An oral (gavage) developmental neurotoxicity study of decabromodiphenyl oxide (DeBDPO) in rats

Jacobi, Sylvia; Silberberg, Hanna; Stedeford, Todd; Biesemeier, John A.; Adriano, John; Beck, Melissa J.

doi:10.1016/j.toxlet.2009.06.382

Cited by 3 publications

(17 citation statements)

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“…In contrast, females in the HBCD-treated groups were not significantly different from control females in performance of the T-maze swim. The results of the locomotor activity tests were similar to those of Jacobi et al (2009) andSchroeder (2002), which found no adverse neurobehavioral effects of perinatal BDE209 or TBBPA treatment, respectively, in the only other GLP-compliant neurodevelopmental studies conducted on these substances. Schroeder (2002); TBBPA Schroeder (2002) conducted a two-generation reproductive toxicity study of TBBPA that included assessment of various behavioral elements.…”

supporting

confidence: 83%

“…These results are similar to those of Eriksson et al (2001), which failed to show an effect of TBBPA on motor activity when the test substance was administered on PND10. These also parallel those of the other two GLP-and guideline-compliant studies reviewed herein (Jacobi et al, 2009;Ema et al, 2008), which showed no significant effects on motor activity associated with gestational and lactational exposure to BDE209 and HBCD, respectively.…”

supporting

confidence: 81%

“…In addition, Rice et al (2007) used the same 20% fat emulsion as Eriksson and Viberg for their dosing vehicle. Interestingly, a preliminary analysis by Jacobi et al (2009) using a similar emulsion vehicle suggests that the emulsion of Erikson and Viberg results in lower bioavailability than a corn oil vehicle. All other studies involved administration of BFR to dams beginning either during gestation or prior to mating and extending through at least PND21, or in the case of two studies (Ema et al, 2008;Schroeder, 2002), through one or two generations.…”

Section: Test Methodologymentioning

confidence: 99%

“…PBDE congeners were the substances of interest in most studies; only four examined HBCD or TBBPA. Three studies (Jacobi et al, 2009;Ema et al, 2008;Schroeder, 2002) were conducted according to recognized guidelines for developmental neurotoxicity, two of which were conducted as components of two-generation reproductive toxicity studies. The results of investigations of motor activity are provided in Tables 2 and 3, and the studies are discussed next.…”

Section: Review Of Studiesmentioning

confidence: 99%

“…The results of these studies are presented in Table 3 and the studies are discussed individually next. Jacobi et al (2009); BDE209 Jacobi et al (2009) conducted a Good Laboratory Practices (GLP)-compliant developmental neurotoxicity study of BDE209 that followed both Organization for Economic Cooperation and Development (OECD) and U.S. EPA guidelines. This study is also described in a recent review article (Hardy et al, 2009).…”

Section: Tablementioning

confidence: 99%

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The Potential of Selected Brominated Flame Retardants to Affect Neurological Development

Williams

DeSesso

2010

Journal of Toxicology and Environmental Health, Part B

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Various brominated flame retardants (BFR), including polybrominated diphenyl ether (PBDE) congeners, hexabromocyclododecane (HBCD), and tetrabromobisphenol A (TBBPA), are commonly used in household items and electronics and have been detected in the environment and/or the bodily fluids of people, including children. Some studies in animals suggest that exposure to PBDE congeners, HBCD, or TBBPA during the perinatal period may affect locomotor activity and/or memory and learning. Epidemiological studies showing similar effects in humans, however, are lacking. To assess whether an association exists between perinatal exposure and development of consistent neurobehavioral alterations, published animal studies investigating perinatal exposure to PBDE congeners, HBCD, or TBBPA with specific neurobehavioral evaluations-particularly, assessments of motor activity-were reviewed for consistency of results. Our analysis shows that although the majority of studies suggest that perinatal exposure affects motor activity, the effects observed were not consistent. This lack of consistency includes the type of motor activity (locomotion, rearing, or total activity) affected, the direction (increase or decrease) and pattern of change associated with exposure, the existence of a dose response, the permanency of findings, and the possibility of gender differences in response. Interestingly, Good Laboratory Practices (GLP)-compliant studies that followed U.S. Environmental Protection Agency (EPA)/Organization for Economic Cooperation and Development (OECD) guidelines for developmental neurotoxicity testing found no adverse effects associated with exposure to PBDE209, HBCD, or TBBPA at doses that were orders of magnitude higher and administered over longer durations than those used in the other studies examined herein. The lack of consistency across studies precludes establishment of a causal relationship between perinatal exposure to these substances and alterations in motor activity.

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supporting

confidence: 83%

supporting

confidence: 81%

Section: Test Methodologymentioning

confidence: 99%

Section: Review Of Studiesmentioning

confidence: 99%

Section: Tablementioning

confidence: 99%

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The Potential of Selected Brominated Flame Retardants to Affect Neurological Development

Williams

DeSesso

2010

Journal of Toxicology and Environmental Health, Part B

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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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Effects of maternal exposure to BDE209 on neuronal development and transcription of iodothyronine deiodinase in offspring mice

Qian

Wang

Zhao

et al. 2019

Toxicology Mechanisms and Methods

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An oral (gavage) developmental neurotoxicity study of decabromodiphenyl oxide (DeBDPO) in rats

Cited by 3 publications

References 0 publications

The Potential of Selected Brominated Flame Retardants to Affect Neurological Development

The Potential of Selected Brominated Flame Retardants to Affect Neurological Development

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

Effects of maternal exposure to BDE209 on neuronal development and transcription of iodothyronine deiodinase in offspring mice

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