Mistaken Science Caused Erroneous Diagnosis and the Underestimation of Damage
to the Cerebral Cortex from Methylmercury (MeHg) Poisoning
Dr. Shigeo Ekino (MD)
Professor, Graduate School of Medical Sciences, Kumamoto University
Honjo 1-1-1, Kumamoto City 860-8556 Japan
Dr. Tadashi Ninomiya (MD)
Assistant Professor, Graduate School of Medical Sciences, Kumamoto University
Associate Professor of Law, Kumamoto University
April 25, 2006
The anthropogenic release of methylmercury into Minamata Bay led to extremely high concentrations of this toxic substance in fish and shellfish resulting in widespread, acute methylmercury poisoning by1960 known as "Minamata disease". Subsequent discharge of methylmercury into the Minamata River from 1958 to 1968 caused chronic methylmercury poisoning throughout the surrounding Shiranui Sea area resulting in diffuse damage to the cerebral cortex and persistent sensory disturbance among residents on the coast of the Shiranui Sea. Systematic research of the damage is yet to be undertaken. This research should take place to protect future generations. We propose the establishment of a special hospital for Minamata disease in order to research damage to the cerebral cortex by methylmercury as well as to provide medical treatment for those suffering from this poisoning.
Acute Methylmercury (MeHg) Poisoning
The mass MeHg poisoning of residents living around Minamata Bay, a small inlet located on the southwestern coast of Kyushu island, Japan in the early 1950's first raised awareness of this severe neurological disease. Since the victims lived near the bay, the disease was soon named "Minamata disease". The primary route of exposure to MeHg was the consumption of fish and shellfish contaminated with a high concentration of MeHg. MeHg chloride, which was produced as a by-product in the acetaldehyde plant of the chemical factory facing the bay was detected in the wastewater from the plant. This contaminant had been released in large quantities into Minamata Bay for more than a decade. This caused 121 cases of severe acute poisoning in the areas around Minamata by 1960.
Chronic MeHg Poisoning Caused by Increase and Extension of MeHg Pollution.
Since acetaldehyde is an intermediate in the manufacture of plastics, its production expanded steadily to meet growing demands. In order to increase production, the factory built up the manufacturing plant and changed the drainage site from Minamata Bay to the mouth of the Minamata River. This resulted in further expansion of the pollution into the surrounding Shiranui Sea, since the factory continued production of acetaldehyde discharging MeHg in the effluent until 1968. MeHg concentrations in the umbilical cords of people on the coast of Shiranui Sea from 1950 to 1968 was much higher than that of Tokyo inhabitants in 1975. Furthermore, Kumamoto Prefectural Institute of Public Health reported that the median value of T-Hg in hairs of 1,644 residents of the coastal areas was 23.4 ppm (range 0 - 920 ppm) in 1960, while the median value of non-polluted Japanese was 2.1 ppm (range 0.1 - 8 ppm). These data suggest that methylmercury had already spread into the Shiranui Sea in 1960 and the release of methylmercury to the Shiranui Sea continued until 1968. Because fishing in the Shiranui Sea area has never been restricted, people living around the sea, many of whom were dependent on the sea for a large part of their food supply, were suspected to be exposed for almost 20 years to MeHg by ingestion of polluted fish. This led to chronic MeHg poisoning in the residents of the coastal areas.
Minamata Disease and MeHg Poisoning
Since the outbreak of Minamata disease in 1953, the number of patients has reached 2,264 by 2000. It is estimated that at most, in the order of 200,000 people could be suspected cases of MeHg poisoning, considering the coastal areas around the Shiranui Sea had a population of about 200,000 in 1960. In Japan, these two terms, "Minamata disease" and "methylmercury poisoning" are used in different ways. Although Minamata disease is MeHg poisoning, to be "Minamata disease" patients, people who were affected by MeHg are required to come forward for official recognition of their suffering. Once they are certified as Minamata disease patients, they are eligible to receive compensation. The Diagnostic Guidelines for Minamata disease were set up for the compensation scheme under the Law Concerning Special Measures for the Relief of Pollution-related Health Damage, which was put into effect in 1969. So far, only about 17,000 of residents had applied for this certification, and among them the abovementioned 2,264 were certified.
Lack of Systematic Research on Minamata disease
The expansion of MeHg pollution to the Shiranui Sea caused neurological disorders in many residents on the coast of the Shiranui Sea. However, the authorities have not performed systematic research of the affected area. The authorities made the diagnostic guidelines for Minamata disease in 1977, and this has remained unchanged for 30 years.
There is no Scientific Evidence of Damage to Human Peripheral Nerves by MeHg
Chronic MeHg poisoning patients principally have often complained of paresthesia at the distal parts of the extremities and around the lips 30 years after the cessation of exposure to anthropogenic MeHg. When they were examined with conventional sensory examinations using a painting brush and pinprick, they reported the sensory reduction at the distal extremities in the pattern of the so-called "stocking-glove distribution", which is a characteristic feature of peripheral neuropathy. In Japan, paresthesia at these parts has been believed to be caused by damage to the peripheral nervous system. Definitive scientific data on damage to human peripheral nervous system by MeHg have not been reported. Nagaki et al. and Tokuomi et al. proved that the peripheral nerves were not injured in MeHg poisoning patients. Those certified as having Minamata disease and chronic MeHg poisoning patients reported sensory reduction in the distal extremities with conventional sensory examinations. However, the quantifiable sensory tests revealed that sensory reduction is systemic, but not restricted to the distal extremities. These results confirm that the lesion of the persistent somatosensory disturbances in Minamata disease patients is not in the peripheral nerves. Scientists in Japan, examining human cases without a satisfactory control group, made errors in studying sensory disturbances in MeHg poisoning.
Long-term and Low-dose MeHg Exposure Causes Diffuse Damage to the Cerebral Cortex
Tokuomi et al. clarified that persistent sensory disturbance in MeHg poisoning patients were caused by damage to the somatosensory cortex, but neither the peripheral nerves nor the spinal cord nor the thalamus. The quantifiable examinations of MeHg poisoning patients confirmed that the persisting somatosensory disorders after discontinuation of exposure to MeHg are induced by diffuse damage to the somatosensory cortex (Neurotoxicology and Teratology 27 (2005) 643-653)).
Research Needs to Protect the Generations to Come
Neurotoxic substances such as MeHg cause the loss of nerve cells in the cerebral cortex. Damage to the brain causes persistent disorders of the nervous system. This kind of degeneration of the nervous system may imply the retrogression of human beings in the future. Thus, it is a matter of urgent concern not only for Japan but also for the world over. MeHg pollution which started locally in the Minamata area expanded to a wider area and extended for a longer period of time than previously thought. The fact that lower levels of MeHg cause damage to the human brain make us reconsider its implications. The "out of sight, out of mind" attitude must be abandoned. In order to overcome our past mistakes and look to the future, we propose the establishment of a special hospital for those suffering from Minamata disease and to help finding those who remain unrecognized.
All scientists at all times commit errors; they seem to be unavoidable. One should search for errors, analyze them when found, and learn from them; it is an unforgivable sin to conceal errors. (Karl Popper in 1981)