Characterization of maternal transfer of decabromodiphenyl ether (BDE-209) administered to pregnant Sprague–Dawley rats

Cai, Yunmei; Zhang, Wenbing; Hu, Junjie; Sheng, Guoying; Chen, Dunjin; Fu, Jiamo

doi:10.1016/j.reprotox.2010.08.005

Cited by 23 publications

(13 citation statements)

References 37 publications

(63 reference statements)

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“…Trace of octa-BDEs was also detected but below the quantification detection limit. So in our article the purity of BDE-209 was given as >98% [2]. In addition, we also noted that the purity of >98% BDE-209 in this commercial product has also been reported by other researchers [3,4].…”

supporting

confidence: 79%

Response to comment on “Characterization of maternal transfer of decabromodiphenyl ether (BDE-209) administered to pregnant Sprague-Dawley rats” by Biesemeier et al.

Cai¹,

Zhang²,

Hu³

et al. 2012

Reproductive Toxicology

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supporting

confidence: 79%

Response to comment on “Characterization of maternal transfer of decabromodiphenyl ether (BDE-209) administered to pregnant Sprague-Dawley rats” by Biesemeier et al.

Cai¹,

Zhang²,

Hu³

et al. 2012

Reproductive Toxicology

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“…This may explain the very low levels or absence of BDE-209 in fetal or umbilical cord blood (see Section 5 and Table 4), though placental BDE-209 levels may be relatively higher than other PBDEs in relationship to maternal blood levels (Frederiksen et al 2009). A recent study reported that administration of BDE-209 (98% pure) to rats from GD 7 to lactational day (LD) 4, at the oral dose of 5 umol/kg/day, resulted in 10-fold lower levels in fetuses and pups than in the dams (Cai et al 2010). In another recent experimental study, BDE-209 (97.5% pure) was given by gavage in corn oil to rats from GD 6 to LD 4 at the doses of 100, 300, and 1000 mg/kg/day (Biesemeier et al 2010).…”

Section: General Toxicology Of Bde-209mentioning

confidence: 99%

Is decabromodiphenyl ether (BDE-209) a developmental neurotoxicant?

2011

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Polybrominated diphenyl ether (PBDE) flame retardants have become ubiquitous environmental pollutants. The relatively higher body burden in toddlers and children has reaised concern for their potential developmental neurotoxicity, which has been suggested by animal studies, in vitro experiments, and recent human epidemiological evidence. While lower brominated PBDEs have been banned in several countries, the fully brominated decaBDE (BDE-209) is still utilized, though manufacturers will discontinue production in the U.S.A. in 2013. The recent decision by the U.S. Environmental Protection Agency to base the Reference Dose (RfD) for BDE-209 on a developmental neurotoxicity study has generated some controversy. Because of its bulky configuration, BDE-209 is poorly absorbed and does not easily penetrate the cell wall. Its acute and chronic toxicities are relatively low, with the liver and the thyroid as the primary targets, though there is some evidence of carcinogenicity. A few animal studies have indicated that BDE-209 may cause developmental neurotoxicity, affecting motor and cognitive domains, as seen for other PBDEs. Limited in vivo and in vitro studies have also evidenced effects of BDE-209 on thyroid hormone homeostasis and direct effects on nervous cells, again similar to what found with other lower brominated PBDEs. In contrast, a recent developmental neurotoxicity study, carried out according to international guidelines, has provided no evidence of adverse effects on neurodevelopment, and this should be considered in a future re-evaluation of BDE-209. While estimated exposure to BDE-209 in children is believed to be several orders of magnitude below the most conservative RfD proposed by the USEPA, questions remain on the extent and relevance of BDE-209 metabolism to lower brominated PBDEs in the environment and in humans.

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“…In our study three nona-BDEs 207 and 208) and five octa-BDEs 197/204,198/203) were identified and quantified in pup tissues. Like the distribution in dams (Cai et al, 2011), nonaBDEs were also the predominant debrominated congeners in the pup tissues. BDE-206 was the most abundant metabolite while BDE-197/204 was the major congener of octa-BDE.…”

Section: Discussionmentioning

confidence: 74%

Tissue distribution of decabrominated diphenyl ether (BDE-209) and its metabolites in sucking rat pups after prenatal and/or postnatal exposure

et al. 2011

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Characterization of maternal transfer of decabromodiphenyl ether (BDE-209) administered to pregnant Sprague–Dawley rats

Cited by 23 publications

References 37 publications

Response to comment on “Characterization of maternal transfer of decabromodiphenyl ether (BDE-209) administered to pregnant Sprague-Dawley rats” by Biesemeier et al.

Response to comment on “Characterization of maternal transfer of decabromodiphenyl ether (BDE-209) administered to pregnant Sprague-Dawley rats” by Biesemeier et al.

Is decabromodiphenyl ether (BDE-209) a developmental neurotoxicant?

Tissue distribution of decabrominated diphenyl ether (BDE-209) and its metabolites in sucking rat pups after prenatal and/or postnatal exposure

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