Minamata disease revisited: An update on the acute and chronic manifestations of methyl mercury poisoning

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Abstract

The first well-documented outbreak of acute methyl mercury (MeHg) poisoning by consumption of contaminated fish occurred in Minamata, Japan, in 1953. The clinical picture was officially recognized and called Minamata disease (MD) in 1956. However, 50 years later there are still arguments about the definition of MD in terms of clinical symptoms and extent of lesions. We provide a historical review of this epidemic and an update of the problem of MeHg toxicity. Since MeHg dispersed from Minamata to the Shiranui Sea, residents living around the sea were exposed to low-dose MeHg through fish consumption for about 20 years (at least from 1950 to 1968). These patients with chronic MeHg poisoning continue to complain of distal paresthesias of the extremities and the lips even 30 years after cessation of exposure to MeHg. Based on findings in these patients the symptoms and lesions in MeHg poisoning are reappraised. The persisting somatosensory disorders after discontinuation of exposure to MeHg were induced by diffuse damage to the somatosensory cortex, but not by damage to the peripheral nervous system, as previously believed.

Introduction

In the early 1950s, massive methyl mercury (MeHg) poisoning of residents living around Minamata Bay, a small inlet located on the southwestern coast of Kyushu island, Japan, (Fig. 1) first raised awareness of the resulting severe neurological disease [33]. Since the victims lived near the Bay, this neurological disorder was named Minamata disease (MD). The primary route of exposure to MeHg in this incident was the consumption of fish and shellfish contaminated with a high concentration of MeHg [33]. MeHg chloride, which was produced as a by-product in the acetaldehyde plant of the chemical factory located there, was detected in the wastewater from the acetaldehyde plant, but not from its vinyl chloride plant [12], [13]. Initially, this contaminant had been released into Minamata Bay for more than a decade [13] causing severe acute poisoning cases in the vicinity [33]. Acetaldehyde is an intermediate by-product in the manufacture of plastics and its production had expanded steadily to meet the growing demands for plastics at that time. In order to increase production, the factory had expanded the manufacturing plants and changed the drainage site from Minamata Bay to the mouth of the Minamata River [18], [24]. This resulted in further dissemination of the pollution into the surrounding waters of the Shiranui Sea (Fig. 2A). The factory continued the production of acetaldehyde and the release of MeHg into the sea waters until 1968 [40], [47]. Because fishing in that part of the Shiranui Sea was never restricted, people living in coastal areas–many of whom depended on the sea for a large part of their food supply–were exposed to MeHg by ingestion of polluted fish for almost 20 years [24], [25] resulting in chronic MeHg poisoning.

In this article, the clinical symptoms of the acute poisoning cases are first reviewed. Neurological effects in adult cases and fetal cases are discussed separately. Secondly, we discuss the features of chronic MeHg poisoning and the neurological sequelae observed in the population with continued MeHg exposure, after the acute exposure in former years had apparently ceased.

Section snippets

Incidence in local residents

Since the initial outbreak of MD in 1953, the number of affected patients has reached 2264 as of the year 2000 [20]. Nonetheless, it is estimated that there are at least 200,000 suspected cases of MeHg poisoning since the coastal areas around the Shiranui Sea had a population of about 200,000 in 1960 [20], [25]. In Japan, the terms MD and MeHg poisoning, are used in different ways. Although MD certainly is a form of MeHg poisoning, to be diagnosed as suffering from MD, patients affected by MeHg

Clinical features

Methyl mercury poisoning observed in the areas around Minamata Bay and then on the coast of the Shiranui Sea is classified into two types: acute and chronic poisoning. As mentioned above, MD is a certified MeHg poisoning according to the Diagnostic Guidelines [36]. This was caused by consumption of polluted fish containing high levels of MeHg in Minamata Bay around 1953. Such severe acute cases had not been found since about 1960, because the residents stopped consuming highly contaminated fish

Acknowledgments

This work was supported by Kumamoto University Library. By the courtesy of Dr. J. Nagaki and Dr. H. Tokuomi, we were permitted to use data and figures in this article. We thank them for their cooperation. We are grateful to Dr. S. Kawamura for his encouragement.

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