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Hexabromocyclododecane (HBCD)

Action Plan 

I. Overview

 HBCD is a brominated flame retardant found world-wide in the environment and 

wildlife. Human exposure is evidenced from its presence in breast milk, adipose tissue and 

blood. It bioaccumulates and biomagnifies in the food chain. It persists and is transported long 

distances in the environment, and highly toxic to aquatic organisms. It also presents human 

health concerns based on animal test results indicating potential reproductive, developmental and 

neurological effects. For these reasons, the Environmental Protection Agency (EPA) intends to 

consider initiating action under the Toxic Substances Control Act to address the manufacturing, 

processing, distribution in commerce, and use of HBCD. 

 

As part of the Agency's efforts to address HBCD, EPA also intends to evaluate the 

potential for disproportionate impact on children and other sub-populations. 

II. Introduction 

 As part of EPA’s efforts to enhance the existing chemicals program under the Toxic 

Substances Control Act (TSCA)1, the Agency has identified certain widely recognized 

chemicals, including HBCD, for action plan development based on their presence in humans; 

persistent, bioaccumulative, and toxic (PBT)2 characteristics; use in consumer products; 

production volume; or other similar factors. This Action Plan is based on EPA’s initial review of 

readily available use, exposure, and hazard information on HBCD. EPA considered which of the 

various authorities provided under TSCA and other statutes might be appropriate to address 

potential concerns with HBCD in developing the Action Plan. The Action Plan is intended to 

describe the courses of action the Agency plans to pursue in the near term to address its 

concerns. The Action Plan does not constitute a final Agency determination or other final 

Agency action. Regulatory proceedings indicated by the Action Plan will include appropriate 

opportunities for public and stakeholder input, including through notice and comment 

rulemaking processes. 

III. Scope of Review

HBCD is a category of brominated flame retardants, consisting of 16 possible isomers. It 

has a molecular formula of C12H18Br6 and its structure consists of a ring of 12 carbon atoms to 

which 18 hydrogen and six bromine atoms are bound. Hexabromocyclododecane may be 

designated as a non-specific mixture of all isomers (Hexabromocyclododecane; CASRN 25637-

99-4) or as a mixture of three main diastereomers (1,2,5,6,9,10-hexabromocyclododecane; 

CASRN 3194-55-6), but both commercial products essentially have the same chemical 

composition. Both CASRNs are listed on the TSCA Inventory. Commercial preparations of 

HBCD may contain some possible impurities, such as tetrabromocyclododecene or other. 

 

1 15 U.S.C. §2601 et seq. 

2 Information on PBT chemicals can be found on the EPA website at: 

http://www.epa.gov/oppt/newchems/pubs/pbtpolcy.htm
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isomeric HBCDs (UNEP, 2009). All isomers of HBCD are the subject of this Action Plan, 

irrespective of the particular CASRN or name used to identify them3

. 

IV. Uses and Substitutes Summary

Uses 

HBCD, with an 8% share in the brominated flame retardant (BFR) global market in 2001, 

is the third most commonly used BFR, following tetrabromobisphenol A (TBBPA; 

approximately 59% of the market), and decabromodiphenyl ether (deca-BDE; 26% market share) 

(Morose, 2006). 

The main use of HBCD is as a flame retardant in expanded polystyrene foam (EPS) and 

extruded polystyrene foam (XPS) (Weil and Levchik, 2009). EPS and XPS are used primarily 

for thermal insulation boards in the building and construction industry (Morose, 2006). HBCD is 

used because it is highly effective at low concentrations; EPS boards contain approximately 

0.5% HBCD by weight in the final product (Morose, 2006). 

HBCD may also be used as a flame retardant in the backcoating of textiles for 

upholstered furniture, upholstery seating in transportation vehicles, draperies, wall coverings, 

mattress ticking, and interior textiles such as roller blinds (Morose, 2006; ECHA, 2009). The 

maximum concentration of CASRN 3194-55-6 for use in fabrics and textiles and in rubber and 

plastic products ranges from 1-30% (US EPA, 2006). The majority of HBCD used in textiles is 

for upholstered furniture, in order to meet the stringent fire safety laws of the United Kingdom 

and California (Morose, 2006). However, according to the 2006 TSCA Inventory Update Rule 

(IUR) data (which includes information for chemicals manufactured and imported in amounts of 

25,000 pounds or greater at a single site), less than 1% of the total commercial and consumer use 

of HBCD was used for fabrics, textiles and apparel (US EPA, 2006). 

In addition, HBCD is used as a flame retardant in high impact polystyrene (HIPS) for 

electrical and electronic appliances such as audio-visual equipment, and some wire and cable 

applications (Morose, 2006 and ECHA, 2009). Less than 10% of all HBCD used in Europe is 

used in HIPS (ECHA, 2009). 

Production 

The annual United States (U.S.) import/production volume of CASRN 25637-99-4 was 

between 10,000 and 500,000 pounds as reported to EPA in 2002; no import/production was 

reported in 2006 (US EPA, 2006). The annual U.S. import/production volume of CASRN 3194-

55-6 was 10-50 million pounds reported in 2002 and 2006 (US EPA, 2006). The U.S. 

International Trade Commission reported that 380,000 pounds of HBCD (1,3,5,7,9,11-HBCD 

isomer) were imported in 2008 (US ITC, 2010). In 2006, five facilities reported either the 

manufacture or importation of at least 25,000 pounds of HBCD: Albemarle (2 facilities), BASF, 

LG Chem America and Chemtura (US EPA, 2006). 

 

3

 For example, The U.S. International Trade Commission December 2009 Publication 4121 reports importation of 

the 1,3,5,7,9,11-HBCD isomer which would be subject to this action plan. 
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Substitutes 

According to the European Chemicals Agency (ECHA) there are currently no 

commercially or technically viable alternatives for HBCD as a flame retardant in polystyrene 

foam, as all alternative flame retardants it noted impair the structure and properties of the foam, 

making it unsuitable for use (ECHA, 2009). Some commercially available brominated flame 

retardants may be used in EPS foam (e.g., tetrabromo-cyclooctane, dibromoethyldibromocyclohexane and TBBPA), but their effectiveness in this application when compared with HBCD 

is unknown (Morose, 2006). There are commercially available substitutes for XPS and EPS 

foam board in the construction process that do not use brominated flame retardants. Polyester 

and polyether polyols, as well as phenolic foam may be used to produce insulation boardstock 

from rigid foam. Other substitutes include alternative insulation types such as blanket, loose-fill, 

and reflective insulation (Morose, 2006). 

Several chemicals may be used as alternatives for HBCD in textile applications. For 

textile backing, these include deca-BDE, chloroparaffins and ammonium polyphosphate (ECHA, 

2009). There are several alternatives to HBCD for use in high-impact polystyrene (HIPS). 

Deca-BDE is currently the most widely used flame retardant in HIPS (Weil and Levchik, 2009) 

and is also used in electronic wire insulation. Deca-BDE and chloroparaffins may not be suitable 

for use as substitutes for HBCD since EPA has already developed Action Plans for these 

chemicals due to concerns about their persistent, bioaccumulative and toxic properties. Other 

chemicals used in HIPS include both halogenated flame retardants used in conjunction with 

antimony trioxide (ATO) and organic aryl phosphorus compounds (ECHA, 2009). 

V. Hazard Identification Summary

Human Health Effects 

HBCD is absorbed via the gastro-intestinal tract and accumulates in the adipose tissue 

(body fat), muscle and liver in experimental animals. Bioaccumulation was observed to be 

higher in female than male rats. The elimination of HBCD from body fat is markedly slower than 

from other tissues with an elimination half-life of weeks to months (Chengelis, 2001). Repeated 

exposure of HBCD to rats showed disturbances in thyroid hormone system and effects on the 

thyroid males and females (Chengelis, 2001). A study by Eriksson, et al. (2006), concluded that 

neonatal exposure of HBCD to mice affected spontaneous motor behavior, learning and memory 

processes in adult mice. However, this study was not conducted according to established test 

guidelines. In a recently conducted, more robust, two-generation reproductive toxicity study in 

rats conducted according to established test guidelines, HBCD showed treatment-related 

reproductive effect (a significant decrease in the number of primordial follicles in the F1 

females). Although this decrease in ovarian follicles did not affect any reproductive parameters 

in this study, this effect is suggestive of potential reproductive toxicity. Developmental effects 

were observed including delays in eye opening in the second (F2) generation and transient 

changes in learning and memory in F1 males, but exposure did not cause any changes in 

spontaneous behavior. In addition, there was high and dose-dependent pup mortality during 

lactation (Ema, et al., 2008).
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Environmental Effects 

Laboratory studies have shown that HBCD is capable of producing adverse effects in a 

variety of organisms including algae, fish, invertebrates and soil-dwelling organisms at 

environmentally relevant concentrations. HBCD is toxic to algae and acutely toxic to fish 

embryos (Desjardins, et al., 2004; Deng, et al., 2009). A number of sub-lethal effects have also 

been observed in fish (Palace, et al., 2008; Kling and Förlin, 2009; Zhang, et al., 2008; Ronisz, et 

al., 2004). Drottar and Krueger (1998) reported a reduced number and size of daphnid offspring 

in first and second generations. Thyroid hormone-dependent developmental effects were 

observed in tadpoles (Xenopus laevis) exposed to HBCD (Schriks, et al., 2006). HBCD has been 

reported to reduce egg production and lower biomass in soil dwelling organisms (Lumbriculus 

variegatus) (Oetken, et al., 2001). HBCD administered to chicken (Gallus domesticus) 

embryonic hepatocytes in vitro resulted in significant alterations in expression of genes (mRNA) 

associated with liver and thyroid function (Crump, et al., 2008). Thinner egg shells were 

measured in American kestrels exposed to a combination of PBDEs and HBCD (Fernie, et al., 

2009). 

VI. Physical-Chemical Properties and Fate Characterization Summary 

 

The members of the HBCD flame retardants category are solids with negligible to low 

vapor pressure and negligible to low water solubility. [Molecular Weight = 642; Melting Point = 

175 - 190 °C; Vapor Pressure < 5 x 10-7 mm Hg at 20°C; log Kow = 5.8; and Water Solubility < 

50 ppb (μg/L) (EC 2000; EC 2008; Guerra, et al., 2009)] 

Persistence 

 Limited data are available on the degradation of HBCD in soil, water or sediment. 

Laboratory studies have shown that HBCD is degraded by abiotic and biotic processes in soil 

and aquatic sediment with reported half-lives of 2 days to 2 months (Davis, et al., 2005; 2006). 

These data are consistent with low persistence according to half-life criteria set forth in the PMN 

program (64 FR 60194, November 4, 1999) and international Persistent Organic Pollutants 

(POPs) protocols (UNEP, 2007; Norden, 2008). However, environmental monitoring data shows 

frequent occurrence of HBCD in biota over large areas and in remote locations where no 

demonstrable sources have been shown to account for the exposures (see discussion of 

environmental exposures in Section VII below), supporting the finding that HBCD is sufficiently 

persistent to be of concern within the scope of these international protocols. Measured levels of 

HBCD in dated sediment core samples also provide evidence of persistence. The frequent 

detection of HBCD over a large geographic area, with increasing exposure in remote locations 

such as the Arctic, where no demonstrable local sources exist that can account for these 

exposures, suggest that HBCD is persistent and undergoes long-range atmospheric transport. 

 
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Bioaccumulation 

HBCD has high bioaccumulation potential. Veith, et al. (1979) reported a measured 

bioconcentration factor (BCF) of 18,100 for HBCD in fathead minnows, and this value was later 

confirmed by a kinetic study with rainbow trout (Drottar, et al., 2001), for which the mean BCF 

was 19,200. A monitoring study by deBoer, et al. (2002) included a wide variety of biota 

(invertebrates, fish, birds and marine mammals) and showed that HBCD bioaccumulates easily 

and biomagnifies in food chains. In a Swedish monitoring study (Sellstrom, et al. 1998), a fishto-sediment ratio (biota/sediment accumulation factor; BSAF) of 15 was reported for one of two 

sites, indicating that HBCD is bioavailable and bioaccumulative. Isomer-specific 

biomagnification has been demonstrated based on monitoring of a Lake Ontario food web 

(Tomy, et al. 2004). Monitoring in Sweden found much higher levels of HBCD in eggs from 

wild peregrine falcons than from captive populations feeding on chickens (Lindberg, et al., 2004) 

or guillemot from the Baltic Sea (Sellstrom, et al., 2003), demonstrating that HBCD may also 

bioaccumulate in terrestrial organisms and food chains. 

 

VII. Exposure Characterization Summary

Releases 

HBCD is not reported in the Toxics Release Inventory. No readily available quantitative 

release information in the U.S. was found. ECHA reported a total of about 3,100 kg/year of 

HBCD released to the environment in Europe in 2008, of which 50% were to wastewater, 29% to 

surface water and 21% to air (ECHA, 2009). The overall volume used in 2007 was estimated at 

11.6 million kg/year (ECHA, 2009). A Swedish article indicates the primary source of release of 

HBCD in Europe is from textile applications (KEMI, 2006). Based on IUR data, the volume of 

HBCD used for textile application in the U.S. is estimated to be < 1 % of the total volume of 

HBCD produced/imported and hence releases from this use in the U.S. are expected to be 

relatively small (as a percentage of overall volume produced/imported). 

Information from the United Kingdom indicates that the primary sources of HBCD in the 

environment are from fugitive emissions during its manufacture and use in subsequent products, 

potentially from leaching in landfills, and from incinerator emissions (UKEA, 2009). As an 

additive flame retardant, HBCD is not chemically bound to the matrix of the material it protects, 

and thus has the potential to enter the environment from the finished products in use or after 

disposal (US EPA, 2008b). ECHA states: “A substantial proportion of articles containing 

HBCD will have very long service life (30+ years for typical insulation like EPS and XPS) and 

environmental releases will continue for a long time into the future.” (ECHA, 2009). It is not 

known how comparable the releases of HBCD from manufacturing and use operations in the 

U.S. are to those reported in Europe. 

Human Exposure 

HBCD is typically manufactured as a powder of approximately 100 microns in size; 

however, a portion of the materials is micronized to 1 micron during manufacture (U.S. Patent 

4980382), which poses the potential of deep lung particulate exposure (Rozman, et al., 2001)). 
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Workers who do not wear appropriate respiratory protection have the high potential for deep 

lung exposure of the 1 micron material. Particles 1 micron and smaller penetrate to the alveolar 

sacs of the lungs. They may be absorbed into blood or cleared through the lymphatics. The 

overall removal of particles from the alveoli is relatively inefficient; on the first day only about 

20 percent of particles are cleared, and the portion remaining longer than 24 hours is cleared very 

slowly. Some particles may remain in the alveoli indefinitely (Rozman, et al., 2001). 

Commercial workers also may have potential dermal and inhalation exposure to the chemical 

during application. The Occupational Safety and Health Administration (OSHA) has not 

established a Permissible Exposure Limit for HBCD. An occupational exposure study at an 

industrial plant in Europe producing EPS, reported measured elevated airborne dust levels and 

measured HBCD in the blood of workers (Thomsen, et al., 2007). No readily available HBCD 

occupational exposure information (including biomonitoring data) was found for U.S. workers. 

Based on available IUR reporting, the maximum total number of industrial workers likely to be 

exposed to this chemical during manufacturing and industrial processing and use is between 100 

and 999 (US EPA, 2006); however, this is likely an underestimate since it does not include the 

commercial workers and some IUR submitters did not have to report numbers of workers or the 

information was reported to be not readily obtainable. 

HBCD has been detected in human adipose tissue, milk, and blood (Covaci, et al, 2006; 

Johnson-Restrepo, et al, 2008; Arnot, et al., 2009). General population exposure to HBCD is 

likely from its presence in food (Hiebl and Vetter, 2007; Fernandes, et al., 2008; van Leeuwen 

and de Boer, 2008), outdoor air, particularly near point sources (Covaci, et al., 2006), and indoor 

air (Law, et al., 2008). HBCD has also been detected in indoor dust (Covaci, et al., 2006; Law, 

et al., 2008; Roosens, et al., 2009). 

The IUR information suggests either that HBCD will not be used in children’s consumer 

products or that this type of information is not readily available. However, to the extent it is 

present in household applications (e.g., building foam, furniture upholstery, carpeting), children 

could be exposed, especially given children’s increased exposure via dust and the hand-to-mouth 

ingestion pathway. In vitro experiments conducted to demonstrate leaching of HBCD from 

textiles showed that the presence of simulated biological fluids (sweat, saliva) and fruit juices 

enhances the leaching of HBCD from back-coated samples (Ghanem, 2009). Children’s 

exposure to HBCD from mouthing of textiles and from pica ingestion of dust has been estimated 

(EC, 2008). 

Environmental Exposure 

 

HBCD has been measured in air and sediment in Scandinavian countries, North America 

and Asia (Covaci, et al., 2006, Arnot, et al., 2009). HBCD has been measured in marine and 

arctic mammals, freshwater and marine fish, aquatic invertebrates, birds and bird eggs, and one 

plant species (Covaci, et al., 2006; Arnot, et al., 2009). HBCD has been detected in Arctic air in 

northern Scandinavia and in Arctic birds and bird eggs, Arctic fish, ringed seals and polar bears 

(UNEP, 2009). It has been detected in freshwater, marine, and avian organisms, and in upper 

trophic-level mammals (polar bears and seals). The majority of these studies are European, some 

are from North America, and a few are from Asia. A study reported decreased levels of HBCD 

in biota once a United Kingdom manufacturing plant was closed (Law, et al., 2008b). 
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VIII. Risk Management Considerations

HBCD is of international concern because of its PBT properties. HBCD is on the 

ECHA’s list of Substances of Very High Concern (SVHCs). HBCD is under consideration for 

listing under the POPs Protocol to the Convention on Long-Range Transboundary Air Pollution, 

as technical review has concluded that HBCD is persistent, bioaccumulative, can cause adverse 

effects to humans or the environment, and has the potential to be transported long distances 

within the meaning of the Protocol (UNECE, 2010). Under the Stockholm Convention for 

Persistent Organic Pollutants, the POPs Review Committee decided in October 2009 that Annex 

D screening criteria have been met for HBCD; further determinations have not been made 

(UNEP, 2010). 

HBCD is persistent, bioaccumulative and toxic, especially to aquatic organisms. HBCD 

biomagnifies in food chains. Given its presence at increasing levels in the environment 

including wildlife, and the high hazard for HBCD to algae and aquatic invertebrates, EPA has a 

concern for the potential risk to these aquatic organisms. 

 EPA has presented evidence which strongly suggests there is potential for exposure to the 

general population from HBCD in the environment, as well as exposure to HBCD from products 

and dust in the home and workplace. HBCD shows repeated dose toxicity. There may be some 

human health hazard concern based on thyroid effects and indications of developmental and 

transient neurobehavioral effects. These health effects combined with potential exposures 

suggests some concern for a potential risk to the general population from HBCD is warranted. 

Greater concern is warranted for workers who manufacture the chemical and produce products 

that contain it, given available expose information. 

 Availability of substitutes for HBCD uses is an unresolved issue, especially for EPS and 

XPS building foam board applications, where other, more suitable flame retardants may not be 

readily available. 

HBCD is currently on the Integrated Risk Information System (IRIS) program agenda. 

The anticipated date for a completed assessment has not yet been determined. (US EPA, 2010). 

HBCD is under consideration for inclusion in the NHANES human bio-monitoring program, 

which could provide data on exposure in the U.S. 

 

Potential Impacts on Children 

HBCD is found in household dust, and it is used in the U.S. in certain consumer products 

that could provide direct exposure pathways to children. HBCD has been measured in blood 

serum and breast milk, so that a developing fetus or nursing infant could be exposed to it. The 

reproductive, developmental and neurotoxic health hazards that could result from exposures to 

HBCD are an important consideration in protecting children’s health. These factors suggest that 

concerns for potential risks to children and pregnant women should be considered with any 

actions taken to manage this chemical. 
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IX. Next Steps

 

 In conducting this review of HBCD, EPA considered a number of potential risk 

management actions, including regulatory actions under TSCA sections 4 and 5 and under the 

Emergency Planning and Community Right-to-Know Act (EPCRA) 313, as well as voluntary 

actions through such programs as Design for the Environment (DfE). 

 Based on its screening-level review of hazard and exposure information, EPA intends to 

initiate actions to protect humans and the environment from exposure to HBCD due to 

manufacture (including import) use, or disposal of commercial HBCD. In addition, as part of the 

Agency’s efforts to address these chemical substances, EPA also intends to evaluate the potential 

for disproportionate impact of exposure to HBCD on children and other sub-populations. 

On the basis of existing information, the Agency believes that the following actions would be 

warranted: 

 Initiate rulemaking under TSCA Section 5(b)(4) of TSCA to add HBCD to the list of 

chemicals which present or may present an unreasonable risk of injury to health or the 

environment. EPA intends to publish a notice of proposed rulemaking by the end of 

2011. 

 Initiate rulemaking under TSCA section 5(a)(2) to designate manufacture or processing 

of HBCD for use in consumer textiles as a flame retardant as a significant new use which 

would require manufacturers and processors to notify EPA before manufacturing or 

processing HBCD for the significant new use. This Significant New Use Rule (SNUR) 

also would be proposed to apply to imports of consumer textiles articles containing 

HBCD. EPA has evidence to suggest that the use of HBCD in textiles may be limited to 

specialty commercial applications, and that general consumer textile use may be so 

limited it would be appropriate for SNUR regulation. If information shows this 

assumption to be incorrect, EPA will consider initiating rulemaking under TSCA section 

6(a) to address general consumer textile use. 

 Consider rulemaking under TSCA section 6(a) to regulate HBCD. A section 6(a) action 

could take the form of a comprehensive ban on the manufacturing, processing, 

distribution in commerce and use of a chemical substance, or a more targeted regulation 

to address specific activities. The extent of the rule for HBCD would be determined 

during the rulemaking process. 

 Inititate rulemaking in late 2011 to add HBCD to the Toxics Release Inventory. HBCD 

is currently not listed by any CASRN on the Emergency Planning and Community Rightto-Know (EPCRA) section 313 list of toxic substances. Listing will require 

manufacturers or importers to provide environmental release information not currently 

captured by IUR. 

 Conduct a Design for the Environment and Green Chemistry alternatives assessment of 

HBCD. The information developed could be used to encourage industry to move away 
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from HBCD instead of, in addition to, or as part of any regulatory action taken under 

TSCA. The alternatives assessment would build upon existing knowledge and would 

consider various exposed populations, including sensitive human subpopulations, as well 

as environmental exposure. The work will begin in 2011, with completion expected in 

2013. 
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X. References 

Arnot, J., McCarty, L., Armitage, J., Toose-Reid, L., Wania, F., and Cousins, I. 2009. An evaluation of 

hexabromocyclododecane (HBCD) for Persistent Organic Pollutant (POP) properties and the potential for adverse 

effects in the environment. Submitted to European Brominated Flame Retardant Industry Panel (EBFRIP). 26 May 

2009. 

Chengelis, C. 2001. An oral (gavage) 90 day toxicity study of HBCD in rats. Study No. WIL-186012. WIL Research 

Laboratories, Inc., Ashland, Ohio. 

Covaci, A., Gerecke, A.C., Law, R.J., Voorspoels, S., Kohler, M., Heeb, N.V., Leslie, H., Allchin, C.R., and De 

Boer, J. 2006. Hexabromocyclododecanes (HBCDs) in the Environment and Humans: A Review. Environ. Sci. 

Technol. 40, 3679-3688. 

Crump, D. ; Chiu, S. ; Egloff, C. ; Kennedy. S.W. 2008. Effects of hexabromocyclododecane and polybrominated 

diphenyl ethers on mRNA expression in chicken (Gallus domesticus) hepatocytes. Toxicol. Sci. 2008, 106, 479-487. 

Davis JW, S Gonsior, G Marty, J Ariano. 2005. The transformation of hexabromocyclododecane in aerobic and 

anaerobic soils and aquatic sediments. Water Res. 39:1075-1084. 

Davis JW, SJ Gonsior, DA Markham, URS Friederich, RW Hunziker, JM Ariano. 2006. Biodegradation and product 

identification of [14C]hexabromocyclododecane in wastewater sludge and freshwater sediment. Environ. Sci. 

Technol. 40:5395-5401. 

DeBoer J.; Allchin, C.; Zegers, B.; Boon, J.P.; Brandsma, S.A.; Morris, S.; Kruijt, A.W.; van der Veen, I.; 

Hesselingen, J.M.; Haftka, J.J.H.. 2002. HBCD and TBBP-A in sewage sludge, sediments and biota, including 

interlaboratory study. Ymuiden, The Netherlands: Netherlands Institute for Fisheries Research (RIVO) BV. Report 

number C033/02. 

Deng, J. ; Yu, L, ; Liu, C. ; Yu , K. ; Shi,, X. ; Yeung, L.W.Y. ; Lam, P.K.S. ; Wu, R.S.S. ;Zhou B. 2009. 

Hexabromcyclododecane-induced developmental toxicity and apoptosis in zebrafish embryos. Aquatic Toxicol. 

2009, 93, 29-36. 

Desjardins D.; MacGregor, J.A.; Krueger, H.O. 2004. Hexabromocyclododecane (HBCD): A 72-hour toxicity test 

with the marine diatom (Skeletonema costatum). Final Report. Wildlife International, Ltd., Easton, Maryland, USA. 

pp 66. 

Drottar KR and Krueger HO. 1998. Hexabromocyclododecane (HBCD): An flow-through life-cycle toxicity test 

with the cladoceran (Daphnia magna). Final report. 439A-108, Wildlife International, Ltd, Easton, Maryland, USA. 

1998. 78pp. 

Drottar, K.R.; MacGregor, J.A.; Krueger, H.O. 2001. Hexabromocyclododecane (HBCD): An early life-stage 

toxicity test with the rainbow trout (Oncorhynchus mykiss). Final 

Report. Wildlife International, Ltd, Easton, Maryland, USA. 2001. pp 1-102. 

EC 2000. European Commission 2000 IUCLID Dataset for Hexabromocyclododecane [25637-99-4] 

EC 2008. European Commission. Risk Assessment: Hexabromocyclododecane CAS-No.: 25637-99-4 EINECS-No.: 

247-148-4, Final Report May 2008. Office for Official Publications of the European Communities: Luxembourg, 

2008. 

ECHA, 2009. European Chemicals Agency. Data on Manufacture, Import, Export Uses and Releases of HBCDD as 

well as Information on Potential Alternatives to Its Use. December 1, 2009. 

http://echa.europa.eu/doc/consultations/recommendations/tech_reports/tech_rep_hbcdd.pdf 
U.S. Environmental Protection Agency OMB Review Draft, 04/28/10 

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release 

11

Ema, M., Fujii, S., Hirata-Koizumi, M., and Matsumoto, K. 2008. Two-generation reproductive toxicity study of the 

flame retardant hexabromcyclododecane in rats. Reproductive Toxicology, 25:335-351. 

Eriksson, P.; Fisher, C.; Wallin, M.; Jakobsson, E.; Fredriksson, A. 2006. Impaired behaviour, 

learning and memory, in adult mice neonatally exposed to hexabromocyclododecane (HBCDD). Environ. Toxicol. 

Pharmacol. 2006, 21, 317-322. 

Fernandes, A., Dicks, P., Mortimer, D., Gem, M., Smith, F., Driffield, M., White, S., and Rose, M. 2008. 

Brominated and chlorinated dioxins, PCBs, and brominated flame retardants in Scottish shellfish: methodology, 

occurrence and human dietary exposure. Mol. Nutr. Food Res. 52, 238-249. 

Fernie, K.J. ; Shutt, J.L. ; Letcher, R.J. ; Ritchie, I.J. ; Bird, D.M. 2009. Environmentally relevant concentrations of 

DE-71 and HBCD alter eggshell thickness and reproductive success of American kestrels. Environ. Sci. Technol. 

2009, 43, 2124-30. 

Ghanem, R. 2009. Kinetics of Thermal and Photolytic Segregation of Hexabromocyclododecane in Backcoated 

Textile Samples. Jordan J Chem. 4, 171-181. 

Guerra, P.,et al.; (2009); Transfer of hexabromocyclododecane from industrial effluents to sediments and biota: 

Case study in Cinca river (Spain). Journal of Hydrology, 2009, 378, 355. 

Heibl, J., and Vetter W. 2007. Detection of hexabromocyclododecane and its metabolite pentabromocyclodedecane 

in chicken egg and fish from the official food control. J. Agric. Food Chem. 55, 3319-3324. 

Johnson-Restrepo, B., Adams, D.H., and Kannan, K. 2008. Tetrabromobisphenol A (TBBPA) and 

hexabromocyclododecanes (HBCDs) in tissues of humans, dolphins, and sharks from the United States. 

Chemosphere 2008, 70, 1935-1944. 

Kemi 2006. Survey and Technical Assessment of Alternatives to TBBPA and HBCDD’, KEMI Swedish Chemicals 

Agency, Jan 2006 http://www.kemi.se/upload/Trycksaker/Pdf/PM/PM1_06.pdf 

Kling, P.; Förlin, L. 2009. Proteomic studies in zebrafish liver cells exposed to the brominated flame retardants 

HBCD and dTBBPA. Ecotoxicol. Environ. Saf. 2009, 72, 985-1993. 

Law, R.J., Herzke, D., Harrad, S., Morris, S., Bersuder, P., and Allchin, C.R. 2008. Levels and trends of HBCD and 

BDEs in the European and Asian environments, with some information for other BFRs. Chemosphere 2008, 73, 

223-241. 

Law, RJ, Bersuder, P., Barry, J., Wilford, B.H., Allchin, C.R. and Jepson, P.D. 2008b. “A Significant Downturn in 

Levels of Hexabromocyclododecane in the Blubber of Harbor Porpoises (Phocoena phocoena) Stranded or Bycaught 

in the UK: An Update to 2006 Environ. Sci. Technol. 2008, 42, 9104–9109. 

Lindberg, P.; Sellstrom, U.; Haggberg, L.; de Wit, C.A.. 2004. Higher brominated diphenyl ethers and 

hexabromocyclododecane found in eggs of peregrine falcons (Falco peregrinus) breeding in Sweden. Environ. Sci. 

Technol. 38:93-96. 

Morose, G. 2006. An Overview of Alternatives to Tetrabromobisphenol A (TBBPA) and Hexabromocyclododecane 

(HBCD)”. A Publication of the Lowell Center for Sustainable Production University of Massachusetts – Lowell, 

Lowell, MA. http://www.chemicalspolicy.org/downloads/AternativestoTBBPAandHBCD.pdf. (accessed April 1, 

2010). 

Norden, 2008. Hexabromocyclododecane as a possible global POP. TemaNord 2008:520. Nordic Council of 

Ministers, Copenhagen 2007 ISBN 978-92-893-1665-1 
U.S. Environmental Protection Agency OMB Review Draft, 04/28/10 

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release 

12

Oetken, M.; Ludwichowski, K-U.; Nagel, R. 2001. Validation of the preliminary EU-concept of assessing the 

impact of chemicals to organisms in sediment by using selected substances. UBA-FB 299 67 411, Institute of 

Hydrobiology, Dresden University of Technology, Dresden, Germany. 2001, pp 97. 

Palace, V.P.; Pleskach, K.; Halldorson, T.; Danell, R.; Wautier, K.; Evans, B.; Alaee, M.; Marvin, C.; Tommy, G.T. 

2008. Biotransformation enzymes and thyroid axis disruption in juvenile rainbow trout (Oncorhynchus mykiss) 

exposed to hexabromocyclododecane diastereoisomers. Environ. Sci. Technol. 2008, 42:1967-1972. 

Ronisz, D.; Farmen, E.; Finne, E.;, Karlsson, H.; Förlin, L. 2004. Sublethal effects of the flame retardants 

hexabromocyclododecane (HBCDD), and tetrabromobisphenol A (TBBPA), on 

hepatic enzymes and other biomarkers in juvenile rainbow trout and feral eelpout. Aquatic Toxicol. 2004,69, 229-

245. 

Roosens, L., Abdallah, M.A., Harrad, S., Neels, H. and Covaci, A. 2009. Exposure to Hexabromocyclododecanes 

(HBCDs) via Dust Ingestion, but not Diet, Correlates with Concentration in Human Serum—Preliminary Results. 

Environ. Health Perspect. doi:10.1289/ehp.0900869. http://dx.doi.org/. Online 13 July 2009. 

Rozman, K. K.; Klaassen, C. D. Absorption, Distribution, and Excretion of Toxicants. In Casarett and Doull’s 

Toxicology: The Basic Science of Poisons, 6th edition; Seils, A.; Noujaim, S. R.; Sheinis, L. A., Eds.; McGrawHill: New York, 2001; pg 117. 

Schriks, M. ; Zninavashe, E. ; Furlow, J.D. ; Murk, A.J. 2006. Disruption of thyroid hormone-mediated Zenopus 

laevis tadpole tail tip regression by hexabromocyclododecane (HBCD) and 2,2’,3,3’,4,4’,5,5’, 6-nona brominated 

diphenyl ether (BDE206). Chemosphere 2006, 65, 1904-1908. 

Sellstrom, U.; Soderstrom, G.; deWit, C.; Tysklind, M. 1998. Photolytic debromination of decabromodiphenyl ether 

(DeBDE). Organohal. Cmpd 35:447-450. 

Sellstrom, U; Bignert, A.; Kierkegaard, A.; Haggberg, L.; de Wit, C.A.; Olsson, M.; Jansson, B.. 2003. Temporal 

trend studies on tetra- and pentabrominated ethers and hexabromocyclododecane in Guillemot egg from the Baltic 

Sea. Environ. Sci. Technol. 37:5496-5501 

Thomsen, C.; Molander, P.; Daae, H. L.; Janak, K.; Froshaug, M.; Liane, V. H.; Thorud, S.; Becher, G.; Dybing, E. 

2007. Occupational Exposure to Hexabromocyclododecane At An Industrial Plant. Environ. Sci. Technol. 2007, 

41 (15), 5210-5216. 

Tomy, G.T.; Budakowski, W.; Halldorson, T.; Whittle, D.M.; Keir, M.J.; Marvin, C.; Macinnis, G.; Alaee, M.. 

2004. Biomagnification of α- and γ-hexabromocyclododecane isomers in a Lake Ontario food web. Environ. Sci. 

Tehcnol. 38:2298-2303. 

UKEA, 2009. United Kingdom Environment Agency. Hexabromocyclododecane in the Environment. 

http://www.environment-agency.gov.uk/business/topics/pollution/39137.aspx 

UNECE, 2010. Economic Commission for Europe. Executive Body for CLRTAP; Report of the Executive Body 

on its 27th Session. ECE/EB.AIR/99. 9 March 2010, p.9 

http://www.unece.org/env/documents/2009/EB/eb/ece.eb.air.99.pdf 

UNEP, 2007. Stockholm Convention on Persistent Organic Pollutants. Persistent Organic Pollutants Review 

Committee, Third meeting, Geneva, 19–23 November 2007, Item 7 of the provisional agenda, Presentation on 

environmental transport and modeling. The OECD screening tool for overall persistence and long-range transport 

potential. UNEP/POPS/POPRC.3/INF/7 

UNEP, 2009. Stockholm Convention on Persistent Organic Pollutants. “Summary of the proposal for the listing of 

hexabromocyclododecane (HBCDD) in Annex A to the Convention.” July 9, 2009. 

http://chm.pops.int/Convention/POPsReviewCommittee/hrPOPRCMeetings/POPRC5/POPRC5Followupcommunic

ations/HBCDAnnexEInformationRequest/tabid/645/language/en-US/Default.aspx 
U.S. Environmental Protection Agency OMB Review Draft, 04/28/10 

U.S. Government Internal Deliberative Document, Do Not Quote, Cite, or Release 

13

UNEP, 2010. Stockholm Convention on Persistent Organic Pollutants. Invitation to review and provide comments 

on draft risk profile on hexabromocyclododecane (HBCD). 

http://chm.pops.int/Convention/POPsReviewCommittee/hrPOPRCMeetings/POPRC5/POPRC5Followupcommunic

ations/HBCDInvitationforcommentsondraftRP/tabid/742/language/en-US/Default.aspx (accessed April 24, 2010). 

US EPA. 2006. U.S. Environmental Protection Agency. Toxic Substance Control Act (TSCA) Chemical Substance 

Inventory. 2006 Inventory Update Rule Public Database. Office of Pollution and Prevention of Toxics: Washington, 

D.C., 2006. 

US EPA, 2008. Exposure Characterization for HPV Challenge Chemical, Exposures to the General Population and 

the Environment, March 14, 2008 

US EPA, 2010. Integrated Risk Information System. IRISTrack Report for Hexabromocyclododecane Assessment 

(http://cfpub.epa.gov/ncea/iristrac/index.cfm?fuseaction=viewChemical.showChemical&sw_id=1102). Accessed 

April 6, 2010. 

US ITC, 2010. US International Trade Commission. Interactive Tariff and Data Web: US Imports for Consumption. 

http://dataweb.usitc.gov/ (accessed April 1, 2010). 

US Patent 4980382 - Process for the preparation of expandable vinyl aromatic polymer particles containing 

hexabromocyclododecane, http://www.google.com/patents?vid=USPAT4980382 

van Leeuwen, S.P., and de Boer, J. 2008. Brominated flame retardants in fish and shellfish – levels and contribution 

of fish consumption to dietary exposure of Dutch citizens to HBCD. Mol. Nutr. Food Res. 2008, 52, 194-203. 

Veith, G.D.; Defoe, D.L.; Bergstedt, B.V.. 1979. Measuring and estimating the bioconcentration factor in fish. J. 

Fish Res. Bd. Can. 36:1040-1048. 

Weil E.D.; Levchik, S.V. 2009. Flame Retardants for Plastics and Textiles Practical Applications. Hanser Gardner 

Publications. Cincinnati, OH, 2009. 

Zhang, X., Yang, F., Zhang, X., Xu, Y., Liao, T., Song, S., Wang J. 2008. Induction of hepatic enzymes and 

oxidcative stress in Chinese rare minnow (Gobiocypris rarus) exposed to waterborne hexabromocyclododecane 

(HBCD). Aquatic. Toxicol. 2008, 86, 4-11.