Impaired oligodendroglial development by decabromodiphenyl ether in rat offspring after maternal exposure from mid-gestation through lactation

Fujimoto, Hitoshi; Woo, Gye‐Hyeong; Inoue, Kaoru; Takahashi, Miwa; Hirose, Masao; Nishikawa, Akiyoshi; Shibutani, Makoto

doi:10.1016/j.reprotox.2010.09.003

Cited by 27 publications

(35 citation statements)

References 42 publications

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“…PTU is a model anti-thyroid drug that acts primarily at the central hypothalamic-pituitary-thyroid (HPT) axis to reduce T4 by inhibiting thyroid peroxidase iodination of tyrosine residues in thyroglobulin in thyroid follicles. While this is the first study to examine BDE-209 effects on circulating thyroid hormone levels in adult fish, data here are consistent with studies showing that PBDEs, including BDE-209, can elicit reductions in plasma thyroid hormone levels in other species at various life-stages 23, 38–41 .…”

Section: Discussionsupporting

confidence: 87%

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Low Level Exposure to the Flame Retardant BDE-209 Reduces Thyroid Hormone Levels and Disrupts Thyroid Signaling in Fathead Minnows

Noyes

Lema

Macaulay

et al. 2013

Environ. Sci. Technol.

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Polybrominated diphenyl ether (PBDE) flame retardants have been shown to disrupt thyroid hormone regulation, neurodevelopment, and reproduction in some animals. However, effects of the most heavily used PBDE, decabromodiphenyl ether (BDE-209), on thyroid functioning remain unclear. This study examined low-dose effects of BDE-209 on thyroid hormone levels and signaling in fathead minnows. Adult males received dietary exposures of BDE-209 at a low dose (~3 ng/g bw-day) and high dose (~300 ng/g bw-day) for 28 days followed by a 14-day depuration to evaluate recovery. Compared to controls, fish exposed to the low dose for 28 days experienced a 53% and 46% decline in circulating total thyroxine (TT4) and 3,5,3'-triiodothyronine (TT3), respectively, while TT4 and TT3 deficits at the high dose were 59% and 62%. Brain deiodinase activity (T4-ORD) was reduced by ~65% at both doses. BDE-209 elevated the relative mRNA expression of genes encoding deiodinases, nuclear thyroid receptors, and membrane transporters in the brain and liver in patterns that varied with time and dose, likely in compensation to hypothyroidism. Declines in the gonadal-somatic index (GSI) and increased mortality were also measured. Effects at the low dose were consistent with the high dose, suggesting non-linear relationships between BDE-209 exposures and thyroid dysfunction.

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Section: Discussionsupporting

confidence: 87%

“…Doses tested in this study were generally less than those administered in rodent studies conducted to date with BDE-209 38–40 . Further study is needed to determine whether non-monotonic dose-responses are occurring in fish exposed to BDE-209 as have been detected with other endocrine disruptors 78 .…”

Section: Discussionmentioning

confidence: 99%

Low Level Exposure to the Flame Retardant BDE-209 Reduces Thyroid Hormone Levels and Disrupts Thyroid Signaling in Fathead Minnows

Noyes

Lema

Macaulay

et al. 2013

Environ. Sci. Technol.

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“…In another recent study, BDE-209 (purity > 98%) was given to pregnant rats in the diet at levels of 10, 100 and 1000 ppm, from GD 10 to LD 20 (Fujimoto et al 2010). No reproductive effects were observed, in agreement with previous findings by Hardy et al (2002).…”

Section: Evidence Of Developmental Neurotoxicity Of Bde-209mentioning

confidence: 99%

“…Body weights in male pups were slightly increased at the two lowest dose levels, while thyroid hormones were decreased at the highest dosage, with hypertrophy of thyroid follicular cells. In brain, a decrease of CNPase (2’,3’- cyclic nucleotide 3’- phosphodiesterase, a marker of oligodendrocytes) was found in the cingulated deep cortex at postnatal week 11 at the two highest dose levels, indicating white matter hypoplasia (Fujimoto et al 2010). In the amphibian Xenopus laevis , exposure of tadpoles to the technical decabromodiphenyl ether mixture DE-83R (containing 96 to 99% BDE-209, as well as other PBDEs) in water, from stage 46/47 (free swimming larvae) to stage 62, at the concentrations of 1 to 1000 ng/L, did not cause any malformation or abnormal behavior.…”

Section: Evidence Of Developmental Neurotoxicity 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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“…Experimental evidence suggests that PBDEs in maternal blood can partially cross the placenta [40,41,42] and disrupt thyroid function [17,43,44]. Thyroid disruption has been considered a crucial pathway linking PEP and IBO.…”

Section: Discussionmentioning

confidence: 99%

Correlation between Prenatal Exposure to Polybrominated Diphenyl Ethers (PBDEs) and Infant Birth Outcomes: A Meta-Analysis and an Experimental Study

Zhao

Peng

Xiang

et al. 2017

IJERPH

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Only a few epidemiological studies have focused on the correlation between prenatal exposure to polybrominated diphenyl ethers (PBDEs) and infant birth outcomes (IBO), and the results of these epidemiological studies are contradictory. The objective of this study was to assess the correlation between prenatal exposure to PBDEs (PEP) and IBO (i.e., birth weight) in an analysis of epidemiological studies and an experimental animals study. We searched databases of the medical literature (PubMed, Excerpta Medica Database, Cochrane Library, and China National Knowledge Infrastructure) for articles and pooled the results of the included epidemiological studies. In parallel, birth outcomes (i.e., birth weights of pups) were collected from female Sprague-Dawley (SD) rats exposed to decabromodiphenyl ether (DecaBDE) in the diet from five weeks of age to delivery. A significant negative relationship was found between human PBDE burden and birth weight in the analysis of seven epidemiological studies based on a random-effects model (β = −50.598; 95% confidence interval (CI) −95.914, −5.282; I2 = 11.8%; p = 0.029). In the experimental animal study, a significant decrease in birth weight in the DecaBDE-treated group was also observed (5.26 ± 0.39 vs. 5.8 ± 0.58, p = 0.0132). The results of our study contribute to increasing evidence suggesting that PEP adversely impacts IBO, especially birth weight.

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Impaired oligodendroglial development by decabromodiphenyl ether in rat offspring after maternal exposure from mid-gestation through lactation

Cited by 27 publications

References 42 publications

Low Level Exposure to the Flame Retardant BDE-209 Reduces Thyroid Hormone Levels and Disrupts Thyroid Signaling in Fathead Minnows

Low Level Exposure to the Flame Retardant BDE-209 Reduces Thyroid Hormone Levels and Disrupts Thyroid Signaling in Fathead Minnows

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

Correlation between Prenatal Exposure to Polybrominated Diphenyl Ethers (PBDEs) and Infant Birth Outcomes: A Meta-Analysis and an Experimental Study

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