Photography's Underappreciated Contributions to Neuropsychiatry: The Photographs of W. Eugene Smith in Minamata, Japan.

Photographers and filmmakers have made important contributions to the international mental health community through documentation and social commentary, leveraging the power of visual imagery. To illustrate, this article uses the example of W. Eugene Smith who photographed the catastrophic effects of methylmercury poisoning from industrial pollution in the region around Minamata Bay, Japan. Although many art forms have been comfortably integrated into mainstream psychiatry and neuropsychiatry, photography has been underappreciated and underutilized.

Saint Ioannis Lampadistis, the first possible case of blindness due to organic mercury poisoning in history.

Saint Ioannis Lampadistis is a Cypriot saint of the Greek Orthodox Church, widely venerated in his island of origin. He lived during the 11th century and was blinded by ingesting contaminated fish in the mountainous area of Galata, withdrew from civil life when he was 18, and died at the age of 22. The reason for his blindness remains unknown, though it is widely attributed to an unknown poison related to the copper mines of the region. As fish is the end reservoir of organic mercury, it is quite possible that his blindness was the result of heavy metal toxicity. Organic mercury is associated with CNS atrophy and hypoplasia, and blindness is a frequent presenting symptom. While not much is known about the saint's clinical symptoms (as his ecclestiastical biography focuses on his example and miracles), organic mercury poisoning could explain his sudden loss of vision, thus possibly making him the first-recorded case of organic mercury poisoning in history.

The blood of my veins - mercury, Minamata and the soul of Japan.

The methylmercury contamination of Minamata Bay during the WWII postwar period resulted in thousands of Japanese citizens suffering horrific neurological injury. Fear and miscommunication destroyed and changed family and social structure. In addition, the Minamata poisoning caused momentous changes in the civic discourse in Japan and was an instrumental event in the democratization of the country. This manuscript describes the effects that the environmental contamination and human poising had in the transition of Japan from a feudal society to a democratic one.

[History of ignorance of methylmercury toxicity and intoxication in Japan in relation to Minamata disease].

The first reports of methylmercury intoxication appeared in 1865 and 1866. These reports had sensational effects in European countries, and were introduced not only in journals but also in newspapers. These two reports were referable in Japan at the latest in 1927. The formation of organic mercury in the production of acetoaldehyde was also referable in 1906 in Japan. In 1931 (one year before the start of acetoaldehyde production in Minamata) these important reports cited above were referable in Kumamoto University, and there were warnings about the toxicity of organic mercury and environmental pollution prior to the start of acetoaldehyde production. However, not only the plant, authorities (Ministry of Welfare), and Kumamoto Prefectural Office, but also the scientists completely ignored these reports. Waste was dumped into the environment without any treatment. Serious pollution of the environment by organic mercury started, which resulted in the outbreak of Minamata disease (=methylmercury intoxication).

[Bibliographical study of the toxicity of organic mercury compounds].

OBJECTIVES: The aim of this study is to correct the misunderstanding that the toxicity of organic mercury compounds is unknown at the time of the outbreak of Minamata disease (May 1, 1956). RESULTS AND DISCUSSION: Two case reports of organic mercury (methylmercury) intoxication were published already in 1865 and 1866. The conversion of inorganic mercury added in acetoaldehyde synthesis was already pointed out in 1921. In 1930 several cases of organic mercury poisoning among workers engaged in acetoaldehyde production were reported. Many reports on not only in occupational exposure but a oral exposure via the ingestion of flour made from grains treated with organic mercurials were available at the time of the outbreak of Minamata disease (May 1, 1956). These reports pointed out the toxic effects of organic mercury on the central nervous system, and indicated cleary that the causal substance of Minamata disease must be the organic mercury compounds (methylmercury) from the Chisso plant. The identification of methylmercury as the causal substance by the authority was presented in 1968 when acetoaldehyde production in the Chisso plant was closed. Most of these reports except that of (Hunter et al.) were not referred to in the study of Minamata disease . Inadequate referencing should be pointed out. CONCLUSION: Several reports indicated that the causal substance of Minamata disease must be methylmercury from the Chisso Plant. However, most of these reports were not referred to during the study of Minamata disease. Inadequate referencing of literatures should be pointed out.

[An examination of "Minamata disease general investigation and research liaison council"--The process of making uncertain the organic mercury causal theory].

Minamata disease occurred because inhabitants consumed the polluted seafood. The official confirmation of Minamata disease was in 1956. However, the material cause of that disease was uncertain at that time. The Minamata Food Poisoning Sub-committee, under authority of the Food Hygiene Investigation Committee of the Ministry of Health and Welfare, determined the material cause of Minamata disease to be a certain kind of organic mercury in 1959. The sub-committee was dissolved after their report. The discussion about the investigation of the cause was performed in a conference initiated by the Economic Planning Agency, which was titled "Minamata Disease General Investigation and Research Liaison Council". The Participants were eight scientists; four fishery scientists, two chemists, and only two medical scientists, which implied that only examination of the organic mercury was to be discussion. The conference was held four times from 1960 to 1961. In the first and second conferences, the organic mercury research from a medical perspective progressed in cooperation with fishery sciences. In the third conference, it was reported that UCHIDA Makio, professor of Kumamoto University, had found organic mercury crystal in the shellfish found in Minamata-bay. Authorities of biochemistry and medicine in the third conference criticized UCHIDA's research. At the fourth conference, reports contradicting his research were presented. Although those anti-UCHIDA reports were not verified, AKAHORI Shiro, the highest authority of biochemistry, not only accepted them, but also expressed doubt in the organic mercury causal theory. Therefore, this theory was recognized as uncertain.

The pathology of methylmercury poisoning (Minamata disease): The 50th Anniversary of Japanese Society of Neuropathology.

Methylmercury (Me-Hg) poisoning (Minamata disease: MD) is one of the most severe types of disease caused by humans to humans in Japan. The disease is a special class of food-borne methylmercury intoxication in humans as typified by the outbreak that began in 1953 in Minamata and its vicinity in Kumamoto Prefecture, Japan. There are 450 autopsy cases in Kumamoto and 30 autopsy cases in Niigata Prefecture related to MD in Japan. Two hundred and one cases in Kumamoto and 22 cases in Niigata showed pathological changes of MD. This report provides a brief research history and overview of the pathological changes of MD, and also presents representative cases of adult, infantile and fetal forms of MD among the 450 MD-related autopsy cases in Kumamoto Prefecture.

[Development of neurology in Japan and its contribution to elucidate and resolve the sociomedical problems].

Japanese Society of Neurology (JSN) was established in 1960 with 643 members, and in 2009 it has grown up to a big society having more than 8,000 members including 3,600 neurology board specialists. JSN has greatly contributed in elucidating and resolving many socio-medical problems. I will take three topics including SMON (subacute myelo-optico-neuropathy), infectious Creutzfeldt-Jakob disease (CJD) and Minamata disease. SMON was a new epidemic disease characterized by subacute optic neuritis and myeloneuropathy associated with diarrhea and abdominal symptoms. The research committee clarified that it was a neurological complication of chinoform, a drug for gastroenteritis. CJD surveillance started in 1996 for variant CJD, and uncovered many patients who developed CJD after human dura draft. The government prohibited to use non-inactivated human dura. Minamata disease is an organic mercury poisoning of people who took fish contaminated by mercury in Minamata bay in Kumamoto or in Aganogawa river in Niigata. The factories discharged water contaminated with mercury which was accumulated in fish and shellfish. Still many victims claim for compensation to the companies and government. Neurologists in Kumamoto and Niigata greatly contributed to diagnose and treat the victims and to clarify the cause of the disease.

Minamata disease: catastrophic poisoning due to a failed public health response.

We present the history of Minamata disease in a chronological order from the public health point of view. Because the appropriate public health response - to investigate and control the outbreak - as set out in the Food Sanitation Act was not conducted, no one knew how many became ill following the outbreak. Exposure could not be stopped. In our discussion, we offer two reasons as to why the Japanese public health agencies did not apply the Act: social circumstances in the 1950s and 1960s that placed emphasis on industrial development, and the Japanese medical community's lack of knowledge about the Act. The history of Minamata disease shows us the consequences when public health responses are not implemented. Minamata disease should be an invaluable lesson for future public health responses.

John Martin Wood (1938-2008)--pioneering biochemist, educator and communicator.

John Martin Wood, Emeritus Professor of Medical Biochemistry at the University of Bradford died in Wieck by Greifswald, Germany after a short illness on February 5, 2008 - just short of his 70(th) year. John worked as a pioneering biochemist and educator in the US and in Britain across two research careers. He devoted the first twenty-five years to the role of transition metals in biology, and his last twenty-years to cutaneous enzymology and melanogenesis. Working together with his wife Professor Karin U. Schallreuter, his research on oxidative stress handling in skin and on the expression of a cutaneous catecholaminergic system will help direct research in these fields for many years to come. John impressed on his fellow cutaneous researchers and students the critical importance of appreciating the true role of enzymes in skin health and disease. This obituary aims to contextualize the significant contributions made by this remarkable man to experimental dermatology.

The delayed appearance of a mercurial warning.

The publication of a 1971 study from Japan on chronic methylmercury poisoning in adults provides an occasion to reexamine the history of Minamata disease and its social and political repercussions. Research findings were suppressed or held back due to controversies that were tearing the Japanese scientific community apart. Similar controversies occurred outside of Japan as well. Only now are the long-term adverse effects of environmental methylmercury exposure becoming clear. The delayed release of the 1971 results therefore reminds us as epidemiologists of our obligation, even in the presence of scientific uncertainty, to call attention to preventable risks.

The severity of Minamata disease declined in 25 years: temporal profile of the neurological findings analyzed by multiple logistic regression model.

Minamata disease (MD) was caused by ingestion of seafood from the methylmercury-contaminated areas. Although 50 years have passed since the discovery of MD, there have been only a few studies on the temporal profile of neurological findings in certified MD patients. Thus, we evaluated changes in neurological symptoms and signs of MD using discriminants by multiple logistic regression analysis. The severity of predictive index declined in 25 years in most of the patients. Only a few patients showed aggravation of neurological findings, which was due to complications such as spino-cerebellar degeneration. Patients with chronic MD aged over 45 years had several concomitant diseases so that their clinical pictures were complicated. It was difficult to differentiate chronic MD using statistically established discriminants based on sensory disturbance alone. In conclusion, the severity of MD declined in 25 years along with the modification by age-related concomitant disorders.

Mercury exposure and child development outcomes.

Mercury is ubiquitous in the global environment, ensuring universal exposure. Some forms of mercury are especially neurotoxic, including clinical signs at high doses. However, typical human exposures occur at low to moderate doses. Only limited data about neurotoxicity at low doses are available, and scientists differ in their interpretation. Dose-response data on neurodevelopment are particularly limited. Despite or perhaps because of the lack of sufficient or consistent scientific data, public concern about a link between mercury exposure and developmental disabilities has been rising. After reviewing the data, the US Environmental Protection Agency proposed a reference dose (an estimate of a daily dose that is likely to be without a risk of adverse effects over a lifetime) for methyl mercury that is substantially lower than previous guidelines from the World Health Organization, the US Agency for Toxic Substances and Disease Registry, and the US Food and Drug Administration. Some questions have been raised about the Environmental Protection Agency's guidelines, but the issue remains unresolved. Meanwhile, consumer groups have raised questions about the potential link between mercury exposure and autism spectrum disorders as well as other adverse neurodevelopmental outcomes. This hypothesis has prompted some parents to seek regulatory, legal, or medical remedies in the absence of firm evidence. This article reviews what is known about mercury neurotoxicity and neurodevelopmental risk. Our intent is to focus the debate about mercury on 1) additional research that should be sought and 2) defining the principal issues that public policy makers face.

Reappraisal of the historic 1959 cat experiment in Minamata by the Chisso Factory.

Autopsy specimens from the historic cat experiment were recently discovered in a storage area at the Kumamoto University School of Medicine. The specimens were from an experiment prompted by physicians in the Chisso Minamata Plant following the announcement made by the Study Group for Minamata disease. On July 14, 1959 the Group announced that the disease was most likely caused by a kind of organic mercury. In order to prove or disprove that industrial waste from the Chisso Factory was the culprit in Minamata disease, a total of ten cats were fed food mixed with industrial waste produced in the acetaldehyde-producing plant. One of the ten cats, No. 717, was subsequently autopsied but the autopsy findings have never been published or recorded in the literature despite their historic significance. The rediscovered specimens were studied pathologically and biochemically, and were analyzed chemically with currently available techniques. Characteristic lesions of methylmercury poisoning were observed in the central nervous system, and the mercury levels in the cerebrum, cerebellum, liver and kidney were found to be markedly elevated in this animal.