데카브로모디페닐에테르

Other Classes -> Halogenated Polyaromatics

Polybrominated diphenyl ether

Plastics -> N.a.

Plastics -> Flame retardants

log Kow = 9.97 /HPLC method/

6.27

9.56

3 (NTP, 1992) - Denser than water; will sink

3.4

Relative density (water = 1): 3.0

Yellow prisms from toluene

White powder

less than 1 mg/mL at 68 °F (NTP, 1992)

In water, <1.0X10-4 mg/L at 25 °C /OECD Guideline 105 (Water Solubility)/

Solubility (wt%): 0.05 acetone; 0.1 toluene; 0.48 benzene; 0.42 methylene bromide; 0.87 xylene

Solubility in water: none

This chemical does not meet GHS hazard criteria for 71.3% (191 of 268) of all reports.

Warning

H302 (10.8%): 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 268 reports by companies from 11 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Danger

Chemical: Benzene, 1,1'-oxybis[2,3,4,5,6-pentabromo-

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

Hazard Traits - Bioaccumulation; Environmental Persistence

Regulation (EC) No 178/2002 (amended)

Benzene, 1,1'-oxybis[2,3,4,5,6-pentabromo- is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Benzene, 1,1'-oxybis[2,3,4,5,6-pentabromo- are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

R - indicates a substance that is the subject of a TSCA section 6 risk management rule.

Flash point data for this chemical are not available; however, it is probably combustible. (NTP, 1992)

Not combustible.

A skin, eye, mucous membrane, and respiratory tract irritant; May cause kidney and liver injury; [CAMEO] Low acute oral toxicity in animal experiments; [HSDB] An irritant; Targets spleen, thyroid, liver, and kidneys; [MSDSonline] Practically nontoxic on acute toxicity testing; Not considered a reproductive hazard; Lesions of the liver, kidney, and thyroid gland in high-dose, subchronic feeding studies of rats; [AIHA] In high-dose animal experiments, polybrominated diphenyls (PBDEs) cause increased cancer, reproductive toxicity, and behavioral changes. Several human studies found associations between PBDE serum levels and reproductive adverse effects. [Reference #1]

European Chemicals Bureau; European Union Risk Assessment Report, Bis(pentabromophenyl) ether (1163-19-5) (July 2002).[Available from, as of October 9, 2008: http://esis.jrc.ec.europa.eu/]

US EPA; Toxicological Review of Decabromodiphenyl Ether (BDE-209) (CAS No. 1163-19-5) In Support of Summary Information on the Integrated Risk Information System (IRIS) (June 2008)[Available from, as of Septermber 12, 2008: http://www.epa.gov/ncea/iris/subst/0035.htm]

National Academies of Science/Commission on Life Sciences; Toxicological Risks of Selected Flame-Retardant Chemicals (2000)[Available from, as of November 4, 2008: http://books.nap.edu/openbook.php?record_id=9841&page=84]

DHHS/NTP; Toxicology & Carcinogenesis Studies of Decabromodiphenyl Oxide in F344/N Rats and B6C3F1 Mice (Feed Studies) Technical Report Series No. 309 (1986) NIH Publication No. 86-2565[Available from, as of April 4, 2003: http://ntp.niehs.nih.gov/ntp/htdocs/LT_rpts/tr309.pdf]

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. Decabromodiphenyl ether is included on this list. Effective date 1/11/90; Sunset date: 6/30/98.

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. A water spray may also be used. (NTP, 1992)

In case of fire in the surroundings, use appropriate extinguishing media.

Fresh air, rest.

Rinse and then wash skin with water and soap.

Rinse with plenty of water (remove contact lenses if easily possible).

Rinse mouth. Give one or two glasses of water to drink.

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

TIH (Toxic Inhalation Hazard) - Term used to describe gases and volatile liquids that are toxic when inhaled. Some are TIH materials themselves, e.g., chlorine, and some release TIH gases when spilled in water, e.g., chlorosilanes. [ERG 2016].

Wear self contained breathing apparatus for fire fighting if necessary.

Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Avoid breathing dust.; Environmental precautions: Do not let product enter drains.; Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

SMALL SPILLS AND LEAKAGE: If you spill this chemical, you should dampen the solid spill material with water, then transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: 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 air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contaminated packaging: Dispose of as unused product.

Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday

Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

Five composite samples of the fiscal year 1987 National Human Adipose Tissue Survey(FY87 NHATS) were analyzed for decabromodiphenyl ether(1). Concns of this compound ranged from 73 to 140 pg/g (lipid basis)(1). 3 of 5 selected human adipose tissue samples from the FY87 NHATS contained decabromodiphenyl ether(1). A study of 48 composite samples from the FY87 NHATS contained decabromodiphenyl ether at concns of 5 to 20 pg/g (lipid basis) (38 of 48 samples contained undetectable concentrations of this compound)(1). Decabromodiphenyl ether was detected at concns up to 5 ppb in human hair in communities near the bromine industry in Magnolia and El Dorado, AK(2). Decabromobiphenyl ether was found in human adipose tissue obtained from a hospital in Osaka, Japan(3). Blood serum concentrations of decabromodiphenyl ether in hospital cleaners (n=20), computer clerks (n=20) and electronics dismantlers (n=19) ranged from <0.3 to 3.9, <0.3 to 8.0, and <0.3 to 9.9 pmol/g lipid, respectively(4). Decabromodiphenyl ether was present in nearly all blood serum samples collected during this study(4). Decabromodiphenyl ether was analyzed in breast milk from 23 mothers in Dallas, TX and detected in 7 at concentrations of less than detection limit to 8.24 ng/g lipid(5). Decabromodiphenyl ether was detected in the serum of computer tech, test facility workers, shredder workers, smelter workers, rubber polybromodiphenyl ether mixers, wire manufacturers, and abattoirs at 1.5, 2.9, 3.8, <0.1, 1.2-145, 7.3-278, and 0.92-9.3 pmol/g lipid, industries in Sweden(6). In 1999, 19 full time computer technicians had serum levels of decabromodiphenyl ether of <2-7.1 pmol/g lipid weight(7). Serum from US blood donors in 1988 contained decabromodiphenyl ether at a concn range of <1-35 pmol/g lipid weight(8).

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.

The aim of this study was to see how a mixture of cadmium (Cd) and decabrominated diphenyl ether (BDE209) affect thyroid function, namely thyroid-stimulating hormone (TSH), thyroxin (T4), free thyroxin (FT4), triiodothyronin (T3), and free triiodothyronin (FT3) in Wistar rats (eight per group) receiving either a single substance or their combination by gavage for 28 days. Three groups were receiving Cd alone in the doses of 2.5 mg/kg, 7.5 mg/kg, or 15 mg/kg bw a day, three groups were receiving BDE209 in the doses of 1000 mg/kg, 2000 mg/kg, or 4000 mg/kg bw a day, while nine groups were receiving different mixtures of Cd and BDE209 in these doses (3x3 design). The results have indicated that the Cd+BDE209 mixtures more potently disrupt thyroid hormone homeostasis than would be expected from these chemicals alone.

Decabromodiphenyl ether (BDE-209) and its commercial alternative decabromodiphenyl ethane (DBDPE) are two structurally similar brominated flame retardants, with evidence of their ubiquitous existence in aquatic ecosystems. The present study was conducted to investigate the hepatic oxidative stress inducing potential of BDE-209, DBDPE, and their mixture in Carassius auratus after exposure to different doses (10, 50 and 100 mg/kg) for 7, 14 and 30 days. Results showed that oxidative stress was evoked evidently for the experimental groups with longer exposure duration, as indicated by significant inhibition in the antioxidant enzymes activities and decrease in the reduced glutathione level, as well as simultaneous elevation of lipid peroxidation level measured by malondialdehyde content. In addition, it was found that BDE-209 possessed a higher oxidative stress inducing ability than DBDPE. Considering the more pronounced antioxidant responses in combined exposure, the interaction of BDE-209 and DBDPE was presumed to be additive action.

Polybrominated diphenyl ether (PBDE) flame retardants are ubiquitous in the environment and in humans. A deca-bromodiphenyl ether mixture (deca-BDE) is the dominating commercial PBDE product today. Deca-BDE is degraded by UV to PBDEs with fewer bromines. We hypothesized that photodegradation of deca-BDE results in the formation of free radicals. We employed electron paramagnetic resonance (EPR) with spin trap agents to examine the free radicals formed from UV irradiation of a deca-BDE mixture (DE-83R). The activating wavelength for deca-BDE photochemistry was in the UVA to UVB range. The yields of radicals from irradiated deca-BDE in tetrahydrofuran, dimethylformamide, and toluene were about 9-, 4-, and 7-fold higher, respectively, than from irradiated solvent alone. Radical formation increased with deca-BDE concentration and irradiation time. The quantum yield of radical formation of the deca-BDE mixture was higher than with an octa-BDE mixture (DE-79; approximately 2-fold), decabromobiphenyl (PBB 209; approximately 2-fold), decachlorobiphenyl (PCB 209; approximately 3-fold), and diphenyl ether (DE; approximately 6-fold), indicating the positive effects of bromine and an ether bond on radical formation. Analysis of hyperfine splittings of the spin adducts suggests that radical formation is initiated or significantly enhanced by debromination paired with hydrogen abstraction from the solvents. To our knowledge this is the first study that uses EPR to demonstrate the formation of free radicals during the photolytic degradation of PBDEs. Our findings strongly suggest the potential of negative consequences due to radical formation during UV exposure of PBDEs in biological systems.

Globally, brominated diphenyl ether-209 (BDE-209) is the most widely used polybrominated diphenyl ether (PBDEs). It has been reported that BDE-209 induces developmental neurotoxicity in vivo. The purpose of this study was to use an antioxidant, N-acetylcysteine (NAC), as an antidote for the neurotoxic effect of BDE-209. We used primary hippocampal neurons from rats for the in vitro cultures. BDE-209 was added to the cultures in increasing concentrations and co-cultured with NAC in order to assess the effect of NAC on BDE-209-induced neurotoxicity. We measured cell viability, apoptosis, expression of phosphorylated p38 mitogen-activated protein kinases (MAPK), intracellular calcium content, and intracellular reactive oxygen species (ROS) levels. The difference between the BDE-209 groups without NAC and the blank control groups was significant (P<0.05). The difference between the NAC treatment groups and the BDE-209 groups without NAC was also significant (P<0.05), showing that BDE-209 increased apoptosis, the expression of p38 MAPK, the calcium ion concentration, and the ROS level and decreased cell viability. In contrast, NAC reduced the degree of cellular cytotoxicity induced by BDE-209. The results suggested that NAC may be able to attenuate BDE-209-induced neurotoxicity.

LC50; Species: Eisenia fetida (Earthworm) mature organism; environmental exposure using filter paper >1000 ug/sq cm

LC50; Species: Oryzias latipes (Japanese medaka); Concentration: >500 mg/L for 48 hr /Conditions of bioassay not specified in source examined/

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 2.8X10+5(SRC), determined from a structure estimation method(2), indicates that decabromodiphenyl ether is expected to be immobile in soil(SRC). Volatilization of decabromodiphenyl ether from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.2X10-8 atm-cu m/mole(SRC), using a fragment constant estimation method(2). Decabromodiphenyl ether is not expected to volatilize from dry soil surfaces(SRC) based upon an extrapolated vapor pressure of 6.96X10-11 mm Hg(3). A 0% of theoretical BOD using activated sludge in the Japanese MITI test indicates that decabromodiphenyl ether is not readily biodegradable(4). A soil degradation study found that soils spiked with 1, 10, and 100 mg/kg decabromodiphenyl ether showed no degradation after 160 days of incubation(5). Anaerobic biodegradation is very slow(5). In the absence of sunlight, the compound persists in soils and sediments(6). In sunlight, decabromodiphenyl ether readily photodegrades to the lower brominated congeners (such as tetra- and hexabrominated biphenyl ethers) which can bioaccumulate(7). The extrapolated primary degradation half-life in sludge-amended soil under both aerobic and anaerobic conditions was found to be >360 days assuming exponential decay(8).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 2.8X10+5(SRC), determined from a structure estimation method(2), indicates that decabromodiphenyl ether 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 1.2X10-8 atm-cu m/mole(SRC), developed using a fragment constant estimation method(2). According to a classification scheme(4), BCF values of 0.3 to <50(5-7), suggest the potential for bioconcentration in aquatic organisms is low(SRC). A 0% of theoretical BOD using activated sludge in the Japanese MITI test indicates that decabromodiphenyl ether is not readily biodegradable(7). A soil biodegradation study found that decabromodiphenyl ether showed no degradation after 160 days of incubation(8). Anaerobic biodegradation is very slow(8). In the absence of sunlight, decabromodiphenyl ether persists in sediments(9). Photodegradation may occur in the surface layer of water(10,11). In sunlight, decabromodiphenyl ether readily degrades to the lower brominated congeners (such as tetra- and hexabrominated biphenyl ethers) which can bioaccumulate(8). Decabromobiphenyl ether does not hydrolyze in water(8).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), decabromodiphenyl ether, which has an extrapolated vapor pressure of 6.96X10-11 mm Hg at 25 °C(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase decabromodiphenyl ether may be removed from the air by wet and dry deposition(SRC). Photodegradation of decabromodiphenyl ether may occur in the atmosphere, where decabromodiphenyl ether is likely to be adsorbed onto atmospheric particulates(3). Theoretically, direct photodegradation may be fairly rapid(SRC) based upon studies with sunlight irradation(3-5). However, photodegradation of atmospheric particulate matter is difficult to assess(SRC). Global monitoring that has detected decabromodiphenyl ether at numerous remote sites around the world indicate that decabromodiphenyl ether is transported long distances through the atmosphere(6-9) suggesting that atmospheric photodegradation is not a rapid fate process for decabromodiphenyl ether(SRC).

A market basket study conducted in Osaka, Japan in 2012 detected decabromodiphenyl ether in sugar and confectionary (153 pg/g), oils and fats (75.9 pg/g wet wt), legumes and their products (74.6 pg/g), fish, shellfish and their products (31.8 pg/g wet wt), meat and eggs (87.2 pg/g wet wt) and seasonings and other processed foods (186 pg/g)(1). Decabromodiphenyl ether was detected in US baby foods at median cocnentrations of 26.5, 14, 41 pg/g fresh wt in baby formula, cereal and puree, respectively(2).

The substance can be absorbed into the body by inhalation.

Oral (L628) ; inhalation (L628) ; dermal (L628)

ENVIRONMENTAL: Decabromodiphenyl ether was analyzed in breast milk from 23 mothers in Dallas, TX and detected in 7 at concentrations of not detected to 8.24 ng/g lipid(1). Human milk samples collected in Beijing in 2011 (103 samples) contained median decabromodiphenyl ether concentrations of 2.14 and 1.44 ng/g in urban and suburban samples respectively(2).

ENVIRONMENTAL: The findings /reported/ from a recent survey of the levels of decabromodiphenyl ether in human milk and commercial foods from Canada. The analysis of decabromodiphenyl ether in these samples was reported to be difficult, and the presence of decabromodiphenyl ether in laboratory blanks made quantification in the samples uncertain. However, little or no decabromodiphenyl ether could be detected in 72 human milk(1).

ENVIRONMENTAL: ... The breast milk was obtained from /39/ primiparous mothers from Uppsala county, Sweden aged 22 to 36 years. The year of the collection was not indicated, however the study is part of a current and ongoing investigation on persistent and organic pollutants in blood and breast milk from mothers planning to include 250 mothers. The women had to answer a questionnaire focusing on the present pregnancy, including symptoms, dietary habits and other habits (including smoking and alcohol consumption). The levels of polybromodiphenyl ethers detected in the breast milk samples were generally within 1,000 to 10,000 pg/g fat weight with one individual presenting a high peak value (28,170 pg/g fat). ... Within this small group of samples there was no correlation between the concentrations of polybromodiphenyl ethers and the mothers' age, the alcohol or the fish consumption, the place of residence or the birth weight of the child, the computer usage frequency although an increase in concentration with increasing cigarette smoking was suggested. However it is not established if smoking habits is a causal effect for the increase of polybromodiphenyl ethers in human breast milk. No data on /decabromobiphenyl ether/ were reported. ... /Polybromodiphenyl ethers/

ENVIRONMENTAL: Breast-milk excretion is one of the concerns for some PBDPOs and at least for PeBDPOs, it was deemed useful to include in this report the available data on PBDPOs breast-milk excretion. Studies which focused mainly on analytical techniques and extraction and purification methods, samples of human milk were analyzed for PBDPO content. The milk was collected during different periods from 1972 to 1997 and supplied by the Mothers' Milk Centre in Stockholm. The milk samples were collected from differing numbers (ranging from 20 to 116) of women with an average age between 27 and 31 years, over a 25-year period from 1972 to 1997. TriBDPO, TeBDPOs, PeBDPOs and HxBDPOs congeners were differentiated. Recovery studies were performed by adding a standard solution of TriBDPOs, TeBDPOs, PeBDPOs and HxBDPO to one of the samples before extraction.. The average recoveries of these substances ranged from 86 to 102% except for one internal standard with a recovery of 70-111%. /Polybromobiphenyl ethers/

For more Milk Concentrations (Complete) data for DECABROMODIPHENYL ETHER (6 total), please visit the HSDB record page.

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. Decabromodiphenyl ether is included on this list. Effective date 1/11/90; Sunset date: 6/30/98.

T4 levels in the blood of C57BL6/J mice /were evaluated/ (1 male, 1 female/litter) on PND 21 following exposure to 0.6 or 20 mg/kg-day BDE during postnatal days 2-15. In this instance, there was a dose-related reduction in the T4 levels for males but not females. Despite the possibility of thyroid hormone involvement in the neurodevelopmental impact of BDE-209 on the habituation response in male mice exposed to a single dose on postnatal day 3, there are no mode-of-action data that link thyroid hormones to the neurobehavioral observations reported.

The interference of decaBDE with thyroid hormone homeostasis /was evaluated/ in weanling rats exposed to decaBDE (>98% purity) up to 100 mg/kg-day for 4 consecutive days. Results indicated that decaBDE did not affect hepatic enzyme activities or serum T4, T3, TSH, and hepatic UDPGT activity at doses up to 100 mg/kg-day.

DecaBDE may share the general property of organohalogen compounds in which in vivo exposure in rodents results in reduction of serum total and free thyroid hormone (T4) levels. Thyroid hormone disruption has been hypothesized to arise from at least two different mechanisms, one of which is the induction of liver enzymes of different enzyme families, including CYP-1A1 and CYP-2B. Induction of liver UDPGTs may increase the rate of T4 conjugation and excretion, which is believed to be a mechanism for TCDD-induced thyroid effects. An increase in the metabolism of T4 will result in enhanced excretion and thus a drop in its circulating levels. The other mechanism involves alteration of thyroid homeostasis through hormone mimicry. Potential thyroid toxicants may be metabolized by liver enzymes to metabolites that compete with the thyroid transport protein, transthyretin, a key protein involved in the transport of T4 through the blood and into the developing tissues in rodents.

A large percentage of absorbed decabromodiphenyl oxide (DBDPO) appears to be rapidly metabolized in the liver and excreted in the bile with a half-life of <24 hr.

Pulmonary clearance was evaluated in rats following a single intratracheal injection of 0 or 20 mg decabromodiphenyl oxide (DBDPO) dust (purity 77.4%) suspended in rat serum. Based on determinations of total bromine content in the lungs 3, 10, 30, 91, and 365 d following exposure, the half-life for elimination of DBDPO from the lungs was estimated to be 150 d.

...The distribution and elimination half-lives of parent BDE-209 and several debrominated nonhydroxylated metabolites based on assays of plasma, excreta, liver, and carcass over a 21-day period that followed 21 days of dosing with 0.36 ug/day /were modeled/. The BDE-209 data showed the best fit to a biphasic depletion pattern. The distribution half-lives were 1.0 and 1.2 days for liver and plasma, respectively. The elimination half-lives for the same tissues were 20.2 and 75.9 days, respectively. A plasma first order half-life for octaBDE-207 (7.9 days) was twice that of BDE-209 (3.9 days). In the liver, the first order half-life estimates for congeners 208, 191, and 197 (approximately 6 days) were greater than those for 206 and 207 (approximately 1 day). First-order estimates for 207 and 196 were intermediate (4-5 days). These values reflect the behavior of the parent BDE-209 and the debrominated, nonhydroxylated metabolites after absorption, distribution, and excretion but do not reflect the distribution and elimination of the hydroxylated metabolites.

Half-lives were determined from the slope of the total concentration-time curve by linear regression. The disposition of decaBDE in male rats after oral dosing was described by a two-compartment model with t1/2 beta and t1/2 gamma values of 6.9 hours and 51 hours, respectively. The results from the i.v. study were consistent with a three-compartment model with half-lives (t1/2 alpha, t1/2 beta, and t1/2 gamma) of 1.6 hours, 12 hours, and 58 hours, respectively. This value is lower than the 15-day half-life for humans.

For more Biological Half-Life (Complete) data for DECABROMODIPHENYL ETHER (7 total), please visit the HSDB record page.

... The unconjugated phenolic fractions isolated from the feces were examined by gas chromatography/mass spectrometry (GC/MS). Methoxyhydroxylated penta- to heptabrominated diphenyl ethers were identified. ... The methoxy and hydroxy substituents were on the same phenyl ring when both were present. In addition, trace amounts of debrominated metabolites and nonaBDEs were also found in the feces and bile, indicating debromination may have been the first step in decaBDE metabolism. A small proportion of monohydroxylated metabolites was found in tissues and feces, indicating a role for reductive dehalogenation followed by an oxidation step or direct oxidative dehalogenation reactions.

About 20% of the decaBDE-derived radioactivity in urine from noncannulated rats was protein bound at 72 hours (compared to >73% not associated with protein). Eighteen percent of the bound material was bound to albumin, a serum protein with the ability to bind (nonspecific protein binding) short chain fatty acids. In cannulated rats, 18.2% of the decaBDE-derived radioactivity was unbound, and all the remaining 68.3% was associated with albumin. Two polar metabolites were noted but not identified. Under the assumption that the bound materials are less polar than the unbound materials, this observation supports the concept that a substantial portion, but not all, of the metabolites in the fecal matter originate from the bile. About 90% of the biliary radiolabel was associated with an unidentified 79-kDa protein, with the percent of bound label decreasing from 94 to 87% in bile samples pooled at 1-24 hours, 24-48 hours, and 48-72 hours. Approximately 17% of the protein-bound biliary radioactivity collected over the first 24 hours was parent compound (and the remainder was unidentified metabolites); no parent compound was detected at 48 and 72 hours. The percent of total bound label in the bile samples also declined over time. None of the label in the bile was found to be unbound.

The metabolism of unlabeled decaBDE /was evaluated/ in male rats after gavage or i.v. injection. Blood samples were collected at specific intervals for up to 6 days. Pooled plasma samples from all 6 days were extracted and decaBDE and its metabolites were quantified. Analysis of the pooled samples indicated that the major neutral compound in the plasma was unmodified decaBDE with trace amounts of three nonaBDEs. Thirteen phenolic metabolites were determined in the plasma of both the orally and i.v. dosed rats, but only three phenolic metabolites were present in sufficiently high concentration for further analysis. These metabolites were characterized as a hydroxy-octaBDE, an hydroxy-nonaBDE, and an hydroxy/methoxy hexaBDE. The relative amount of each metabolite recovered was not reported, but the concentration of phenolic radioactivity in the plasma collected 3 and 7 days after oral gavage was four times higher than that of the neutral compounds (i.e., the parent or debrominated decaBDE). The authors indicated that reductive debromination may be the first step in the metabolic pathway of decaBDE, followed by oxidation to form phenolic metabolites. It was also suggested that the hydroxy/methoxy metabolites were probably formed via an arene oxide hydrolyzed to a dihydrodiol and further rearomatized followed by a methylation reaction.

DecaBDE metabolism /was studied/ in rats given a single oral dose by gavage. Results indicated that in noncannulated rats about 90% of the dose was excreted in the feces within 3 days after a single oral dose of 14C-labeled decaBDE and the majority of this radioactivity (65%) represented decaBDE metabolites. Measurement of bile radioactivity indicated that close to 10% of the total dose was excreted in the bile during the same period, with almost all of the excreted dose in bile in the form of metabolites. Analysis of radiolabeled materials from tissues of these rats at day 3 after decaBDE administration revealed that 42% of the radioactivity in the liver represented solvent extractable lipid-bound metabolites and 30% was in the form of extractable unconjugated metabolites (4 and 26% of which were hydroxylated and neutral metabolites, respectively). Twenty-seven percent of the radiolabel could not be extracted and was tissue bound. Only 1% of the extractable material was water soluble. A larger percentage (61%) of the radioactivity in the small intestine wall was tissue bound. Lipid-bound metabolites accounted for 7% of the label, water-soluble compounds for 11%, and unbound parent or metabolites for 20%. The percentage of the radiolabel found as water-soluble compounds in the intestinal wall was 10 times greater than the water-soluble metabolites in the liver, providing some support for the hypothesis that oxidative metabolism can occur in the intestinal mucosa. Most of the radioactivity (71-80%) in the lung, adipose tissue, and kidney was unbound parent or metabolites; 15-21% represented lipid-bound metabolites, and 1.5-8% was tissue bound. Formation of adducts was indicative of covalent and/or noncovalent interactions with cellular macromolecules.

For more Metabolism/Metabolites (Complete) data for DECABROMODIPHENYL ETHER (19 total), please visit the HSDB record page.

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)

After admin of (14)C-decabromodiphenyl oxide by intragastric intubation, all (14)C activity was eliminated by way of feces within 2 days.

Several studies have demonstrated that decabromodiphenyl oxide (DBDPO) is very poorly absorbed in rats following oral exposure, generally <1% of the amount ingested.

Studies with (14)C labeled decabromodiphenyl oxide administered orally to Sprague Dawley rats indicate that more than 99% of the administered label was excreted in feces within 2 days following administration. An analysis of bromine in tissues following long term exposure in diets that provided 0.1 mg/kg per day to rats indicated a slight increase in bromine content in liver and adipose tissue at 90 days but no significant increase following 12 months of exposure. A significant increase in the bromine content of adipose, but no other tissues, was observed following a similiar dose of decabromodiphenyl oxide for 2 years but not at lower doses. There was no indication as to whether the failure of decabromodiphenyl oxide to accumulate in tissues was due to lack of absorption from the gastrointestinal tract or rapid metabolism and clearance.

Retention of decabromodiphenyl oxide in the brain of neonatal mice /had recently reported/. A single oral dose of 14(C)-labelled decabromodiphenyl oxide (purity >98%) was given on postnatal day 3, 10 or 19 to neonatal NMRI mice. Two litters in each age categories were given 1.5 14(C) MBq/kg body weight. The radioactivity in the brain was determined after 24 hours or 7 days after dosing in each of the two litters from the three different age categories. The results of the study showed that 14(C) was taken up into the brain, but there were differences in the amount of radioactivity found in the different age mice. The mice exposed on postnatal day 3 or 10 had around 4% of the total administered dose of 14(C) in the brain at 24-hours after dosing, whereas only 0.6 % of the total administered dose was found at 24-hours in the brains of mice dosed on postnatal day 19. At day-7 after administration the amount of radioactivity in the brain had increased by around a factor of 2 in the mice exposed on postnatal days 3 or 10, whereas no noticeable change in the amount of radioactivity present had occurred in brains of the mice dosed on postnatal day.

For more Absorption, Distribution and Excretion (Complete) data for DECABROMODIPHENYL ETHER (36 total), please visit the HSDB record page.

Used in high impact polystyrene and other polymers; Used as a flame retardant in thermoplastic resins, thermoset resins, textiles, and adhesives; [HSDB] Used as flame retardants since the 1970s in carpet lining, mattresses, chairs and sofas (polyurethane foam), and casings for televisions and computers; 209 congeners of polybrominated diphenyl ethers (PBDEs) exist, but only 13 are usually found in commercial mixtures; Electronic recycling workers have increased blood levels; [Reference #1]

Textiles (Fiber & Fabric Manufacturing) [Category: Industry]

Brominated additive flame retardant. ... /Used in:/ ABS: Acrylonitrile-butadiene-styrene polymers; HIPS: High-impacted polystyrene; PBT: Poly(butylene terephthalate); PE: Polyethylene; PP: Polypropylene; UPE: Unsaturated polyester. /From table/

Decabromodiphenyl oxide is an unreactive, additive flame retardant widely used for its thermal stability and its low cost in thermoplastic resins, thermoset resins, textiles and adhesives. The major applications are in high impact polystyrene, glass reinforced thermoplastic polyester and moulding resins, low density polyethylene extrusion coatings, polypropylene (homo- and copolymers), acrylonitrile butadiene styrene rubber, nylon and polyvinyl chloride.

Decabromodiphenyl ether is used as a flame retardant. It is mostly used in applications in the plastics and textile industries. It is an additive flame retardant, i.e. it is physically combined with the material being treated rather than chemically combined (as in reactive flame retardants).

The largest volume use of decabromodiphenyl ether is in high impact polystyrene that is used to manufacture television cabinets ... used in virtually every class of polymer, including ABS, engineering thermoplastics such as polyamides and polyesters, polyolefins, thermosets (i.e., epoxies and unsaturated polyesters), PVC, and elastomers. It is also widely used in textile applications as the flame retardant in latex-based back coatings.

2022: 22,000 lb

(1973) MORE THAN 5X10+5 G

(1975) MORE THAN 5X10+5 G

Production volumes for non-confidential chemicals reported under the Inventory Update Rule. [Table#4285]

Benzene, 1,1'-oxybis[2,3,4,5,6-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).[EPA/Office of Pollution Prevention and Toxics; High Production Volume (HPV) Challenge Program. Benzene, 1,1'-oxybis

For more U.S. Production (Complete) data for DECABROMODIPHENYL ETHER (6 total), please visit the HSDB record page.

Decabromobiphenyl ether is manufactured by the exhaustive bromination of phenyl ether. ... Lewis acid catalysis and an excess of bromine are used to obtain high conversions of the less reactive under-brominated intermediates to decabromobiphenyl ether.

Decabromobiphenyl ether can be prepared at atmospheric pressure by reacting bromine with phenyl ether in ethylene dibromide solvent and in the presence of aluminum bromide catalyst.

... Production of decabromodiphenyl ether is carried out by using bromine as both the reactant and reaction medium. Diphenyl ether is added to the bromine in the presence of a catalyst and the rate of addition of diphenyl ether effectively controls the rate of reaction. The reaction is a batch process and the temperature of the reaction is around the boiling point of the bromine solvent (~59 °C).

Plastics -> Flame retardants

Plastics -> Polymer Type -> N.a.

Plastics Material and Resin Manufacturing

Benzene, 1,1'-oxybis[2,3,4,5,6-pentabromo-: ACTIVE

Decabromodiphenyl oxide (DBDPO) is commonly used in conjunction with antimony trioxide, which acts as a synergist, contributing to the flame retardancy of the textile. Typically, the flame retardant mixture consists of about 66 to 75% DBDPO and 25 to 33% antimony trioxide. The amount of DBDPO added to the mixture varies depending on the desired flame-retardant properties of the fabric.

Often plastic additives may be released by leaching. However, decabromodiphenyl ether in acrylonitrile-butadiene-styrene and acrylonitrile-butadiene-styrene-polystyrene polymers did not leach into water even under conditions of elevated temperatures in the presence of 3% acetic acid (detection limit=0.5 ppm bromide).

In the 1990's, two types of flame retardants are preferred for outdoor fabrics, ... an antimony-bromine system based on decabromodiphenyl ether and antimony(III)oxide.