Additive Brominated Flame Retardants Research Articles

Neurotoxicity of tetrabromobisphenol-A-bis(2,3-dibromopropyl ether) through the GABAergic and serotonergic neurotransmission in Caenorhabditis elegans

Tetrabromobisphenol-A-bis(2,3-dibromopropyl ether) (TBBPA-BDBPE), a novel additive brominated flame retardant, is being developed for use in polyolefin and copolymers. Despite its emerging application, the neurotoxicity and mechanisms of action of TBBPA-BDBPE remain unexplored. Caenorhabditis elegans was utilized as the model organism to study the neurotoxic effects of TBBPA-BDBPE across environmental concentrations ranging from 0 to 100 μg/L. This investigation focused on various toxicological endpoints such as locomotive behavior, neuronal injury, neurotransmitter transmission, and the regulation of nervous system-related gene expression. Acute exposure to TBBPA-BDBPE at concentrations of 10–100 μg/L significantly impaired nematode movement, indicating potential neurotoxicity. In transgenic nematodes, this exposure also caused damage to γ-aminobutyric acid (GABAergic) and serotonergic neurons, along with notable changes in the levels of GABAergic and serotonergic neurotransmitters. Further molecular studies indicated alterations in neurotransmission-related genes (cat-4, mod-1, unc-25, and unc-47). Molecular docking analysis confirmed the binding affinity of TBBPA-BDBPE to key neurotransmission proteins—CAT-4, MOD-1, UNC-25, and UNC-47. These findings demonstrate that TBBPA-BDBPE exerts neurotoxic effects by impacting GABAergic and serotonergic neurotransmission in nematodes. This study provides new insights into the potential environmental risks of TBBPA-BDBPE.

Physiologically based pharmacokinetic (PBPK) modeling of BDE-209 following oral exposure in Chinese population.

The wide usage of decabromodiphenyl ether (BDE-209) as additive brominated flame retardant has caused its widespread occurrence in the environment and high exposure risk in humans. Estimating its internal exposure dose and reconstruction of external exposure dose using physiologically based pharmacokinetic (PBPK) modelling approach is a key step in the risk assessment of BDE-209. However, the PBPK model for BDE-209 is currently unavailable. This study has established two oral permeability-limited PBPK models of BDE-209 without enterohepatic recirculation (EHR) (model 1) and with EHR (model 2) for Chinese population. Using the in vitro experiments, the average binding of BDE-209 to human plasma protein (99.64%±2.97%) was obtained. Moreover, blood sample analysis and systematic literature review were performed to obtain internal and external exposure data of BDE-209 used for model calibration and validation. The predictions of both models were within 2-fold of the observed, and a longer half-life of serum BDE-209 was observed in model 2 than model 1. Based on the models, a human biomonitoring guidance value (HBM-GV) of 93.61μg/g lw was derived for BDE-209, and there is no health risk found for Chinese population currently. This study provides new quantitative assessment tools for health risk assessment of BDE-209.

Contamination status, emission sources, and human health risk of brominated flame retardants in urban indoor dust from Hanoi, Vietnam: the replacement of legacy polybrominated diphenyl ether mixtures by alternative formulations.

This study investigated the occurrence, distribution of several additive brominated flame retardants (BFRs) such as polybrominated diphenyl ethers (PBDEs) and some novel brominated flame retardants (NBFRs) in urban indoor dust collected from ten inner districts of Hanoi, Vietnam to assess the contamination status, emission sources, as well as their associated human exposure through indoor dust ingestion and health risks. Total concentrations of PBDEs and NBFRs in indoor dust samples ranged from 43 to 480 ng g-1 (median 170 ng g-1) and from 56 to 2200 ng g-1 (median 180 ng g-1), respectively. The most abundant PBDE congener in these dust samples was BDE-209 with concentrations ranging from 29 to 360 ng g-1, accounting for 62.6-86.5% of total PBDE levels. Among the NBFRs analyzed, decabromodiphenyl ethane (DBDPE) was the predominant compound with a mean contribution of 98.6% total NBFR amounts. Significant concentrations of DBDPE were detected in all dust samples (median 180 ng g-1, range 54-2200 ng g-1), due to DBDPE as a substitute for deca-BDE. Other NBFRs such as 1,2-bis(2,4,6-tribromophenoxy) ethane (BTBPE), pentabromoethylbenzene (PBEB) and 2,2',4,4',5,5'-hexabromobiphenyl (BB-153) were found at very low levels. Based on the measured BFR concentrations, daily intake doses (IDs) of PBDEs and NBFRs via dust ingestion at exposure scenarios using the median and 95th percentile levels for both adults and children were calculated for risk assessment. The results showed that the daily exposure doses via dust ingestion of all compounds, even in the high-exposure scenarios were also lower than their reference dose (RfD) values. The lifetime cancer risks (LTCR) were much lower than the threshold level (10-6), which indicated the acceptable health risks resulting from indoor BFRs exposure for urban residents in Hanoi.

A novel management strategy for removal and degradation of polybrominated diphenyl ethers (PBDEs) in waste printed circuit boards

Waste printed circuit boards (PCBs) contain a high level of brominated flame retardants (BFRs), among which polybrominated biphenyl ethers (PBDEs) are the most widely used additive BFRs. PBDEs are considered to be a type of persistent organic pollutants (POPs). The efficient removal/degradation of PBDEs in waste PCBs is an urgent problem in electronic waste treatment, but the degradation of PBDEs is a great challenge due to their extreme stability and persistence in nature. In this study, a novel management strategy was developed for removal and degradation of PBDEs in waste PCBs by using a simple subcritical methanol (SubCM) process. The results showed that reaction temperature, residence time, solid-to-liquid ratio, and additive NaOH are key factors influencing the removal of PBDEs from waste PCBs. Under optimal conditions (200 °C, 60 min, 1:20 g/mL), the removal efficiency of ∑8PBDEs from waste PCBs could reach 91.3% and 98.8% for the proposed process of SubCM and SubCM + NaOH, respectively. When the temperature is below 200 °C, highly brominated PBDEs congeners in waste PCBs were degraded into 2,'3,4′,6-Tetrabromodiphenyl ether (BDE71) and 2,4,4′-Tribromodiphenyl ether (BDE28) after SubCM treatment. 4-Bromophenyl ether (BDE4) and diphenyl ether were generated by the further debromination of BDE71 and BDE28 with the increase of treatment temperature. The debromination temperature of PBDEs congeners in SubCM could be markedly lowered by adding 4 g/L of NaOH. The complete debromination of PBDEs congeners in waste PCBs could be achieved at 300 °C and 250 °C for the developed process of SubCM and SubCM + NaOH, respectively.

Enhanced dehalogenation and coupled recovery of complex electronic display housing plastics by sub/supercritical CO2

Electronic display housing plastics contain a high amount of halogenated compounds such as brominated flame retardants (BFRs) and polyvinyl chloride (PVC). Compared with moderate critical conditions of conventional eco-friendly sub/supercritical carbon dioxide (Sc−CO2), a novel and sustainable procedure by using improved Sc−CO2 was developed for disposal of this type of plastic. The main merit of the process was that complex halogen-containing plastics were safely disposed and halogen-free products were recycled without using catalysts or additives. It was discovered that additive BFRs were initially extracted by Sc−CO2 technique and then it decomposed accompanied with PVC rapidly to form HBr and HCl, which could be separated by traditional bromine stripping techniques from seawater. Based on response surface methodology (RSM), the maximum debromination and dechlorination efficiencies were achieved at 99.51% and 99.12% respectively. After the treatment, halogen-free products such as solid carbon materials and organic chemical feedstocks were obtained. Mechanism study elucidated that free radicals reaction involving chain initiation, growth and termination induced the polymer decomposition to form these products. This study provides an applicable and green approach for disposal and recovery of halogen-containing plastics.

The molecular mechanism of the antagonistic activity of hydroxylated polybrominated biphenyl (OH-BB80) toward thyroid receptor β

Polybrominated biphenyls (PBBs) were widely used as additive brominated flame retardants. Their hydroxylated products (OH-PBBs) have been detected frequently in various marine mammals, causing an increased health risk. Till now, there lacks information on the potential disruption of OH-PBBs toward thyroid hormone receptor (TR) and the molecular characteristics of their interactions remain largely unknown. We herein in vitro and in silico evaluated the disrupting effect of 3,3′,5,5′-tetrabromobiphenyl (BB80) and its metabolite 2,2′-dihydroxy- 3,3′,5,5′-tetrabromobiphenyl (OH-BB80) toward human TR. The recombinant human TRβ two-hybrid yeast assay reveals the moderate antagonistic activity of OH-BB80 with IC20 at 2 μmol/L, while BB80 shows no agonistic or antagonistic activity. OH-BB80 binds at the binding cavity of TRβ ligand binding domain (LBD) and forms one hydrogen bond with Phe272. Electrostatic interactions and hydrophobic interactions contribute much to their interactions. The binding of OH-BB80 quenches the intrinsic fluorescence of TRβ LBD at static quenching mode. Our study extends knowledge on the endocrine disrupting effect of OH-PBBs and suggests the full consideration of the biotransformation for further health risk assessment of PBBs and related structurally similar emerging contaminants.

Hexabromocyclododecanes promoted autophagy through the PI3K/Akt/mTOR pathway in L02 cells

As additive brominated flame retardants, hexabromocyclododecanes (HBCDs) are being widely used in diverse artificial materials and products, including thermal insulation building materials, housings of electronic equipment, and upholstery textiles. Toxicology studies have shown that HBCDs exposure are closely related to hepatotoxicity and liver diseases. The present study is designed to explore how HBCDs affect cell apoptosis and autophagy process in a human hepatocyte cell line (L02) and to reveal the underline molecular mechanisms. Firstly, HBCDs could elevate the apoptosis rate of L02 cells dose-dependently. Three apoptosis related proteins (apoptotic protease activating factor 1 (Apaf-1), cysteinyl aspartate specific proteinase 3 (caspase-3) and cysteinyl aspartate specific proteinase 9 (caspase-9)) were observed to be up-regulated using western blotting method. Autophagy process was also started by HBCDs in L02 cells as indicated by the increased expressions of LC3-phosphatidylethanolamine conjugate (LC3-II) and other autophagic protein markers (Beclin-1, autophagy related protein 3 (Atg3), autophagy related protein 5 (Atg5), autophagy related protein 7 (Atg7) and autophagy related protein 16L1(Atg16L1)). The results of the green fluorescent protein (GFP)-microtubule-associated protein 1 light chain 3 (LC3) intracellular localization and fluorescence intensity further evidenced the activation of autophagy in L02 cells after treated with HBCDs. In addition, phosphatidylinositide 3-kinases/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway was activated in L02 cells by HBCDs, suggested by the increased expressions of related proteins. The inhibitors of PI3K (LY294002), DNA-activated protein kinase catalytic subunit (DNA-PKcs) (NU7441), Akt (MK2206), and mTOR (KU0063794) could obviously reduce the autophagic proteins prompted by HBCDs. The fluorescence intensities of GFP-LC3 transfected L02 cells were also decreased significantly after the application of these inhibitors. These results indicated that PI3K/Akt/mTOR pathway was participated in regulating autophagy process promoted by HBCDs. In above, HBCDs could induce mitochondrial-dependent apoptosis and autophagy in L02 cells, which was modulated by PI3K/Akt/mTOR pathway.

Tetrabromoethylcyclohexane affects gonadal differentiation and development in the frog Pelophylax nigromaculatus

Tetrabromoethylcyclohexane (TBECH), an additive brominated flame retardant, has been shown to have an androgenic activity in vitro. In the present study, we aimed to investigate the effects of TBECH on gonadal differentiation and development in the frog Pelophylax nigromaculatus, an amphibian species sensitive to androgenic chemicals, and to assess the androgenic activity of TBECH in vivo. P. nigromaculatus tadpoles were exposed to TBECH (1, 10, 100nM) from Gosner stage 24 to complete metamorphosis, and to 5α-dihydrotestosterone (DHT) as a positive control. We found that 1nM DHT resulted in 100% males, while the sex ratio in the solvent control group was close to 1:1. In all the TBECH treatment groups, sexually ambiguous gonads based on gross morphology and intersexualities with testicular and ovarian histological structures were found, but no abnormality occurred in the solvent control. In the 1, 10, 100nM TBECH treatment groups, the female percentages were 52%, 31%, 17%, with 36%, 56%, 66% for males and 12%, 13%, 17% for abnormal sexes, respectively. X2-test revealed significant differences in sex ratios between the three TBECH groups and the solvent control group, and the sex ratios in the two higher concentration groups were male-biased. These observations show that TBECH has a masculinizing effect on gonadal differentiation and development in P. nigromaculatus, suggesting an androgenic activity of TBECH in vivo. To our knowledge, this is the first study demonstrating that TBECH could induce gonadal masculinization in an animal, which raises new concerns for reproductive risk of TBECH exposure.

Enantioselective Analytical- and Preparative-Scale Separation of Hexabromocyclododecane Stereoisomers Using Packed Column Supercritical Fluid Chromatography.

Hexabromocyclododecane (HBCDD) is an additive brominated flame retardant which has been listed in Annex A of the Stockholm Convention for elimination of production and use. It has been reported to persist in the environment and has the potential for enantiomer-specific degradation, accumulation, or both, making enantioselective analyses increasingly important. The six main stereoisomers of technical HBCDD (i.e., the (+) and (−) enantiomers of α-, β-, and γ-HBCDD) were separated and isolated for the first time using enantioselective packed column supercritical fluid chromatography (pSFC) separation methods on a preparative scale. Characterization was completed using published chiral liquid chromatography (LC) methods and elution profiles, as well as X-ray crystallography, and the isolated fractions were definitively identified. Additionally, the resolution of the enantiomers, along with two minor components of the technical product (δ- and ε-HBCDD), was investigated on an analytical scale using both LC and pSFC separation techniques, and changes in elution order were highlighted. Baseline separation of all HBCDD enantiomers was achieved by pSFC on an analytical scale using a cellulose-based column. The described method emphasizes the potential associated with pSFC as a green method of isolating and analyzing environmental contaminants of concern.

Disposition of the emerging brominated flame retardant, bis(2-ethylhexyl) tetrabromophthalate, in female Sprague Dawley rats: effects of dose, route and repeated administration

1. Bis(2-ethylhexyl)-tetrabromophthalate (BEH-TEBP; CAS No. 26040-51-7; PubChem CID: 117291; MW 706.15 g/mol, elsewhere: TeBrDEPH, TBPH, or BEHTBP) is used as an additive brominated flame retardant in consumer products.2. Female Sprague Dawley rats eliminated 92–98% of [14C]-BEH-TEBP unchanged in feces after oral administration (0.1 or 10 μmol/kg). A minor amount of each dose (0.8–1%) was found in urine after 72 h. Disposition of orally administered BEH-TEBP in male B6C3F1/Tac mice was similar to female rats.3. Bioaccumulation of [14C]-radioactivity was observed in liver and adrenals following 10 daily oral administrations (0.1 μmol/kg/day). These tissues contained 5- and 10-fold higher concentrations of [14C]-radioactivity, respectively, versus a single dose.4. IV-administered [14C]-BEH-TEBP (0.1 μmol/kg) was slowly eliminated in feces, with >15% retained in tissues after 72 h. Bile and fecal extracts from these rats contained the metabolite mono-ethylhexyl tetrabromophthalate (TBMEHP).5. BEH-TEBP was poorly absorbed, minimally metabolized and eliminated mostly by the fecal route after oral administration. Repeated exposure to BEH-TEBP led to accumulation in some tissues. The toxicological significance of this effect remains to be determined. This work was supported by the Intramural Research Program of the National Cancer Institute at the National Institutes of Health (Project ZIA BC 011476).

Single and 14-day repeated dose inhalation toxicity studies of hexabromocyclododecane in rats

Limited toxicological information is available for hexabromocyclododecane (HBCD),a widely used additive brominated flame retardant. Inhalation is a major route of human exposure to HBCD. The aim of this study was to determine the acute inhalation toxicity and potential subchronic inhalation toxicity of HBCD in Sprague-Dawley rats exposed to HBCD only through inhalation. The acute inhalation toxicity of HBCD was determined using the limit test method on five male and five female Sprague-Dawley rats at a HBCD concentration of 5000 mg/m3. Repeated-dose toxicity tests were also performed, with 20 males and 20 females randomly assigned to four experimental groups (five rats of each sex in each group). There were three treatment groups (exposed to HBCD concentrations of 125,500, and 2000 mg/m3) and a blank control group (exposed to fresh air). In the acute inhalation toxicity study, no significant clinical signs were observed either immediately after exposure or during the recovery period. Gross pathology examination revealed no evidence of organ-specific toxicity in any rat. The inhalation LC50(4 h) for HBCD was higher than 5312 ± 278 mg/m3 for both males and females. In the repeated dose inhalation study, daily head/nose-only exposure to HBCD at 132 ± 8.8, 545.8 ± 35.3, and 2166.0 ± 235.9 mg/m3 for 14 days caused no adverse effects. No treatment-related clinical signs were observed at any of the test doses. The NOAEL for 14-day repeated dose inhalation toxicity study of HBCD is 2000 mg/m3.

Hexabromocyclododecane affects benthic-pelagic coupling in an experimental ecosystem

Hexabromocyclododecane (HBCDD) is an additive brominated flame retardant and a recognized PBT chemical. However, little is known about its effects on coastal species, and even less on ecosystem effects. We investigated the dose–response effects of HBCDD over 8 months in 1000 L experimental mesocosms assembled from coastal Baltic Sea ecosystem components. HBCDD was added via spiked plankton material and a range of structural and functional endpoints were measured during the experiment. Increasing HBCDD concentration decreased the biomass of large Macoma balthica, resulting in a decreased recirculation of nutrients to the water. Changes in plankton communities were also observed, either due to direct toxic HBCDD effects or indirect via changes in benthic-pelagic coupling of nutrients. Such complex ecosystem responses can only be quantified and understood by using realistic experimental set-ups, and including knowledge of system-specific ecological interactions. This is the first study of HBCDD effects on ecosystem level.

Simulating long-term occupational exposure to decabrominated diphenyl ether using C57BL/6 mice: Biodistribution and pathology

Decabrominated biphenyl ether (BDE-209) is a fully brominated diphenyl ether compound used widely as an additive brominated flame retardant in a variety of consumer products. In recent years, BDE-209 has been reported to be abundant and persistent in the environment, and comparatively high burdens have been found in occupational environmental compartments and exposed individuals. In the present study, an animal model for simulating long-term occupational exposure to BDE-209 was set up. Female C57BL/6 mice (n=10) were intragastrically administered BDE-209 at a dose of 800mgkg−1bw at 2-d intervals for 2years with an internal blood level of approximately 200ngmL−1, which was comparable to the high level of BDE-209 detected in the occupational population, and the biodistribution and biological effects were evaluated systematically. The results showed that large amounts of the chemical accumulated in most tissues, and the preferential organs were the ovary and uterus, liver and lung. Decreased survival was observed in the exposed mice. The subsequent pathological analysis revealed hepatomegaly in the exposed mice, accompanied by obvious histopathological changes in the liver, lung, brain, spleen, kidney and ovary. No neoplastic lesions were observed in this lifetime exposure study. Although the number of experimental mice was limited, our observations offer a comprehensive understanding of the chronic toxicology of BDE-209 after continuous high-dose exposure.

Occurrence of additive brominated flame retardants in aquatic organisms from Tai Lake and Yangtze River in Eastern China, 2009–2012

Since the phase-out of PBDEs, reports regarding occurrences of these compounds in the environment have become less frequent. To characterize potential influences of the phase-out of PBDEs’ on concentrations in the environment, trends in concentrations as a function of time were investigated for two additive brominated flame retardants, PBDEs and HBCDs. Three aquatic species, including shrimp, common carp, and yellow catfish, were collected from Meiliang Bay of Tai Lake, 2009–2012. The analysis of PBDEs in three aquatic organisms has shown a downward-trend in the first three years but a significant upward-trend in the final year. Concentrations of HBCDs have not shown temporal increases in the investigated environments. Concentrations of both PBDEs and HBCDs in the three studied organisms increased as a function of trophic level, which suggested that these additive flame retardants can be biomagnified through the food web of Tai Lake. In accordance with previous publications, PBDE-47 contributed the greatest proportion of ∑PBDEs and had a detection frequency of 100%. α-HBCD was the predominate isomer that contributed to ∑HBCDs. Both β-HBCD and γ-HBCD were likely detected at lesser concentrations than the α-isomer due to differences in bioavailability. Concentrations of ∑PBDEs in the three aquatic organisms from Tai Lake ranged from 1.13 to 97.59ngg−1 lipid. These concentrations were generally less than those in biota from other countries, but equal to those found at other locations in China. Specimens from the Yangtze River had greater concentrations of ∑HBCDs (169.6–316.5ngg−1 lipid) than those collected at Tai Lake, which were comparatively greater than many reported concentrations in freshwater organisms from other countries.

Mechanisms of hexabromocyclododecanes induced developmental toxicity in marine medaka (Oryzias melastigma) embryos

Hexabromocyclododecanes (HBCDs) are widely used as additive brominated flame retardants, and are now ubiquitous contaminants in the environmental media and biota, including the marine environment and marine organisms. However, the impacts of HBCDs on marine fish are not well known. In this study the embryos of marine medaka (Oryzias melastigma) were used to assess the developmental toxicity of HBCDs. Freshly fertilized marine medaka embryos were exposed to various concentrations of technical HBCD (tHBCD, 0, 5, 20 and 50μg/L) until the first fry stage, and hatch success, morphology and cardiac function were examined. In all the exposure groups (5, 20 and 50μg/L) tHBCD significantly increased the embryo heart beats. The measurement of sinus venosus–bulbus arteriosus (SV–BA) distance indicated that tHBCD significantly enlarged the SV–BA distance at exposure concentrations of 20 and 50μg/L. The malformation rate at the first fry stage was also induced by tHBCD in a dose dependent manner, with the formation of pericardial edema and yolk sac edema as the most frequently observed malformation. In addition, the concentrations of total HBCD isomers (ΣHBCDs) in embryos in the current study were comparative with environmental levels and increased with increasing exposure duration. Furthermore, exposure to tHBCD also induced the level of 8-oxodG, a representative oxidative DNA damage. The mechanisms of HBCD-induced developmental toxicity were further explored by TUNEL assay, gel-based quantitative proteomic approach and measurement of the expression of several stress responsive genes, such as p53, TNF-α, IL-1β, CYP1A, COX-1 and COX-2, together with the activities of caspases. The results suggested that HBCDs exposure at environmentally realistic concentrations induced oxidative stress and apoptosis, and suppressed nucleotide and protein synthesis, which all together resulted in developmental toxicity, particularly in the cardiovascular system, in the embryos of O. melastigma.

Decabrominated diphenyl ether (BDE-209) and/or BDE-47 exposure alters protein expression in purified neural stem/progenitor cells determined by proteomics analysis

Polybrominateddiphenyl ethers (PBDEs) are widely utilized as the additive brominated flame retardants in electronic devices, furniture, plastics, rubber foam, and textiles, which exhibit many negative biological effects, especially potential toxic effects on neurodevelopment. In the present study, we applied a proteomics approach to study the effects of decabromodiphenyl ether (BDE-209) and/or tetrabromodiphenyl ether (BDE-47) on the expression of proteins extracted from neural stem/progenitor cells and further explored mechanisms on neurodevelopmental toxicity. We sub-cultured 3–4 generations of neural stem/progenitor cells which were exposed to BDE-209 and/or BDE-47. After a 72-h exposure, we applied two-dimensional gel (2-DE) to identify differentially expressed proteins and matrix-assisted laser desorption ionization time of flight mass spectrometry (MALDI–TOF–MS) to determine the protein identity of 25 spots. Western blot analysis was applied to determine the expression of cofilin-1 and vimentin. A total of 39 differential expression protein spots were identified by 2-DE after BDE-209 and/or BDE-47 exposure in the neural stem/progenitor cells, and 19 differentially expressed proteins were identified by MALDI-TOF-MS. Western blot analysis revealed that cofilin-1 and vimentin were differentially expressed in all groups. Expression of both proteins was decreased when the neural stem/progenitor cells were exposed to BDE-209 and were absent when exposed to both BDE-47 and BDE-209. BDE-209 and/or BDE-47 might alter the expression of some proteins of neural stem/progenitor cells. Nineteen proteins were identified by MALDI-TOF-MS, which will provide a useful basis for further study of the mechanisms underlying PBDE-mediated neurotoxicity.

실내 먼지 중 브롬화난연제 함유특성 연구

본 연구에서는 전기전자제품에 브롬화난연제로 널리 사용되고 있는 폴리브롬화디페닐에테르가 우리의 생활에서 어떻게 배출되는지 파악하고자 가정에서 발생되는 먼지 시료를 2011년 1월부터 12월까지 채취 분석하여 이성체 함량특성을 조사하였다. 아파트와 실험실에서 채취한 실내 먼지 중 총 22종의 PBDEs (47, 49, 66, 71, 77, 85, 99, 100, 119, 126, 138, 153, 154, 156, 183, 184, 191, 196, 197, 206, 207, 209)를 분석하여 정량한 결과, 아파트 실내 먼지에서 검출된 PBDEs 농도는 35.22~575.88 ng/g으로 나타났으며, 실험실에서 겨울에 채취된 먼지 중에서는 PBDEs가 524.44 ng/g 검출되었다. 분석시료 중 1ng/g 이상 검출된 이성체는 BDE-47, 153, 183, 196, 197, 206, 207, 209 등 8종으로 조사되었으며, 모든 시료에서는 BDE-206, 207, 209 3종의 이성체가 검출되었다. The objective of this study was to understand the content characteristic of polybrominated biphenyl ethers in indoor household dust. Polybrominated diphenyl ethers (PBDEs) are widely used as additive brominated flame retardants (BFR) in electrical and electronic equipment, and insulation in the indoor environment, and may be released indoors via volatilization or as dusts. The indoor household dust samples were collected from January to December in 2011 and measured for the concentrations, congener profiles and possible sources of PBDEs. The concentrations of 22 congeners of PBDEs (the sum of PBDEs 47, 49, 66, 71, 77, 85, 99, 100, 119, 126, 138, 153, 154, 156, 183, 184, 191, 196, 197, 206, 207 and 209) were 35.22~575.88 ng/g for apartment dust samples and 524.44 ng/g for laboratory dust sample. The eight congeners of BDE-47, 153, 183, 196, 197, 206, 207, and 209 are detected in the more than 1 ng/g. The three congeners of BDE-206, 207 and 209 in all dust samples were detected.

Acute effects of hexabromocyclododecane on Leydig cell cyclic nucleotide signaling and steroidogenesis in vitro

Hexabromocyclododecane (HBCDD), an additive brominated flame retardant routinely added to various consumer products, was reported to have toxic effects upon biota, including endocrine disruption. In this study, the potential toxicity of HBCDD was tested in peripubertal rat Leydig cells in vitro during 6h exposure. HBCDD inhibited human chorionic gonadotropin- and forskolin-supported cAMP accumulation and steroidogenesis. It also inhibited basal cAMP production, but elevated basal steroidogenesis. The expression of several cAMP-dependent genes, including steroidogenic acute regulatory protein, cholesterol side chain cleavage enzyme, and 3β-hydroxysteroid dehydrogenase, was also inhibited by HBCDD treatment. Nevertheless, this was not accompanied by a decrease in steroidogenic acute regulatory protein expression, as documented by western blot analysis, and activity of steroidogenic enzymes, as documented by unaffected steroidogenesis in the presence of permeable 22(R)-hydroxycholesterol. However, HBCDD caused significant decrease in mitochondrial membrane potential in untreated and human chorionic gonadotropin-treated cells. This indicates that HBCDD acute toxicity in Leydig cells reflects changes in mitochondrial membrane potential-dependent cAMP production and basal and cAMP-regulated cholesterol transport. This in turn facilitates basal but inhibits cAMP-dependent steroidogenesis. Acute effects of HBCDD treatment on transcription are also indicative of its sustained effects on Leydig cell function.

Contamination of indoor dust and air by polychlorinated biphenyls and brominated flame retardants and relevance of non-dietary exposure in Vietnamese informal e-waste recycling sites

This study investigated the occurrence of polychlorinated biphenyls (PCBs), and several additive brominated flame retardants (BFRs) in indoor dust and air from two Vietnamese informal e-waste recycling sites (EWRSs) and an urban site in order to assess the relevance of these media for human exposure. The levels of polybrominated diphenyl ethers (PBDEs), hexabromocyclododecane (HBCD), 1,2-bis-(2,4,6-tribromophenoxy)ethane (BTBPE) and decabromodiphenyl ethane (DBDPE) in settled house dust from the EWRSs (130–12,000, 5.4–400, 5.2–620 and 31–1400ngg−1, respectively) were significantly higher than in urban house dust but the levels of PCBs (4.8–320ngg−1) were not higher. The levels of PCBs and PBDEs in air at e-waste recycling houses (1000–1800 and 620–720pgm−3, respectively), determined using passive sampling, were also higher compared with non-e-waste houses. The composition of BFRs in EWRS samples suggests the influence from high-temperature processes and occurrence of waste materials containing older BFR formulations. Results of daily intake estimation for e-waste recycling workers are in good agreement with the accumulation patterns previously observed in human milk and indicate that dust ingestion contributes a large portion of the PBDE intake (60%–88%), and air inhalation to the low-chlorinated PCB intake (>80% for triCBs) due to their high levels in dust and air, respectively. Further investigation of both indoor dust and air as the exposure media for other e-waste recycling-related contaminants and assessment of health risk associated with exposure to these contaminant mixtures is necessary.

日本全国の淡水域に生息するギンブナ<I>(Carassius auratus (gibelio) langsdorfii )</I> 中のヘキサブロモシクロドデカン蓄積量調査 -濃度レベル,地域分布及び産卵期の卵への移行-

Hexabromocyclododecanes (HBCDs), widely used as additive brominated flame retardants, were determined in muscle of crucian carp (Carassius auratus (gibelio) langsdorfii) taken from 14 freshwater areas throughout Japan during 2003-2005; these sampling sites comprised 10 rivers and 4 ponds and were categorized into 4 groups based on local circumstances; large cities, small cities, agricultural areas and remote areas. HBCDs were detected in all samples analyzed, and total HBCDs ranged from 0.068 to 150 (average: 12, median: 0.37) ng/g wet wt. and 5.0 to 15000 (average: 1200, median: 29) ng/g lipid wt. The higher levels of HBCDs were found in urban areas. α -HBCD was the predominant isomer of HBCDs except for 5 rivers in urban areas where γ -HBCD was abundant. Minor isomers of technical HBCD, δ - and ε -HBCD were not found. To estimate maternal transfer rates of HBCDs, samples (male and female) were taken at the Murasaki River in the spawning season and analyzed their muscles and eggs. Maternal transfer rates of α -, β - and γ -HBCD were 11, 20 and 14%, respectively, which were slightly lower than those of dioxins and organochlorine pesticides.