Toxicology and human health assessment of decabromodiphenyl ether

Abstract

Recent public concern has focused on potential reproductive and developmental effects from exposure to low levels of bisphenol A (BPA, CAS number 80-05-7). Two previous published reviews (Gray et al., 2004a; Goodman et al., 2006) conducted weight-of-evidence evaluations of in vivo reproductive/developmental toxicity from BPA exposure < or = 5 mg/kg-d based on studies published through February 2006. Here, an update of those analyses presents additional relevant studies that were published through July 25, 2008, and a weight-of-evidence analysis of the studies evaluated in all three reviews. As with the earlier literature, positive findings: (1) are countered by null findings in more numerous studies; (2) have not been replicated; (3) do not exhibit coherence and plausibility; (4) do not show consistency across species, doses, and time points; and/or (5) were from studies using non-oral exposure routes. Owing to the lack of first-pass metabolism, results from non-oral studies are of limited relevance to human exposure. Exposure levels in most of the low-dose oral and non-oral animal studies are generally much higher than those experienced by even the most exposed people in the general population. The weight of evidence does not support the hypothesis that low oral doses of BPA adversely affect human reproductive and developmental health.

Response to the Letter from Biesemeier et al.

“…We agree that no adverse biological effects of BDE-209 have also been reported in the literatures (Biesemeier et al, 2011;Hardy et al, 2002Hardy et al, , 2009Johnson et al, 2010), however, a comprehensive review of the toxicity of BDE-209 is beyond the scope of our paper. The purpose of our paper was to demonstrate the maternal transfer of BDE-209 and its metabolites to sucking rat pups after prenatal and/or postnatal exposure.…”

Scientific Opinion on Polybrominated Diphenyl Ethers (PBDEs) in Food

“…The early works regarding BDE-209 were conducted in rats fed this compound at high dietary concentrations (> 230 mg/kg feed) and suggested that BDE-209 was poorly absorbed from the gastrointestinal tract (NTP, 1986;ATSDR, 2004;Hardy et al, 2009). However, in a more recent study carried out in rats dosed by gavage with radiolabelled BDE-209 (2.8 mg/kg b.w.)…”

Effects of Dose, Administration Route, and/or Vehicle on Decabromodiphenyl Ether Concentrations in Plasma of Maternal, Fetal, and Neonatal Rats and in Milk of Maternal Rats

“…In 2000, the U.S. National Research Council issued a chronic oral reference dose 1 for DecaBDE of 4 mg/(kg ⅐ day) (National Research Council, 2000). This value was derived from DecaBDE's extensive toxicology database, which includes evaluations on subchronic and chronic toxicity, development, reproduction, mutagenicity, and carcinogenicity (Norris et al, 1973(Norris et al, , 1974Kociba et al, 1975;National Toxicology Program, 1986;el Dareer et al, 1987;Hardy et al, 2002Hardy et al, , 2009). The European Union (EU) independently reviewed these same studies and concluded that the manufacture and use of DecaBDE did not present a risk to human health (European Commission, 2002).…”

“…Until the report by Viberg et al (2001), DecaBDE's mammalian toxicology database supported its safe use as a flame retardant, as evidenced by no-observed-effect levels and no-observed-adverseeffect levels of Ն1000 mg/(kg ⅐ day) in repeated-dose studies (Hardy et al, 2009). DecaBDE's limited bioavailability 3 was considered a factor in its general lack of mammalian toxicity (National Toxicology Program, 1986;el Dareer et al, 1987;Zhou et al, 2001).…”