![]() Are you okay to go to such a place as a bride?” Naming me, the person said to her, “the man you are trying to marry is a Minamata disease victim. I got married at the age of 20, but on the day of our engagement, my wife had a phone call. Rumours spread though, and people would say that no one should marry a member of the Ogata family. We came to understand that it was caused by methylmercury poisoning but we couldn’t really make it public that we were victims, because people thought that Minamata disease was contagious. I work as a joiner and, when I was younger, would often cut my finger on the whetstone when sharpening knives, because my finger would droop. When I became an adult, I noticed that I had very little sensation in my limbs. My sister Hitomi, who was born a week before her grandfather developed the illness, was born with a disability, again without explanation, then other members of the Ogata family started falling ill one after another. However, we were never told what caused the illness. That was the first tragedy caused by Minamata disease in the Ogata family. Two months later, he passed away in the isolation and infectious diseases ward at the Minamata City Hospital. However, a correct diet, a careful surveillance of neurodevelopment with attentive learning stimulations, can counterbalance the effects of this neurotoxic substance.Minamata Disease is a neurological disease caused by severe mercury poisoning. Methylmercury-induced cognitive and psychomotor impairments are not always completely corrected by the decrease of internal methylmercury dose. Mercury chelation should be considered only in those cases where severe neurological complications are possible. Biomonitoring and search for neurodevelopmental disorders are recommended for children with hair or whole-blood mercury levels above 10 µg/g or 40 µg/L, respectively or born from mothers who exceeded these levels during pregnancy. Fish consumption should be reduced in individuals with hair or whole-blood mercury levels of more than 2.5 µg/g or 10 µg/L, and without delay, when these levels exceed 10 µg/g or 40 µg/L, respectively. Since exposure to methylmercury is primarily through fish consumption, it is recommended to consume not more than 2 portions of fish per week, especially for children and women of childbearing age. The responsibility of methylmercury should be considered when a high fish consumption is characterized. The clinical picture in prenatal or postnatal severe methylmercury poisoning is one of unspecific encephalopathy. In most individuals from the general population, they are under 2 µg/g and 8 µg/L, respectively. The best biomarkers of methylmercury exposure and internal dose are mercury concentrations in hair and whole-blood. Methylmercury is also excreted in milk (where its concentration is about 5 % of the concentration in the maternal blood). Elimination is mainly through the fecal route about 10 % of the amount excreted is in the urine, in the form of inorganic mercury. ![]() In cells, methylmercury is partly demethylated into inorganic mercury which is mostly distributed in the liver and kidneys. It is transported through the placenta to the fetus and accumulated in fetal brain. ![]() In blood, methylmercury being lipophilic is mostly in red cells. Most of the human exposure is through food ingestion. Methylmercury is absorbed from the intestinal tract, through the skin and by inhalation. They are associated with increased risks of preterm delivery, lower birth weight, and impaired postnatal growth. In populations with high fish consumption, the only manifestations of methylmercury encephalopathy are impaired psychomotor and cognitive performances. ![]() In severe cases, the clinical picture of prenatal methylmercury poisoning is one of unspecific infantile cerebral palsy, with ataxic motor disturbances, psychomotor retardation and seizures. Large cohort studies in New-Zealand, the Faroe Islands and the Seychelles have documented a risk of less severe prenatal (and/or postnatal) methylmercury poisoning associated with frequent fish consumption (more than 2 or 3 times a week) in thousands of individuals. Iraqi cases resulted from contaminated flour consumption. ![]() The Japanese cases resulted from local seafood consumption and sea mercury pollution by a local industrial installation. Severe methylmercury poisoning cases were reported in the context of two large epidemics: in the Minamata area, in Japan, and in Iraq, both affecting hundreds of people. ![]()
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