Minamata disease is a well-known mercury contamination that happened in Japan in 1953. Due to demand during world war, second mercury disaster occurred in Niigata Prefecture in 1965. This is a review on the Niigata Minamata disease based on available documents and local expert opinions on the disaster. The aims of this paper are to record exposure history like the source of mercury in Agano River and specific fish that was associated with the disease. It is for an appraisal of the basic mercury exposure control, particularly to protect Japanese and world population during that time. There was indication that initial exposure limit for mercury was calculated incorrectly, and higher safe dose was applied. This epidemiological study is very useful and significant in comprehend the correct estimation of the human exposure to any hazardous substances.
Mercury Poisoning, Nervous System

BACKGROUND: Humans are exposed to mercury via many different routes and in different forms. Studies concerned with the exposure in the general population were done many times in the past. But, the treatment of mercury exposure and mercury intoxication is limited. Therefore, chelators such as birth anti lewistite, 2,3-dimercaptopropanol (BAL), dimercaptopropane-1-sulphonate (DMPS), and dimercaptosuccinic acid (DMSA) were given to patients with acute symptoms resulting from the central nervous system due to confirmed mercury poisoning. In this paper, we reported the effects of oral Vitamin C on mercury excretion. METHODS: This study has been reviewed in the clinical findings of 213 patients aged 30-80 who visited Kosin University Gospel Hospital during 3 months from March to September 2007. We measured hair mercury levels at the initial visit and at 3-4 months after the oral vitamin C (4 g/day) treatment. RESULTS: The number of patients who had initial hair mercury level over 1.5 ppm were 57 patients among 213 patients, and 41 patients rechecked the hair mercury level. Twenty patients who had hair mercury level over 1.5 ppm were treated with oral vitamin C for 3 months and rechecked the hair mercury level and 21 patients without vitamin C treatment. The vitamin treatment group had a hair mercury level that was three times lower than the non-treated group. CONCLUSION: The vitamin C oral treatment significantly decreased the level of hair mercury.
Aged ; Ascorbic Acid ; Central Nervous System ; Chelating Agents ; Dimercaprol ; Hair ; Humans ; Mercury Poisoning ; Parturition ; Succimer ; Vitamins

This is a case of 27-year-old male who sustained multiple metallic embolism from non-accidental self-injection of elemental mercury through the intravenous route. The patient allegedly self-injected at least twenty thermometers' worth of elemental mercury in a span of one year. The patient presented with generalized body fatigue, difficulty in position sense, distal hand weakness, tremors, labile mood, insomnia, and emotional instability. Physical examination showed multiple subcutaneous granulomas in the extremities at the sites of elemental mercury injection. Radiographic studies in the lungs, abdomen and extremities showed multiple dense spherules and pinpoint opacities indicative of metallic mercury embolism. Serum mercury levels were elevated. The patient underwent multiple hemodialysis sessions due to acute renal failure and tubular nephropathy secondary to mercury poisoning. The patient was eventually referred to the anesthesia department for excision of foreign body granulomas. Fentanyl, Propofol, Atracurium and Sevoflurane were used to induce and maintain anesthesia. Intra-operative course was unremarkable. Chelation therapy with DMSA (2,3-dimercaptosuccinic acid) was done postoperatively. Serum mercury was undetectable 20 days after surgery and chelation therapy. There were no postoperative complications. The patient was discharged well after 43 days of admission.
Human ; Male ; Adult ; EMBOLISM ; CHELATION THERAPY ; MERCURY POISONING, NERVOUS SYSTEM ; CUSHING SYNDROME

Mercury occurs in various chemical forms, and it is different to health effects according to chemical forms. In consideration of the point, the evaluation of the mercury exposure to human distinguished from occupational and environmental exposure. With strict to manage occupational exposure in factory, it is declined mercury intoxication cases by metallic and inorganic mercury inhalation to occupational exposure. It is increasing to importance in environmental exposure and public health. The focus on the health impact of exposure to mercury is more on chronic, low or moderate grade exposure—albeit a topic of great controversy—, not high concentration exposure by methylmercury, which caused Minamata disease. Recently, the issue of mercury toxicity according to the mercury exposure level, health effects as well as the determination of what mercury levels affect health are in the spotlight and under active discussion. Evaluating the health effects and Biomarker of mercury exposure and establishing diagnosis and treatment standards are very difficult. It can implement that evaluating mercury exposure level for diagnosis by a provocation test uses chelating agent and conducting to appropriate therapy according to the result. but, indications for the therapy of chelating agents with mercury exposure have not yet been fully established. The therapy to symptomatic patients with mercury poisoning is chelating agents, combination therapy with chelating agents, plasma exchange, hemodialysis, plasmapheresis. But the further evaluations are necessary for the effects and side effects with each therapy.
Chelating Agents ; Diagnosis* ; Environmental Exposure ; Humans ; Inhalation ; Mercury Poisoning ; Mercury Poisoning, Nervous System ; Occupational Exposure ; Plasma Exchange ; Plasmapheresis ; Public Health ; Renal Dialysis

BACKGROUND: It is known that methylmercury poisoning, Minamata disease is very toxic to human body. But, cardiotoxic mechanism of methylmercury is left unknown, Recent study has been reported that the cleavage of methylmercury produce oxygen radicals as well as methyl radicals, and also these radicals induce the release of excitotoxic amino acids(EAAs). So, oxygen radicals and EAA are regarded as a causative factors in the various diseases such as heart disease induced by toxicity of methylmercury. We studied to know the cardiotoxic effect of methylmercury on cultured myocardial cells derived from neonatal rat in order to evaluate the toxic mechanism of methylmercury. METHODS: Myocardial cells of neonatal rat were incubated with various concentrations of methylmercuric chloride for 1-96 hours. MTT90 and MTT50 values were measured and cell viability was determined by MTT assay. In addition, morphological study was performed by light microscope after cultured myocardial cells that were exposed to methymercuric chloride. RESULTS: MTT90 and MTT50 values were 1microM and 15microM of methylmercuric chloride in cultured myocardial cells of neonatal rat respectively. Exposure of cultured rat myocardial cells to methylmercuric chloride resulted in a significant cell death in a time-dependent manner. In the observation of morphological changes, cultured cells treated with methlymercuric chloride showed decrease of cell number and disconnection between cultured myocardial cells. CONCLUSION: These observation suggest that methylmercury has a severe myocardiotoxicity on cultured myocardial cells derived from neonatal rat by the decrease of cell viability and morphological changes.
Animals ; Cell Count ; Cell Death ; Cell Survival ; Cells, Cultured ; Heart Diseases ; Human Body ; Mercury Poisoning, Nervous System ; Poisoning ; Rats* ; Reactive Oxygen Species

Mercury poisoning affects various organs including peripheral and central nervous systems, especially cerebellum. We report a case of mercury intoxication presenting cerebellar ataxia. From several days after exposure to mercury vapor, scanning speech, head titubation, bilateral limb and truncal ataxia developed and progressed slowly. On admission, brain MRI did not show remarkable change. However, nine months later, atrophic changes in both cerebellar hemispheres on follow-up brain MRI and perfusion defects in same areas on brain SPECT were found.
Ataxia ; Brain ; Central Nervous System ; Cerebellar Ataxia* ; Cerebellum ; Extremities ; Follow-Up Studies ; Head ; Magnetic Resonance Imaging ; Mercury Poisoning ; Perfusion ; Poisoning ; Tomography, Emission-Computed, Single-Photon

Mercury is traditionally used as a dye for making amulets in Korea. Inhaling the vapor produced by burning mercury damages major organs, such as the lungs, kidneys, and brain. We herein present a case of a 41-year-old man who complained of abdominal pain and dyspnea. A chest X-ray and computed tomography scan showed infiltration in both upper lung lobes. A thorough medical history revealed that the patient had made amulets prior to developing symptoms, and blood and urine tests confirmed elevated levels of mercury. Dimercaptosuccinic acid was used to chelate the mercury, and methylprednisolone was used to treat the acute lung injury. No kidney or nervous system complications were detected during follow-up. Inhalation of mercury vapor should be suspected in patients with acute lung injury involving both upper lobes.
Abdominal Pain ; Acute Lung Injury* ; Adult ; Brain ; Burns ; Dyspnea ; Follow-Up Studies ; Humans ; Inhalation* ; Kidney ; Korea ; Lung ; Mercury Poisoning ; Methylprednisolone ; Nervous System ; Succimer ; Thorax

Methylmercury is a hazardous substance that is of interest with regard to environmental health, as inorganic mercury circulating in the general environment is dissolved into freshwater and seawater, condensed through the food chain, ingested by humans, and consequently affects human health. Recently, there has been much interest and discussion regarding the toxicity of methylmercury, the correlation with fish and shellfish intake, and methods of long-term management of the human health effects of methylmercury. What effects chronic exposure to a low concentration of methylmercury has on human health remains controversial. Although the possibility of methylmercury poisoning the heart and blood vessel system, the reproductive system, and the immune system is continuously raised and discussed, and the carcinogenicity of methylmercury is also under discussion, a clear conclusion regarding the human health effects according to exposure level has not yet been drawn. The Joint FAO/WHO Expert Committee on Food Additives proposed to prepare additional fish and shellfish intake recommendations for consumers based on the quantified evaluation of the hazardousness of methylmercury contained in fish and shellfish, methylmercury management in the Korea has not yet caught up with this international trend. Currently, the methylmercury exposure level of Koreans is known to be very high. The starting point of methylmercury exposure management is inorganic mercury in the general environment, but food intake through methylation is the main exposure source. Along with efforts to reduce mercury in the general environment, food intake management should be undertaken to reduce the human exposure to methylmercury in Korea.
Animals ; *Environmental Exposure ; Fishes/metabolism ; Food Chain ; Humans ; Mercury Poisoning, Nervous System/etiology ; Methylmercury Compounds/chemistry/*metabolism/toxicity ; Neurons/drug effects ; Oxidative Stress/drug effects ; Public Health ; Reproduction/drug effects ; Thymocytes/cytology/drug effects

Acrodynia is caused by chronic mercury poisoning and/or mercury, hypersensitivity occuring in infants and children only. Ingestion or inhalation of mercury contained in some house paints, calomel ingestion, the use of mercury ointments and other mercurial preparations can be the causes of acrodynia. We herein report a 3-year-old boy with typical acrodynia after expoaure to house paints and lacquer for 2 months. His hands and feet were erythematous and edematous vesiculo-bullous lesion with acral dark bluish discoloration. Mercury levels of blood and urine were significantly incresed by 61. 2ug/dl and 264ug/L (normal; below 30ug/dl and 100ug/L).
Acrodynia* ; Child ; Child, Preschool ; Eating ; Foot ; Hand ; Humans ; Hypersensitivity ; Infant ; Inhalation ; Lacquer ; Male ; Mercury Poisoning ; Ointments ; Paint

Previously, we reviewed biological evidence that mercury could induce autoimmunity and coronary arterial wall relaxation as observed in Kawasaki syndrome (KS) through its effects on calcium signaling, and that inositol 1,4,5-triphosphate 3-kinase C (ITPKC) susceptibility in KS would predispose patients to mercury by increasing Ca2+ release. Hg2+ sensitizes inositol 1,4,5-triphosphate (IP3) receptors at low doses, which release Ca2+ from intracellular stores in the sarcoplasmic reticulum, resulting in delayed, repetitive calcium influx. ITPKC prevents IP3 from triggering IP3 receptors to release calcium by converting IP3 to inositol 1,3,4,5-tetrakisphosphate. Defective IP3 phosphorylation resulting from reduced genetic expressions of ITPKC in KS would promote IP3, which increases Ca2+ release. Hg2+ increases catecholamine levels through the inhibition of S-adenosylmethionine and subsequently catechol-O-methyltransferase (COMT), while a single nucleotide polymorphism of the COMT gene (rs769224) was recently found to be significantly associated with the development of coronary artery lesions in KS. Accumulation of norepinephrine or epinephrine would potentiate Hg2+-induced calcium influx by increasing IP3 production and increasing the permeability of cardiac sarcolemma to Ca2+. Norepinephrine and epinephrine also promote the secretion of atrial natriuretic peptide, a potent vasodilator that suppresses the release of vasoconstrictors. Elevated catecholamine levels can induce hypertension and tachycardia, while increased arterial pressure and a rapid heart rate would promote arterial vasodilation and subsequent fatal thromboses, particularly in tandem. Genetic risk factors may explain why only a susceptible subset of children develops KS although mercury exposure from methylmercury in fish or thimerosal in pediatric vaccines is nearly ubiquitous. During the infantile acrodynia epidemic, only 1 in 500 children developed acrodynia whereas mercury exposure was very common due to the use of teething powders. This hypothesis mirrors the leading theory for KS in which a widespread infection only induces KS in susceptible children. Acrodynia can mimic the clinical picture of KS, leading to its inclusion in the differential diagnosis for KS. Catecholamine levels are often elevated in acrodynia and may also play a role in KS. We conclude that KS may be the acute febrile form of acrodynia.
Acrodynia ; Arterial Pressure ; Autoimmunity ; Calcium ; Calcium Signaling ; Catechol O-Methyltransferase ; Catecholamines ; Child ; Coronary Vessels ; Diagnosis, Differential ; Epinephrine ; Heart Rate ; Humans ; Hydrazines ; Hypertension ; Inositol ; Inositol 1,4,5-Trisphosphate ; Inositol 1,4,5-Trisphosphate Receptors ; Inositol Phosphates ; Mucocutaneous Lymph Node Syndrome ; Norepinephrine ; Permeability ; Phosphorylation ; Polymorphism, Single Nucleotide ; Powders ; Relaxation ; Risk Factors ; S-Adenosylmethionine ; Sarcolemma ; Sarcoplasmic Reticulum ; Tachycardia ; Thimerosal ; Thrombosis ; Tooth ; Tooth Eruption ; Vaccines ; Vasoconstrictor Agents ; Vasodilation