What neurological syndrome caused by severe mercury poisoning is named after a Japanese city where it was first discovered?
"Nations communities, the federal government's Indian Act governance system has made it difficult for band councils and chiefs to negotiate for their people. Chief Sakatcheway was the first leader of community when the treaty was signed and mainly wanted education for the community. Ontario Minamata disease Ontario Minamata disease is a neurological syndrome caused by severe mercury poisoning. It occurred in the Canadian province of Ontario, in 1970, and severely affected two First Nation communities in Northwestern Ontario following consumption of local fish contaminated with mercury, and one First Nation in Southern Ontario due to illegal disposal of industrial chemical"
"on a daily basis in the Amazon. The most serious case of mercury poisoning in recent history was in the Japanese city of Minamata, in the 1950s. Minamata poisoning proves that significant prenatal and postnatal exposure to high levels of methylmercury causes serious neurological problems. Minamata victims also show higher than normal signs of psychiatric diseases, along with those diseases being caused by underlying neurological issues. A 2014 USGS survey of mercury levels in the United States water system found that methylmercury concentrations in fish were typically highest in wetland areas including the coastal plain streams in the Southeast. Fish"
"made public from several disasters that occurred globally. In 1965, it was recognized that extensive mercury pollution by the Chisso chemical factory in Minamata, Japan due to improper handling of industrial wastes resulted in significant effects to the humans and organisms exposed. Mercury was released into the environment as methyl mercury (bioavailable state) into industrial wastewater and was then bioaccumulated by shellfish and fish in Minamata Bay and the Shiranui Sea. When the contaminated seafood was consumed by the local populace it caused a neurological syndrome, coined Minamata disease. Symptoms include general muscle weakness, hearing damage, reduced field of vision,"
"occurred in Minamata Bay, Japan in the 1950s demonstrated the frightening effects of exposure to extremely high concentrations of mercury. Adult patients experienced extreme salivation, limb deformity, and irreversible dysarthria and intelligence loss. In children and fetuses (exposed to mercury through the mother's consumption of contaminated seafood), extensive brain lesions were observed and the patients experienced more serious effects like cerebral palsy, mental retardation, and primitive reflexes. In order to avoid the toxic effects of mercury exposure, the United States EPA advises a mercury dose limit of 0.1 µg/kg/day. In addition to human health, animal health is also seriously threatened"
"is known to produce adverse nervous system effects, especially during brain development. Eating fish is the main source of mercury exposure in humans and some fish may contain enough mercury to harm the developing nervous system of an embryo or fetus, sometimes leading to learning disabilities. Mercury is present in many types of fish, but it is mostly found in certain large fish. One well-documented case of widespread mercury ingestion and subsequent fetal development complication took place in the 1950s in Minamata Bay, Japan. Used by a nearby industrial plant in the manufacture of plastics, methyl mercury was discharged into"
"contaminated with high levels of methylmercury, notably the dumping of industrial waste that resulted in the pollution and subsequent mass poisoning in Minamata and Niigata, Japan and the situation in Iraq in the 1960s and 1970s in which wheat treated with methylmercury as a preservative and intended as seed grain was fed to animals and directly consumed by people (see Basra poison grain disaster). These episodes resulted in neurological symptoms including paresthesias, loss of physical coordination, difficulty in speech, narrowing of the visual field, hearing impairment, blindness, and death. Children who had been exposed in-utero through their mothers' ingestion were"
"The plant discharged wastewater from its acetaldehyde plant into Minamata Bay via Hyakken Harbour. The wastewater contained many pollutants and poisonous substances including methylmercury, a highly toxic chemical. This chemical was absorbed by fish and shellfish and bioaccumulated up the food chain. People who unknowingly ate the fish over many years suffered from severe mercury poisoning. Hajime Hosokawa, a doctor at a Shin Nichitsu's company hospital, officially reported on May 1, 1956 an ""epidemic of an unknown disease of the central nervous system"", marking the official discovery of Minamata disease. In 1963, doctors at Kumamoto University concluded that the cause"
"as many, as towns mentioned in the study, such as Hiezuson, Tottori (699). The chief of the NIMD, Kōji Okamoto, said, ""We presume that the high mercury concentrations are due to the intake of dolphin and whale meat. There were not any particular cases of damaged health, but seeing as how there were some especially high concentration levels found, we would like to continue conducting surveys here."" NIMD ran further tests in 2010 and 2011. Hair from 700 Taiji residents were tested for mercury; 117 males and 77 females who showed over 10 ppm underwent further neurological tests. Again, no"
"include damage to the brain, kidneys and lungs. Mercury poisoning can result in several diseases, including acrodynia (pink disease), Hunter-Russell syndrome, and Minamata disease. Symptoms typically include sensory impairment (vision, hearing, speech), disturbed sensation and a lack of coordination. The type and degree of symptoms exhibited depend upon the individual toxin, the dose, and the method and duration of exposure. Case–control studies have shown effects such as tremors, impaired cognitive skills, and sleep disturbance in workers with chronic exposure to mercury vapor even at low concentrations in the range 0.7–42 μg/m. A study has shown that acute exposure (4–8 hours)"
"1917. Ingestion of radioactive materials caused many radiation-induced cancers in the 1930s, but no one was exposed to high enough doses at high enough rates to bring on acute radiation syndrome. Marie Curie died of aplastic anemia caused by radiation, a possible early incident of acute radiation syndrome. The atomic bombings of Hiroshima and Nagasaki resulted in high acute doses of radiation to a large number of Japanese, allowing for greater insight into its symptoms and dangers. Red Cross Hospital Surgeon Terufumi Sasaki led intensive research into the syndrome in the weeks and months following the Hiroshima bombings. Dr Sasaki"
"ingestion of contaminated fish from Minamata Bay. The methylmercury inside the contaminated fish attacked the afflicted patient’s central nervous system, which caused a variety of symptoms. Most patients exhibited combinations of symptoms and did not show all symptoms. National-institute-for-minamata-disease says 182 taiji-residents have extremely-high-mercury-level but do not display any symptoms of mercury-poisoning. The cause of this contamination in Minamata bay was then traced back to Chisso Corporation’s dumping of methylmercury into Minamata Bay. Chisso Corporation produced acetaldehyde using water, acetylene, mercury(II) sulfate as a catalyst and manganese dioxide or since August 1951, ferric sulfide as a co-catalyst. Acetaldehyde reacts with"
"mercury, such as that commonly experienced by affected hatters, include mental confusion, emotional disturbances, and muscular weakness. Severe neurological damage and kidney damage can also occur. Neurological effects include Korsakoff's dementia and erethism (the set of neurological symptoms characteristically associated with mercury poisoning). Signs and symptoms can include red fingers, red toes, red cheeks, sweating, loss of hearing, bleeding from the ears and mouth, loss of appendages such as teeth, hair, and nails, lack of coordination, poor memory, shyness, insomnia, nervousness, tremors, and dizziness. A survey of exposed U.S. hatters revealed predominantly neurological symptomatology, including intention tremor. After chronic exposure"
"Disease (NIMD). The NIMD published the full data of the research online a few days later. It has been pointed out that the amount of methyl-mercury, which causes neurological damage, was not exceedingly high, and the mercury in hair showed rapid decrease since tests carried out by other institutions a few months ago to the same people. The NIMD agreed to help monitor the health of Taiji residents. In 2010, hair samples from 1,137 Taiji residents were tested for mercury by the National Institute for Minamata Disease. The average amount of methyl mercury found in the hair samples was 11.0"
"several places in Japan during the 1950s due to industrial discharges of mercury into rivers and coastal waters. The best-known instances were in Minamata and Niigata. In Minamata alone, more than 600 people died due to what became known as Minamata disease. More than 21,000 people filed claims with the Japanese government, of which almost 3000 became certified as having the disease. In 22 documented cases, pregnant women who consumed contaminated fish showed mild or no symptoms but gave birth to infants with severe developmental disabilities. Since the industrial Revolution, mercury levels have tripled in many near-surface seawaters, especially around"
"go mad and die: ""...one cat ran into a small clay cooking stove containing burning charcoal. With the pupils of its eyes dilated, salivating, convulsing and uttering a strange cry, the cat breathed its last breath."" These strange symptoms eventually began to appear in people, too. Professor Tadao Tsubaki of Niigata University examined two patients in April and May 1965 and suspected Minamata disease. One patient's hair was found to have a mercury level of 390 ppm. On 31 May, he reported an outbreak of organic mercury poisoning in the Agano River basin to the prefectural government and made his"
"including mercury poisoning. Elders in the community recall collecting mercury from the local toxic waste dump by pouring water, then selling the collected mercury on the black market. In the late 1960s, people in the Grassy Narrows and Whitedog First Nations populations started to suffer symptoms of mercury poisoning. Several Japanese doctors who had been involved in studying Minamata disease in Japan travelled to Canada to investigate the mercury poisoning in these people. Blood mercury levels were above 100 ppb in a significant number of individuals and above 200 ppb in several others. Symptoms included sensory disturbances, such as narrowing"
"methylmercury as well as ethylmercury, have significant differences from the brains of people with autism. Previous episodes of widespread mercury toxicity in a population such as in Minamata Bay, Japan would also be expected to lead to documentation of a significant rise in autism or autism-like behavior in children should autism be caused by mercury poisoning. However, research on several episodes of acute and chronic mercury poisoning have not documented any such rise in autism-like behavior. Although some parents cite an association between the timing of onset of autistic symptoms with the timing of vaccinations as evidence of an environmental"
"Erethism Erethism, also known as erethism mercurialis, Mad hatter disease, or mad hatter syndrome is a neurological disorder which affects the whole central nervous system, as well as a symptom complex derived from mercury poisoning. Erethism is characterized by behavioral changes such as irritability, low self-confidence, depression, apathy, shyness and timidity, and in some extreme cases with prolonged exposure to mercury vapors, delirium, personality changes and memory loss. People with erethism often have difficulty with social interactions. Associated physical problems may include a decrease in physical strength, “headaches, general pain, and tremors after exposure to metallic mercury” as well as"
"contain higher concentrations of mercury than others. This is because mercury is stored in the muscle tissues of fish, and when a predatory fish eats another fish, it assumes the entire body burden of mercury in the consumed fish. Since fish are less efficient at depurating than accumulating methylmercury, fish-tissue concentrations increase over time. Thus species that are high on the food chain amass body burdens of mercury that can be ten times higher than the species they consume. This process is called biomagnification. The first occurrence of widespread mercury poisoning in humans occurred this way in Minamata, Japan, now"
"to calculated elemental mercury levels of 1.1 to 44 mg/m resulted in chest pain, dyspnea, cough, hemoptysis, impairment of pulmonary function, and evidence of interstitial pneumonitis. Acute exposure to mercury vapor has been shown to result in profound central nervous system effects, including psychotic reactions characterized by delirium, hallucinations, and suicidal tendency. Occupational exposure has resulted in broad-ranging functional disturbance, including erethism, irritability, excitability, excessive shyness, and insomnia. With continuing exposure, a fine tremor develops and may escalate to violent muscular spasms. Tremor initially involves the hands and later spreads to the eyelids, lips, and tongue. Long-term, low-level exposure has"
"Prefecture were poisoned by methylmercury drained from the chemical factory, known as the ""Minamata disease"". The number of casualties in Minamata is 6,500 as of November 2006. In Yokkaichi, a port in Mie Prefecture, air pollution caused by sulfur dioxide and nitrogen dioxide emissions led to a rapid increase in the number of people suffering from asthma and bronchitis. In urban areas photochemical smog from automotive and industrial exhaust fumes also contributed to a rise in respiratory problems. In the early 1970s, chronic arsenic poisoning attributed to dust from arsenic mines occurred in Shimane and Miyazaki Prefectures. Consumers Union of"
"the Anti-Hazardous Drug Day in several parts of the world. Subacute myelo-optic neuropathy Subacute myelo-optic neuropathy (SMON) is an iatrogenic disease of the nervous system leading to a disabling paralysis, blindness and even death. Its defining manifestation was as an epidemic in Japan during the 1960s: the Japanese government estimated 11,000 were affected; however, the College of Medicine at the University of Tokyo put the number at 30,000, citing a lack of preservation of medical records for longer than five years and a lack of cooperation from doctors as the reasons for the discrepancy. On August 3, 1978, the Tokyo"
"patients must exhibit all symptoms of Hunter-Russell syndrome – the standard diagnosis of organic mercury poisoning at the time – which originated from an industrial accident in the United Kingdom in 1940. The committee certified only patients exhibiting explicit symptoms of the British syndrome, rather than basing their diagnosis on the disease in Japan. This resulted in many applicants being rejected by the committee, leaving them confused and frustrated. As of March 2001, 2,265 victims had been officially certified (1,784 of whom have died) and over 10,000 people had received financial compensation from Chisso, although they were not recognised as"
"primarily by the United States Environmental Protection Agency. Case–control studies have shown effects such as tremors, impaired cognitive skills, and sleep disturbance in workers with chronic exposure to mercury vapor even at low concentrations in the range 0.7–42 μg/m. A study has shown that acute exposure (4 – 8 hours) to calculated elemental mercury levels of 1.1 to 44 mg/m resulted in chest pain, dyspnea, cough, hemoptysis, impairment of pulmonary function, and evidence of interstitial pneumonitis. Acute exposure to mercury vapor has been shown to result in profound central nervous system effects, including psychotic reactions characterized by delirium, hallucinations, and"
"parts per million for men and 6.63 ppm for women, compared with an average of 2.47 ppm for men and 1.64 ppm for women in tests conducted in 14 other locations in Japan. One hundred eighty-two Taiji residents showing extremely high mercury levels underwent further medical testing to check for symptoms of mercury poisoning. None of the Taiji residents displayed any of the traditional symptoms of mercury poisoning, according to the Institute. Japan's National Institute of Population and Social Security Research, however, reports that the mortality rate for Taiji and nearby Koazagawa, where dolphin meat is also consumed, is over"
"concentrations of mercury than others. As mercury and methylmercury are fat soluble, they primarily accumulate in the viscera, although they are also found throughout the muscle tissue. When this fish is consumed by a predator, the mercury level is accumulated. Since fish are less efficient at depurating than accumulating methylmercury, fish-tissue concentrations increase over time. Thus species that are high on the food chain amass body burdens of mercury that can be ten times higher than the species they consume. This process is called biomagnification. Mercury poisoning happened this way in Minamata, Japan, now called Minamata disease. In the European"
"have been to some extent poisoned by mercury. Mercury poisoning in Minamata, Japan, is now known as Minamata disease. Mercury in fish Fish and shellfish concentrate mercury in their bodies, often in the form of methylmercury, a highly toxic organic compound of mercury. Fish products have been shown to contain varying amounts of heavy metals, particularly mercury and fat-soluble pollutants from water pollution. Species of fish that are long-lived and high on the food chain, such as marlin, tuna, shark, swordfish, king mackerel and tilefish (Gulf of Mexico) contain higher concentrations of mercury than others. Mercury is known to bioaccumulate"
"disease affected Japan. The recorded death toll was 459 people, but figures at least ten times greater have been suggested. The 1971 poisoning was the largest mercury poisoning disaster when it occurred, with cases peaking in January and February 1972 and stopping by the end of March. Reports after the disaster recommended tighter regulation, better labelling and handling of mercury-treated grain, and wider involvement of the World Health Organization in monitoring and preventing poisoning incidents. Investigation confirmed the particular danger posed to fetuses and young children. The properties of mercury make it an effective fungicide. Methylmercury had been banned in"
"2009, hair samples from 1,137 Taiji residents were tested for mercury by the National Institute for Minamata Disease (NIMD). The average amount of methylmercury found in the hair samples was 11.0 parts per million for men and 6.63 ppm for women, compared with an average of 2.47 ppm for men and 1.64 ppm for women in tests conducted in 14 other locations in Japan. From the total population, 182 Taiji residents who showed relatively high mercury levels over 7.2 ppm, including 18 men and 5 women over 50 ppm, underwent further medical testing to check for neurological symptoms of mercury"
"disease (it originally occurred in Japan in the Minamata Bay area during 1952–60). About 850 First Nations people were living on the two reserves when the mercury issue arose, and they were told to stop eating fish and drinking water. Also, the commercial fishery and fishing guides services were forced to close, resulting in mass unemployment in the community. Furthermore, ""the impact of the mercury poisoning on the local economy had not received attention for a long time."" And the Ontario government did not address the issue for a long time. In 2015, a former employee claimed he had participated"
"the mercury recovered from the sludge. Hair samples were taken from the victims of the disease and also from the Minamata population in general. In patients, the maximum mercury level recorded was 705 parts per million (ppm), indicating very heavy exposure and in nonsymptomatic Minamata residents, the level was 191 ppm. This compared to an average level of 4 ppm for people living outside the Minamata area. On November 12, 1959, the Ministry of Health and Welfare's Minamata Food Poisoning Subcommittee published its results: During the investigation by researchers at Kumamoto University, the causal substance had been identified as a"
"petrochemical and plastics company, contaminated the waters of Minamata Bay with an estimated 27 tons of methylmercury, contaminating the local water supply. This led to many people in the area developing what became known as the “Minamata Disease”. Because methylmercury is a teratogen, the mercury poisoning of those residing by the bay resulted in neurological defects in the offspring. Infants exposed to mercury poisoning in utero showed predispositions to cerebral palsy, ataxia, inhibited psychomotor development, and mental retardation. Landfill sites have been shown to have adverse effects on fetal development. Extensive research has been shown that landfills have several negative"
"popular expressions like ""mad as a hatter"" (see below) and ""the hatters' shakes"". The first description of symptoms of mercury poisoning among hatters appears to have been made in St Petersburg, Russia, in 1829. In the United States, a thorough occupational description of mercury poisoning among New Jersey hatters was published locally by Addison Freeman in 1860. Adolph Kussmaul's definitive clinical description of mercury poisoning published in 1861 contained only passing references to hatmakers, including a case originally reported in 1845 of a 15-year-old Parisian girl, the severity of whose tremors following two years of carroting prompted opium treatment. In"