Minamata disease is methylmercury poisoning from consuming fish and shellfish contaminated by industrial waste. The polluted seafood was widely consumed in the area around Minamata, but many individuals were never examined for or classified as having Minamata disease. Following the determination of the Supreme Court of Japan in October 2004 that the Japanese Government was responsible for spreading Minamata disease, over 13,000 residents came forward to be examined for Minamata disease. We studied 197 residents from the Minamata area who had a history of fish consumption during the polluted period to determine the importance of sensory symptoms and findings in making a diagnosis of Minamata disease. We divided the exposed subjects into non-complicated (E) and complicated (E+N) groups based on the absence or presence of other neurological or neurologically related disorders and compared them to residents in control area (C) after matching for age and sex. We quantitatively measured four somatosensory modalities (minimal tactile sense by Semmes-Weinstein monofilaments, vibration sense, position sense, and two-point discrimination) and did psychophysical tests of fine-surface-texture discrimination. Subjective complaints were higher in groups E and E+N than C. Over 90% of E+N and E subjects displayed a sensory disturbance on conventional neurological examination and 28% had visual constriction. About 50% of the E and E +N groups had upper and lower extremity ataxia and about 70% had truncal ataxia. The prevalence of these neurological findings was significantly higher in exposed subjects than controls. All sensory modalities were impaired in the E and E+N groups. All four quantitatively measured sensory modalities were correlated. The prevalence of complaints, neurological findings, and sensory impairment was similar or a little worse in group E+N than in group E. We conclude that sensory symptoms and findings are important in making the diagnosis of Minamata disease and that they can be determined even in the presence of neurological or neurologically related diseases.
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http://dx.doi.org/10.1016/j.envres.2007.05.012 | DOI Listing |
Sci Total Environ
December 2024
CAS-HKU Joint Laboratory of Metallomics on Health and Environment, & CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, & Beijing Metallomics Facility, & National Consortium for Excellence in Metallomics, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing 100049, China; University of Chinese Academy of Sciences, Beijing 100049, China. Electronic address:
J Obstet Gynaecol Res
January 2025
Department of Environmental Health, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Int J Mol Sci
October 2024
Faculty of Pharmaceutical Sciences, Tokyo University of Science, 2641 Yamazaki, Noda 278-8510, Chiba, Japan.
Sensory disturbances and central nervous system symptoms are important in patients with Minamata disease. In the peripheral nervous system of these patients, motor nerves are not strongly injured, whereas sensory nerves are predominantly affected. In this study, we investigated the mechanisms underlying the sensory-predominant impairment of the peripheral nervous system caused by methylmercury.
View Article and Find Full Text PDFArch Toxicol
October 2024
Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, 700‑8530, Japan.
Methylmercury (MeHg) is an environmental neurotoxin that induces damage to the central nervous system and is the causative agent in Minamata disease. The mechanisms underlying MeHg neurotoxicity remain largely unknown, and there is a need for effective therapeutic agents, such as those that target MeHg-induced endoplasmic reticulum (ER) stress and the unfolded protein response (UPR), which is activated as a defense mechanism. We investigated whether intraperitoneal administration of the chemical chaperone, 4-phenylbutyric acid (4-PBA), at 120 mg/kg/day can alleviate neurotoxicity in the brains of mice administered 50 ppm MeHg in drinking water for 5 weeks.
View Article and Find Full Text PDFToxicology
December 2024
Children's Health and Environment Program, Child Health Research Centre, The University of Queensland, South Brisbane, QLD 4101, Australia.
Electronic waste (e-waste) contains hazardous elements such as lead (Pb), cadmium (Cd), mercury (Hg), and other toxic elements that pose significant health risks to the population directly exposed. We recruited 199 e-waste recycling workers and 104 non-exposed workers in Bangladesh and analyzed heavy metals in blood and hair, as well as hematological and cardiovascular parameters including, blood lipids and blood pressure. We fitted quantile regression models at 0.
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