Synopsis

Pursuant to section 74 of the Canadian Environmental Protection Act, 1999 (CEPA 1999), the Ministers of the Environment and of Health have conducted a screening assessment of Cyclododecane, 1,2,5,6,9,10-hexabromo-, more commonly referred to as hexabromocyclododecane (HBCD), Chemical Abstracts Service Registry Number 3194-55-6. HBCD was one of 123 substances on the Domestic Substances List (DSL) selected for a pilot project for screening assessments. During the categorization of the DSL, the substance was identified as a high priority for screening assessment as it met the criteria for persistence, bioaccumulation and inherent toxicity to aquatic life. Therefore, the focus of this assessment relates principally to ecological risk.

The primary application of HBCD is as a flame retardant in polystyrene foams that are used as thermal insulation materials in the construction industry. A second application is the flame retarding of textiles for usage in residential and commercial upholstered furniture, transportation seating, wall coverings and draperies. Minor uses include addition to latex binders, adhesives and paints and to high-impact polystyrene and styrene-acrylontrile resins for electrical and electronic equipment.

Global demand for HBCD was estimated at 16 700 tonnes in 2001, representing 8.2% of total demand for brominated flame retardants that year. Results from a section 71 Notice with Respect to Certain Substances on the Domestic Substances List (DSL)conducted for the year 2000 indicated that HBCD was not manufactured in Canada in 2000. Amounts imported into the country in that year were in the range of 100 000 to 1 000 000 kg.

Monitoring studies document the presence of HBCD in many environmental media, sometimes at high concentrations. Analyses of sediment core samples show a clear trend of increasing concentrations of HBCD since the 1970s, confirming stability in deep sediments for periods of more than 25 to 30 years. As well, there is evidence of increasing HBCD levels in North American and European biota, both within species and along food chains.

Measured and modelled data indicate that HBCD will undergo primary degradation; however, ultimate degradation in the environment has not been definitively established. Laboratory studies conducted using water, sediment, soil and sludge confirm the presence of primary degradation products, including 1,5,9-cyclododecatriene, a substance that is not readily biodegradable and may be stable in the environment. Available evidence indicates that 1,5,9-cyclododecatriene is potentially very toxic to aquatic life (with measured and predicted median lethal concentrations (LC₅₀s) < 1 mg/L) and is potentially highly bioaccumulative in aquatic organisms.

Considered together, the lines of evidence from degradation studies and monitoring data establish that HBCD can remain stable in the environment for a period exceeding one year. The substance therefore meets the criteria for persistence as outlined in the Persistence and Bioaccumulation Regulations under CEPA 1999 (i.e., half-life in water and soil of 182 days or more and half-life in sediment of 365 days or more). Additionally, HBCD meets the criteria for persistence in air set out in the same regulations (i.e., half-life of two days or more, or being subject to atmospheric transport from the source to a remote area), based on a predicted atmospheric half-life of 2.13 days and evidence of occurrence in regions considered remote from potential sources, including the Arctic.

The weight of experimental and predicted data indicate that HBCD meets the criteria for bioaccumulation as specified in the Persistence and Bioaccumulation Regulations under CEPA 1999--bioaccumulation (BAF) or bioconcentration factors (BCF) of 5000 or more?and is likely to have significant bioaccumulation potential in the environment. Bioconcentration factors of 18 100 (rainbow trout) and 12 866 (steady state, fathead minnow) were obtained in laboratory studies. Field studies show evidence that bioaccumulation and biomagnification are occurring within food webs.

HBCD has demonstrated toxicity in both aquatic and terrestrial species, with significant adverse effects on survival, reproduction and development reported in algae, daphnids and annelid worms. Recent studies indicate potential impacts on the normal functioning of liver enzymes and thyroid hormones in fish. In mammals, sublethal exposures have been associated with potential toxicological effects on the liver and thyroid system, including cellular damage, significantly increased hepatic enzyme activity, significant reductions in circulating thyroid hormone levels and increases in thyroid weight.

Combustion of HBCD under certain conditions may lead to production of polybrominated dibenzo-p-dioxins (PBDDs) and dibenzofurans (PBDFs). Trace levels of these compounds and their precursors have been measured during combustion of flame-retarded polystyrene materials containing HBCD. These transformation products are brominated analogues of the Toxic Substances Management Policy Track 1 polychlorinated dibenzofurans and dibenzo-p-dioxins.

The analysis of risk quotients determined that HBCD concentrations in the Canadian environment have the potential to cause adverse effects in populations of pelagic and benthic organisms but are unlikely to result in direct adverse effects to soil organisms and wildlife. However, it must be considered that the presence of HBCD in the environment warrants concern in light of strong evidence that the substance is environmentally persistent and bioaccumulative.

While recent detailed production and use information are not available for HBCD, monitoring studies suggest that North American and global use of the substance may be on the rise. As well, there is evidence that HBCD may be replacing some polybrominated diphenyl ether (PBDE) flame retardants (notably the commercial Decabromodiphenyl Ether formulation).

Based on the information in this draft screening assessment, it is proposed that HBCD is entering the environment in a quantity or concentration or under conditions that have or may have an immediate or long-term harmful effect on the environment or its biological diversity.

Exposures of the general population of Canada to HBCD may occur through oral and inhalation routes. Known sources of human exposure to HBCD include environmental media (ambient air, water, soil, sediment), household dust, indoor air, human breast milk, and HBCD-treated consumer products. HBCD may be released from the matrix of a product over time through abrasion and usage, as it is not covalently bound. As HBCD has a low vapour pressure, it will not volatilize or off-gas from a product.

The human health hazard risk characterization for HBCD was based primarily upon the assessment of the European Union, with more recent data taken into consideration. The critical effect for the characterization of risk to human health is reproductive toxicity, with reported effects including decreased fertility and effects upon the thyroid. The highest upper-bounding estimated intake of HBCD is expected to be in infants from ingestion of human breast milk and the mouthing of consumer products. A comparison of these exposure estimates with the critical effect levels identified in the two-generation reproductive toxicity assay results in margins of exposure that are considered adequately protective of human health. Based on the available information it is proposed that HBCD is not entering the environment in a quantity or concentration or under conditions that constitute or may constitute a danger in Canada to human life or health.

Based on the information available for environment and human health considerations, it is proposed that HBCD meets one or more of the criteria set out in section 64 of CEPA 1999.

In addition, it is proposed that HBCD meets the criteria for persistence and bioaccumulation potential as set out in the Persistence and Bioaccumulation Regulations, and its presence in the environment results primarily from human activity.

Where relevant, research and monitoring will support verification of assumptions used during the screening assessment and, where appropriate, the performance of potential control measures identified during the risk management phase.