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      The Vernix Caseosa is the Main Site of Dioxin Excretion in the Human Foetus

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          Abstract

          Dioxins are highly toxic to foetuses and prenatal exposure leads to adverse health effects; however, the metabolic pathways involved in dioxin excretion are poorly understood. We determined the dynamics of maternal-to-foetal dioxin transfer during normal pregnancy and how foetuses eliminate polychlorinated dibenzo- p-dioxins, polychlorinated dibenzofurans, and non- ortho polychlorinated biphenyls. Dioxin levels in maternal blood, cord blood, placenta, vernix caseosa, meconium, and amniotic fluid were analysed by high-resolution gas chromatography/mass spectrometry. The average levels of total dioxins, expressed as picograms of toxic equivalency quantity per gram of lipid and in parentheses, dioxin fraction, with maternal blood levels arbitrarily set as 100%, were as follows: maternal blood, 15.8 (100%); placenta, 12.9 (81.5%); cord blood, 5.9 (37.2%); vernix caseosa, 8.4 (53.2%); meconium, 2.9 (18.2%); and amniotic fluid, 1.5 (9.2%). Similar proportions were observed for each dioxin congener. Thus, the highest content of foetal dioxins was observed in the vernix caseosa, indicating that this is the major site of dioxin excretion in human foetuses.

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          The 2005 World Health Organization reevaluation of human and Mammalian toxic equivalency factors for dioxins and dioxin-like compounds.

          Martin van den Berg, Linda S. Birnbaum, Michael H. Denison … (2006)
          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.
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            Non-invasive matrices in human biomonitoring: a review.

            Marta Esteban, Argelia Castaño (2009)
            Humans and other living organisms are exposed to a variety of chemical pollutants that are released into the environment as a consequence of anthropogenic activities. Environmental pollutants are incorporated into the organism by different routes and can then be stored and distributed in different tissues, which leads to an internal concentration that can induce different alterations, adverse effects and/or diseases. Control measures should be taken to avoid these effects and human biomonitoring is a very useful tool that can contribute to this aim. Human biomonitoring uses different matrices to measure the target chemicals depending on the chemical, the amount of matrix necessary for the analysis and the detection limit (LOD) of the analytical technique. Blood is the ideal matrix for most chemicals due to its contact with the whole organism and its equilibrium with organs and tissues where chemicals are stored. However, it has an important disadvantage of being an invasive matrix. The development of new methodology and modern analytical techniques has allowed the use of other matrices that are less or non-invasive, such as saliva, urine, meconium, nails, hair, and semen or breast milk. The presence of a chemical in these matrices reflects an exposure, but correlations between levels in non-invasive matrices and blood must be established to ensure that these levels are related to the total body burden. The development of new biomarkers that are measurable in these matrices will improve non-invasive biomonitoring. This paper reviews studies that measure Cd, Pb, Hg, polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), polycyclic aromatic hydrocarbons (PAHs), polybrominated diphenyl ethers (PBDEs), organochlorine pesticides and phthalates in non-invasive matrices, the most used techniques for measurements and what alternative techniques are available.
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              Role of AhR/ARNT system in skin homeostasis

              Masutaka Furue, Masakazu Takahara, Takeshi Nakahara … (2014)
              Aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor that binds to structurally diverse synthetic and naturally occurring chemicals including dioxins, flavonoids, tryptophan photoproducts, and Malassezia metabolites. Upon binding to its ligands, cytoplasmic AhR translocates to the nucleus, heterodimerizes with aryl hydrocarbon receptor nuclear translocator (ARNT), and mediates numerous biological and toxicological effects by inducing the transcription of various AhR-responsive genes. AhR ligation controls oxidation/antioxidation, epidermal barrier function, photo-induced response, melanogenesis, and innate immunity. This review summarizes recent advances in the understanding of the regulatory mechanisms of skin homeostasis mediated by the AhR/ARNT system.
              Article 0 comments Cited 54 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Seiichi Morokuma: morokuma@med.kyushu-u.ac.jp
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 7 April 2017
                Publication date PMC-release: 7 April 2017
                Publication date Collection: 2017
                Volume: 7
                Electronic Location Identifier: 739
                Affiliations
                [1 ]GRID grid.411248.a, Department of Obstetrics and Gynecology, , Kyushu University Hospital, ; Fukuoka, Japan
                [2 ]GRID grid.410810.c, Department of Obstetrics, , Fukuoka Children’s Hospital, ; Fukuoka, Japan
                [3 ]GRID grid.415138.a, , Fukuoka Institute of Health and Environmental Science, ; Fukuoka, Japan
                [4 ]GRID grid.177174.3, Department of Obstetrics and Gynecology, Graduate School of Medical Sciences, , Kyushu University, ; Fukuoka, Japan
                [5 ]GRID grid.411248.a, Research and Clinical Center for Yusho and Dioxin, , Kyushu University Hospital, ; Fukuoka, Japan
                [6 ]GRID grid.177174.3, Department of Dermatology, Graduate School of Medical Sciences, , Kyushu University, ; Fukuoka, Japan
                Article
                Publisher ID: 863
                DOI: 10.1038/s41598-017-00863-9
                PMC ID: 5429709
                PubMed ID: 28389640
                SO-VID: 89e57276-2800-4429-a3e8-4a6e0d3851d4
                Copyright © © The Author(s) 2017
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 13 December 2016
                Date accepted : 15 March 2017
                Categories
                Subject: Article
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                issue-copyright-statement © The Author(s) 2017

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