Chronic Neurological Disease Due to Methylmercury Poisoning

Organic mercury, especially methylmercury, poisoning causes chronic neurological disease predominantly affecting the brain. There have been documented exposures from eating fish from contaminated waters in Japan and in northwestern Ontario and in Iraq from eating bread made from seed wheat treated with methylmercuric fungicide. The neurological disease is called Minamata disease in Japan. Visual field constriction due to involvement of the calcarine cortex, sensory disturbance due to involvement of the somatosensory cortex, and cerebellar ataxia due to involvement of granule cell neurons of the cerebellum are common and characteristic features due to methylmercury poisoning. Other neurological features include dysarthria, postural and action tremor, cognitive impairment, and hearing loss and dysequilibrium. In contrast, peripheral nerve disease is more characteristic of inorganic mercury intoxication. Similarly, psychosis is more typical of exposure to inorganic mercury, which has been documented in the felt hat industry (“mad hatter”). Laboratory tests (e.g., on blood and hair and toenail samples) are of limited value in the assessment of chronic neurological disease due to mercury poisoning because they may not reflect remote neuronal injury due to mercury. Methylmercury also causes injury to fetal brains during development. There is no effective treatment.

Survey of the Extent of the Persisting Effects of Methylmercury Pollution on the Inhabitants around the Shiranui Sea, Japan

In 1956 methylmercury poisoning, known as Minamata disease, was discovered among the inhabitants around the Shiranui Sea, Kyushu, Japan. Although about five hundred thousand people living in the area had supposedly been exposed to methylmercury, administrative agencies and research institutes had not performed any subsequent large scale, continuous health examination, so the actual extent of the negative health effects was not clearly documented. In 2009, we performed health surveys in order to examine residents in the polluted area and to research the extent of the polluted area and period of pollution. We analyzed data collected on 973 people (age = 62.3 ± 11.7) who had lived in the polluted area and had eaten the fish there and a control group, consisting of 142 persons (age = 62.0 ± 10.5), most of whom had not lived in the polluted area. Symptoms and neurological signs were statistically more prevalent in the four groups than in the control group and were more prevalent and severe in those who had eaten most fish. The patterns of positive findings of symptoms and neurological findings in the four groups were similar. Our data indicates that Minamata disease had spread outside of the central area and could still be observed recently, almost 50 years after the Chisso Company’s factory had halted the dumping of mercury polluted waste water back in 1968.