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  • 1.
    Carvalho, Raquel N.
    et al.
    Institute for Environment and Sustainability, European Commission-DG Joint Research Centre, Ispra, Italy.
    Arukwe, Augustine
    Norwegian University of Science & Technology, Trondheim, Norway.
    Ait-Aissa, Selim
    National Institute for Industrial Environment and Risks, Verneuil en Halatte, France.
    Bado-Nilles, Anne
    National Institute for Industrial Environment and Risks, Verneuil en Halatte, France; Reims University, Reims, France.
    Balzamo, Stefania
    Istituto Superiore per la Protezione e la Ricerca Ambientale (ISPRA), Rome, Italy.
    Baun, Anders
    Department of Environmental Engineering,Technical University of Denmark, Kgs Lyngby, Denmark.
    Belkin, Shimshon
    Institute of Life Sciences, The Hebrew University, Jerusalem, Israel.
    Blaha, Ludek
    Faculty of Science, RECETOX, Masaryk University, Brno, Czech Republic.
    Brion, Francois
    National Institute for Industrial Environment and Risks, Verneuil en Halatte, France.
    Conti, Daniela
    Istituto Superiore per la Protezione e la Ricerca Ambientale (ISPRA), Rome, Italy.
    Creusot, Nicolas
    National Institute for Industrial Environment and Risks, Verneuil en Halatte, France.
    Essig, Yona
    Analytical and Environmental Sciences Division, King's College, London, UK.
    Ferrero, Valentina E. V.
    European Commission-DG Joint Research Centre, Institute for Environment and Sustainability, Ispra, Italy.
    Flander-Putrle, Vesna
    Marine Biology Station Piran, National Institute of Biology, Ljubljana, Slovenia.
    Furhacker, Maria
    University of Natural Resources and Life Sciences, Vienna, Austria.
    Grillari-Voglauer, Regina
    University of Natural Resources and Life Sciences, Vienna, Austria.
    Hogstrand, Christer
    Diabetes and Nutritional Sciences Division, King's College London, London, UK.
    Jonas, Adam
    Faculty of Science, RECETOX, Masaryk University, Brno, Czech Republic.
    Kharlyngdoh, Joubert B.
    Örebro University, School of Science and Technology.
    Loos, Robert
    European Commission-DG Joint Research Centre, Institute for Environment and Sustainability, Ispra, Italy.
    Lundebye, Anne-Katrine
    National Institute of Nutrition and Seafood Research, Bergen, Norway.
    Modig, Carina
    Örebro University, School of Science and Technology. Life Science Center, Örebro University, Örebro, Sweden.
    Olsson, Per-Erik
    Örebro University, School of Science and Technology. Life Science Center, Örebro University, Örebro, Sweden.
    Pillai, Smitha
    University of Natural Resources and Life Sciences, Vienna, Austria.
    Polak, Natasa
    Analytical and Environmental Sciences Division, King's College, London, UK.
    Potalivo, Monica
    Istituto Superiore per la Protezione e la Ricerca Ambientale (ISPRA), Rome, Italy.
    Sanchez, Wilfried
    National Institute for Industrial Environment and Risks, Verneuil en Halatte, France.
    Schifferli, Andrea
    Swiss Centre for Applied Ecotoxicology, Eawag-EPFL, Dübendorf, Switzerland.
    Schirmer, Kristin
    Swiss Centre for Applied Ecotoxicology, Eawag-EPFL, Dübendorf, Switzerland.
    Sforzini, Susanna
    Department of Environmental and Life Sciences, Universita del Piemonte Orientale Vercelli Novara Alessandria, Alessandria, Italy.
    Sturzenbaum, Stephen R.
    Analytical and Environmental Sciences Division, King's College, London, UK.
    Søfteland, Liv
    National Institute of Nutrition and Seafood Research, Bergen, Norway.
    Turk, Valentina
    Marine Biology Station Piran, National Institute of Biology, Ljubljana, Slovenia.
    Viarengo, Aldo
    Department of Environmental and Life Sciences, Università del Piemonte Orientale Vercelli Novara Alessandria, Alessandria, Italy.
    Werner, Inge
    Swiss Centre for Applied Ecotoxicology, Swiss Federal Institute of Aquatic Science and Technology ( Eawag-EPFL), Dübendorf, Switzerland.
    Yagur-Kroll, Sharon
    Institute of Life Sciences, The Hebrew University, Jerusalem, Israel.
    Zounkova, Radka
    Faculty of Science, RECETOX, Masaryk University, Brno, Czech Republic.
    Lettieri, Teresa
    European Commission-DG Joint Research Centre, Institute for Environment and Sustainability, Rome, Italy.
    Mixtures of chemical pollutants at European legislation safety concentrations: how safe are they?2014In: Toxicological Sciences, ISSN 1096-6080, E-ISSN 1096-0929, Vol. 141, no 1, p. 218-233Article in journal (Refereed)
    Abstract [en]

    The risk posed by complex chemical mixtures in the environment to wildlife and humans is increasingly debated, but has been rarely tested under environmentally relevant scenarios. To address this issue, two mixtures of 14 or 19 substances of concern (pesticides, pharmaceuticals, heavy metals, polyaromatic hydrocarbons, a surfactant, and a plasticizer), each present at its safety limit concentration imposed by the European legislation, were prepared and tested for their toxic effects. The effects of the mixtures were assessed in 35 bioassays, based on 11 organisms representing different trophic levels. A consortium of 16 laboratories was involved in performing the bioassays. The mixtures elicited quantifiable toxic effects on some of the test systems employed, including i) changes in marine microbial composition, ii) microalgae toxicity, iii) immobilization in the crustacean Daphnia magna, iv) fish embryo toxicity, v) impaired frog embryo development, and vi) increased expression on oxidative stress-linked reporter genes. Estrogenic activity close to regulatory safety limit concentrations was uncovered by receptor-binding assays. The results highlight the need of precautionary actions on the assessment of chemical mixtures even in cases where individual toxicants are present at seemingly harmless concentrations.

  • 2.
    Guruge, K S
    et al.
    Toxico-Biochemistry Section, National Institute of Animal Health, Kannondai 3-1-5, Tsukuba, Ibaraki, Japan.
    Yeung, L W Y
    Toxico-Biochemistry Section, National Institute of Animal Health, Kannondai 3-1-5, Tsukuba, Ibaraki, Japan;Department of Biology and Chemistry, City University of Hong Kong, Tat Chee Avenue, Kowloon, Hong Kong SAR, Hong Kong.
    Yamanaka, N
    Toxico-Biochemistry Section, National Institute of Animal Health, Kannondai 3-1-5, Tsukuba, Ibaraki, Japan.
    Miyazaki, S
    Toxico-Biochemistry Section, National Institute of Animal Health, Kannondai 3-1-5, Tsukuba, Ibaraki, Japan.
    Lam, P K S
    Department of Biology and Chemistry, City University of Hong Kong, Tat Chee Avenue, Kowloon, Hong Kong SAR, Hong Kong.
    Giesy, J P
    Department of Biology and Chemistry, City University of Hong Kong, Tat Chee Avenue, Kowloon, Hong Kong SAR, Hong Kong;Zoology Dept., National Food Safety and Toxicology Center, Michigan State University, East Lansing, MI, United States.
    Jones, P D
    Zoology Dept., National Food Safety and Toxicology Center, Michigan State University, East Lansing, MI, United States.
    Yamashita, N
    Environmental Measurement Group, National Institute of Advance Industrial Science and Technology, Onogawa 16-1, Tsukuba, Ibaraki, Japan.
    Gene expression profiles in rat liver treated with perfluorooctanoic acid (PFOA)2006In: Toxicological Sciences, ISSN 1096-6080, E-ISSN 1096-0929, Vol. 89, no 1, p. 93-107Article in journal (Refereed)
    Abstract [en]

    Perfluorooctanoic acid (PFOA; Pentadecafluorooctanoic acid) is widely used in various industrial applications. It is persistent in the environment and does not appear to undergo further degradation or transformation. PFOA is found in tissues including blood of wildlife and humans; however, the environmental fate and biological effects of PFOA remain unclear. Microarray techniques of gene expression have become a powerful approach for exploring the biological effects of chemicals. Here, the Affymetrix, Inc. rat genome 230 2.0 GeneChip was used to identify alterations in gene regulation in Sprague-Dawley rats treated with five different concentrations of PFOA. Male rats were exposed by daily gavage to 1, 3, 5, 10, or 15 mg PFOA/kg, body weight (bw)/day for 21 days and at the end of the exposure, liver was isolated and total liver RNA were used for the gene chip analysis. Over 500 genes, whose expression was significantly (p < 0.0025) altered by PFOA at two-fold changes compared to control, were examined. The effects were dose-dependent with exposure to 10 mg PFOA/kg, bw/day, causing alteration in expression of the greatest number of genes (over 800). Approximately 106 genes and 38 genes were consistently up- or down-regulated, respectively, in all treatment groups. The largest categories of induced genes were those involved in transport and metabolism of lipids, particularly fatty acids. Other induced genes were involved in cell communication, adhesion, growth, apoptosis, hormone regulatory pathways, proteolysis and peptidolysis and signal transduction. The genes expression of which was suppressed were related to transport of lipids, inflammation and immunity, and especially cell adhesion. Several other genes involved in apoptosis; regulation of hormones; metabolism; and G-protein coupled receptor protein signaling pathways were significantly suppressed.

  • 3.
    Shi, Xiongjie
    et al.
    State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China.
    Yeung, Leo W. Y.
    Department of Biology and Chemistry, City University of Hong Kong, Hong Kong SAR, Hong Kong.
    Lam, Paul K. S.
    Department of Biology and Chemistry, City University of Hong Kong, Hong Kong SAR, Hong Kong.
    Wu, Rudolf S. S.
    State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China.
    Zhou, Bingsheng
    State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China.
    Protein Profiles in Zebrafish (Danio rerio) Embryos Exposed to Perfluorooctane Sulfonate2009In: Toxicological Sciences, ISSN 1096-6080, E-ISSN 1096-0929, Vol. 110, no 2, p. 334-340Article in journal (Refereed)
    Abstract [en]

    Perfluorooctane sulfonate (PFOS) is widely distributed and persistent in the environment and in wildlife, and it has the potential for developmental toxicity. However, the molecular mechanisms that lead to these toxic effects are not well known. In the present study, proteomic analysis has been performed to investigate the proteins that are differentially expressed in zebrafish embryos exposed to 0.5 mg/l PFOS until 192 h postfertilization. Two-dimensional electrophoresis coupled with mass spectrometry was employed to detect and identify the protein profiles. The analysis revealed that 69 proteins showed altered expression in the treatment group compared to the control group with either increase or decrease in expression levels (more than twofold difference). Of the 69 spots corresponding to the proteins with altered expression, 38 were selected and subjected to matrix-assisted laser desorption/ionization tandem time-of-flight mass spectrometry (TOF/TOF) analysis; 18 proteins were identified in this analysis. These proteins can be categorized into diverse functional classes such as detoxification, energy metabolism, lipid transport/steroid metabolic process, cell structure, signal transduction, and apoptosis. Overall, proteomic analysis using zebrafish embryos serves as an in vivo model in environmental risk assessment and provides insight into the molecular events in PFOS-induced developmental toxicity.

  • 4.
    Van den Berg, Martin
    et al.
    World Health Organization Collaborating Centre for Research on Environmental Health Risk Assessment and Institute for Risk Assessment Sciences, Faculties of Veterinary Medicine, Science and University Medical Center, Universiteit Utrecht, Utrecht, The Netherlands.
    Birnbaum, Linda S.
    National Health & Environmental Effects Research Laboratory, United States Environmental Protection Agency Research Triangle Park, North Carolina, USA.
    Denison, Michael
    Department of Environmental Toxicology, University of California at Davis, Davis, California, USA.
    De Vito, Mike
    National Health & Environmental Effects Research Laboratory, United States Environmental Protection Agency Research Triangle Park, North Carolina, USA.
    Farland, William
    Office of Research and Development, U.S. Environmental Protection Agency (EPA), NW, Washington, District of Columbia, USA.
    Feeley, Mark
    Chemical Health Hazard Assessment Division, Bureau of Chemical Safety, Health Canada, Tunney’s Pasture, Ottawa, Ontario, Canada.
    Fiedler, Heidelore
    United Nations Environment Program Chemicals, International Environment House, Châtelaine (GE), Switzerland.
    Håkansson, Helen
    Institute of Environmental Medicine, Karolinska Institutet, Unit of Environmental Health Risk Assessment, Stockholm, Sweden.
    Hanberg, Annika
    Institute of Environmental Medicine, Karolinska Institutet, Unit of Environmental Health Risk Assessment, Stockholm, Sweden.
    Haws, Laurie
    ChemRisk, Austin, Texas, USA.
    Rose, Martin
    Central Science Laboratory, Sand Hutton, York, United Kingdom.
    Safe, Stephen
    Veterinary Physiology and Pharmacology, Texas A&M University, Texas, USA.
    Schrenk, Dieter
    Department of Food Chemistry and Environmental Toxicology, University of Kaiserslautern, Kaiserslautern, Germany.
    Tohyama, Chiharu
    Division of Environmental Health Sciences, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo Japan.
    Tritscher, Angelika
    nternational Programme on Chemical Safety, World Health Organization, Geneva, Switzerland.
    Tuomisto, Jouko
    National Public Health Institute, Department of Environmental Health, Kuopio, Finland.
    Tysklind, Mats
    Environmental Chemistry, Umeå University, Sweden.
    Walker, Nigel
    National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA.
    Peterson, Richard E.
    School of Pharmacy and Molecular and Environmental Toxicology Center, University of Wisconsin, Madison, Wisconsin, USA.
    The 2005 World Health Organization reevaluation of human and mammalian toxic equivalency factors for dioxins and dioxin-like compounds2006In: Toxicological Sciences, ISSN 1096-6080, E-ISSN 1096-0929, Vol. 93, no 2, p. 223-241Article in journal (Refereed)
    Abstract [en]

    In June 2005, a World Health Organization (WHO)-International Programme on Chemical Safety expert meeting was held in Geneva during which the toxic equivalency factors (TEFs) for dioxin-like compounds, including some polychlorinated biphenyls (PCBs), were reevaluated. For this reevaluation process, the refined TEF database recently published by Haws et al. (2006, Toxicol. Sci. 89, 4-30) was used as a starting point. Decisions about a TEF value were made based on a combination of unweighted relative effect potency (REP) distributions from this database, expert judgment, and point estimates. Previous TEFs were assigned in increments of 0.01, 0.05, 0.1, etc., but for this reevaluation, it was decided to use half order of magnitude increments on a logarithmic scale of 0.03, 0.1, 0.3, etc. Changes were decided by the expert panel for 2,3,4,7,8-pentachlorodibenzofuran (PeCDF) (TEF = 0.3), 1,2,3,7,8-pentachlorodibenzofuran (PeCDF) (TEF = 0.03), octachlorodibenzo-p-dioxin and octachlorodibenzofuran (TEFs = 0.0003), 3,4,4',5-tetrachlorbiphenyl (PCB 81) (TEF = 0.0003), 3,3',4,4',5,5'-hexachlorobiphenyl (PCB 169) (TEF = 0.03), and a single TEF value (0.00003) for all relevant mono-ortho-substituted PCBs. Additivity, an important prerequisite of the TEF concept was again confirmed by results from recent in vivo mixture studies. Some experimental evidence shows that non-dioxin-like aryl hydrocarbon receptor agonists/antagonists are able to impact the overall toxic potency of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds, and this needs to be investigated further. Certain individual and groups of compounds were identified for possible future inclusion in the TEF concept, including 3,4,4'-TCB (PCB 37), polybrominated dibenzo-p-dioxins and dibenzofurans, mixed polyhalogenated dibenzo-p-dioxins and dibenzofurans, polyhalogenated naphthalenes, and polybrominated biphenyls. Concern was expressed about direct application of the TEF/total toxic equivalency (TEQ) approach to abiotic matrices, such as soil, sediment, etc., for direct application in human risk assessment. This is problematic as the present TEF scheme and TEQ methodology are primarily intended for estimating exposure and risks via oral ingestion (e.g., by dietary intake). A number of future approaches to determine alternative or additional TEFs were also identified. These included the use of a probabilistic methodology to determine TEFs that better describe the associated levels of uncertainty and "systemic" TEFs for blood and adipose tissue and TEQ for body burden.

  • 5.
    van den Berg, Martin
    et al.
    Institute for Risk Assessment Sciences (IRAS) and WHO Collaborating Centre for Environmental Health Risk Assessment, Utrecht University, Utrecht, The Netherlands.
    Denison, Michael S.
    Department of Environmental Toxicology, University of California, Davis CA, USA.
    Birnbaum, Linda S.
    National Cancer Institute and National Institute of Environmental Health Sciences, Research Triangle Park NC, USA.
    DeVito, Michael J.
    Environmental Health Sciences, Research Triangle Park NC, USA.
    Fiedler, Heidelore
    United Nations Environment Programme (UNEP), Geneva, Switzerland.
    Falandysz, Jerzy
    University of Gdańsk, Gdańsk, Poland.
    Rose, Martin
    Food and Environment Research Agency, York, United Kingdom.
    Schrenk, Dieter
    Department of Food Chemistry & Environmental Toxicology, Technische Universität Kaiserslautern, Kaiserslautern, Germany.
    Safe, Stephen
    Veterinary Physiology and Pharmacology, Texas A&M University, College Station TX, USA.
    Tohyama, Chiharu
    Laboratory of Environmental Health Sciences, University of Tokyo, Tokyo, Japan.
    Tritscher, Angelika
    Department of Food Safety and Zoonoses, World Health Organization (WHO), Geneva, Switzerland.
    Tysklind, Mats
    Department of Chemistry, Umeå University, Umeå, Sweden.
    Peterson, Richard E.
    Department of Pharmaceutical Sciences, University of Wisconsin, Madison WI, USA.
    Polybrominated Dibenzo-p-Dioxins, Dibenzofurans, and Biphenyls: Inclusion in the Toxicity Equivalency Factor Concept for Dioxin-Like Compounds2013In: Toxicological Sciences, ISSN 1096-6080, E-ISSN 1096-0929, Vol. 133, no 2, p. 197-208Article, review/survey (Refereed)
    Abstract [en]

    In 2011, a joint World Health Organization (WHO) and United Nations Environment Programme (UNEP) expert consultation took place, during which the possible inclusion of brominated analogues of the dioxin-like compounds in the WHO Toxicity Equivalency Factor (TEF) scheme was evaluated. The expert panel concluded that polybrominated dibenzo-p-dioxins (PBDDs), dibenzofurans (PBDFs), and some dioxin-like biphenyls (dl-PBBs) may contribute significantly in daily human background exposure to the total dioxin toxic equivalencies (TEQs). These compounds are also commonly found in the aquatic environment. Available data for fish toxicity were evaluated for possible inclusion in the WHO-UNEP TEF scheme (van den Berg et al., 1998). Because of the limited database, it was decided not to derive specific WHO-UNEP TEFs for fish, but for ecotoxicological risk assessment, the use of specific relative effect potencies (REPs) from fish embryo assays is recommended. Based on the limited mammalian REP database for these brominated compounds, it was concluded that sufficient differentiation from the present TEF values of the chlorinated analogues (van den Berg et al., 2006) was not possible. However, the REPs for PBDDs, PBDFs, and non-ortho dl-PBBs in mammals closely follow those of the chlorinated analogues, at least within one order of magnitude. Therefore, the use of similar interim TEF values for brominated and chlorinated congeners for human risk assessment is recommended, pending more detailed information in the future.

  • 6.
    Yu, Ke
    et al.
    State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China; Department of Biology and Chemistry, City University of Hong Kong, Kowloon, SAR, Hong Kong.
    He, Yuhe
    Graduate School of the Chinese Academy of Sciences, Beijing, China.
    Yeung, Leo W. Y.
    Graduate School of the Chinese Academy of Sciences, Beijing, China.
    Lam, Paul K. S.
    Graduate School of the Chinese Academy of Sciences, Beijing, China.
    Wu, Rudolf S. S.
    Graduate School of the Chinese Academy of Sciences, Beijing, China.
    Zhou, Bingsheng
    State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China.
    DE-71-induced apoptosis involving intracellular calcium and the Bax-mitochondria-caspase protease pathway in human neuroblastoma cells In vitro2008In: Toxicological Sciences, ISSN 1096-6080, E-ISSN 1096-0929, Vol. 104, no 2, p. 341-351Article in journal (Refereed)
    Abstract [en]

    Polybrominated diphenyl ethers (PBDEs) are used extensively as flame-retardants and are ubiquitous in the environment and in wildlife and human tissue. Recent studies have shown that PBDEs induce neurotoxic effects in vivo and apoptosis in vitro. However, the signaling mechanisms responsible for these events are still unclear. In this study, we investigated the action of a commercial mixture of PBDEs (pentabrominated diphenyl ether, DE-71) on a human neuroblastoma cell line, SK-N-SH. A cell viability test showed a dose-dependent increase in lactate dehydrogenase leakage and 3-(4,5-dimethylthia-zol-2-yl)-2, 5-diphenyl-tetrazolium bromide reduction. Cell apoptosis was observed through morphological examination, and DNA degradation in the cell cycle and cell apoptosis were demonstrated using flow cytometry and DNA laddering. The formation of reactive oxygen species was not observed, but DE-71 was found to significantly induce caspase-3, -8, and -9 activity, which suggests that apoptosis is not induced by oxidative stress but via a caspase-dependent pathway. We further investigated the intracellular calcium ([Ca2+]i) levels using flow cytometry and observed an increase in the intracellular Ca2+ concentration with a time-dependent trend. We also found that the N-methyl d-aspartate (NMDA) receptor antagonist MK801 (3μM) significantly reduced DE-71-induced cell apoptosis. The results of a Western blotting test demonstrated that DE-71 treatment increases the level of Bax translocation to the mitochondria in a dose-dependent fashion and stimulates the release of cytochrome c (Cyt c) from the mitochondria into the cytoplasm. Overall, our results indicate that DE-71 induces the apoptosis of [Ca2+]i in SK-N-SH cells via Bax insertion, Cyt c release in the mitochondria, and the caspase activation pathway.

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