Toxicity of PBDEs

Both animal model and in vitro studies suggest adverse developmental, reproductive, and neurotoxic as well as endocrine disruptive effects associated with exposure to PBDEs. Evidences for ElXI activity of PBDEs are based primarily on animal model studies (Van der Ven et al., 2008). Mice and rat studies on deca-DBE at a dose level of about 5 mg/kg bw/day or above resulted in B-cell activation and a reduced number of natural killer (NK) cells in the offspring (Teshima et al., 2008). The limited human toxicity data reported are summarized in Table 7.10. 

An interesting recent study (Gaylor et al., 2012) showed house aickets (Acheta domesticus) provided with free access to polyurethane foam with 8.7 wt. % of penta-BDE as well as uncontaminated food for 28 days accumulated substautial body bur-deus of 13.4mg/kg of EDC. Even with food and water available ad libitum, the crickets still ingested PBDE-contaminated foam and showed no apparent distress despite the high body burdens. However, effects on the larval stages and the role of these as vectors for PBDE transfer have not been investigated. 

The San Antonio Statement on Brominated and Chlorinated Elame Retardants (DiGangi et al., 2010), agreed upon at the 30th International Symposium on Halogenated Persistent Organic Pollutants (DiGangi et al., 2010), in San Antonio, Texas, summarizes the concerns of expert scientists on PBDEs. Abont 145 scientists 

TABLE 7.10 A Summary of Effects of Human Exposure To PBDEs 

System affected Adverse effect reported References 

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PBDEs are a class of brominated flame retardants (BFRs) used in textiles, plastics and electronic products. The effects of BFRs are associated with three commercial mixtures of PBDEs decaBDE, octaBDE and pentaBDE. In laboratory animal experiments, the toxicity of PBDEs was linked to damage to liver function and,... 

Polybrominated Diphenyl Ethers. Information on the reproductive toxicity of PBDEs is limited to a single one-generation oral study of decaBDE in rats that found no exposure-related functional effects (Dow Chemical Co. 1975 Norris et al. 1975a, 1975b). Tests of octaBDE and/or pentaBDE, particularly second-... 

There is hardly any information available on the toxicity of PBDEs in organisms in the environment. A case study has been described of a young man who developed Yusho-like health effeccts after having watched to a newly bought television set in a small non-ventilated insulated room for several hours a day during 8 consecutive months at the age of 13. PBDEs were determined in a fat biopsy and a blood sample of this man at the age of 21. PBDE levels above the detection limit were only found in the fat biopsy. PBDEs, but also tetrabromo-... 

Toxicity Results in Aqueous Samples of PBDE Degradation. 

No mortality was found in any embryo exposed to the controls. On the contrary, all the embryos exposed to the non-diluted samples of penta-, octa-, and deca-BDE commercial mixtures were dead after 24 h (Fig. 10). When the untreated PBDEs samples were diluted at 50%, a gradient of toxicity was observed penta > octa > deca. After dilution at 5%, no embryos exposed to untreated samples were dead. In agreement with our results, it has been demonstrated that the toxicity of deca-BDE is commonly lower than for octa- and penta-BDE commercial products exposures with mammalian models [64]. The different toxicity found in mammalian models and also in zebrafish should be related to the higher accumulation of lower brominated congeners in the body, because of their greater partitioning and retention in lipid-rich tissues and lower rates of metabolism and elimination in relation to deca-BDE. 

T. and Jiang, G. (2006) Quantitative structure-activity relationship for prediction of the toxicity of polybrominated diphenyl ether (PBDE) congeners. Chemosphere, 64, 515—524. 

Available intermediate- and chronic-duration oral studies in animals indicate that the thyroid and liver are the main systemic targets of PBDE toxicity as shown by effects mainly including enlargement and histological alterations in both organs and changes in serum levels of thyroid hormones. Several acute-duration studies of pentaBDE suggest that immunosuppression may also be an important health end point. Very little information is available on potential neurotoxic effects of PBDEs, mainly the results of three... 

Developmental Effects. Oral developmental toxicity studies of deca-, octa-, and pentaBDE have shown no evidence of teratogenicity in animals. Gestational exposure to a high (1,000 mg/kg/day) but maternally nontoxic dose of decaBDE was fetotoxic in rats as shown by subcutaneous edema and delayed skull bone ossification. Commercial mixtures of octaBDE caused skeletal ossification variations in rats and rabbits at maternally toxic levels and other indications of fetotoxicity at lower doses. Effects of gestational exposure to octaBDE included minimally increased postimplantation loss in rats at >10 mg/kg/day, increased resorptions in rats at 25 mg/kg/day, and increased skeletal variations in rabbits at 15 mg/kg/day and rats at 50 mg/kg/day. No evidence of fetotoxicity was found in the only available study of pentaBDE in rats at maternally toxic doses < 200 mg/kg/day. No studies are available on developmental effects of PBDEs in humans. Based on the evidence in animals, PBDEs are unlikely to cause developmental toxicity at expected levels of exposure. 

The assumption that PBBs and PBDEs share many toxicological characteristics with PCBs also does not consider geometrical differences due to the higher atomic weight and considerably larger molecular volume of bromine compare to chlorine (Hardy 2000, 2002). These differences contribute to dissimilar physical/chemical properties that can influence the relative toxicokinetics and toxicities of the chemicals. 

Polybrominated Diphenyl Ethers. No specific infonnation was located regarding interactions between PBDEs and other chemicals. PBDEs are inducers of hepatic microsomal enzymes (Carlson 1980a, 1980b Fowles et al. 1994 Hallgren et al. 2001 Zhou et al. 2001, 2002) and therefore could potentially enhance or decrease the toxicity of any substance that is metabolized by the P-450 system. 

Zhou et al. 2001, 2002). The available data indicate that the thyroid is a particularly sensitive target of acute oral exposure and justify using thyroid effects as the basis for an acute oral MRL, but acute effects of PBDEs on the liver are not as well characterized as thyroid effects. Other studies indicate that immunosuppression and neurobehavior are important and potentially critical health end points for acute exposure to PBDEs that need to be further investigated (see discussions of data needs for Immunotoxicity and Neurotoxicity). Studies in other species would help to clearly establish the most sensitive target and species for acute exposure, as well as which animal toxicity data are the most relevant to humans and useful for assessing acute health risks. 

Polybrominated Diphenyl Ethers. The mechanism by which PBDEs enter the blood stream is not known, there are no established methods for reducing body burden of PBDEs, and the mechanisms of toxic action of PBDEs are incompletely understood. Types of studies that could address these data gaps and possibly provide information on reducing to dc effects of PBDEs are discussed in the preceding subsection on PBBs. 

PBDEs Considered the new PCBs, polybrominated diphenyl ethers are a group of brominated flame retardants used in lots of products, including the foam in couches and mattresses, and plastic TV and computer monitors (Dell and HP, among others, have banned them). One of the reasons PBDEs are so hard to avoid is that they re not bound to the molecules in materials, so toxic residue can escape in the form of dust. Most kinds of PBDEs have been banned in Europe since 2004, and American women carry ten to seventy times as many PBDEs in their breast milk, tissues, and blood as Europeans do. Exposure to PBDEs during fetal development can negatively affect how the brain functions. 

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