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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).
Additional recommended knowledge
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. The term decaBDE alone refers to only decabromodiphenyl ether, the single "fully brominated" PBDE.
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." DecaBDE is also used for "polypropylene drapery and upholstery fabric" by means of backcoating and "may also be used in some synthetic carpets."
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. 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.
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." 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." 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."
DecaBDE is released by different processes into the environment, such as emissions from manufacture of decaBDE-containing products and from the products themselves. Elevated concentrations can be found in air, water, soil, food, sediment, sludge, and dust. A 2006 study concluded "in general, environmental concentrations of BDE-209 [i.e., decaBDE] appear to be increasing."
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. Debromination may be "biotic" (caused by biological means) or "abiotic" (caused by nonbiological means). 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." 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." In September 2004 an Agency for Toxic Substances and Disease Registry (ATSDR) report asserted that "DecaBDE seems to be largely resistant to environmental degradation."
In May 2006, the EPHA Environment Network (now The Health and Environment Alliance) released a report reviewing the available scientific literature and concluding the following:
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." In addition, the BSEF reiterated the findings of the May 2004 EU report.
Subsequently, many studies have been published concerning decaBDE debromination. Common anaerobic soil bacteria debrominated decaBDE and octaBDE in a 2006 study. In 2006-2007 studies, metabolic debromination of decaBDE was demonstrated in fish, birds, cows, and rats. 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." 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.
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." 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."
Exposure to decaBDE is thought to occur by means of ingestion. Humans and animals do not absorb decaBDE well; at most, perhaps 2% of an oral dose is absorbed. It is believed that "the small amount of decaBDE that is absorbed can be metabolized".
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." 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.
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. 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.
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." Based on animal studies, the possible health effects of decaBDE in humans involve the liver, thyroid, reproductive/developmental effects, and neurological effects.
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 ]."
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." 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.
"Significant data gaps" exist in the scientific literature on a possible relationship between decaBDE and reproductive/developmental effects. A 2006 study of mice found that decaBDE decreased some "sperm functions."
A single study in 2003 on neurotoxicity in mice was "criticized for certain procedural and statistical problems." 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." 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."
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. 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." A 2006 study concluded "current levels of Deca in the United States are unlikely to represent an adverse health risk for children." 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.
Voluntary and governmental actions
In Germany, plastics manufacturers and the textile additives industry "declared in 1986 a voluntary phase-out of the use of PBDEs, including Deca-BDE." 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. A case in the European Court of Justice against the RoHS exemption is pending. Sweden, an EU member, banned decaBDE as of 2007. 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." 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.
A representative of the BSEF stated in 2007 "There's no reason to ban deca ... it's not a scientifically supportable position." 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." 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." As of 2007, other states considering restrictions on decaBDE include California, Connecticut, Hawaii, Illinois, Massachusetts, Michigan, Minnesota, Montana, and New York.
A number of reports have examined alternatives to decaBDE as a flame retardant. 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.” At least three U.S. states have evaluated decaBDE alternatives:
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Decabromodiphenyl_ether". A list of authors is available in Wikipedia.|