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      Survey of the Extent of the Persisting Effects of Methylmercury Pollution on the Inhabitants around the Shiranui Sea, Japan

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          Abstract

          In 1956 methylmercury poisoning, known as Minamata disease, was discovered among the inhabitants around the Shiranui Sea, Kyushu, Japan. Although about five hundred thousand people living in the area had supposedly been exposed to methylmercury, administrative agencies and research institutes had not performed any subsequent large scale, continuous health examination, so the actual extent of the negative health effects was not clearly documented. In 2009, we performed health surveys in order to examine residents in the polluted area and to research the extent of the polluted area and period of pollution. We analyzed data collected on 973 people (age = 62.3 ± 11.7) who had lived in the polluted area and had eaten the fish there and a control group, consisting of 142 persons (age = 62.0 ± 10.5), most of whom had not lived in the polluted area. Symptoms and neurological signs were statistically more prevalent in the four groups than in the control group and were more prevalent and severe in those who had eaten most fish. The patterns of positive findings of symptoms and neurological findings in the four groups were similar. Our data indicates that Minamata disease had spread outside of the central area and could still be observed recently, almost 50 years after the Chisso Company’s factory had halted the dumping of mercury polluted waste water back in 1968.

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          Evidence on the Human Health Effects of Low-Level Methylmercury Exposure

          Background: Methylmercury (MeHg) is a known neuro-toxicant. Emerging evidence indicates it may have adverse effects on the neuro-logic and other body systems at common low levels of exposure. Impacts of MeHg exposure could vary by individual susceptibility or be confounded by bene-ficial nutrients in fish containing MeHg. Despite its global relevance, synthesis of the available literature on low-level MeHg exposure has been limited. Objectives: We undertook a synthesis of the current knowledge on the human health effects of low-level MeHg exposure to provide a basis for future research efforts, risk assessment, and exposure remediation policies worldwide. Data sources and extraction: We reviewed the published literature for original human epidemio-logic research articles that reported a direct biomarker of mercury exposure. To focus on high-quality studies and those specifically on low mercury exposure, we excluded case series, as well as studies of populations with unusually high fish consumption (e.g., the Seychelles), marine mammal consumption (e.g., the Faroe Islands, circumpolar, and other indigenous populations), or consumption of highly contaminated fish (e.g., gold-mining regions in the Amazon). Data synthesis: Recent evidence raises the possibility of effects of low-level MeHg exposure on fetal growth among susceptible subgroups and on infant growth in the first 2 years of life. Low-level effects of MeHg on neuro-logic outcomes may differ by age, sex, and timing of exposure. No clear pattern has been observed for cardio-vascular disease (CVD) risk across populations or for specific CVD end points. For the few studies evaluating immunologic effects associated with MeHg, results have been inconsistent. Conclusions: Studies targeted at identifying potential mechanisms of low-level MeHg effects and characterizing individual susceptibility, sexual dimorphism, and non-linearity in dose response would help guide future prevention, policy, and regulatory efforts surrounding MeHg exposure.
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            Methylmercury Poisoning in Iraq

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              Methylmercury-induced neurotoxicity and apoptosis.

              Methylmercury is a widely distributed environmental toxicant with detrimental effects on the developing and adult nervous system. Due to its accumulation in the food chain, chronic exposure to methylmercury via consumption of fish and sea mammals is still a major concern for human health, especially developmental exposure that may lead to neurological alterations, including cognitive and motor dysfunctions. Mercury-induced neurotoxicity and the identification of the underlying mechanisms has been a main focus of research in the neurotoxicology field. Three major mechanisms have been identified as critical in methylmercury-induced cell damage including (i) disruption of calcium homeostasis, (ii) induction of oxidative stress via overproduction of reactive oxygen species or reduction of antioxidative defenses and (iii) interactions with sulfhydryl groups. In vivo and in vitro studies have provided solid evidence for the occurrence of neural cell death, as well as cytoarchitectural alterations in the nervous system after exposure to methylmercury. Signaling cascades leading to cell death induced by methylmercury involve the release of mitochondrial factors, such as cytochrome c and AIF with subsequent caspase-dependent or -independent apoptosis, respectively; induction of calcium-dependent proteases calpains; interaction with lysosomes leading to release of cathepsins. Interestingly, several pathways can be activated in parallel, depending on the cell type. In this paper, we provide an overview of recent findings on methylmercury-induced neurotoxicity and cell death pathways that have been described in neural and endocrine cell systems. Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
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                Author and article information

                Journal
                Toxics
                Toxics
                toxics
                Toxics
                MDPI
                2305-6304
                20 July 2018
                September 2018
                : 6
                : 3
                : 39
                Affiliations
                [1 ]Kyoritsu Neurology and Rehabilitation Clinic, 2-2-28 Sakurai-cho, Minamata 867-0045, Japan
                [2 ]Kikuyou Hospital, 5587 Haramizu, Kikuyou 869-1102, Japan; tds-fujino@ 123456jcom.zaq.ne.jp
                [3 ]Minamata Kyoritsu Hospital, 2-2-12 Sakurai-cho, Minamata 867-0045, Japan; mkkawa@ 123456fsinet.or.jp (Y.K.); shigeoka@ 123456mk-kyouritu.com (S.-i.S.)
                [4 ]Department of Human Ecology, Graduate School of Environmental and Life Science, Okayama University, 3-1-1 Tsushima-naka, Kita-ku, Okayama 700-8530, Japan; yorichan@ 123456md.okayama-u.ac.jp
                Author notes
                [* ]Correspondence: stakaoka@ 123456x.email.ne.jp ; Tel.: +81-966-63-6835
                Author information
                https://orcid.org/0000-0003-1318-0488
                Article
                toxics-06-00039
                10.3390/toxics6030039
                6160922
                30037044
                bd4d1a1c-6f0a-48c0-a736-a5e97cddcb34
                © 2018 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 28 June 2018
                : 18 July 2018
                Categories
                Article

                methylmercury,long term exposure,symptoms,neurological findings,severity,delayed toxicity,correlation of signs and symptoms,dose-response relationship

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