Report III Industrial wastes containing mercury compounds from Minamata Factory

Irukayama, Katsuro; Fujiki, Motoo; Kai, Fumiaki; Kondo, Takako

doi:10.1265/jjh.16.476

Cited by 7 publications

(9 citation statements)

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“…The similarity in clinical symptoms was in fact noted ( Tokuomi et al 1960 ), as were the pathology findings from autopsies of deceased victims ( Matsumoto 1961 ; Takeuchi et al 1959 , 1960 ). However, thin-layer chromatography identification of methylmercury was not successful until 1962, when the substance was identified in sludge from the acetaldehyde plant and the bottom sediment of the effluent channel ( Irukayama et al 1962 ). Elevated methylmercury concentrations were subsequently documented in seafood and in tissues of deceased patients.…”

Section: Unexpected Exposure Pathwaysmentioning

confidence: 99%

Adverse Effects of Methylmercury: Environmental Health Research Implications

Grandjean

Satoh

Murata

et al. 2010

Environ Health Perspect

264

168

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BackgroundThe scientific discoveries of health risks resulting from methylmercury exposure began in 1865 describing ataxia, dysarthria, constriction of visual fields, impaired hearing, and sensory disturbance as symptoms of fatal methylmercury poisoning.ObjectiveOur aim was to examine how knowledge and consensus on methylmercury toxicity have developed in order to identify problems of wider concern in research.Data sources and extractionWe tracked key publications that reflected new insights into human methylmercury toxicity. From this evidence, we identified possible caveats of potential significance for environmental health research in general.SynthesisAt first, methylmercury research was impaired by inappropriate attention to narrow case definitions and uncertain chemical speciation. It also ignored the link between ecotoxicity and human toxicity. As a result, serious delays affected the recognition of methylmercury as a cause of serious human poisonings in Minamata, Japan. Developmental neurotoxicity was first reported in 1952, but despite accumulating evidence, the vulnerability of the developing nervous system was not taken into account in risk assessment internationally until approximately 50 years later. Imprecision in exposure assessment and other forms of uncertainty tended to cause an underestimation of methylmercury toxicity and repeatedly led to calls for more research rather than prevention.ConclusionsCoupled with legal and political rigidity that demanded convincing documentation before considering prevention and compensation, types of uncertainty that are common in environmental research delayed the scientific consensus and were used as an excuse for deferring corrective action. Symptoms of methylmercury toxicity, such as tunnel vision, forgetfulness, and lack of coordination, also seemed to affect environmental health research and its interpretation.

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Section: Unexpected Exposure Pathwaysmentioning

confidence: 99%

Adverse Effects of Methylmercury: Environmental Health Research Implications

Grandjean

Satoh

Murata

et al. 2010

Environ Health Perspect

264

168

View full text Add to dashboard Cite

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“…239 In addition to neuron loss in the visual area of the calcarine cortex and granule cells of the cerebellum, methylmercury also produces degeneration of neurons in the DRG along with their associated axons while sparing the peripheral nerve motor axons. [239][240][241][242][243] Methylmercury exerts its neurotoxic affects in DRG partly through the ability to accumulate there due to the high density of fenestrated capillaries. [26][27][28][29] Although the molecular targets and mechanisms of methylmercury are still being delineated, the experimental evidence supports contributions from several processes including disrupted calcium homeostasis, increased oxidative stress, and altered glutamate homeostasis leading to excitotoxicity.…”

Section: Methylmercurymentioning

confidence: 99%

Toxic Peripheral Neuropathies: Agents and Mechanisms

Valentine¹

2019

Toxicol Pathol

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Toxic peripheral neuropathies are an important form of acquired polyneuropathy produced by a variety of xenobiotics and different exposure scenarios. Delineating the mechanisms of neurotoxicants and determining the degenerative biological pathways triggered by peripheral neurotoxicants will facilitate the development of sensitive and specific biochemical-based methods for identifying neurotoxicants, designing therapeutic interventions, and developing structure–activity relationships for predicting potential neurotoxicants. This review presents an overview of the general concepts of toxic peripheral neuropathies with the goal of providing insight into why certain agents target the peripheral nervous system and produce their associated lesions. Experimental data and the main hypotheses for the mechanisms of selected agents that produce neuronopathies, axonopathies, or myelinopathies including covalent or noncovalent modifications, compromised energy or protein biosynthesis, and oxidative injury and disruption of ionic gradients across membranes are presented. The relevance of signaling between the main components of peripheral nerve, that is, glia, neuronal perikaryon, and axon, as a target for neurotoxicants and the contribution of active programmed degenerative pathways to the lesions observed in toxic peripheral neuropathies is also discussed.

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“…CH 3 HgCl was extracted from mercury sludge (mixture of inorganic mercury and activated charcoal which was used as the catalyst) in the acetaldehyde plant (Irukayama et al 1962c) and from sediments in the drainage close to Hyakken Port (Irukayama et al 1962d). Irukayama et al (1964a) concluded that the causative agent of MPM was CH 3 HgCl and that the functional group is methylmercury (CH 3 Hg-).…”

Section: Extraction Of Organic Mercury From the Factorymentioning

confidence: 99%

Lecture on Methylmercury Poisoning in Minamata (MPM)

Yokoyama

2018

Mercury Pollution in Minamata

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This chapter outlines the methylmercury poisoning in Minamata (MPM): about the history, symptom pathogenesis, research on the causal agent, and responses of the national and local governments and the responsible company, i.e., Chisso, to the outbreak of MPM. A book written by Nishimura and Okamoto (2001) played an important role to clarify the mechanism of the MPM outbreak. Based on this book and the published data on mercury concentrations of aquatic organisms and newborns' umbilical cords, how methylmercury generated in the plant, flew into the sea, transferred to aquatic organisms, and was consumed by residents are explained. Victims of MPM, compensation and environmental restructure, and court ruling against this incident are described. Based on lecture notes from a university course, students' suggestions for avoiding a repeat of the tragedy are also introduced.

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Report III Industrial wastes containing mercury compounds from Minamata Factory

Cited by 7 publications

References 0 publications

Adverse Effects of Methylmercury: Environmental Health Research Implications

Adverse Effects of Methylmercury: Environmental Health Research Implications

Toxic Peripheral Neuropathies: Agents and Mechanisms

Lecture on Methylmercury Poisoning in Minamata (MPM)

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