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5. D1 Immunotoxicology

Author

Pieters, Raymond, Vos, Joseph G., van der Laan, Jan Willem, van Loveren, Henk, Nijkamp, F.P., editor, and Parnham, Michael J., editor

Published
2011
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6. Immunotoxicology

Author

Vos, Joseph G., van der Laan, Jan Willem, van Loveren, Henk, Albers, Ruud, Pieters, Raymond, Nijkamp, Frans P., editor, and Parnham, Michael J., editor

Published
2005
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9. Persistent hematologic and immunologic disturbances in 8-year-old Dutch children associated with perinatal dioxin exposure

Author

ten Tusscher, Gavin W., Steerenberg, Peter A., van Loveren, Henk, Vos, Joseph G., von dem Borne, Albert E.G.K., Westra, Matthijs, van der Slikke, Johannes W., Olie, Kees, Pluim, Hendrik J., and Koppe, Janna G.

Abstract

Perinatal exposure to Dutch "background" dioxin levels in 1990 was high, but comparable with that of other industrialized Western European countries. Exposure during the sensitive perinatal period may cause permanent [...]

Published
2003

20. LETTER TO THE EDITOR

Author

Ezendam, Janine, Vos, Joseph G., and Pieters, Raymond

Published
2004

25. Immune System

Author

Schuurman, Henk-Jan, primary, Krajnc-Franken, Magda A.M., additional, Kuper, C. Frieke, additional, van Loveren, Henk, additional, and Vos, Joseph G., additional

Published
1991
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31. Brominated flame retardants and endocrine disruption

Author

Vos, Joseph G., Georg Becher, Martin Van Den Berg, Pim Leonards, E&H: Environmental Bioanalytical Chemistry, AIMMS, and Institute for Environmental Studies

Subjects
SDG 14 - Life Below Water
Abstract

From an environmental point of view, an increasing important group of organo-halogen compounds are the brominated flame retardants (BFRs), which are widely used in polymers and textiles and applied in construction materials, furniture, and electronic equipment. BFRs with the highest production volume are the polybrominated diphenyl ethers (PBDEs), tetrabromobisphenol A (TBBP-A), and hexabromocyclododecane (HBCD). Because of their persistence and low biodegradation profile, several of the PBDE congeners accumulate in biota and are widely found in the aquatic food chain. Their levels in the environment and in humans have increased during the last decades, in contrast to compounds such as polychlorinated biphenyls (PCBs) and dichlorodiphenyltrichloroethane (DDT), for example. Humans may be exposed to PBDEs mainly through consumption of fatty food of animal origin (e.g., fish), but exposure through skin contact with textiles protected with flame retardants or through inhalation of BFRs volatilized from electronic and electric equipment may also occur. The levels of PBDEs in Swedish human milk showed a doubling in concentration every five years over the period 1972 to 1997 (2,2′,4,4′-tetraBDE being the predominant congener). The levels of penta- and hexa-BDEs increased at the same rate in ringed seals collected in the Canadian Arctic from 1981 to 2000. PBDEs exhibit a great variety of biological effects, depending on the bromine substitution pattern. PBDEs are potential endocrine disrupters, based on shared toxicity with the structurally related PCBs, polychlorinated dibenzofurans (PCDFs), and polychlorinated dibenzo-p-dioxins (PCDDs) (partial aryl hydrocarbon- [Ah-] receptor agonist and antagonist activity in vitro, thyroid toxicity, and immune effects), including developmental toxicity. The potency of TBBP-A to interact with thyroid hormone homeostasis is indicated from in vitro studies in which the compound competes with thyroxin (T4) for binding to transthyretin (TTR). So far, the toxicological profile of many BFRs is too incomplete and insufficient to perform an adequate risk assessment, and further information is required regarding the potential for endocrine disruption of these compounds that are of increasing environmental concern.

Published
2003

33. p53 Heterozygosity Results in an Increased 2-Acetylaminofluorene-Induced Urinary Bladder but not Liver Tumor Response in DNA Repair-DeficientXpaMice

Author

Hoogervorst, Esther M., primary, van Oostrom, Conny Th. M., additional, Beems, Rudolf B., additional, van Benthem, Jan, additional, Gielis, Siska, additional, Vermeulen, Jolanda P., additional, Wester, Piet W., additional, Vos, Joseph G., additional, de Vries, Annemieke, additional, and van Steeg, Harry, additional

Published
2004
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50. Research Articles Mechanisms of Hexachlorobenzene-Induced Adverse Immune Effects in Brown Norway Rats.

Author

Ezendam, Janine, Vos, Joseph G., and Pieters, Raymond

Subjects
*HEXACHLOROBENZENE, *FUNGICIDES, *RATS, *ORGANOCHLORINE compounds, *IMMUNOTOXICOLOGY, *IMMUNOPATHOLOGY
Abstract

Hexachlorobenzene (HCB) is an environmental pollutant that induces adverse immune effects in humans and rats. Brown Norway rats (BN) appear to be very susceptible to HCB-induced immune effects. Oral exposure causes inflammatory skin and lung lesions, enlarged spleen and lymph nodes (LN) and elevated humoral responses. This review describes recent experiments that were performed to elucidate the mechanisms underlying these adverse immune effects. The metabolites tetrachlorohydroquinone and tetrachlorobenzoquinone are capable of generating neoantigen-specific T-cells in the mouse reporter antigen popliteal lymph node assay with 2,4,6-trinitrophenyl-Ficoll. Additional experiments in BN rats have shown that T-cells are involved in the development of HCB-induced skin lesions, the increase in auricular LN weight, lung eosinophilia, and humoral responses. However, splenomegaly and macrophage infiltration in the spleen and lung occur independent of T-cells. Remarkably, HCB does not induce T-cell sensitization in BN rats, suggesting that T-cells are activated nonspecifically, for example by macrophages. Transcriptome profiles obtained after subchronic HCB exposure to BN rats reveal that HCB induces a systemic inflammatory response in which several innate immune cells, such as macrophages, and pro-inflammatory cytokines are involved. Additional experiments have shown that macrophages are implicated in HCB-induced skin lesions, in particular in the aggravation of skin effects. Also, HCB-induced lung eosinophilia and elevation of anti-ssDNA IgM antibodies are less pronounced after macrophage elimination. Presumably, HCB activates macrophages, thereby generating pro-inflammatory adjuvant signals that induce a systemic inflammatory response. Subsequently, this may lead to polyclonal activation of T- and B-cells, eosinophilia, and eventually visible clinical effects. [ABSTRACT FROM AUTHOR]

Published
2004
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