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Kurunthachalam Kannan - One of the best experts on this subject based on the ideXlab platform.
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persistent organic pollutants including polychlorinated and polybrominated dibenzo p dioxins and dibenzofurans in firefighters from northern california
Chemosphere, 2013Co-Authors: Susan D Shaw, Kurunthachalam Kannan, Sehun Yun, Michelle L Berger, Jennifer H Harris, Chunyang Liao, Arlene Blum, Anthony StefaniAbstract:Polychlorinated and polybrominated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs and PBDD/Fs) were measured in serum of twelve firefighters sampled after a fire event in San Francisco, California, along with polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), p,p'-DDE, hexachlorobenzene (HCB), perfluorinated chemicals (PFCs), bisphenol-A (BPA) and tetrabromobisphenol-A (TBBPA). TEQPCDD/F concentrations were relatively low (mean 5pgg(-1) (lipid weight), lw, range 1-11pgg(-1)lw), but concentrations of 1,2,3,4,6,7,8-HpCDD, a congener indicative of exposure during firefighting, were elevated. Tentative WHO2005-TEQs calculated for PBDD/Fs in our samples (mean 104pgg(-1)lw, range 0.2-734pgg(-1)lw) suggested that PBDD/Fs may contribute substantially to dioxin-like toxicity in individual firefighters. PBDE concentrations were elevated in firefighter serum (mean 135ngg(-1)lw, range 48-442ngg(-1)lw). PBDE-209, PBDE-47 and PBDE-153 were prevalent congeners; PBDE-209 contributed >50% of the total PBDE concentration in four individuals, implying continuous occupational exposure to deca-BDE. Perfluorooctanesulfonate (PFOS) was the dominant PFC in serum (mean 12ngml(-1) (wet weight), ww, range 3ngml(-1)ww to 59ngml(-1)ww), followed by perfluorooctanoic acid (PFOA) (mean 7ngml(-1)ww, range 2ngml(-1)ww to 12ngml(-1)ww). Concentrations of perfluorononanoic acid (PFNA) (mean 2ngml(-1)ww, range 1-4ngml(-1)ww) were higher than those reported in the high-smoke exposure group of World Trade Center fire responders, suggesting that the California firefighters were exposed to PFNA in smoke during firefighting. Given their elevated rates of cancers, these results illustrate the importance of monitoring halogenated contaminants including PBDD/Fs in firefighters.
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polybrominated dibenzo p dioxins dibenzofurans and polybrominated diphenyl ethers in soil vegetation workshop floor dust and electronic shredder residue from an electronic waste recycling facility and in soils from a chemical industrial complex in ea
Environmental Science & Technology, 2009Co-Authors: Rudolf Addink, Wenhua Wang, Jinping Cheng, Sehun Yun, Kurunthachalam KannanAbstract:The formation and release of polybrominated dibenzo-p-dioxins and dibenzofurans (PBDD/Fs) from the incineration of electronic wastes (e-waste) that contain brominated flame retardants (BFRs) are a concern. However, studies on the determination of PBDD/Fs in environmental samples collected from e-waste recycling facilities are scarce. In this study, 11 2,3,7,8-substituted PBDD/Fs and 10 polybrominated diphenyl ether (PBDE) congeners were determined in electronic shredder waste, workshop-floor dust, soil, and leaves (of plants on the grounds of the facility) from a large-scale e-waste recycling facility and in surface soil from a chemical-industrial complex (comprising a coke-oven plant, a coal-fired power plant, and a chlor-alkali plant) as well as agricultural areas in eastern China. Total PBDD/F concentrations in environmental samples were in the range of 113−818 pg/g dry wt (dw) for leaves, 392−18500 pg/g dw for electronic shredder residues, 716−800000 pg/g dw for soil samples, and 89600−143000 pg/g dw ...
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polybrominated dibenzo p dioxins dibenzofurans and polybrominated diphenyl ethers in soil vegetation workshop floor dust and electronic shredder residue from an electronic waste recycling facility and in soils from a chemical industrial complex in eastern china
Environmental Science & Technology, 2009Co-Authors: Rudolf Addink, Wenhua Wang, Jinping Cheng, Sehun Yun, Kurunthachalam KannanAbstract:The formation and release of polybrominated dibenzo-p-dioxins and dibenzofurans (PBDD/Fs) from the incineration of electronic wastes (e-waste) that contain brominated flame retardants (BFRs) are a concern. However, studies on the determination of PBDD/Fs in environmental samples collected from e-waste recycling facilities are scarce. In this study, 11 2,3,7,8-substituted PBDD/Fs and 10 polybrominated diphenyl ether (PBDE) congeners were determined in electronic shredder waste, workshop-floor dust soil, and leaves (of plants on the grounds of the facility) from a large-scale e-waste recycling facility and in surface soil from a chemical-industrial complex (comprising a coke-oven plant, a coal-fired power plant, and a chlor-alkali plant) as well as agricultural areas in eastern China. Total PBDD/F concentrations in environmental samples were in the range of 113-818 pg/g dry wt (dw) for leaves, 392-18500 pg/g dw for electronic shredder residues, 716-800000 pg/g dw for soil samples, and 89600-pg/g dw for workshop-floor dust from the e-waste recycling facility and in a range from nondetect (ND) to 427 pg/g dw in soil from the chemical-industrial complex. The highest mean concentrations of total PBDD/Fs were found in soil samples and workshop-floor dust from the e-waste recycling facility. The dioxin-like toxic equivalent (measured as TEQ) concentrations of PBDD/Fs were greater than the TEQs of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) reported in our previous study for the same set of samples. The concentrations of PBDFs were several orders of magnitude higher than the concentrations of PBDDs in samples from the e-waste facility or from soil from the chemical-industrial complex. A significant correlation was found between the concentrations of sigmaPBDD/Fs and sigmaPBDEs (r = 0.769, p < 0.01) and between sigmaPBDD/Fs and the previously reported sigmaPCDD/F concentrations (r = 0.805, p < 0.01). The estimated daily human intakes of TEQs contributed by PBDD/Fs via soil/dust ingestion and dermal exposures in e-waste recycling facilities were higher than the intakes of TEQs contributed by PCDD/ Fs, calculated in our previous study.
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polybrominated diphenyl ethers and polychlorinated biphenyls in human adipose tissue from new york
Environmental Science & Technology, 2005Co-Authors: Boris Johnsonrestrepo, Kurunthachalam Kannan, David P Rapaport, Bruce D RodanAbstract:Human adipose tissue samples (n = 52) collected in New York City during 2003−2004 were analyzed for the presence of polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs). Concentrations of PBDEs in adipose tissues ranged from 17 to 9630 ng/g, lipid wt (median: 77; mean: 399 ng/g, lipid wt; sum all di- through hexa-BDE congeners). Average PBDE concentrations in human adipose tissues from New York City were 10- to 100-times greater than those reported for European countries. A concentration of 9630 ng/g, lipid wt, found in a sample of adipose tissue, is one of the highest concentrations reported to date. PBDE 47 (2,2‘,4,4‘-tetraBDE) was the major congener detected in human tissues, followed by PBDE congeners #99 (2,2‘,4,4‘,5-pentaBDE), 100 (2,2‘,4,4‘,6-pentaBDE), and 153 (2,2‘,4,4‘,5,5‘-hexaBDE). A few individuals contained PBDE 153 as the predominant congener in total PBDE concentrations, suggesting alternative exposure sources, possibly occupational. Principal component analysis of...
Fangxing Yang - One of the best experts on this subject based on the ideXlab platform.
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apoptosis induction on human hepatoma cells hep g2 of decabrominated diphenyl ether PBDE 209
Toxicology Letters, 2007Co-Authors: Yang Hui, Fangxing YangAbstract:Polybrominated diphenyl ethers (PBDEs) are an important class of halogenated organic brominated flame retardants. Because of their presence in abiotic and biotic environments widely and their structural similarity to polychlorinated biphenyls (PCBs), concern has been raised on their possible adverse health effects to humans. This study was designed to determine the anti-proliferative, apoptotic properties of decabrominated diphenyl ether (PBDE-209), using a human hepatoma Hep G2 line as a model system. Hep G2 cells were cultured in the presence of PBDE-209 at various concentrations (1.0-100.0 mu mol/L) for 72 h and the percentage of cell viability was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. The results showed that PBDE-209 inhibited the cells viability in time and concentration-dependent characteristics at concentrations (10.0-100.0 mu mol/L). We found that anti-proliferative effect of PBDE-209 was associated with apoptosis on Hep G2 cells by determinations of morphological changes, cell cycle and apoptosis. Mechanism study showed that PBDE-209 could increase the generation of intracellular reactive oxygen species (ROS) concentration-dependently. Antioxidant N-acetylcyteine partially inhibited the increase of ROS. The mechanism for its hepatoma-inhibitory effects was the induction of cellular apoptosis through ROS generation. In addition, activity of lactate dehydrogenase (LDH) release increased when the cells incubated with PBDE-209 at various concentrations and times. These results suggested that PBDE-209 had the toxicity activity of anti-proliferation and induction of apoptosis in tumor cells in vitro. (c) 2007 Elsevier Ireland Ltd. All rights reserved.
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apoptosis induction on human hepatoma cells hep g2 of decabrominated diphenyl ether PBDE 209
Toxicology Letters, 2007Co-Authors: Xiaozhong Hu, Ying Xu, Decong Hu, Fangxing YangAbstract:Polybrominated diphenyl ethers (PBDEs) are an important class of halogenated organic brominated flame retardants. Because of their presence in abiotic and biotic environments widely and their structural similarity to polychlorinated biphenyls (PCBs), concern has been raised on their possible adverse health effects to humans. This study was designed to determine the anti-proliferative, apoptotic properties of decabrominated diphenyl ether (PBDE-209), using a human hepatoma Hep G2 line as a model system. Hep G2 cells were cultured in the presence of PBDE-209 at various concentrations (1.0-100.0 mu mol/L) for 72 h and the percentage of cell viability was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. The results showed that PBDE-209 inhibited the cells viability in time and concentration-dependent characteristics at concentrations (10.0-100.0 mu mol/L). We found that anti-proliferative effect of PBDE-209 was associated with apoptosis on Hep G2 cells by determinations of morphological changes, cell cycle and apoptosis. Mechanism study showed that PBDE-209 could increase the generation of intracellular reactive oxygen species (ROS) concentration-dependently. Antioxidant N-acetylcyteine partially inhibited the increase of ROS. The mechanism for its hepatoma-inhibitory effects was the induction of cellular apoptosis through ROS generation. In addition, activity of lactate dehydrogenase (LDH) release increased when the cells incubated with PBDE-209 at various concentrations and times. These results suggested that PBDE-209 had the toxicity activity of anti-proliferation and induction of apoptosis in tumor cells in vitro. (c) 2007 Elsevier Ireland Ltd. All rights reserved.
Penny Swanson - One of the best experts on this subject based on the ideXlab platform.
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dietary exposure to 2 2 4 4 tetrabromodiphenyl ether PBDE 47 alters thyroid status and thyroid hormone regulated gene transcription in the pituitary and brain
Environmental Health Perspectives, 2008Co-Authors: Sean C Lema, Irvin R Schultz, Jon T Dickey, Penny SwansonAbstract:BACKGROUND: Polybrominated diphenyl ether (PBDE) flame retardants have been implicated as disruptors of the hypothalamic-pituitary-thyroid axis. Animals exposed to PBDEs may show reduced plasma thyroid hormone (TH), but it is not known whether PBDEs impact TH-regulated pathways in target tissues. OBJECTIVE: We examined the effects of dietary exposure to 2,2´,4,4´-tetrabromodiphenyl ether (PBDE-47)—commonly the highest concentrated PBDE in human tissues—on plasma TH levels and on gene transcripts for glycoprotein hormone a-subunit (GPHa) and thyrotropin s-subunit (TSHs) in the pituitary gland, the autoinduced TH receptors a and s in the brain and liver, and the TH-responsive transcription factor basic transcription element-binding protein (BTEB) in the brain. METHODS: Breeding pairs of adult fathead minnows (Pimephales promelas) were given dietary PBDE-47 at two doses (2.4 µg/pair/day or 12.3 µg/pair/day) for 21 days. RESULTS: Minnows exposed to PBDE-47 had depressed plasma thyroxine (T4), but not 3,5,3´-triiodothyronine (T3). This decline in T4 was accompanied by elevated mRNA levels for TSHs (low dose only) in the pituitary. PBDE-47 intake elevated transcript for TH receptor a in the brain of females and decreased mRNA for TH receptor s in the brain of both sexes, without altering these transcripts in the liver. In males, PBDE-47 exposure also reduced brain transcripts for BTEB. CONCLUSIONS: Our results indicate that dietary exposure to PBDE-47 alters TH signaling at multiple levels of the hypothalamic-pituitary-thyroid axis and provide evidence that TH-responsive pathways in the brain may be particularly sensitive to disruption by PBDE flame retardants. KEY WORDS: basic transcription element-binding protein, brain, endocrine disruption, PBDE-47, polybrominated diphenyl ethers, thyroid hormone, thyroid hormone receptor, thyroid-stimulating hormone, thyrotropin. Environ Health Perspect 116:1694–1699 (2008). doi:10.1289/ehp.11570 available via http://dx.doi.org/ [Online 1 August 2008]
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neural defects and cardiac arrhythmia in fish larvae following embryonic exposure to 2 2 4 4 tetrabromodiphenyl ether PBDE 47
Aquatic Toxicology, 2007Co-Authors: Sean C Lema, Irvin R Schultz, Nathaniel L Scholz, John P Incardona, Penny SwansonAbstract:Polybrominated diphenyl ethers (PBDEs) are added to plastics, polyurethane foam, and textiles as a flame retardant. While PBDEs play a key role in reducing loss of human life and property from fires, these flame retardants have become pervasive organic contaminants in the environment and in the tissues of fish, birds, marine mammals, and humans. Levels of PBDEs in wildlife and humans continue to rise, raising concerns about potential ecological and health risks associated with exposure to these chemicals. Nevertheless, there is little currently known about the toxicological effects of PBDE exposure. Here, we examined the developmental toxicity of the PBDE congener 2,2',4,4'-tetrabromodiphenyl ether (PBDE 47) using the zebrafish (Danio rerio) as an ontogenetic model. Zebrafish embryos were exposed continuously to dissolved phase PBDE 47 (100-5000 microg/l) beginning 3-5 h post-fertilization (hpf). Fish treated with the highest concentrations of PBDE 47 delayed hatching, had reduced growth post-hatching, and displayed an abnormal dorsal curvature of the body with flexion at the hindbrain. By 96h post-fertilization larvae exposed to PBDE 47 had significant tachycardia, which progressed into atrioventricular block arrhythmias. Microinjection of fluorescent dye into the hindbrain ventricle revealed that cerebrospinal fluid in the neural tube and brain ventricles flowed more slowly in fish larvae exposed to PBDE 47, a likely etiology for the dorsal curvature. Similar, though much less pronounced, developmental toxicity also occurred in larvae exposed to PBDE 47 only for a 20h period during early embryogenesis (3-23 hpf), suggesting that PBDEs incorporated in lipid of the egg are bioavailable and cause toxicity later in life. Taken together, this work indicates that exposure to PBDE 47 can cause morphological abnormalities, impair cardiovascular function and cerebrospinal fluid flow, and provides a tractable starting point for using the zebrafish model to explore molecular mechanisms of PBDE toxicity.
Kwangsoo Kim - One of the best experts on this subject based on the ideXlab platform.
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a direct role of the homeodomain proteins phox2a 2b in noradrenaline neurotransmitter identity determination
Journal of Neurochemistry, 2002Co-Authors: Hyemyung Seo, Su Guo, Arnon Rosenthal, Seok Jong Hong, Heesun Kim, Chunhyung Kim, Dong Youn Hwang, Ole Isacson, Kwangsoo KimAbstract:Development of noraderenergic (NA) neurons in the vertebrate brain is dependent on the homeodomain proteins Phox2a and 2b. Here, we show that Phox2a directly controls the NA identity by activating NA-synthesizing dopamine β-hydroxylase (DBH) gene. Single point mutations in the homeodomain of Phox2a resulted in a failure to transactivate the DBH promoter in vitro and resulted in the loss of NA neurons in vivo. In addition, injection of Phox2a-specific antisense oligonucleotide induced the loss of NA neurons in developing zebrafish. Phox2a and 2b activate the DBH promoter and bind to three domains (PBD1–3). PBD1 is composed of two overlapping sites with which monomers of Phox2a can interact. In contrast, PBD2 and 3 interact with the dimeric form of Phox2a. Mutations in three or four, but not one or two, of the binding sites completely abolished activation of the DBH promoter by Phox2a or 2b, while the conversion of PBD3 to a consensus motif (ATTA) improved the DBH promoter activity by > 10-fold. Taken together, these findings establish that Phox2a and 2b control the development of NA neurons in part by directly transactivating DBH transcription through interactions with four binding sites clustered in the proximal promoter.
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a direct role of the homeodomain proteins phox2a 2b in noradrenaline neurotransmitter identity determination
Journal of Neurochemistry, 2002Co-Authors: Hyemyung Seo, Su Guo, Arnon Rosenthal, Seok Jong Hong, Heesun Kim, Chunhyung Kim, Dong Youn Hwang, Ole Isacson, Kwangsoo KimAbstract:Development of noraderenergic (NA) neurons in the vertebrate brain is dependent on the homeodomain proteins Phox2a and 2b. Here, we show that Phox2a directly controls the NA identity by activating NA-synthesizing dopamine beta-hydroxylase (DBH ) gene. Single point mutations in the homeodomain of Phox2a resulted in a failure to transactivate the DBH promoter in vitro and resulted in the loss of NA neurons in vivo. In addition, injection of Phox2a-specific antisense oligonucleotide induced the loss of NA neurons in developing zebrafish. Phox2a and 2b activate the DBH promoter and bind to three domains (PBD1-3). PBD1 is composed of two overlapping sites with which monomers of Phox2a can interact. In contrast, PBD2 and 3 interact with the dimeric form of Phox2a. Mutations in three or four, but not one or two, of the binding sites completely abolished activation of the DBH promoter by Phox2a or 2b, while the conversion of PBD3 to a consensus motif (ATTA) improved the DBH promoter activity by > 10-fold. Taken together, these findings establish that Phox2a and 2b control the development of NA neurons in part by directly transactivating DBH transcription through interactions with four binding sites clustered in the proximal promoter.
Irvin R Schultz - One of the best experts on this subject based on the ideXlab platform.
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dietary exposure to 2 2 4 4 tetrabromodiphenyl ether PBDE 47 alters thyroid status and thyroid hormone regulated gene transcription in the pituitary and brain
Environmental Health Perspectives, 2008Co-Authors: Sean C Lema, Irvin R Schultz, Jon T Dickey, Penny SwansonAbstract:BACKGROUND: Polybrominated diphenyl ether (PBDE) flame retardants have been implicated as disruptors of the hypothalamic-pituitary-thyroid axis. Animals exposed to PBDEs may show reduced plasma thyroid hormone (TH), but it is not known whether PBDEs impact TH-regulated pathways in target tissues. OBJECTIVE: We examined the effects of dietary exposure to 2,2´,4,4´-tetrabromodiphenyl ether (PBDE-47)—commonly the highest concentrated PBDE in human tissues—on plasma TH levels and on gene transcripts for glycoprotein hormone a-subunit (GPHa) and thyrotropin s-subunit (TSHs) in the pituitary gland, the autoinduced TH receptors a and s in the brain and liver, and the TH-responsive transcription factor basic transcription element-binding protein (BTEB) in the brain. METHODS: Breeding pairs of adult fathead minnows (Pimephales promelas) were given dietary PBDE-47 at two doses (2.4 µg/pair/day or 12.3 µg/pair/day) for 21 days. RESULTS: Minnows exposed to PBDE-47 had depressed plasma thyroxine (T4), but not 3,5,3´-triiodothyronine (T3). This decline in T4 was accompanied by elevated mRNA levels for TSHs (low dose only) in the pituitary. PBDE-47 intake elevated transcript for TH receptor a in the brain of females and decreased mRNA for TH receptor s in the brain of both sexes, without altering these transcripts in the liver. In males, PBDE-47 exposure also reduced brain transcripts for BTEB. CONCLUSIONS: Our results indicate that dietary exposure to PBDE-47 alters TH signaling at multiple levels of the hypothalamic-pituitary-thyroid axis and provide evidence that TH-responsive pathways in the brain may be particularly sensitive to disruption by PBDE flame retardants. KEY WORDS: basic transcription element-binding protein, brain, endocrine disruption, PBDE-47, polybrominated diphenyl ethers, thyroid hormone, thyroid hormone receptor, thyroid-stimulating hormone, thyrotropin. Environ Health Perspect 116:1694–1699 (2008). doi:10.1289/ehp.11570 available via http://dx.doi.org/ [Online 1 August 2008]
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neural defects and cardiac arrhythmia in fish larvae following embryonic exposure to 2 2 4 4 tetrabromodiphenyl ether PBDE 47
Aquatic Toxicology, 2007Co-Authors: Sean C Lema, Irvin R Schultz, Nathaniel L Scholz, John P Incardona, Penny SwansonAbstract:Polybrominated diphenyl ethers (PBDEs) are added to plastics, polyurethane foam, and textiles as a flame retardant. While PBDEs play a key role in reducing loss of human life and property from fires, these flame retardants have become pervasive organic contaminants in the environment and in the tissues of fish, birds, marine mammals, and humans. Levels of PBDEs in wildlife and humans continue to rise, raising concerns about potential ecological and health risks associated with exposure to these chemicals. Nevertheless, there is little currently known about the toxicological effects of PBDE exposure. Here, we examined the developmental toxicity of the PBDE congener 2,2',4,4'-tetrabromodiphenyl ether (PBDE 47) using the zebrafish (Danio rerio) as an ontogenetic model. Zebrafish embryos were exposed continuously to dissolved phase PBDE 47 (100-5000 microg/l) beginning 3-5 h post-fertilization (hpf). Fish treated with the highest concentrations of PBDE 47 delayed hatching, had reduced growth post-hatching, and displayed an abnormal dorsal curvature of the body with flexion at the hindbrain. By 96h post-fertilization larvae exposed to PBDE 47 had significant tachycardia, which progressed into atrioventricular block arrhythmias. Microinjection of fluorescent dye into the hindbrain ventricle revealed that cerebrospinal fluid in the neural tube and brain ventricles flowed more slowly in fish larvae exposed to PBDE 47, a likely etiology for the dorsal curvature. Similar, though much less pronounced, developmental toxicity also occurred in larvae exposed to PBDE 47 only for a 20h period during early embryogenesis (3-23 hpf), suggesting that PBDEs incorporated in lipid of the egg are bioavailable and cause toxicity later in life. Taken together, this work indicates that exposure to PBDE 47 can cause morphological abnormalities, impair cardiovascular function and cerebrospinal fluid flow, and provides a tractable starting point for using the zebrafish model to explore molecular mechanisms of PBDE toxicity.
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oral exposure of PBDE 47 in fish toxicokinetics and reproductive effects in japanese medaka oryzias latipes and fathead minnows pimephales promelas
Environmental Science & Technology, 2006Co-Authors: Elisabeth K Muirhead, Ann D Skillman, Sharon E Hook, Irvin R SchultzAbstract:The toxicokinetics of 2,2,4,4-tetrabromodiphenyl ether (PBDE-47) was studied in the Japanese Medaka (Oryzias latipes) after a single oral exposure followed by termination at specific time points. The effects of repeated oral exposure to PBDE-47 on reproductive performance was assessed using a pair breeding experimental design with fathead minnows (Pimephales promelas) given daily PBDE-47 exposures for 25 days, during which fecundity was measured as an indicator of reproductive performance. Medaka and fathead minnows were orally exposed to PBDE-47 by bioencapsulation in brine shrimp, Artemia sp. In the medaka studies, measurable levels of PBDE-47 were detected in the carcass within 0.25 h with peak levels occurring at 8 h. The body levels of PBDE-47 slowly declined and were still 25% of peak levels at 624 h after dosing. Assimilation of the bioencapsulated dose was at least 80% and may well approach 100%. The PBDE-47 concentration-time profile was fitted to a one-compartment clearance-volume toxicokinetic model and the model-predicted value for elimination half-life was determined to be 281 h and the first-order absorption rate constant was Ka = 0.26 hr(-1). In the fathead minnow study, egg laying in the PBDE-treated breeding pairs stopped after 10 days. The condition factor of PBDE-treated males was significantly reduced (P <0.011) compared with control males, whereas no significant difference was observed in females. Histological examination revealed a greater than 50% reduction in mature sperm in PBDE-47 exposed minnows compared to controls. Collectively, these results suggest PBDE-47 is selectively toxic to sexually mature male fathead minnows.
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oral exposure of PBDE 47 in fish toxicokinetics and reproductive effects in japanese medaka oryzias latipes and fathead minnows pimephales promelas
Environmental Science & Technology, 2006Co-Authors: Elisabeth K Muirhead, Ann D Skillman, Sharon E Hook, Irvin R SchultzAbstract:The toxicokinetics of 2,2,4,4-tetrabromodiphenyl ether (PBDE-47) was studied in the Japanese Medaka (Oryzias latipes) after a single oral exposure followed by termination at specific time points. The effects of repeated oral exposure to PBDE-47 on reproductive performance was assessed using a pair breeding experimental design with fathead minnows (Pimephales promelas) given daily PBDE-47 exposures for 25 days, during which fecundity was measured as an indicator of reproductive performance. Medaka and fathead minnows were orally exposed to PBDE-47 by bioencapsulation in brine shrimp, Artemia sp. In the medaka studies, measurable levels of PBDE-47 were detected in the carcass within 0.25 h with peak levels occurring at 8 h. The body levels of PBDE-47 slowly declined and were still 25% of peak levels at 624 h after dosing. Assimilation of the bioencapsulated dose was at least 80% and may well approach 100%. The PBDE-47 concentration−time profile was fitted to a one-compartment clearance-volume toxicokinetic ...