Decabromodiphenyl ether (also referred to as decaBDE, DBDE, BDE-209) is a brominated flame retardant which belongs to the group of polybrominated diphenyl ethers (PBDEs). It was commercialised in the 1970s and was initially thought to be safe, but is now recognised as a hazardous and persistent pollutant. It was added to Annex A of the Stockholm Convention on Persistent Organic Pollutants in 2017,Reference: C.N.766.2017.TREATIES-XXVII.15 (Depositary Notification) which means that treaty members must take measures to eliminate its production and use. The plastics industry started switching to decabromodiphenyl ethane as an alternative in the 1990s, but this is now also coming under regulatory pressure due to concerns over human health.
Composition, uses, and production Commercial decaBDE is a technical mixture of various PBDE congeners (related compounds). Congener number 209 (decabromodiphenyl ether) and nonabromodiphenyl ether are the main components.Joint Research Centre European inventory of Existing Commercial chemical Substances The term decaBDE alone refers to only decabromodiphenyl ether, the single "fully brominated" PBDE.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.
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. In 2012 between 2500 and 5000 metric tonnes of Deca-BDE was sold in Europe. As of 2007, Albemarle in the U.S., Chemtura in the U.S., ICL-IP in Israel, and Tosoh Corporation in Japan are the main manufacturers of DecaBDE.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.
Despite its listing in Annex A to the Stockholm Convention, decaBDE is still produced in China, namely in the provinces Shandong and Jiangsu.
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." 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 diverse 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). 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 literatureStapleton, Heather M. Brominated Flame Retardants: Assessing DecaBDE Debromination in the Environment. Brussels, Belgium: EPHA Environment Network, May 2006. 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."
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."Illinois Environmental Protection Agency. Report on Alternatives to the Flame Retardant DecaBDE: Evaluation of Toxicity, Availability, Affordability, and Fire Safety Issues. March 2007. In September 2010, the UK Advisory Committee on Hazardous Substances issued an opinion that ‘there is strong but incomplete, scientific evidence indicating that Deca-BDE has the potential to undergo transformation to lower brominated congeners in the environment'.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
Pharmacokinetics 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.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.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. 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. A 2004 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.WWF Detox Campaign. Bad Blood? A Survey of Chemicals in the Blood of European Ministers. October 2004.
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. 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.Illinois Environmental Protection Agency. DecaBDE Study: A Review of Available Scientific Research. January 2006.
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 ]."
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." 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.
Reproductive/developmental effects "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."
Neurological effects EPA has determined that daily Deca exposures should be less than 7 μg/kg-d (micrograms per kilogram bodyweight per day) to minimize the chance of brain and nervous system toxicity.EPA. 2008. Final Integrated Risk Information System Assessment for Decabromodiphenyl ether (BDE-209). Available: EPA based its assessment on a study in 2003 on neurotoxicity in mice, which some have "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