헥사브로모사이클로도데케인(헥사브로모사이클로도데칸)

This compound is not very flammable but any fire involving this compound may produce dangerous vapors. You should evacuate the area. All firefighters should wear full-body protective clothing and use self-contained breathing apparatuses. You should extinguish any fires involving this chemical with a dry chemical, carbon dioxide, foam, or halon extinguisher. (NTP, 1992)

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

Fresh air.

Rinse and then wash skin with water and soap.

Rinse with plenty of water (remove contact lenses if easily possible). Refer for medical attention if irritation persists.

Rinse mouth.

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.

SMALL SPILLS AND LEAKAGE: Should a spill occur while you are handling this chemical, you should dampen the solid spill material with alcohol, then transfer the dampened material to a suitable container. Use absorbent paper dampened with alcohol to pick up any remaining material. Seal the absorbent paper, and any of your clothes, which may be contaminated, in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with alcohol followed by washing with a strong soap and water solution. Do not reenter the contaminate 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.

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Then store and dispose of according to local regulations.

Median hexabromocyclododecane plasma levels in 2002 from 10 pregnant women living in Bodo, Norway were 19, 7, and 23 pg/mL plasma for the alpha-, beta-, and gamma-isomers, respectively; levels of plasma samples from 10 women living in Taimyr, Russia were 21, 8, and 33 pg/mL plasma, respectively(1). Hexabromocyclododecane levels in mothers' milk from the Stockholm, Sweden area increased from 0.13 pmol/g lipid in 1980 to 0.60 pmol/g lipid in 2004, with the highest levels reported in 2001 and 2002, 0.83 and 0.93 pmol/g lipid, respectively. Levels in Norwegian breast milk samples ranged from 0.25-2 ng/g lipids over a study period of 1986-2001(1).

The National Food Administration in Sweden has analyzed HBCDD and other substances in mother's milk from Swedish women in two different studies. The first study detected HBCDD in 12 of 33 samples. The samples were taken from primiparous, age 19-40, living in Uppsala County, Sweden, two weeks after delivery. The limit of detection was /leas than/ 15 pg HBCDD/g mothers milk (fresh weight). On a lipid weight basis, the mean and max concentrations were 0.45 and 2.4 ng/g fat, respectively(1).

Hexabromocyclododecane (HBCD) is a type of brominated flame retardant. We investigated the time trend of the stereoisomer-specific concentrations of HBCD (alpha, beta, and gamma) in breast milk samples of Japanese women by using liquid chromatography-tandem mass spectrometry (LC/MS/MS). The pooled milk lipid samples collected in 1973, 1978, 1983, 1988, 1993, 1999, and from 2000 to 2006 were analysed. The concentration was below the detection limit in the samples collected between 1973 and 1983 and increased in those collected since 1988. Between 1988 and 2006, alpha-HBCD was detected in all 11 breast milk samples collected from 25 to 29-year-old Japanese women; gamma-HBCD, in 7; and beta-HBCD, in none of the samples. Time trend of summation operatorHBCD appeared to be related to that of the industrial HBCD consumption level in Japan.

Concentrations of tetrabromobisphenol A (TBBPA) and alpha-, beta-, and gamma-isomers of hexabromocyclododecanes (HBCDs) were determined by liquid chromatography-tandem mass spectrometry (LC-ESI-MS/MS) in human adipose tissue obtained in New York City. ... The overall mean concentrations (mean+/-SD) of TBBPA and HBCDs were 0.048+/-0.102 and 0.333+/-0.571 ng/g lipid wt in human adipose tissue samples. ... Overall mean concentrations of HBCDs were 5-10-fold higher than mean TBBPA concentrations, in all of the samples analyzed. ... In the human adipose tissue samples, the concentrations of HBCDs were 3-4 orders of magnitude lower than the concentrations of polybrominated diphenyl ethers (PBDEs) previously reported for the same set of tissue samples. Concentrations of HBCDs in human samples from the United States were 1-5-fold lower than the concentrations reported from several European countries.

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.

Thyroid hormone (TH) plays an essential role in growth and differentiation of the central nervous system. Deficiency of TH during perinatal period results in abnormal brain development known as cretinism in human. We recently reported that an environmental chemical 1,2,5,6,9,10-a-hexabromocyclododecane (HBCD) suppressed TH receptor (TR)-mediated transcription. To examine the effect of HBCD on cerebellar granule cells, we used purified rat cerebellar granule cells in reaggregate culture. Low dose HBCD (10(-10)M) significantly suppressed TH-induced neurite extension of granule cell aggregate. To clarify further the mechanisms of such suppression, we added brain-derived neurotrophic factor (BDNF) into culture medium, since BDNF plays a critical role in promoting granule cell development and is regulated by TH. BDNF completely rescued HBCD-induced suppression of granule cell neurite extension in the presence of T3. These results indicate that HBCD may disrupt TH-mediated brain development at least in part due to a disruption of the T3 stimulated increase in BDNF and BDNF may possess ability to ameliorate the effect of HBCD in granule cells.

Hexabromocyclododecane (HBCD), a type of brominated flame retardants (BFR), has become ubiquitous organic contaminants in recent years. However, studies on HBCD toxicity and the related molecular mechanisms are so far limited. The objective of the present study was to investigate the effects of oligomeric proanthocyanidins (OPCs) on cytotoxicity induced by HBCD and the underlying molecular mechanisms. HepG2 cells were treated with HBCD and/or OPCs at different concentrations, and cell viability, cell apoptosis, reactive oxygen species (ROS) production, cellular Ca(2+) level, mitochondrial membrane potential, cytochrome C (Cyt-c) release, and nuclear factor-erythroid 2-related factor 2 (Nrf2) proteins expression were evaluated. Results showed that HBCD induced toxic effects in HepG2 cells in a concentration-dependent manner. HBCD at high concentrations (40 and 60 uM) caused a significant decrease of cell viability and led to elevated cell apoptosis ratio, intracellular Ca(2+) level, cytoplasmic Cyt-c level, and ROS production, together with a loss of /mitochondrial membrane potential/ and mobilization of Nrf2. Pretreatment with OPCs effectively attenuated the cytotoxic effects and ROS production, as well as mitochondrial responses induced by HBCD. Thus, OPCs could alleviate cytotoxicity in HepG2 cells induced by HBCD through regulation on intracellular Ca(2+) level and ROS formation in a mitochondrial pathway.

Proteomic effect screening in zebrafish liver cells was performed to generate hypotheses regarding single and mixed exposure to the BFRs HBCD and TBBPA. Responses at sublethal exposure were analysed by two-dimensional gel electrophoresis followed by MALDI-TOF and FT-ICR protein identification. Mixing of HBCD and TBBPA at sublethal doses of individual substances seemed to increase toxicity. Proteomic analyses revealed distinct exposure-specific and overlapping responses suggesting novel mechanisms with regard to HBCD and TBBPA exposure. While distinct HBCD responses were related to decreased protein metabolism, TBBPA revealed effects related to protein folding and NADPH production. Overlapping responses suggest increased gluconeogenesis (GAPDH and aldolase) while distinct mixture effects suggest a pronounced NADPH production and changes in proteins related to cell cycle control (prohibitin and crk-like oncogene). We conclude that mixtures containing HBCD and TBBPA may result in unexpected effects highlighting proteomics as a sensitive tool for detecting and hypothesis generation of mixture effects.

Bromine vapour causes irritation and direct damage to the mucous membranes. Elemental bromine also burns the skin. The bromide ion is a central nervous system depressant and chronic exposure produces neuronal effects. This is called bromism and can result in central reactions reaching from somnolence to coma, cachexia, exicosis, loss of reflexes or pathologic reflexes, clonic seizures, tremor, ataxia, loss of neural sensitivity, paresis, papillar edema of the eyes, abnormal speech, cerebral edema, delirium, aggressiveness, and psychoses. (L625, L626, L627)

EC50; Species: Hyalella azteca (amphipod); Conditions: flow-through, 5% total organic carbon in sediment; Concentration: >1000 mg/kg dry weight of sediment for 28 days; Effect: survival and growth (dry weight)

EC50; Species: Leuciscus idus L. (Golden orfe); Conditions: static; Concentration: >10000 mg/L for 96 hr (nominal concentration); Effect: no abnormal behavior was observed in any of the concentrations tested

EC50; Species: Daphnia magna (Water flea) neonate; Conditions: flow through, 20 +/-2 °C; Concentration: >3.2 ug/L for 48 hr; Effect: mortlaity, immobility /The test substance consisted of a composite of HBCDD samples from three manufacturers. The composite contained 8.5% beta- diastereomer, 6.0% alpha- diastereomer and 79.1% gamma- diastereomer (total HBCDD 93.6%)/

EC50; Species: Selenastrum capricornutum (algae); Conditions: freshwater, static, 24 +/-2 °C, pH ranged from 7.4-7.5 on day 0 and 8.0-8.4 on day 4; Concentration: >2.5 ug/L for 72 hr (measured concentration); Effect: growth inhibition /The test substance consisted of a composite of HBCDD samples from three manufacturers. The composite contained 8.5% beta- diastereomer, 6.0% alpha- diastereomer and 79.1% gamma- diastereomer (total HBCDD 93.6%)/

For more Ecotoxicity Values (Complete) data for HEXABROMOCYCLODODECANE (10 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 91,000(SRC), determined from a structure estimation method(2), indicates that hexabromocyclododecane is expected to be immobile in soil(SRC). Volatilization of hexabromocyclododecane from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 6.1X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 4.7X10-7 mm Hg(3), and water solubility, 0.0656 mg/L(3). However, adsorption to soil is expected to attenuate volatilization(SRC). Hexabromocyclododecane is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). Results of screening studies(3) indicate that biodegradation of hexabromocyclododecane can range from not degradable to being inherently biodegradable depending on test conditions(SRC). Aerobic soil degradation tests have determined half-lives ranging from 63-441 days(3,4). Dissipation half-lives were roughly 2-4 times longer in biologically-inhibited soil indicating that biodegradation is an important fate process(3). One microcosm study found biotransformation half-lives of 63 and 6.9 days in aerobic and anaerobic soil, respectively(4).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 91,000(SRC), determined from a structure estimation method(2), indicates that hexabromocyclododecane 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 6.1X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 4.7X10-7 mm Hg(4), and water solubility, 0.0656 mg/L(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 15.6 days and 122 days, respectively(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The estimated volatilization half-life from a model pond is >10 years if adsorption is considered(5). According to a classification scheme(6), measured BCF values of 18,200 in fathead minnows (Pimephales promelas)(7) and 8,974 in rainbow trout (Oncorhynchus mykiss)(8), suggest that bioconcentration in aquatic organisms is very high, provided the compound is not metabolized by the organism(SRC). Results of screening studies(4) indicate that biodegradation of hexabromocyclododecane can range from not degradable to being inherently biodegradable depending on test conditions(SRC). In a microcosm study using two river waters, the biotransformation half-lives of hexabromocyclododecane in aerobic and anaerobic river water were 11-32 and 1.1-1.5 days, respectively(9). Sediment half-lives of 101 and 191 days have been reported for 20 and 12 °C, respectively(10). Aqueous hydrolysis tests conducted over 39-day periods detected no hydrolysis of hexabromocyclododecane(4).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), hexabromocyclododecane, which has a vapor pressure of 4.7X10-7 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase hexabromocyclododecane 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 2.6 days(SRC), calculated from its rate constant of 6.1X10-12 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase hexabromocyclododecane may be removed from the air by wet or dry deposition(SRC). UV spectral data suggest that hexabromocyclododecane does not absorb at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC). Monitoring data from remote areas of the globe indicate that hexabromocyclododecane is subject to long-range environmental transport in the atmosphere(5,6). The majority of long-range environmental transport is likely to occur in aerosol form(5).

Home-produced eggs collected form free-foraging chickens in Belgium in 2006 and 2007 contained hexabromocyclododecane concentrations of <0.4 and 2.9 ng/g lw, respectively(1). A monitoring study comparing results from up to 13 laboratories found mean 1,2,5,6,9,10-hexabromocyclododecane concentrations (in pg/g fresh weight) in the following foods: chicken meat, 50; butter, 211(2).

Exposure mainly occurs via inhalation of dust.

Oral (L626) ; inhalation (L626) ; dermal (L626)

ENVIRONMENTAL: Average hexabromocyclododecane levels in mothers' milk from the Stockholm, Sweden area increased from 0.13 pmol/g lipid in 1980 to 0.60 pmol/g lipid in 2004, with the highest levels reported in 2001 and 2002, 0.83 and 0.93 pmol/g lipid, respectively. Levels in Norwegian breast milk samples ranged from 0.25-2 ng/g lipids over a study period of 1986-2001(1).

ENVIRONMENTAL: The National Food Administration in Sweden has analyzed HBCDD and other substances in mother's milk from Swedish women in two different studies. The first study detected HBCDD in 12 of 33 samples. The samples were taken from primiparous, age 19-40, living in Uppsala County, Sweden, two weeks after delivery. The limit of detection was /less than/ 15 pg HBCDD/g mothers milk (fresh weight). On a lipid weight basis, the mean and maximum concentrations were 0.45 and 2.4 ng/g fat, respectively(1).

ENVIRONMENTAL: ... the time trend of the stereoisomer-specific concentrations of HBCD (alpha, beta, and gamma) in breast milk samples of Japanese women by using liquid chromatography-tandem mass spectrometry (LC/MS/MS) was investigated. The pooled milk lipid samples collected in 1973, 1978, 1983, 1988, 1993, 1999, and from 2000 to 2006 were analysed. The concentration was below the detection limit in the samples collected between 1973 and 1983 and increased in those collected since 1988. Between 1988 and 2006, alpha-HBCD was detected in all 11 breast milk samples collected from 25 to 29-year-old Japanese women; gamma-HBCD, in 7; and beta-HBCD, in none of the samples. Time trend of summation operator HBCD appeared to be related to that of the industrial HBCD consumption level in Japan.

Human milk samples were collected from individuals residing in various regions across Canada ... in the years 1992 to 2005. These included five large cities in southern Canada as well as samples from Nunavik in northern Quebec. Comparative samples were also collected from residents of Austin, Texas, USA in 2002 and 2004. More than 300 milk samples were analysed for the brominated flame retardants (BFRs), PBDEs and HBCD, by extraction, purification and quantification using either isotope dilution gas chromatography-mass spectrometry (GC-MS) or liquid chromatography-MS. ...HBCD levels in most milk samples were usually less than 1ppb milk lipid and dominated by the a-isomer. This large data set of BFRs in Canadian human milk demonstrates an increase in the last few decades in human exposure to BFRs which now appears to have stabilized.

For more Milk Concentrations (Complete) data for HEXABROMOCYCLODODECANE (9 total), please visit the HSDB record page.

IDENTIFICATION AND USE: Technical products of Hexabromocyclododecane (HBCDD) predominantly consist of three stereoisomers (alpha-, beta- and gamma-HBCDD). HBCDD is a widely used brominated flame retardant. HBCDD is used in several products, some of which are available to consumers. Some examples of end-products containing HBCDD are: flat and pile upholstered furniture, upholstery seatings in transportation, draperies, and wall coverings, bed mattress ticking, interior textiles, automobile interior textiles, car cushions, insulation boards of transport vehicles, insulation boards in building constructions, parking decks, insulation boards against frost heaves of road and railway embankments, packaging material, electrical and electronic equipment, video cassette housings, polyvinyl chloride wire, cable and textile coating, protecting paints for military purposes. HUMAN EXPOSURE AND TOXICITY: 10% HBCDD did not cause human skin sensitization. Although no enantioselective enrichment was detected in either dust or diet, substantial enrichment of (-)alpha-HBCDD was observed in human serum. Serum concentrations of HBCDD were correlated with the exposure via dust, but not via dietary ingestion. The enrichment of the (-)alpha-HBCDD enantiomer in humans appears to be due to in vivo enantioselective metabolism/excretion rather than ingestion of dust or diet. HBCDD display estrogenic effects in human cells in vitro. HBCDD modulates thyroid receptor-mediated gene expression in HeLaTR cells, but only in the presence of T3. HBCDD has been tested in the in vitro mammalian cytogenetic test using human peripheral blood lymphocytes, from a healthy 40 year adult female, both in the absence and presence of metabolic activation. No statistically significant increases in structural chromosome aberrations were observed in either the non-activated or activated studies, regardless of dose level or harvest time. Nor were there any increases in numerical chromosome aberrations. Cytotoxicities of HBCDD enantiomers were evaluated in Hep G2 cells. The order of cytotoxicity was gamma-HBCDD beta-HBCDD>alpha-HBCDD. In addition, HBCDD decreases the lytic function of human natural killer (NK) cells. ANIMAL STUDIES: Toxicological studies have been carried out using different experimental designs with single or repeated administration during gestation, postnatally or in adulthood using technical HBCDD. The composition of these mixtures differs from the HBCDD profile found in wildlife and in foods. Main targets for HBCDD toxicity were the liver, thyroid hormone homeostasis, the reproductive, the nervous and the immune systems. The activation of constitutive androstane receptor- (CAR) or pregnane-X-receptor (PXR)-dependent gene expression, leading to disruption of thyroid hormone homeostasis, is considered to be associated with neurodevelopmental effects on behavior and may also be responsible for effects on reproduction. The available studies indicate that HBCDDs are not genotoxic. There is limited information from only one long-term toxicity/carcinogenicity study for HBCDDs in mice, indicating that the incidence of altered foci in the liver of males was increased, as was the incidence of liver carcinoma in females, but without a dose-relationship. ECOTOXICITY STUDIES: Environmental study demonstrates that HBCDD affects breeding behavior in American kestrels throughout the reproductive season and behavioral alterations were linked to reproductive changes (egg size). These studies suggested that birds may be more sensitive to HBCDD than mammals. Other studies indicate limited potential for in vivo endocrine disruption of the reproductive and thyroid hormonal system in immature flounder. Juvenile rainbow trout experiments indicate that all HBCDD isomers have the potential to disrupt thyroid homeostasis. In the study the embryos of marine medaka (Oryzias melastigma) HBCDD exposure at environmentally realistic concentrations induced oxidative stress and apoptosis, and suppressed nucleotide and protein synthesis, which all together resulted in developmental toxicity, particularly in the cardiovascular system, in the embryos of O. melastigma. In plants, both the inhibitory effect of the diastereoisomers on the early development of maize and the intensities of hydroxyl radical and histone H2AX phosphorylation in maize exposed to HBCDD followed the order alpha-HBCD > beta-HBCD > gamma-HBCD, indicating the diastereomer-specific oxidative stress and DNA damage in maize.

The estimated UK upper bound average dietary intake in 2004 was 413 ng total hexabromocyclododecanes/day for a 70 kg adult and 240 ng/day for a 10 kg toddler(1). The maximum daily intake for hexabromocyclododecane is 22 ng/kg/day, based on studies on food samples bought in food stores in Sweden(2). The average daily intake by the Dutch population was calculated at 2.9 ng/kg bwt/day, based on 91 samples from dairy, meat, animal fat, eggs, fish and vegetable oil(2). The estimated median daily intake of hexabromocyclododecane for a Romanian adult and toddler was estimated to be 77 and 47 ng/day, respectively, based on consumption meat products, butter, cheese, vegetable oil and eggs(3). The estimated median daily intake of hexabromocyclododecane for a Romanian adult and toddler was estimated to be 6-15 and 15-61 ng/day, respectively, based on intake of indoor house dust(3).

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. /1,2,5,6,9,10-Hexabromocyclododecane/

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. Hexabromocyclododecane is included on this list. Effective date 1/11/90; Sunset date: 12/19/95. /1,2,5,6,9,10-Hexabromocyclododecane/

Widely used brominated flame retardant

Additive to expanded and extruded polystyrene foams for thermal insulation of buildings ... to a lesser extent to high-impact polystyrene used in enclosures for electronic equipment, such as televisions.

...The use of HBCDD in polypropylene (PP), adhesives, latex binders and unsaturated polyester has been reported in the USA. ...The use of HBCDD in polypropylene (PP) is confirmed. HBCDD can be used in adhesives and coatings and in SAN resins (styrene-acrylonitrile copolymer). It may also be used in PVC (wires, cables and textile coatings).

HBCDD is used in several products, some of which are available to consumers. Some examples of end-products containing HBCDD are: flat and pile upholstered furniture, upholstery seatings in transportation, draperies, and wall coverings, bed mattress ticking, interior textiles, automobile interior textiles, car cushions, insulation boards of transport vehicles, insulation boards in building constructions, parking decks, insulation boards against frost heaves of road and railway embankments, packaging material, electrical and electronic equipment, video cassette housings, polyvinyl chloride wire, cable and textile coating, protecting paints for military purposes.

For more Uses (Complete) data for HEXABROMOCYCLODODECANE (7 total), please visit the HSDB record page.

It is a brominated flame retardant used in extruded (XPS) and expanded (EPS) polystyrene foam that is used as thermal insulation in the building industry. Diatomic bromine does not occur naturally, but bromine salts can be found in crustal rock.

Production volumes for non-confidential chemicals reported under the Inventory Update Rule.[Table#7344]

Non-confidential 2012 Chemical Data Reporting (CDR) information on the production and use of chemicals manufactured or imported into the United States. Chemical: Cyclododecane, hexabromo-. National Production Volume: Withheld.

Production volumes for non-confidential chemicals reported under the Inventory Update Rule. /1,2,5,6,9,10-Hexabromocyclododecane/[Table#7345]

Production volume for non-confidential chemicals reported under the 2006 Inventory Update Rule. Chemical: Cyclododecane, 1,2,5,6,9,10-hexabromo-. Aggregated National Production Volume: 10 to < 50 million pounds. /1,2,5,6,9,10-Hexabromocyclododecane/

For more U.S. Production (Complete) data for HEXABROMOCYCLODODECANE (7 total), please visit the HSDB record page.

End products include upholstered furniture, interior textiles, automobile interior textiles, car cushions and insulation blocks in trucks and caravans as well as in building materials such as house walls, cellars, roofs and parking decks, against frost heaving in roads and railway embankments, packing material, video cassette recorder housing and electric equipment.

(2001) World market demand ... was 16,700 tons of which about 9,500 tons was consumed in Europe.

An aliphatic, brominated cyclic alkane produced by bromination of cyclododecatri-1,5,9-ene

Technical grade HBCDD is generally produced from cis, trans, trans-1,5,9-cyclododecatriene (CDT), one of four CDT isomers, (CAS No. 27070-59-3). The reaction, trans-addition of bromine to the double bonds of CDT, results in the three diastereomers alpha-, beta- and gamma- HBCDD.

... Produced by the addition reaction of bromine to trans, trans, cis-1,5,9-cyclododecatriene, the cyclic trimer of butadiene. The hexabromocyclododecane that is obtained from this reaction consists of a mixture of stereoisomers of 1,2,5,6,9,10-hexabromocyclododecane ranging from oils to an isomer with a 205-208 °C melting point. Commercially available hexabromocyclododecane contains a mixture of solid isomers and has a melting point range of 170-180 °C (185-195 °C).

The final distribution of the diastereomers in technical HBCDD varies with a range of about 70-95% gamma-HBCDD and 5-30 % alpha- and beta-HBCDD.

Technical HBCDD is manufactured in two forms, high-melting (HM) and low-melting (LM). The low-melting HBCDD consists of 70-80% gamma-, 20-30% of alpha- and beta-HBCDD. The high-melting HBCDD consists of 90% or more of gamma-HBCDD.

According to Material Safety Data Sheets from Great Lakes /Chemical Corporation/ there are three technical products of hexabromocyclododecane. One product is 100% pure, another product contains an inorganic stabilizer, and a third product contains 40-60% HBCDD, water and a component A. The Dead Sea Bromine Group has two technical products, one which is 99.5% pure and another which is heat stabilized grade. Albemarle also has two technical products, one of high-purity grade available in powder or granular form, the other one of high-purity grade is ground to a fine particle size.

Technical products of HBCDDs (containing 73-74 % Br) predominantly consists of three stereoisomers (alpha-, beta- and gamma-HBCDD) present in relative amounts of 9-13 % alpha-HBCDD, <0.5-12 % beta-HBCDD and 72-90 % gamma-HBCDD. Apart from these three, also delta- and epsilon-HBCDD may be present in the technical product, although at very low concentrations. In addition, the commercial HBCDDs may contain 1-2 % tetrabromocyclododecene.

Cyclododecane, hexabromo-: ACTIVE

May be used as an alternative to the banned PBDE formulations