new use notice.

Section 8(a) of TSCA requires manufacturers of this chemical substance to report preliminary assessment information concerned with production, exposure, and use to EPA as cited in the preamble in 51 FR 41329. Effective date 1/11/90; Reporting date: 3/12/90.

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. Pentabromodiphenyl ether is included on this list. Effective date 1/11/90; Sunset date: 6/30/98.

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.

Avoid inhalation of mist.

SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. The completeness of the cleaning procedures should be considered before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at the end of shift, but should remain at employee's place of work for cleaning.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

Protective gloves. Protective clothing. Safety goggles.

A/P2 filter respirator for organic vapor and harmful dust.

Samples of human milk from 26 women in North Rhine Westfalia, Germany, were analyzed for pentabromodiphenyl ether, measured as Bromkal 70-DE. Concentrations in the milk from 25 of the women were 0.62-11.1 ug/kg fat. In one Chinese woman, a level of 50 ug/kg fat was found(1). The concentration of 2,2',4,4',5-pentabromodiphenyl in human adipose tissue was 1.1 ng/g lipid wt(2). The concentration of 2,2',4,4',5-pentabromodiphenyl ether in the adipose tissue of a patient with non-Hodgkin's lymphoma was 1.1 ng/g lipid basis(3). The concentrations of pentabromodiphenyl ethers in the adipose tissue of two patients with non-Hodgkin's lymphoma and myelodysplastic syndrome were 1.8 and 0.2 ng/g lipid basis, respectively(3). The mean concentration of 2,2',4,4',5-pentabromodiphenyl in U.S. blood donors in 1988 was 0.58 pmol/g lipid wt (range, <0.4-6.6 pmol/g lipid weight; 8 of 12 samples, positive)(4). The mean concentration of 2,2',4,4',6-pentabromodiphenyl in U.S. blood donors in 1988 was 0.30 pmol/g lipid wt (range, <0.2-4.2 pmol/g lipid weight; 10 of 12 samples, positive)(4). Adipose tissue concentrations of 2,2',4,4',5-pentabromodiphenyl ether were reported as not detected-1.6, 0.02-1.14, 0.74-5.51, <0.003-0.36, <0.7-2.1, 0.78-1.7 and 2.17-72 ng/g lipid in samples from Belgium, Czech Republic, Finland, Japan, Spain, Sweden and the United States, respectively(5). These samples also had reported concentrations of 2,2',4,4',6-pentabromodiphenyl ether of 0.18-1.5, 0.01-2.40, <0.003-0.53, 0.15-1.4, 0.15-0.57 and 0.7-61 ng/g lipid in samples from Belgium, Czech Republic, Japan, Spain, Sweden and the United States, respectively(5). Mean concentrations of 2,2',4,4',5-pentabromodiphenyl ether in serum were 0.21-1.2, 2.44, and 1.1 ng/g lipid in samples from Japan, Korea, Sweden(5). Mean concentrations of 2,2',4,4',5-pentabromodiphenyl ether in serum were 5.7, 7.1 and 0.32 ng/g lipid in samples from maternal, umbilical cords, and in the general population from the United States, respectively(5). Mean concentrations of 2,2',4,4',6-pentabromodiphenyl ether in serum were 0.26-0.29 ng/g lipid in samples from Japan and 4.2, 4.1, and 0.17 ng/g lipid in samples from maternal, umbilical cords, and in the general population from the United States, respectively(5). Human milk concentrations of 0.51-3.2, 0.39, not detected to 21.1, and 0.06-4.47 ng/g lipid were reported in the countries of Canada, Finland, Japan, and Sweden, respectively, for 2,2',4,4',5-pentabromodiphenyl ether(5). Human milk concentrations of 0.23-1.9, not detected to 27.2, and 0.05-5.14 ng/g lipid were reported in the countries of Canada, Japan, and Sweden, respectively, for 2,2',4,4',6-pentabromodiphenyl ether(5).

Pentabromodiphenyl ether was reported in adipose tissue from people that had lived in Tarragona, Spain for at least 10 years at concentrations of 0.15-3.5 ng/g(1). Serum samples from 276 California residents contained a geometric mean of 7.4 and 6.0 ng/g lipid for 2,2',4,4',5-and 2,2',4,4',6-pentabromodiphenyl ether, serum samples from 1764 residents of other US states had a geometric mean of 3.8 ng/g lipid for 2,2',4,4',6-pentabromodiphenyl ether(2). Adipose samples taken in 1970 contained 2,2',4,4',5-pentabromodiphenyl ether at <2.5-13.9 pg/g lipid and 2,2',4,4',6-pentabromodiphenyl ether at <2.5-6.1 pg/g lipid, samples taken in 2000 contained 42-362 pg/g lipid of 2,2',4,4',5-pentabromodiphenyl ether and 41-527 pg/g lipid of 2,2',4,4',6-pentabromodiphenyl ether, all samples were collected in Tokyo, Japan(3).

2,2',4,4',5- and 2,2',4,4',6-Pentabromodiphenyl ether body concentrations over time in Northern Hemisphere populations(1).

EYES: irrigate opened eyes for several minutes under running water. INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice. SKIN: should be treated immediately by rinsing the affected parts in cold running water for at least 15 minutes, followed by thorough washing with soap and water. If necessary, the person should shower and change contaminated clothing and shoes, and then must seek medical attention. INHALATION: supply fresh air. If required provide artificial respiration.

... Recently, /it was/ reported that neonatal exposure to PBDEs causes developmental neurotoxic effects. In the present study, 10-day-old Naval Medical Research Institute male mice were given one single oral dose of PCB 52 (1.4 umol/kg bw) + PBDE 99 (1.4 umol), PCB 52 (1.4 umol or 14 umol), or PBDE 99 (1.4 umol or 14 umol). Controls received a vehicle (20% fat emulsion). Animals exposed to the combined dose of PCB 52 (1.4 umol) + PBDE 99 (1.4 umol) and the high dose of PCB 52 (14 umol) or PBDE 99 (14 umol) showed significantly impaired spontaneous motor behavior and habituation capability at the age of 4 and 6 months. The neurobehavioral defects were also seen to worsen with age in mice neonatally exposed to PCB 52 + PBDE 99. /PBDE 99/

... Neonatal coexposure to PBDE 99 (0.8 mg/kg body weight) and MeHg (0.4 or 4.0 mg/kg body weight) can exacerbate developmental neurotoxic effects. These effects are manifested as disrupted spontaneous behavior, reduced habituation, and impaired learning/memory abilities. This is seen in the low dose range, where the sole compounds do not give rise to developmental neurotoxic effects. The effects seen are more than just additive. Furthermore, a significant effect of interaction was seen on the cholinergic nicotinic receptors in the cerebral cortex and hippocampus. This suggests that a mechanism for the observed cognitive defects is via the cholinergic system. Furthermore, PBDE can interact with MeHg causing developmental neurotoxic effects... /PBDE 99/

10-day-old Naval Medical Research Institute male mice were given one single oral dose of PCB 52 (1.4 umol/kg body weight [bw]) + PBDE 99 (1.4 umol), PCB 52 (1.4 umol or 14 umol), or PBDE 99 (1.4 umol or 14 umol). Controls received a vehicle (20% fat emulsion). Animals exposed to the combined dose of PCB 52 (1.4 umol) + PBDE 99 (1.4 umol) and the high dose of PCB 52 (14 umol) or PBDE 99 (14 umol) showed significantly impaired spontaneous motor behavior and habituation capability at the age of 4 and 6 months. The neurobehavioral defects were also seen to worsen with age in mice neonatally exposed to PCB 52 + PBDE 99. /PBDE 99/

Nervous

Hepatic

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 22,000(SRC), determined from a structure estimation method(2), indicates that pentabromodiphenyl ether is expected to be immobile in soil(SRC). Volatilization of pentabromodiphenyl ether from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.0X10-5 atm-cu m/mole(SRC), based upon its vapor pressure, 3.5X10-7 mm Hg(3), and water solubility, 1.3X10-2 mg/L(4). However, adsorption to soil is expected to attenuate volatilization(SRC). Pentabromodiphenyl ether is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). No biodegradation (as CO2 evolution) was seen after 29 days for pentabromodiphenyl ether in an OECD 301B ready biodegradation test(4). The substance tested was a composite sample from two producers with the following composition: 33.7% tetrabromodiphenyl ether; 54.6% pentabromodiphenyl ether; and 11.7% hexabromodiphenyl ether(4). The test was extended to 93 days to allow sufficient opportunity for adaption to occur. At the end of 93 days, 2.4% of the theoretical amount of CO2 had been evolved(4).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 22,000(SRC), determined from a structure estimation method(2), indicates that pentabromodiphenyl ether is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 2.0X10-5 atm-cu m/mole(SRC), derived from its vapor pressure, 3.5X10-7 mm Hg(4), and water solubility, 1.3X10-2 mg/L(5). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 4.6 and 41 days, respectively(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column(SRC). The estimated volatilization half-life from a model pond is 33 years if adsorption is considered(6). According to a classification scheme(7), BCFs of >10,000 in carp(8), suggests the potential for bioconcentration in aquatic organisms is very high(SRC). No degradation (as CO2 evolution) was seen after 29 days for pentabromodiphenyl ether in an OECD 301B ready biodegradation test(5). The substance tested was a composite sample from two producers with the following composition: 33.7% tetrabromodiphenyl ether; 54.6% pentabromodiphenyl ether; and 11.7% hexabromodiphenyl ether(5). The test was extended to 93 days to allow sufficient opportunity for adaption to occur. At the end of 93 days, 2.4% of the theoretical amount of CO2 had been evolved(5). Pentabromodiphenyl ether is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), pentabromodiphenyl ether, which has a vapor pressure of 2.2X10-7 to 5.5X10-7 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase pentabromodiphenyl ether 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 29 days(SRC), calculated from its rate constant of 5.5X10-13 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase pentabromodiphenyl ether may be removed from the air by wet or dry deposition(SRC). Fifteen polybrominated diphenyl ethers, tetra- thru deca-isomers, were reported to absorb at wavelengths >290 nm(4) and therefore are expected to be susceptible to direct photolysis by sunlight(SRC).

Pentabromodiphenyl ether was reported in vegetables, tubers, pulses, cereals, fruits, fish and shellfish, meat and meat products, eggs, milk, dairy products, and fats and oils at 1.4, 0.5, 0.6, 2.2, 0.4, 115.9, 24.9, 25.8, 5.2, 23.4, and 157.7 ng/kg wet weight in products purchased from 7 cities in Catalonia, Spain, sampled June to August 2000(1). 2,2',4,4',5- and 2,2',4,4',6-Pentabromodiphenyl ether were not detected in cod liver oil supplement manufactured in Norway(2). 2,2',4,4',5- and 2,2',4,4',6-Pentabromodiphenyl ether were reported as <0.1 ng/g in dietary fish oil supplements in 28 samples from Belgium, 18 samples from The Netherlands, 12 samples from the United Kingdom and 11 samples from other countries(3).

ENVIRONMENTAL: Pentabromodiphenyl ether, measured as Bromkal 70-DE, was detected in 4 samples of cow's milk at concentrations ranging from 2.5 to 4.5 ug/kg fat(1).

ENVIRONMENTAL: Samples of human milk from 26 women in North Rhine Westfalia, Germany, were analyzed for pentabromodiphenyl ether, measured as Bromkal 70-DE(1). Concentrations in the milk from 25 of the women ranged from 0.62 to 11.1 ug/kg fat. In one Chinese woman, a level of 50 ug/kg fat was found(1). Human milk concentrations of 0.51-3.2, 0.39, not detected to 21.1, and 0.06-4.47 ng/g lipid were reported in the countries of Canada, Finland, Japan, and Sweden, respectively, for 2,2',4,4',5-pentabromodiphenyl ether(2). Human milk concentrations of 0.23-1.9, not detected to 27.2, and 0.05-5.14 ng/g lipid were reported in the countries of Canada, Japan, and Sweden, respectively, for 2,2',4,4',6-pentabromodiphenyl ether(2).

ENVIRONMENTAL: 2,2',4,4',5- and 2,2',4,4',6-Pentabromodiphenyl ether breast milk concentrations over time in Northern Hemisphere populations(1).

ENVIRONMENTAL: Milk samples were collected in 2003 from 40 first-time mothers with 2- to 8-week-old infants and residing in urban areas in the Pacific Northwest of the U.S. (Montana, Oregon, and Washington State) and Canada (British Columbia). Mean and median total concentrations of 12 tri- thru decabromodiphenyl congeners were 96 and 50 ng/g lipid weight, respectively. 2,2',4,4',5-Pentabromodiphenyl ether was found at 5.4 ng/g lipid weight and 2,2',4,4',6-pentabromodiphenyl ether was found at 5.3 ng/g lipid weight. Breast milk was collected from 12 primiparous 24 to 33 year-old nursing women in Japan, at 1 month after delivery and analyzed for six tri- to hexabrominated diphenyl ethers. The sum of the concentrations of six tri- to hexabromodiphenyl ethers ranged from 0.7 to 2.8 ng/g lipid weight. There was a strong positive relationship between total polybrominated diphenyl ether levels in human milk and the frequency of fish consumption. In Japan, 16 tri- to heptabrominated diphenyl ethers were analyzed in eight pooled human milk samples collected between 1973 and 2000. Polybrominated diphenyl ethers were not detected in the samples from 1973 at the limit of detection of 0.01 ng/g lipid weight. In 2000, the sum of the concentration of these polybrominated diphenyl ethers was 1.4 ng/g lipid weight and 2,2',4,4',5- and 2,2',4,4',6-pentabromodiphenyl ethers were reported at approximately 0.2 ng/g lipid weight each. The breast milk concentrations of five congeners tetra- thru hexabromodiphenyl ethers were determined in samples from 93 primiparous women collected from 1996 to 1999 in Uppsala County, Sweden. The women ranged in age from 20-35 years. 2,2',4,4',5-Pentabromodiphenyl ether was reported at 0.6 ng/g lipid weight and 2,2',4,4',6-pentabromodiphenyl ether was reported at 0.4 ng/g lipid weight. No significant relationship was found between breast milk concentrations of polybrominated diphenyl ethers and dietary intakes of polybrominated diphenyl ethers (through fish, meat/poultry, dairy products, and egg consumption), age, body mass index, alcohol consumption, or computer usage. After adjustments for these factors, a weak but significant association between polybrominated diphenyl ether concentrations and smoking was observed. Time-trend analysis for samples collected between 1996 and 2001 indicated a peak in total polybrominated diphenyl ether concentrations around 1998, followed by decreasing levels. Pooled samples of breast milk collected at eight time periods between 1972 and 1997 from primiparous Swedish women were analyzed for tri- to hexabromodiphenyl ethers. In 1997, 2,2',4,4',5-pentabromodiphenyl ether was reported at approximately 0.5 ng/g lipid weight and 2,2',4,4',6-pentabromodiphenyl ether was reported at 0.4 ng/g lipid weight. The sum of the concentrations of these polybrominated diphenyl ether congeners in human milk increased from 0.1 to 4.0 ng/g lipid weight during the 25-year period studied.

Like other halogenated aromatic hydrocarbons, polybrominated diphenyl ethers bind to the cellular aryl hydrocarbon receptor (AhR), which regulates the synthesis of a variety of proteins. Activation of the AhR induces a number of enzymes, including cytochrome P-450-dependent monooxygenases of the CYP1A and CYP2B families, UDP-glucuronosyltransferase, and ethoxyresorufin-o-deethylase. PBDEs are also believed to disrupt the production, transport, and disposition of thyroid hormones. One mechanism of this involves metabolites ot PDBEs competing with thyroxine to bind to transthyretin, decreasing serum thyroid hormone levels. This change in thyroid hormone levels has been linked to both thyroid toxicity and neurobehavioral alterations. Certain PDBEs and their metabolites are also endocrine disruptors and may act as agonists at the estrogen receptors or antagonists at the androgen and progesterone receptors. (L628, A262)

Normal fish intake in Sweden is about 30 g/day, and, if herring is used as a model fish, this will give an estimate of intake of about 0.1 ug pentabromodiphenyl ether/person per day(1). The average intake for breast-fed infants is reported as 0.05 ug/kg/day, for the general population as 0.01 ug/kg/day, for children with parents working in polybromodiphenyl ether manufacturing as 0.9 ug/kg/day and in local residents near production facilities as 48 ug/kg/day(2).

(a) Chemical substances and significant new uses subject to reporting. (1) The chemical substances identified as tetrabromodiphenyl ether, pentabromodiphenyl ether, hexabromodiphenyl ether, heptabromodiphenyl ether, octabromodiphenyl ether, and nonabromodiphenyl ether, or any combination of these substances resulting from a chemical reaction are subject to reporting under this section for the significant new uses described in paragraph (a)(2) of this section. (2) The significant new use is manufacture or import for any use on or after January 1, 2005. (b) Specific requirements. The provisions of subpart A of this part apply to this section except as modified by this paragraph. (1) Persons who must report. Section 721.5 applies to this section except for section 721.5(a)(2). A person who intends to manufacture or import for commercial purposes a substance identified in paragraph (a)(1) of this section and intends to distribute the substance in commerce must submit a significant new use notice.

Section 8(a) of TSCA requires manufacturers of this chemical substance to report preliminary assessment information concerned with production, exposure, and use to EPA as cited in the preamble in 51 FR 41329. Effective date 1/11/90; Reporting date: 3/12/90.

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. Pentabromodiphenyl ether is included on this list. Effective date 1/11/90; Sunset date: 6/30/98.

... Zebrafish (Danio rerio) embryos were exposed to a low concentration (0, 1, 3, and 10 ug/L) of DE-71 from fertilization to 14 days thereafter. The whole-body content of thyroid hormone and transcription of genes in the hypothalamic-pituitary-thyroid (HPT) axis were analyzed. Exposure to up to 10 ug/L of DE-71 significantly reduced thyroxine (T4) levels and significantly up regulated the transcription of corticotrophin-releasing hormone (CRH) and thyroid-stimulating hormone (TSHbeta) genes in a concentration-dependent manner. The transcription of genes involved in the synthesis of TH proteins, sodium/iodide symporter (Slc5a5), and thyroglobulin (TG) and the transcription of marker genes associated with early thyroid development (Pax8 and Nkx2.1) were significantly up regulated upon DE-71 exposure. The expression of thyronine deiodinase (Deio1 and Deio2) mRNAs was also significantly up regulated, possibly as a compensatory response to the decreased T4 levels. However, DE-71 exposure resulted in the down regulation of transthyretin (TTR) gene transcription and did not affect the transcription of thyroid hormone receptors (TRs). Exposure to DE-71 significantly induced the transcription of the uridinediphosphate-glucuronosyltransferase (UGT1ab) gene. The results of /the/ study confirmed the reliability of the zebrafish larvae as models for assessment of the developmental toxicity of PBDEs and transcription of genes of the HPT axis can evaluate the potential mechanisms of thyroid disruption. /DE-71/

In a study primarily designed to investigate the binding of polyBDE-OH metabolites to human transthyretin (T4-TTr) groups of Wistar rats were pre-treated with stimulants of hepatic xenobiotic metabolism. Once day post pre-treatment animals were sacrificed, the livers excised and hepatic microsomes prepared. The microsomes were subsequently incubated in vitro with 1 of 2 pure congeners of pentaBDPE (BDE-47 or BDE-99) (concentration not reported) in the presence of NADPH for 30 min. The microsomes suspension was then used in T4-TTr competion binding studies. The limited results presented (qualitative tabulated information only) indicate that both BDE-47 and BDE-99 inhibit T4-TTr binding in penobarbitol induced microsomes by approx. 60 and 20%, respectively suggesting that the parent molecule may be metabolized to hydroxylated metabolites. /BDE-47 and BDE-99/

Groups of 6 conventional and 6 bile-cannulated Sprague-Dawley rats were administered a single oral dose of 2.2 mg/ rat 2,2',4,4',5-{14C}pentaBDPE (BDE-99) in peanut oil. Urine, feces, and bile (from cannulated animals) were collected at 24 hr intervals over a 72 hr period post-dosing. ... Chromatographic analysis of the bile indicated the presence of 4 metabolites; two monohydroxy pentabromodiphenyl ethers and two dihydroxy pentabromodiphenyl ethers. No glucuronide or sulfate conjugates were identified. ... Of the radioactivity measured in the feces of conventional rats only 72% could be extracted for chromatographic analysis of its nature. Analysis indicated that >90% of the recovered radioactivity was present as parent BDE-99. The remaining recovered radioactivity was determined as being 1 of 4 metabolites, these being: two monomethyoxy pentabromodiphenyl ethers or two debrominated monomethoxy tetrabromodiphenyl ethers.

Polybrominated biphenyls can be absorbed through oral, inhalation, and dermal routes. Once in the body they distribute throughout and bioaccumulate in the blood, breast milk, and adipose tissue. The extent of PBDE metabolism depends on the degree of bromination. Metabolism is believed to involve debromination and methylation, resulting in phenolic metabolites. Metabolized and unmetabolized PDBE compounds are excreted mainly in the faeces. (L628, L881)

The substance accumulates in fat tissues and can be excreted in breast milk.

... As part of a larger study examining the effects of PBDEs on mink (Mustela vison) reproduction and development, ... congener-specific tissue distribution, maternal transfer, biotransformation, and biomagnification of the technical penta-BDE mixture, DE-71, /were examined/ in farmed mink. Adult female mink were fed one of four concentrations of DE-71 (0-2.5 ug/g) in the diet from breeding through gestation and until weaning at 6 weeks postparturition. Parent PBDEs were measured in tissues and excreta of adult mink, kits, and juveniles, whereas hydroxylated PBDEs (OH-PBDEs) were measured in juveniles only. Similar lipid-normalized concentrations of PBDEs were detected in most tissues of adult mink with the exception of brain, in which concentrations were significantly lower. Kits, however, had a higher proportion of PBDEs in brain compared with adults, presumably because of incomplete development of the blood-brain barrier. Maternal transfer favored lower-brominated PBDE congeners, and the bulk of the body burden in kits at weaning resulted from lactational rather than transplacental transfer. Lipid-normalized, whole-body biomagnification factors ranged from 0.5 to 5.2 for the major congeners and were highest for BDEs 47 and 153. Metabolism clearly limited the biomagnification of some PBDEs, and OH-PBDEs were detectable in plasma, liver, and feces. On a mass basis, OH-PBDEs accounted for 28 to 32% of the excreted fraction, indicating metabolism was an important elimination pathway. /DE-71/

Using rats as a model, ... tissue distribution of PBDEs /was investigated/ after oral administration and ... a suitable matrix /was evaluated/ for body burden estimation. Male rats were administered dust or corn oil containing 8 or 6 ug PBDEs/kg bw, respectively, in the diet for 21 days (N=4 rats per treatment), and the concentration of 15 PBDEs were measured in various tissues, plasma, and feces. PBDEs were found in all tissues, including the brain, and showed no difference in distribution patterns between treatments for most PBDEs. Tri- to hexa-BDEs comprised >80% of the total PBDEs in the adipose, brain, kidney, lung, and residual carcass, but <40% in the liver and plasma. The ratio of the lipid-weight concentration of tri- to hexa-BDEs in adipose tissue, residual carcass, and plasma was 1:1:2. For the hepta- to nona-BDEs, lipid-weight concentrations increased from adipose tissue to residual carcass to plasma in the ratio 0.3:1:>4. BDE-209 was the dominant congener in the liver and plasma, but was not detected in the adipose tissue or carcass. In summary, the lower brominated congeners tended to distribute equally into lipids implying both adipose tissue and plasma would be suitable matrices for biomonitoring. Plasma was the best matrix for detection of the higher brominated congeners (especially BDE-209), although on a lipid-weight basis tended to overestimate the total body burdens.

Male and female rats were given a single oral dose of 300 mg/kg Bromkal 70 in peanut oil. Control groups were given vehicle only. Groups of 4 rats of either sex were sacrificed at weekly intervals up to 10 weeks post-dosing for HPLC and GC/MS analysis of the brominated diphenyl ether content of perirenal fat. The results showed the presence of two isomers of pentaBPDE in the perirenal fat, pentaBDPE1 and pentaBDPE2, in addition to tetra- and hexabromodiphenyl ethers. The half-lives of elimination of the pentaBDPE isomers ranged from 25-47 days in males and females respectively. These results provide evidence that pentaBDPE is absorbed across the GI tract with subsequent distribution to adipose tissue from where it is slowly eliminated ... /Bromkal 70/

For more Absorption, Distribution and Excretion (Complete) data for Pentabromodiphenyl ethers (8 total), please visit the HSDB record page.

Used as additive flame retardant; [HSDB]

Use is severely restricted in the EU; [eChemPortal: ESIS]

The commercial pentaBDE product is used predominantly (95-98%) for flame retardant purposes as an additive in consumer products manufactured by the furniture industry (ENVIRON 2003a). It is used almost exclusively for flame retard flexible polyurethane foam (FPUF), which is used in bed mattresses and cushioning in upholstered products. The commercial pentaBDE is typically used in FPUF as an additive mixture with aromatic phosphate esters (e.g., mixture of 75% pentaBDE and 25% aromatic phosphate esters).

/Pentabromodiphenyl ether is used/ as a flame retardant additive in flexible polyurethane foam for furniture and upholstery. Other reported uses include as a flame retardant additive in epoxy resins, phenolic resins, unsaturated polyesters and textiles.

A small percentage is used in commercial adhesive products.

Polybrominated diphenyl ethers (PBDEs) are flame-retardant man-made chemicals found in plastics used in a variety of consumer products to make them difficult to burn. Pentabromodiphenyl ethers are most commonly used as a flame retardant in flexible polyurethane foam. (L628, L701)

Benzene, 1,1'-oxybis-, pentabromo is listed as a High Production Volume (HPV) chemical (65FR81686). Chemicals listed as HPV were produced in or imported into the U.S. in >1 million pounds in 1990 and/or 1994. The HPV list is based on the 1990 Inventory Update Rule. (IUR) (40 CFR part 710 subpart B; 51FR21438).

Production volumes for non-confidential chemicals reported under the Inventory Update Rule. [Table#6726]

The commercial pentaBDE product is produced by the direct bromination of diphenyl ether using a Friedel-Crafts catalyst. The mixture is a viscous liquid or semi-solid at ambient temperature and is supplied drummed as either the pure product or blended with a phosphate ester additive.

Composition of commercial brominated diphenyl ethers. Product: Pentabromodiphenyl ether: 0-1% tribromodiphenyl ether, 24-38% tetrabromodiphenyl ether, 50-62% pentabromodiphenyl ether and 4-8% hexabromodiphenyl ether. /Commercial pentabromodiphenyl ether/

The DE-71 mixture was analyzed on GC/LRMS (gas chromatography/low resolution mass spectrometry) in the NCI (negative chemical ionization) mode (HP5890 GC coupled to a HP MSD) monitoring at m/z 79 and 81 with methane as the chemical ionization gas. The DE-71 mixture contained on a weight basis 0.23% BDE-28 (tri-BDE), 31.8 % BDE 47 (tetra-BDE), 50.9% BDE-99 (penta-BDE), 9.1% BDE-100 (penta- BDE), 3.9% BDE-153 (hexa-BDE), 3.8% BDE-154 (hexa-BDE), 0.2% BDE- 183 (Hepta-BDE).

The dominant congeners in pentaBDE (percent weight basis in parenthesis) are BDE 99 /2,2',4,4',5-pentabromodiphenyl ether/ (35-50%), BDE 47 /2,2',4,4'-tetrabromodiphenyl ether/ (25-37%), BDE 100 /2,2',4,4',6-penta-bromodiphenyl ether/ (6-10%), BDE 153 /2,2',4,4',5,5'-hexa-bromodiphenyl ether/ (3-5%), and BDE 154 /2,2',4,4',5,6'-hexa-bromodiphenyl ether/ (2-4%).

46 congeners for Pentabromodiphenyl ether /From table/

Great Lakes Chemical Corporation (GLCC) is the sole producer of commercial pentaBDE and offers 4 commercial products. The four products are Great Lakes DE-60F Special, DE-61, DE-62, and Great Lakes DE-71, where the number indicates the percent total bromine by weight.

Benzene, 1,1'-oxybis-, pentabromo deriv.: ACTIVE

... /Hexabromodiphenyl ether/ is a component of ... pentabromodiphenyl ether (PeBDE) ... at concentrations ranging from 4 to 12%.