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 Uploading ....Green Screen Rating: Benchmark 1
Greenscreen version: 1.0
Rationale: Meets criteria 1a, 1b, and 1c for Benchmark 1 by way of breakdown products (PentaBDE, OctaBDE). Details and discussion follow.
| Fate | EcoTox | Human - Tier 1 | Human - Tier 2 | Physical | | P | B | AA | CA | C | M | R | D | ED | N | AT | Cr | Rs | Ss | IS | ST | Rx | F | | vH | M | L | L | M | L | L | M | M | M | L | L | L | nd | nd | L | nd | nd
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See Legend Specific Chemical Information | Chemical Name: | Decabromodiphenyl ether | | Also called: | decaBDE, bis(pentabromophenyl) ether | | CAS: | 1163-19-5 | | EINECS: | 214-604-9 | | SMILES Notation: | O(c(c(c(c(c1Br)Br)Br)Br)c1Br)c(c(c(c(c2Br)Br)Br)Br)c2B | Applications/Functional UseDescription (See Guidance): This chemical is used for.... Tags to search for applications/functional uses (See Guidance): Flame retardant (television casings) Flame retardant (textiles) Transformation Products and Ratings | Life-cycle Stage | Transformation Pathway | Transformation Products | CAS Number | Green Screen Rating | | any release | photodegradation, metabolism in fish (ref) | PentaBDE | 32534-81-9 | 1 | | any release | photodegradation, metabolism in fish (ref) | OctaBDE | 32536-52-0 | 1 |
Supporting Chemical Data by Hazard Endpoint
Environmental Fate (see guidance) Persistance (P) Score: vH
“Swedish and Dutch scientists measured atmospheric deposition of PBDEs in the Baltic Sea for the first time in research published in January 2004. Measurements were taken from an island in the central basin of the Baltic Sea far from human settlement; deposition of PBDEs would therefore be the result of long-range transport through the atmosphere. The research compared deposition of PBDEs to the better documented deposition of PCBs. The atmospheric deposition of PBDEs exceeded that of PCBs by a factor of 40, while deposition of PCBs was decreasing. BDE-209 comprised the largest percentage of PBDEs detected, with BDE-47 and BDE-99 representing the next most abundant congeners.”(1)
“Half-life information for Deca-BDE in water and other media indicate that it is persistent in the environment.” (2)
--but--
“While further research is needed, Ecology and DOH believe the following conclusions are appropriate:
1. Deca-BDE undergoes degradation. The most common path in laboratory studies is the debromination of deca-BDE to lower PBDE species. Other degradation products have been found in some studies, including brominated dioxins, phenols and dibenzofurans. The negative impact these degradation products have upon human health and the environment is unquantified, but the abundance of studies that document negative impacts makes this a matter of considerable concern.
2. Debromination of deca-BDE occurs through light exposure (both UV radiation and direct sunlight) and biological activity. These pathways lead to a variety of degradation products.
3. The rate of debromination has been determined in laboratory studies. Further work is needed to determine the debromination rate under environmental conditions. Degradation in the environment occurs more slowly. This phenomenon is consistent with what occurs to halogenated compounds with similar chemical structure, and is supported by knowledge of standard chemical processes.
4. Deca-BDE will continue to be a source of lower brominated diphenyl ethers and other degradation products for some time.” (2)
Bioaccumulation (B) Score: M
“the available data do suggest that uptake by organisms in the environment could occur if the organisms are exposed to decabromodiphenyl ether in a suitable form. The available data also indicate that decabromodiphenyl ether has a relatively short elimination half-life from organisms. This should limit the potential for bioaccumulation of decabromodiphenyl ether, although the fate of metabolites is unclear and the substance can be retained after exposure is stopped, as demonstrated in the study with Grey Seals.” (3)
“Occurrence of BDE-183, BDE-203, and BDE-209 in addition to other major congeners such as BDE-47, BDE-99, and BDE-100 suggests exposure to all technical PBDE formulations (penta-, octa-, and deca-BDE mixtures) for marine fish. Predominance of BDE-209 relative to otherPBDE congeners in sharks is unique and suggests exposure to deca- BDE mixtures. Biomagnification of ΣPBDEs and ΣPCBs in the fish-shark-dolphin foodweb indicates the potential for elevated accumulation
of these contaminants by apex predators. ΣPBDE and ΣPCB concentrations have increased exponentially, with a doubling time of 2–3 years for bull sharks, and 3–4 years for bottlenose dolphin.” (4)
Ecotoxicity(See Guidance) Acute Aquatic (AA) Toxicity Score: L
“The available aquatic toxicity data for decabromodiphenyl ether show no effects at the limit of water solubility of the substance.”(5)
Chronic Aquatic (CA) Toxicity Score: L
“The available aquatic toxicity data for decabromodiphenyl ether show no effects at the limit of water solubility of the substance.”(5)
Human Health -- Tier 1(See Guidance)
Carcinogenicity (C) Score: M
“Based on the limited evidence of carcinogenicity in animals in the NTP bioassay (significantlyincreased incidences of neoplastic liver nodules in rats and combined hepatocellular adenomas and carcinomas in mice), as well as the lack of human data, decaBDE has been classified in EPA Group C (possible human carcinogen) and IARC Group 3 (not classifiable as to its carcinogenicity to humans).” “Information on carcinogenic effects of PBDEs in animals is limited to results of chronic bioassays of decaBDE mixtures in rats and mice (Kociba et al. 1975; Norris et al. 1975b; NTP 1986). As summarized below, these studies provide Limited evidence for the carcinogenicity of decaBDE in animals. No carcinogenicity studies of octaBDE or pentaBDE were located in the available literature.” Mutagenicity (M) Score: L
“Cytogenetic examination of bone marrow cells showed no increase in aberrations in maternal and neonatal rats following maternal oral exposure to ≤100 mg/kg/day of a 77.4% decaBDE mixture (containing 21.8% nonaBDE and 0.8% octaBDE) for 90 days prior to mating and during mating, gestation, and lactation (Norris et al. 1973, 1975a). In vitro assays found that decaBDE did not induce gene mutations in bacterial cells (S. typhimurium TA98, TA100, TA1535, or TA1537) or mammalian cells (mouse lymphoma L5178Y cells), and did not induce sister chromatid exchange or chromosomal aberrations in Chinese hamster ovary cells (NTP 1986).”(8)“On the whole, results from different Salmonella tests can be considered as negative. DBDPO does not exhibit any cytogenetic effects in vitro nor in vivo. It is noticeable that some of these tests present some limitations. However given the absence of alert-structure for genotoxicity according to Tenant and Ashby (1991), the negative results obtained in the mutagenicity tests with DBDPO and also with OBDPO and PeBDPO, no concern about mutagenicity may be assumed.”(9) Reproductive Toxicity (R) Score: L
Information on the reproductive toxicity of PBDEs is limited to a one-generation study of a low-purity decaBDE product (77.4% decaBDE, 21.8% nonaBDE, 0.8% octaBDE) in rats that found no exposure-related functional effects .” (10)
Developmental Toxicity (D) Score: M
"No prenatal developmental toxicity was found in a comprehensive study of commercial decaBDE product (Hardy et al. 2001, 2002 (11)
A lower purity commercial decaBDE product (77% decaDBE, 22% nonaBDE, 0.8% octaBDE) used in the 1970s was fetotoxic in rats at high dose levels that were not maternally toxic. Developmental effects were investigated in rats that were exposed to doses of 10, 100, or 1,000 mg/kg/day by gavage on GDs 6– 15 and examined on GD 21 (Dow Chemical Co. 1985; Norris et al. 1975b). No treatment-related maternal toxicity was observed. The numbers of fetuses with subcutaneous edema and delayed ossification of normally developed skull bones were significantly increased at 1,000 mg/kg/day.Resorptions were significantly (p<0.05) increased at ≥10 mg/kg/day compared to controls as indicated by resorption/implantation site percentages [1% (3/288), 9% (12/141), 10% (13/135), and 4% (9/203)] and percentages of litters with resorptions [12% (3/25), 64% (9/14), 57% (8/14), and 39% (7/18)]. The resorptions were considered secondary to unusually low control values and unrelated to treatment because (1) the data do not follow a dose-response relationship across the three dose levels, and (2) the rates in the high dose group are comparable to historical control values.”
Endocrine Disruption (ED) Score: M
”Van der Ven et al. (2006) studied the effects of a number of PBDE congeners on thyroid hormones, blood biochemistry, and organ weights in adult rats. DecaBDE decreased T3 levels, thymus weight, and brain weight. DecaBDE was less active than other congeners.” (12)
“There is suggestive evidence of hypothyroidisma small group of workers who werein occupationally exposed to decaBDE as well as PBBs (Bahn et al. 1980), as summarized in the preceding subsection on endocrine effects of PBBs. In another study, plasma levels of thyroid hormones (T3 and free T4) and eight PBDE congeners (tetra- to heptaBDEs) were monitored for 198–221 days in three electronic dismantling workers (Pettersson et al. 2002). The hormones remained within normal ranges and there were no correlations between levels of hormones and congeners.” (13)
Neurotoxicity (N) Score: M
“As was discussed in our 2006 report, Swedish investigators documented changes in motor activity in male mice exposed to a single dose of a number of PBDE congeners administered separately during early postnatal development, including PBDE-47, PBDE-99, PBDE-153 or deca BDE. For all congeners, treated mice were less active than controls at the beginning of the one-hour observation period, but did not decrease their activity over time as did controls.
This is referred to as failure of habituation, and may result from cognitive or attentional deficits or changes in arousal level.
The Swedish investigators have replicated the effects of decaBDE on activity using rats (Viberg et al., 2006a). Male rats were given a single dose of decaBDE on postnatal day (PND) 3 and tested during early adulthood. The high dose group exhibited lower activity at the beginning of the observation period, and failed to habituate over the one-hour session. The low dose rats, on the other hand, were more active than controls at the beginning of the session, and habituated normally. Such a bi-phasic dose-effect curve (e.g., increase at lower doses and decrease at higher) is commonly observed for motor activity, for drugs as well as environmental chemicals. (Amphetamine is a classic example.) The cholinergic drug nicotine decreased activity in the high-dose group.”
“Study of endocrine and behavioral effects of deca BDE by USM and the Maine CDC As described in last year’s presentation to the legislature, a study is ongoing at the University of Southern Maine by Dr. Vincent Markowski in collaboration with Dr. Deborah Rice at the Maine CDC, under contract to Maine CDC. Mice were dosed on PND 2-15 with 6 or 20 mg/kg/ day of decaBDE, and locomotor activity and cognitive function were tested during adulthood.
As young adults, males in the higher dose group were more active than controls over a twohour period, but habituated (decreased their activity) over the observation period in the same manner as controls (Rice et al., submitted). There was no effect in the treated females. Treated mice made more errors on a visual discrimination task compared to controls, indicative of cognitive impairment. Blood concentrations of the thyroid hormone T4 were decreased in males at 21 days of age in a dose-dependent manner.”(14)
“Neurobehavioral effects of individual PBDE congeners were evaluated in mice that were exposed during perinatal and/or early postnatal periods to 2,2’,4,4’-tetraBDE (BDE 47), 2,2’,4,4’,5-pentaBDE (BDE 99), 2,2’,4,4’,5,5’-hexaBDE (BDE 153), or 2,2’,3,3’,4,4’,5,5’,6,6’-decaBDE (BDE 209). Most of these studies used similar single oral dose experimental designs and evaluated spontaneous motor behavior and swim maze performance at 2–6 months of age.
The findings collectively indicate that the nervous system is a target of particular PBDE congeners during a defined critical phase of neonatal brain development, as shown by mild impairments in spontaneous motor behavior and learning and memory in older mice.” (15)
Human Health--Tier 2 (See Guidance)
Acute Toxicity (AT) Score: L
“DBDPO [decaBDE] exhibits a low acute oral, dermal and inhalation toxicity.” (16)
Corrosion/Irritation of the Skin/Eyes (Cr) Score: L
“DBDPO [decaBDE] is not an irritant for skin or eyes.” (17)
Sensitization of the Respiratory System (RSen) Score: nd
Sensitization of the Skin (SSen) Score: L “Taking into account the negative results from studies in animals on OBDPO and in regard
with the two quite large human studies reported on DBDPO, this substance can be considered as a non skin sensitizer.” (18)
Immune System Effects (IS) Score: nd (no data)
Systemic/Organ Toxicity (ST) Score: L
“The hepatotoxic potential of lower brominated PBDE mixtures is well-documented in animals by oral exposure. The spectrum of observed hepatic effects includes microsomal enzyme induction, liver enlargement, and degenerative histopathologic alterations that progress to tumors. Repeated dietary exposure to PBDEs typically caused liver enlargement with or without degenerative changes, and effects were generally dose-related in incidence and severity, more frequent and pronounced in males than females, and more severe with octaBDE and pentaBDE than decaBDE. For example, subchronic oral studies in rats showed that commercial pentaBDE mixtures were hepatotoxic at doses ≤10 mg/kg/day. Increased liver weight and hepatocellular enlargement with vacuolation occurred in rats exposed to commercial pentaBDE doses as low as 2–9 mg/kg/day for 4–13 weeks. Increased incidences of degeneration and necrosis of individual hepatocytes were observed 24 weeks following exposure to ≥2 mg/kg/day of commercial pentaBDE for 90 days in rats. In contrast, high purity commercial decaBDE caused no liver pathology in rats and mice at estimated doses as high as 2,000–8,000 and 2,375– 9,500 mg/kg/day, respectively. High purity commercial decaBDE caused liver effects only following lifetime exposure to doses that were still very high. Exposure to 94–97% decaBDE for 103 weeks caused liver thrombosis and degeneration in rats at 2,240 mg/kg/day, and centrilobular hypertrophy and granulomas in mice at ≥3,200 mg/kg/day. No studies are available on hepatic effects of PBDEs in humans. Based on the evidence in animals, lower brominated PBDEs are potentially hepatotoxic in humans.” (19)
Physical Properties (See Guidance)
Reactivity (Rx) Score: vH, H, M, L, or nd in BOLD or ITALICS (See Guidance)
[Supporting studies]
[1) References]
Flammability (F) Score: vH, H, M, L, or nd in BOLD or ITALICS (See Guidance)
[Supporting studies]
[1) References]
ReferencesReferences
1) EU 2004. European Union. 2004. Update of the Risk Assessment of Bis(Pentabromophenyl Ether
(decabromodiphenyl ether). Oxfordshire: United Kingdom, Environment Agency. pg 90
2) Washington State PBDE Chemical Action Plan (WA 2006). pg 29, 35, 52
3) EU 2004. European Union. 2004. Update of the Risk Assessment of Bis(Pentabromophenyl Ether
(decabromodiphenyl ether). Oxfordshire: United Kingdom, Environment Agency. pg 38
4) Johnson-Restrepo 2005. Johnson-Restrepo B, K Kannan, R Addink and DH Adams. 2005.
Polybrominated Diphenyl Ethers and Polychlorinated Biphenyls in a Marine Foodweb of
Coastal Florida. Environmental Science and Technology 39:8243-8250.
5) EU 2004. European Union. 2004. Update of the Risk Assessment of Bis(Pentabromophenyl Ether
(decabromodiphenyl ether). Oxfordshire: United Kingdom, Environment Agency. pg 192
6) Kociba et al. 1975; Norris et al. 1975b; NTP 1986
7) ATSDR 2004. US Department of Health and Human Services, Public Health Service, Agency for
Toxic Substances and Disease Registry. 2004. Toxicological Profile for Polybrominated Biphenyls and
Polybrominated Diphenyl Ethers (http://www.atsdr.cdc.gov/toxprofiles/tp115-p.pdf — accessed
January 22, 2007). pg 45, 224
8) ATSDR 2004. US Department of Health and Human Services, Public Health Service, Agency for
Toxic Substances and Disease Registry. 2004. Toxicological Profile for Polybrominated Biphenyls and
Polybrominated Diphenyl Ethers (http://www.atsdr.cdc.gov/toxprofiles/tp115-p.pdf — accessed
January 22, 2007). pg 241
9) EU 2002. European Union, European Chemicals Bureau. 2002. Risk Assessment Report —
Bis(Pentabromophenyl) ether. Italy: European Chemicals Bureau. pg 143.
10) ATSDR 2004. US Department of Health and Human Services, Public Health Service, Agency for
Toxic Substances and Disease Registry. 2004. Toxicological Profile for Polybrominated Biphenyls and
Polybrominated Diphenyl Ethers (http://www.atsdr.cdc.gov/toxprofiles/tp115-p.pdf — accessed
January 22, 2007). pg 40
11) ATSDR 2004. US Department of Health and Human Services, Public Health Service, Agency for
Toxic Substances and Disease Registry. 2004. Toxicological Profile for Polybrominated Biphenyls and
Polybrominated Diphenyl Ethers (http://www.atsdr.cdc.gov/toxprofiles/tp115-p.pdf — accessed
January 22, 2007). pg 212, 213
12) Maine 2007. Maine Department of Environmental Protection and Maine Center for Disease Control
and Prevention. 2007. Brominated Flame Retardants: Third annual report to the Maine Legislature.
Augusta: Maine DEP. pg 15
13) ATSDR 2004. US Department of Health and Human Services, Public Health Service, Agency for
Toxic Substances and Disease Registry. 2004. Toxicological Profile for Polybrominated Biphenyls and
Polybrominated Diphenyl Ethers (http://www.atsdr.cdc.gov/toxprofiles/tp115-p.pdf — accessed
January 22, 2007). pg 75
14) Maine 2007. Maine Department of Environmental Protection and Maine Center for Disease Control
and Prevention. 2007. Brominated Flame Retardants: Third annual report to the Maine Legislature.
Augusta: Maine DEP. pg 17, 18
15) ATSDR 2004. US Department of Health and Human Services, Public Health Service, Agency for
Toxic Substances and Disease Registry. 2004. Toxicological Profile for Polybrominated Biphenyls and
Polybrominated Diphenyl Ethers (http://www.atsdr.cdc.gov/toxprofiles/tp115-p.pdf — accessed
January 22, 2007). pg 42
16) EU 2002. European Union, European Chemicals Bureau. 2002. Risk Assessment Report —
Bis(Pentabromophenyl) ether. Italy: European Chemicals Bureau.
17) EU 2002. European Union, European Chemicals Bureau. 2002. Risk Assessment Report —
Bis(Pentabromophenyl) ether. Italy: European Chemicals Bureau.. pg 133
18) EU 2002. European Union, European Chemicals Bureau. 2002. Risk Assessment Report —
Bis(Pentabromophenyl) ether. Italy: European Chemicals Bureau. pg 134
19) ATSDR 2004. US Department of Health and Human Services, Public Health Service, Agency for
Toxic Substances and Disease Registry. 2004. Toxicological Profile for Polybrominated Biphenyls and
Polybrominated Diphenyl Ethers (http://www.atsdr.cdc.gov/toxprofiles/tp115-p.pdf — accessed
January 22, 2007). pg 43
Chemical Structure
Legend
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vH
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| Very High | H
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| High | M
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| Medium | L
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| Low | nd
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| No data | X
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| Estimate (vH, H, M, L) | I
|
| Inconclusive/contradictory data |
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