Decabromodiphenyl ether

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Decabromodiphenyl ether
IUPAC name 2,3,4,5,6-Pentabromo-1-(2,3,4,5,6-
pentabromophenoxy)benzene
Other names DecaBDE, Deca-BDE, BDE-209
Identifiers
CAS number [1163-19-5]
SMILES BrC1=C(OC2=C(Br)C(Br)=C(Br)C(Br)
=C2Br)C(Br)=C(Br)C(Br)=C1Br
Properties
Molecular formula C12Br10O
Molar mass 959.17 g/mol
Appearance White or pale yellow solid
Density 3.2 g/cm©¯ solid
Melting point

302.5 °C
Boiling point

425 °C
Solubility in water not soluble
Hazards
R-phrases R40
S-phrases S36/37
Related compounds
Related polybrominated diphenyl ethers pentabromodiphenyl ether, octabromodiphenyl ether
Related compounds Diphenyl ether
Except where noted otherwise, data are given for
materials in their standard state
(at 25 °C, 100 kPa)
Infobox disclaimer and references

Decabromodiphenyl ether (decaBDE, deca-BDE, DBDE, deca, decabromodiphenyl oxide, DBDPO, bis(pentabromophenyl) ether) is a brominated flame retardant which belongs to the group of polybrominated diphenyl ethers (PBDEs).

Contents

[edit] Composition, uses, and production

Commercial decaBDE is a technical mixture of different PBDE congeners, with PBDE congener number 209 (decabromodiphenyl ether) and nonabromodiphenyl ether being the most common.[1] The term decaBDE alone refers to only decabromodiphenyl ether, the single "fully brominated" PBDE.[2]

DecaBDE is a flame retardant. The chemical "is always used in conjunction with antimony trioxide" in polymers, mainly in "high impact polystyrene (HIPS) which is used in the television industry for cabinet backs."[1] DecaBDE is also used for "polypropylene drapery and upholstery fabric" by means of backcoating and "may also be used in some synthetic carpets."[1]

The annual demand worldwide was estimated as 56,100 tonnes in 2001, of which the Americas accounted for 24,500 tonnes, Asia 23,000 tonnes, and Europe 7,600 tonnes.[3] As of 2007, Albemarle in the U.S., Chemtura in the U.S., Dead Sea Bromine in Israel, and Tosoh Corporation in Japan manufacture decaBDE.[4][5]

[edit] Environmental chemistry

As stated in a 2006 review, "Deca-BDE has long been characterized as an environmentally stable and inert product that was not capable of degradation in the environment, not toxic, and therefore of no concern."[6] However, "some scientists had not particularly believed that Deca-BDE was so benign, particularly as evidence to this effect came largely from the industry itself."[6] One problem in studying the chemical was that "the detection of Deca-BDE in environmental samples is difficult and problematic"; only in the late 1990s did "analytical advances... allow[] detection at much lower concentrations."[6]

DecaBDE is released by different processes into the environment, such as emissions from manufacture of decaBDE-containing products and from the products themselves.[2] Elevated concentrations can be found in air, water, soil, food, sediment, sludge, and dust.[7] A 2006 study concluded "in general, environmental concentrations of BDE-209 [i.e., decaBDE] appear to be increasing."[7]

[edit] The question of debromination

An important scientific issue is whether decaBDE debrominates in the environment to PBDE congeners with fewer bromine atoms, since such PBDE congeners may be more toxic than decaBDE itself.[2] Debromination may be "biotic" (caused by biological means) or "abiotic" (caused by nonbiological means).[4] As of 2001, the Bromine Science and Environmental Forum (BSEF), which represents the chemical industry, stated "Studies commissioned by the bromine industry in order to assess the capacity of octa-BDE and deca-BDE to debrominate, i.e. degrade down to form penta-BDE and tetra-BDE, have proven that there is no debromination of BFRs [Brominated Flame Retardants] to these compounds."[8] The European Union (EU) in May 2004 stated "the formation of PBT/vPvB [Persistent, Bioaccumulative, and Toxic / very Persistent, very Bioaccumulative] substances in the environment as a result of degradation [of decaBDE] is a possibility that cannot be quantified based on current knowledge."[9] In September 2004 an Agency for Toxic Substances and Disease Registry (ATSDR) report asserted that "DecaBDE seems to be largely resistant to environmental degradation."[2]

In May 2006, the EPHA Environment Network (now The Health and Environment Alliance) released a report reviewing the available scientific literature[10] and concluding the following:

  • "It is difficult to assess the degree of BDE 209 photolytic debromination in house dust, soils and sediments when exposed to light. However, in cars debromination can be expected to occur more significantly."
  • "In sewage anaerobic bacteria can initiate debromination of BDE 209, albeit at a slower rate than photolytic debromination, but due to the large volumes of DecaBDE in sewage sludge this may be significant."
  • "Some fish appear capable of debrominating BDE 209 through metabolism. The extent of the metabolism varies among fish and it is difficult to determine the extent of debromination that would occur in the wild."

In response, the BSEF claimed in May 2006 that "the Deca-BDE present in the environment is not readily available for photolysis and therefore does not contribute significantly to environmental levels of lower BDEs."[11] In addition, the BSEF reiterated the findings of the May 2004 EU report.[9]

Subsequently, many studies have been published concerning decaBDE debromination. Common anaerobic soil bacteria debrominated decaBDE and octaBDE in a 2006 study.[12] In 2006-2007 studies, metabolic debromination of decaBDE was demonstrated in fish[13], birds[14], cows[15], and rats[16]. A 2007 study by La Guardia and colleagues measured PBDE congeners "from a wastewater treatment plant (sludge) to receiving stream sediments and associated aquatic biota"; it "support[ed] the hypothesis that metabolic debromination of -209 [i.e., decaBDE] does occur in the aquatic environment under realistic conditions."[17] In another 2007 study, Stapleton and Dodder exposed "both a natural and a BDE 209 spiked [house] dust material" to sunlight, and found "nonabrominated congeners" and "octabrominated congeners" consistent with debromination of decaBDE in the environment.[18]

In March 2007 the Illinois Environmental Protection Agency concluded "it can be questioned how much abiotic and microbial degradation [of decaBDE] occurs under normal environmental conditions, and it is not clear whether the more toxic lower-brominated PBDEs are produced in significant quantities by any of these pathways."[19] In September 2007 a U.K. Advisory Committee on Hazardous Substances issued an opinion that "The relevance of this potential degradation [photodegradation, biodegradation, and metabolism of decaBDE] to the real world is questionable. ... it is impossible to say what the level of concern is unless we have reliable figures for the degradation in the field."[20]

[edit] Pharmacokinetics

Exposure to decaBDE is thought to occur by means of ingestion.[2] Humans and animals do not absorb decaBDE well; at most, perhaps 2% of an oral dose is absorbed.[21][22] It is believed that "the small amount of decaBDE that is absorbed can be metabolized"[2].

Once in the body, decaBDE "might leave unchanged or as metabolites, mainly in the feces and in very small amounts in the urine, within a few days," in contrast with "lower brominated PBDEs... [which] might stay in your body for many years, stored mainly in body fat."[2] In workers with occupational exposure to PBDEs, the calculated apparent half-life for decaBDE was 15 days, as opposed to (for example) an octaBDE congener with a half-life of 91 days.[23]

[edit] Detection in humans

In the general population, decaBDE has been found in blood and breast milk, but at lower levels than other PBDE congeners such as 47, 99, and 153.[24] An investigation carried out by the WWF detected decaBDE in blood samples from 3 of 14 ministers of health and environment of European Union countries, while (for example) PBDE-153 was found in all 14.[25]

[edit] Possible health effects in humans

In 2004, ATSDR wrote "Nothing definite is known about the health effects of PBDEs in people. Practically all of the available information is from studies of laboratory animals. Animal studies indicate that commercial decaBDE mixtures are generally much less toxic than the products containing lower brominated PBDEs. Because of its very different toxicity, decaBDE is expected to have relatively little effect on the health of humans."[2] Based on animal studies, the possible health effects of decaBDE in humans involve the liver, thyroid, reproductive/developmental effects, and neurological effects.[26]

[edit] Liver

ATSDR stated in 2004 "We don’t know if PBDEs can cause cancer in people, although liver tumors developed in rats and mice that ate extremely large amounts of decaBDE throughout their lifetime. On the basis of evidence for cancer in animals, decaBDE is classified as a possible human carcinogen by EPA [i.e., the United States Environmental Protection Agency ]."[2]

[edit] Thyroid

One 2006 review concluded "Decreases in thyroid hormone levels have been reported in several studies, and thyroid gland enlargement (an early sign of hypothyroidism) has been shown in studies of longer duration exposure."[26] A 2007 experiment giving decaBDE to pregnant mice found that decaBDE "is likely an endocrine disrupter in male mice following exposure during development" based on results such as decreased serum triiodothyronine.[27]

[edit] Reproductive/developmental effects

"Significant data gaps" exist in the scientific literature on a possible relationship between decaBDE and reproductive/developmental effects.[26] A 2006 study of mice found that decaBDE decreased some "sperm functions."[28]

[edit] Neurological effects

A single study in 2003 on neurotoxicity in mice was "criticized for certain procedural and statistical problems."[26] A 2007 study in mice "suggest[ed] that decaBDE is a developmental neurotoxicant that can produce long-term behavioral changes following a discrete period of neonatal exposure."[29] Administration of decaBDE to male rats at 3 days of age in another 2007 study "was shown to disrupt normal spontaneous behaviour at 2 months of age."[30]

[edit] Overall risks and benefits

In 2002-2003 the American Chemistry Council’s Brominated Flame Retardant Industry Panel, citing an unpublished 1997 study, estimated that 280 deaths due to fires are prevented each year in the U.S. because of the use of decaBDE.[21][22] The American Council on Science and Health, in a 2006 report largely concerning decaBDE, concluded that "the benefits of PBDE flame retardants, in terms of lives saved and injuries prevented, far outweigh any demonstrated or likely negative health effects from their use."[31] A 2006 study concluded "current levels of Deca in the United States are unlikely to represent an adverse health risk for children."[32] A report from the Swedish National Testing and Research Institute concerning the costs and benefits of decaBDE in television sets that was funded by BSEF assumed "no cost for injuries (either to humans or the environment) due to exposure to flame retardants... as there was no indication that such costs exist for DecaBDE"; it found that decaBDE's benefits exceeded its costs.[33]

[edit] Voluntary and governmental actions

[edit] Europe

In Germany, plastics manufacturers and the textile additives industry "declared in 1986 a voluntary phase-out of the use of PBDEs, including Deca-BDE."[34] Although decaBDE was to be phased out of electrical and electronic equipment in the EU by 2006 under the EU's Restriction of Hazardous Substances Directive (RoHS), decaBDE use has been exempted from RoHS beginning in 2005 and continuing for five years.[35][36] A case in the European Court of Justice against the RoHS exemption is pending.[4] Sweden, an EU member, banned decaBDE as of 2007.[24][37] The European Brominated Flame Retardant Industry Panel (EBFRIP), which represents the chemical industry, stated that Sweden's ban on decaBDE "is a serious breach of EU law."[38] The environment agency of Norway, which is a member of the European Free Trade Association but is not a member of the EU, recommended that decaBDE be banned from electronic products; however, the Norwegian coalition government rejected the recommendation.[39]

[edit] United States

A representative of the BSEF stated in 2007 "There's no reason to ban deca ... it's not a scientifically supportable position."[37] Nevertheless, as of mid-2007 two states had instituted measures to phase out decaBDE. In April 2007 the state of Washington passed a law banning the manufacture, sale, and use of decaBDE in mattresses as of 2008; the ban "could be extended to TVs, computers and upholstered residential furniture in 2011 provided an alternative flame retardant is approved."[5][40][41] In June 2007 the state of Maine passed a law "ban[ning] the use of deca-BDE in mattresses and furniture on January 1, 2008 and phas[ing] out its use in televisions and other plastic-cased electronics by January 1, 2010."[42][43] As of 2007, other states considering restrictions on decaBDE include California, Connecticut, Hawaii, Illinois, Massachusetts, Michigan, Minnesota,[44] Montana, and New York.[37][45]

[edit] Alternatives

A number of reports have examined alternatives to decaBDE as a flame retardant.[34][46][47][48][49][50] The BSEF noted in 2007 that "any substance used as an alternative to Deca will carry its own risks, and we may not even be aware just what those risks are because no alternative has been studied as extensively as Deca.”[51] At least three U.S. states have evaluated decaBDE alternatives:

  • Washington concluded in 2006 that "there do not appear to be any obvious alternatives to Deca-BDE that are less toxic, persistent and bioaccumulative and have enough data available for making a robust assessment" and that "there is much more data available on Deca-BDE than for any of the alternatives."[52]
  • Maine in January 2007 stated that bisphenol A diphenyl phosphate (also known as BDP, BPADP, bisphenol A diphosphate, or BAPP) "is not a suitable alternative to decaBDE" because "one of the degradation products is bisphenol A, a potent endocrine disruptor."[4] The report listed resorcinol bis(diphenyl phosphate) (also known as RDP), magnesium hydroxide, and other chemicals as alternatives to decaBDE that are "most likely to be used."[4]
  • A March 2007 report from Illinois categorized decaBDE alternatives as "Potentially Unproblematic," "Potentially Problematic," "Insufficient Data," and "Not Recommended."[19] The "Potentially Unproblematic" alternatives were BAPP, RDP, aluminum trihydroxide, and magnesium hydroxide.[19]

[edit] References

  1. ^ a b c European Union risk assessment report. Bis(pentabromophenyl) ether. Luxembourg: Office for Official Publications of the European Communities, 2002. Publication EUR 20402 EN.
  2. ^ a b c d e f g h i Agency for Toxic Substances and Disease Registry. Toxicological Profile for Polybrominated Biphenyls and Polybrominated Diphenyl Ethers (PBBs and PBDEs). Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service, September 2004.
  3. ^ Bromine Science and Environmental Forum. Major Brominated Flame Retardants Volume Estimates: Total Market Demand By Region in 2001. 21 January 2003.
  4. ^ a b c d e Brominated Flame Retardants: Third annual report to the Maine Legislature. Augusta, Maine: Maine Department of Environmental Protection and Maine Center for Disease Control & Prevention, January 2007.
  5. ^ a b Sissell, Kara. Washington State Signs Law Regulating Deca-PBDE. Chemical Week, May 2, 2007.
  6. ^ a b c Alcock, Ruth E, and Jerry Busby (2006). Risk Migration and Scientific Advance: The Case of Flame-Retardant Compounds. Risk Analysis 26 (2), 369–381, 2006.
  7. ^ a b Hale, Robert C., et al. Brominated flame retardant concentrations and trends in abiotic media. Chemosphere 2005;64(2):181-6. PMID 16434082
  8. ^ Bromine Science and Environmental Forum. Bromine: Frequently Asked Questions. Revised edition, October 2001.
  9. ^ a b Update of the Risk Assessment of Bis(Pentabromophenyl) Ether (Decabromodiphenyl Ether) CAS Number: 1163-19-5 EINECS Number: 214-604-9 Final Environmental Draft of May 2004.
  10. ^ Stapleton, Heather M. Brominated Flame Retardants: Assessing DecaBDE Debromination in the Environment. Brussels, Belgium: EPHA Environment Network, May 2006.
  11. ^ Bromine Science and Environmental Forum. EEN Report: Assessing DecaBDE Debromination in the Environment. 31 May 2006.
  12. ^ He, Jianzhong, et al. Microbial Reductive Debromination of Polybrominated Diphenyl Ethers (PBDEs). Environmental Science & Technology 40(14), 4429-4434, 2006.
  13. ^ Stapleton, Heather M., et al. In Vivo and In Vitro Debromination of Decabromodiphenyl Ether (BDE 209) by Juvenile Rainbow Trout and Common Carp. Environmental Science & Technology 40(15), 4653-4658, 2006.
  14. ^ Van den Steen, E., et al. Accumulation, tissue-specific distribution and debromination of decabromodiphenyl ether (BDE 209) in European starlings (Sturnus vulgaris). Environmental Pollution 2007 Jul;148(2):648-53. PMID 17239511
  15. ^ Kierkegaard, Amelie, et al. Fate of Higher Brominated PBDEs in Lactating Cows. Environmental Science & Technology 41(2), 417-423, 2007.
  16. ^ Huwe, Janice K., and David J. Smith. Accumulation, Whole-Body Depletion, and Debromination of Decabromodiphenyl Ether in Male Sprague-Dawley Rats Following Dietary Exposure. Environmental Science & Technology 41(7), 2371-2377, 2007. (Erratum, 41(12), 4486, 2007.)
  17. ^ La Guardia, Mark J., et al. Evidence of Debromination of Decabromodiphenyl Ether (BDE-209) in Biota from a Wastewater Receiving Stream. Environmental Science & Technology 2007;41(19):6663-6670.
  18. ^ Stapleton, Heather, and Nathan Dodder. Photodegradation of Decabromodiphenyl Ether in House Dust by Natural Sunlight. Environmental Toxicology and Chemistry, in press ("Accepted: August 8, 2007").
  19. ^ a b c Illinois Environmental Protection Agency. Report on Alternatives to the Flame Retardant DecaBDE: Evaluation of Toxicity, Availability, Affordability, and Fire Safety Issues. March 2007.
  20. ^ Advisory Committee on Hazardous Substances. ACHS opinion on the Draft Environmental Risk Assessment Report for Decabromodiphenyl ether (DecaBDE) (CAS 1163-19-5). Department for Environment, Food and Rural Affairs, September 2007.
  21. ^ a b Voluntary Children’s Chemical Evaluation Program (VCCEP) Data Summary: Decabromodiphenyl Ether (a.k.a. Decabromodiphenyl Oxide, DBDPO) CAS # 1163-19-5. American Chemistry Council’s Brominated Flame Retardant Industry Panel (BFRIP), December 17, 2002.
  22. ^ a b Report of the Peer Consultation Meeting On Decabromodiphenyl Ether. American Chemistry Council’s Brominated Flame Retardant Industry Panel for the Voluntary Children's Chemical Evaluation Program (VCCEP), September 30, 2003.
  23. ^ Thuresson, Kaj, et al. Apparent Half-Lives of Hepta- to Decabrominated Diphenyl Ethers in Human Serum as Determined in Occupationally Exposed Workers. Environmental Health Perspectives 2006 February;114(2):176–181.
  24. ^ a b Lorber, Matthew. Exposure of Americans to polybrominated diphenyl ethers. Journal of Exposure Science and Environmental Epidemiology (2007), 1–18.
  25. ^ WWF Detox Campaign. Bad Blood? A Survey of Chemicals in the Blood of European Ministers. October 2004.
  26. ^ a b c d Illinois Environmental Protection Agency. DecaBDE Study: A Review of Available Scientific Research. January 2006.
  27. ^ Tseng LH, et al. Developmental exposure to decabromodiphenyl ether (PBDE 209): Effects on thyroid hormone and hepatic enzyme activity in male mouse offspring. Chemosphere 2007 Aug 13. PMID 17698168
  28. ^ Tseng LH, et al. Postnatal exposure of the male mouse to 2,2',3,3',4,4',5,5',6,6'-decabrominated diphenyl ether: decreased epididymal sperm functions without alterations in DNA content and histology in testis. Toxicology 2006 Jul 5;224(1-2):33-43. PMID 16713668
  29. ^ Rice DC, et al. Developmental delays and locomotor activity in the C57BL6/J mouse following neonatal exposure to the fully-brominated PBDE, decabromodiphenyl ether. Neurotoxicol Teratol. 2007 Jul-Aug;29(4):511-20. PMID 17482428
  30. ^ Viberg H, et al. Changes in spontaneous behaviour and altered response to nicotine in the adult rat, after neonatal exposure to the brominated flame retardant, decabrominated diphenyl ether (PBDE 209). Neurotoxicology 2007 Jan;28(1):136-42. PMID 17030062
  31. ^ Kucewicz, William P. Brominated Flame Retardants: A Burning Issue. New York: American Council on Science and Health, August 2006.
  32. ^ Hays SM, Pyatt DW. Risk assessment for children exposed to decabromodiphenyl (oxide) ether (Deca) in the United States. Integr Environ Assess Manag. 2006 Jan;2(1):2-12. PMID 16640311
  33. ^ Simonson, Margaret, et al. Cost Benefit Analysis Model for Fire Safety Methodology and TV (DecaBDE) Case Study. Swedish National Testing and Research Institute, SP Report 2006:28.
  34. ^ a b Lassen, Carsten, et al. Deca-BDE and Alternatives in Electrical and Electronic Equipment. Danish Environmental Protection Agency, 2006.
  35. ^ Commission Decision of 13 October 2005 amending for the purposes of adapting to the technical progress the Annex to Directive 2002/95/EC of the European Parliament and of the Council on the restriction of the use of certain hazardous substances in electrical and electronic equipment. Official Journal of the European Union 15.10.2005.
  36. ^ Washington State Departments of Health and Ecology. Developments within the European Union Regarding Deca-BDE as Interpreted by Health and Ecology Staff. October 12, 2005.
  37. ^ a b c Stiffler, Lisa. PBDEs: They are everywhere, they accumulate and they spread. Seattle Post-Intelligencer, March 28, 2007.
  38. ^ European Brominated Flame Retardant Industry Panel. [Swedish move to restrict Deca-BDE contradicts scientific conclusions and EU Law.] "Updated 5 September 2006."
  39. ^ Scott, Alex. Norway Takes Pro-Industry Stance on Deca-BDE. Chemical Week, September 20, 2006.
  40. ^ Stiffler, Lisa. Chemical ban puts industry on the defensive. Seattle Post-Intelligencer, April 16, 2007.
  41. ^ Washington Engrossed Substitute House Bill 1024, Chapter 65, Laws of 2007.
  42. ^ Maine Legislature votes to ban toxic Deca flame retardant. Natural Resources Council of Maine, May 24th, 2007.
  43. ^ Maine House Democrats. Governor signs deca ban bill into law: State will require phase-out of the flame retardant in household items. June 14, 2007.
  44. ^ SF0651 Status in Senate for Legislative Session 85
  45. ^ Maine Joins Washington, Bans PBDEs. Washington, DC: National Caucus of Environmental Legislators, June 18, 2007.
  46. ^ Leisewitz, André, et al. Substituting Environmentally Relevant Flame Retardants: Assessment Fundamentals: Results and summary overview. Berlin, Germany: Federal Environmental Agency (Umweltbundesamt), June 2001.
  47. ^ Pure Strategies, Inc. Decabromodiphenylether: An Investigation of Non-Halogen Substitutes in Electronic Enclosure and Textile Applications. Lowell, MA: University of Massachusetts Lowell, Lowell Center for Sustainable Production, April 2005.
  48. ^ Posner, Stefan, and Linda Börås. Survey and technical assessment of alternatives to Decabromodiphenyl ether (DecaBDE) in plastics. Stockholm: Swedish Chemicals Inspectorate, June 2005.
  49. ^ Stuer-Lauridsen, Frank, et al. Health and Environmental Assessment of Alternatives to Deca-BDE in Electrical and Electronic Equipment. Danish Environmental Protection Agency, 2007.
  50. ^ Pakalin, Sazan, et al. Review on production processes of decabromodiphenyl ether (decaBDE) used in polymeric applications in electrical and electronic equipment, and assessment of the availability of potential alternatives to decaBDE. European Chemicals Bureau, January 2007.
  51. ^ Bromine Science and Environmental Forum. Washington State Establishes Flame Retardant Review Process. Initiates process to search for “alternative” to proven flame retardant known as Deca. Press release, April 17, 2007.
  52. ^ Washington State Polybrominated Diphenyl Ether (PBDE) Chemical Action Plan: Final Plan. Washington State Departments of Ecology and Health, January 19, 2006.
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