A 28-day oral dose toxicity study in Wistar rats enhanced to detect endocrine effects of decabromodiphenyl ether (decaBDE)

Ven, Leo T.M. van der; Kuil, Ton van de; Leonards, P.E.G.; Slob, Wout; Cantón, Rocío F.; Germer, Silke; Visser, Theo J.; Litens, Sabina; Håkansson, Helen; Schrenk, Dieter; Berg, Martin van den; Piersma, Aldert H.; Vos, J.G.; Opperhuizen, Antoon

doi:10.1016/j.toxlet.2008.03.003

Cited by 56 publications

(37 citation statements)

References 51 publications

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“…There is increasing evidence that BDE-209, which is contained in decaBDE, is persistent, bioaccumulative, and might be debrominated to lowerbrominated BDEs (Stapleton et al, 2004;He et al, 2006;Kierkegaard et al, 2007;Van den Steen et al, 2007;Schenker et al, 2008). In addition, the scientific discussion about toxic effects of BDE-209 is ongoing (Viberg et al, 2003;Van der Ven et al, 2008).…”

Section: Congener Patternmentioning

confidence: 99%

“…In addition, the EPA announced the phase-out of decaBDE in December 2009 for the end of 2013 (USEPA, 2009). In Europe the use of decaBDE is still permitted for all appliances except for electric and electronic equipment (BSEF, 2009), but the scientific discussion about the toxicity of decaBDE is ongoing (Viberg et al, 2003;Van der Ven et al, 2008). Effects of PBDEs in animal models include endocrine disruption, neurodevelopmental and behavioural effects, hepatic abnormalities, and possibly cancer (McDonald, 2002;Birnbaum and Staskal, 2004;Darnerud, 2008).…”

Section: Introductionmentioning

confidence: 99%

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PBDE exposure from food in Ireland: optimising data exploitation in probabilistic exposure modelling

Trudel

Tlustos

Goetz

et al. 2010

J Expo Sci Environ Epidemiol

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Polybrominated diphenyl ethers (PBDEs) are a class of brominated flame retardants added to plastics, polyurethane foam, electronics, textiles, and other products. These products release PBDEs into the indoor and outdoor environment, thus causing human exposure through food and dust. This study models PBDE dose distributions from ingestion of food for Irish adults on congener basis by using two probabilistic and one semi-deterministic method. One of the probabilistic methods was newly developed and is based on summary statistics of food consumption combined with a model generating realistic daily energy supply from food. Median (intermediate) doses of total PBDEs are in the range of 0.4-0.6 ng/kg bw /day for Irish adults. The 97.5th percentiles of total PBDE doses lie in a range of 1.7-2.2 ng/kg bw /day, which is comparable to doses derived for Belgian and Dutch adults. BDE-47 and BDE-99 were identified as the congeners contributing most to estimated intakes, accounting for more than half of the total doses. The most influential food groups contributing to this intake are lean fish and salmon which together account for about 22-25% of the total doses.

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Section: Congener Patternmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

PBDE exposure from food in Ireland: optimising data exploitation in probabilistic exposure modelling

Trudel

Tlustos

Goetz

et al. 2010

J Expo Sci Environ Epidemiol

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“…The BDE and MeO-BDE standards were purchased from Wellington Laboratories (Ontario, Canada). BDE mixture standards include 27 BDE congeners (BDE3, 7,15,17,28,47,49,66,71,77,85,99,100,119,126,138,153,154,156,183,184,191,196,197,206,207,209). MeO-BDE mixture standards include four tetra-MeOBDEs and four penta-MeO-BDEs: 2,2′,4,4′-tetrabromo-5-methoxydiphenyl ether (5-MeO-BDE47), 2,2′,4,4′-tetrabromo-6-methoxydiphenyl ether (6-MeO-BDE47), 2,2′,4,5′-tetrabromo-4′-methoxydiphenyl ether (4′-MeO-BDE49), 2,3′,4,5′-tetrabromo-2′-methoxydiphenyl ether (2′-MeO-BDE68), 2,2′,4,4′,5-pentabromo-5′-methoxydiphenyl ether (5′-MeO-BDE99), 2,2′,4,4′,6-pentabromo-5′-methoxydiphenyl ether (5′-MeO-BDE100), 2,2′,4,5,5′-pentabromo-4′-methoxydiphenyl ether (4′-MeO-BDE101), and 2,2′,4,5′,6-pentabromo-4′-methoxydiphenyl ether (4′-MeO-BDE103).…”

Section: Standards and Reagentsmentioning

confidence: 99%

“…In addition, the toxicokinetics of BDE47, BDE99, BDE100, BDE153 and BDE154 were also studied in rats and mice, and the results demonstrated that lipophilic tissues were the preferred uptake sites [16]. The toxicity study of BDE209 in rats with oral administration suggested that BDE209 was hazardous to reproductive health [17]. Overall, most of these studies focused on the toxicokinetics of BDEs in mammals, however, little information was available on the toxicokinetics of BDEs in fish.…”

Section: Introductionmentioning

confidence: 99%

Toxicokinetics and the related metabolites in rainbow trout (Oncorhynchus mykiss) after exposure to decabromodiphenyl ether

Feng

Zha

et al. 2010

Sci. China Chem.

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Decabromodiphenyl ether (BDE209) is poorly absorbed by mammals, and little information is available on the toxicokinetics of BDE209 and its metabolites in fish. In the present study, rainbow trout (Oncorhynchus mykiss) were administered to 100 ng/g and 500 ng/g body wet weight of BDE209 via a single intraperitoneal injection and parent BDE209 and its metabolites were sequentially monitored for 28 days. The results showed that toxicokinetic profiles of BDE209 could be described by the one-compartment model. In the higher dose group (500 ng/g wet weight), the calculated half-life (t 1/2 ) and elimination rate (k e ) were 17.7 d and 0.039/d in the liver, and 100.3 d and 0.007/d in the muscle, respectively. Three major methoxylated brominated diphenyl ethers (MeO-BDEs) were detected with 2,2′,4,4′-tetrabromo-5-methoxydiphenyl ether (5-MeO-BDE47) being detected in all tissue samples. There was no significant temporal change of 5-MeO-BDE47 concentration in the muscle, whereas an exponential increase was observed in the liver. Therefore, the metabolism rate of BDE209 depended on the administered dose. BDE209 was hardly accumulated in the muscle of rainbow trout, while the liver was a primary metabolic organ. MeO-BDEs were formed via metabolism of BDE209, which probably played a significant role in fish toxicology as a potential indicator.decabromodiphenyl ether (BDE209), polybrominated diphenyl ethers (PBDEs), methoxylated brominated diphenyl ethers (MeO-BDEs), toxicokinetics, rainbow trout

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“…Though BDE-209 has long been believed to be only minimally toxic, there is growing evidence that it can cause endocrine effects Tseng et al, 2008;Van der Ven et al, 2008), induce neurotoxic effects and result in cognitive deficiencies, especially for the neonates after prenatal and postnatal exposure to BDE-209 (Onos et al, 2007;Viberg et al, 2003Viberg et al, , 2007. For example, BDE-209 can increase the expression of hepatic CYP1A and CYP2B in male rats and decrease activity of CYP17 in female rats, which may result in hazard for reproductive health (Van der Ven et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

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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A 28-day oral dose toxicity study in Wistar rats enhanced to detect endocrine effects of decabromodiphenyl ether (decaBDE)

Cited by 56 publications

References 51 publications

PBDE exposure from food in Ireland: optimising data exploitation in probabilistic exposure modelling

PBDE exposure from food in Ireland: optimising data exploitation in probabilistic exposure modelling

Toxicokinetics and the related metabolites in rainbow trout (Oncorhynchus mykiss) after exposure to decabromodiphenyl ether

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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