Regarding pollution diseases, administrative agencies may recognize persons with certain symptoms on their bodies as pollution diseases.
In the case of pollution caused by a chemical substance, poisoning of the causative substance may be a pollution disease, but depending on the causative substance, the poisoning symptoms of the chemical substance are not specific to the pollution disease, but may be common nonspecific symptoms that are also seen in other diseases.
Symptoms of Minamata disease, which is a typical pollution disease caused by chemical substances, include (1) sensory disturbance, (2) motor disturbance, (3) visual field abnormality, (4) auditory dysarthria, (5) dysarthria, (6) tremor, and (7) komura-rebound (Masatsune HARADA, “Chronic Minamata Disease: What Is the Statue of Disease?” p. 61 (Jitsusho Publishing, 1994)), all of which can be caused by other diseases. Therefore, it is considered difficult to use specific symptoms as labels for the diagnosis of pollution-related diseases.
Of the sensory disturbances described in (1), peripheral sensory disturbances in the extremities (paresthesias occurring at the tips of the hands and feet) are said to be specific to Minamata’s disease. The reason for this seems to be as follows.
Minamata disease is poisoning caused by the oral ingestion of methylmercury-contaminated fish and shellfish inhabited in polluted areas of Minamata disease. The majority of the ingested methylmercury is absorbed from the digestive tract via the amino acid transport system, and the absorbed methylmercury is distributed throughout the body through the circulation of blood. In particular, methylmercury is able to cross the blood-brain barrier and therefore is also distributed in the brain. Because methylmercury has a high affinity for the -SH group, methylmercury is thought to bind to tissue functional -SH, impairing neuronal function and reducing activation (Araki, Toshiichi, ed., Toxicology, pp. 90-93 (Asakura Shoten, 2002)). Therefore, methylmercury that enters the brain is thought to cause a loss of neurons in the first somatosensory cortex (hereinafter referred to as the “first somatosensory cortex”) after the center of the cerebral cortex, which processes human sensation. Autopsy results of patients with Minamata disease who actually died showed extensive thinning-out loss of neurons in the cerebral cortex (p. 312, rough note). However, the mechanism of neuropathy due to the ingestion of methylmercury is not fully understood. Recently, it has been pointed out that methylmercury compounds induce the expression of vascular endothelial growth factor (VEGF) and that VEGF breaks the blood-brain barrier, thereby increasing vascular permeability. Toxic substances other than methylmercury (such as inflammatory cytokines and oxidants) may enter the brain from the blood vessels, causing neuropathy and site-specificity.
The primary somatosensory cortex then undergoes systemic sensory processing, so if neurons in this area are damaged, it is unlikely that sensory disturbances will occur throughout the body. However, the national government and other countries place importance on sensory impairment in the peripheral superiority of the extremities when recognizing Minamata disease. Indeed, considering the area ratio of the primary somatosensory cortex to the entire primary somatosensory cortex (as described below, the area where peripheral sensory processing is performed in the primary somatosensory cortex is relatively larger than the area where sensory processing is performed in other areas), it is reasonable to treat the peripheral sensory disturbance of the extremities as one that is stronger than that of other sensory disturbances for Minamata disease. However, the national government takes the position that there are no patients with Minamata disease who have no sensory impairment with peripheral superiority in the limbs (provided, however, that the national government adopts the “52-year judgment condition” described later for the recognition of patients with Minamata disease, and the recognition of Minamata disease by those who have no sensory impairment with peripheral superiority in the limbs is not necessarily excluded uniformly in places other than lawsuits). Is this reasonable as a judgment?
Generally, peripheral sensory disturbances in the extremities are thought to result from the functional localization of the primary somatosensory cortex. Functional localization of the cerebral cortex means that not all parts of the cerebral cortex are equally involved in all motor and sensory processes, but the primary somatosensory cortex determines which parts of the body are sensorially processed for each detailed region. A look at the Homunkulus of Penfiled (see Haradae, pp. 92-93), which is famous for showing which part of the primary somatosensory cortex processes the sensation of which part of the body, reveals that the area of the primary somatosensory cortex where the sensation of the limbs is processed is larger than the area of the area of the primary somatosensory cortex where the sensation of the trunk is processed. This suggests that neurons in the peripheral sensory areas of the extremities are susceptible to damage.
However, it is not impossible to consider that neurons in the peripheral sensory areas of the extremities are the sole target of attack because of the directivity of methylmercury that has penetrated into the brain. However, among the above symptoms of Minamata disease, (2) motor disorders and (6) tremors are caused by cerebellar disorders. In Minamata disease, the cause of such disorders is thought to be that neurons in the cerebellum have been damaged by methylmercury. In addition, (3) visual field abnormalities, and (4) auditory abnormalities may be caused by methylmercury damage to neurons in the visual cortex above and below the avian talar sulcus in the occipital area of the cerebrum and in the auditory cortex in the lateral temporal gyrus of the cerebral cortex, respectively. In this way, in Minamata’s disease, because neurons in many parts of the brain are damaged, methylmercury is directional, and it is unlikely that the target cells have been identified. Certainly, it may be possible to hypothesize that only neuronal cells in the peripheral sensory region of the limb are affected by the positional relationship between blood vessels, which are the route of methylmercury transport into the brain, and the peripheral sensory region of the primary somatosensory cortex. However, no such literature has been found within the scope of the investigation, and the State has not made such an assertion. Against this backdrop, we believe that such an idea is difficult at the present time.
Next, consider people with generalized sensory impairment. From the former perspective, it can be considered that systemic sensory impairment occurs not only in the area of the primary somatosensory cortex that processes sensation in the periphery of the extremities, but also in the entire area of neurons. Though a person with peripheral sensory disturbance who suffers from only peripheral sensory disturbance of the extremities can be recognized as a patient with Minamata disease and compensated for it, a person who suffers from neuronal disturbance in the entire primary somatic sensory cortex area as well as neuronal cells that treat peripheral sensory disturbance of the extremities cannot be compensated for.
Incidentally, the national government recognizes those who meet the conditions referred to as “52-year judgment conditions” as “patients with Minamata disease” and pays compensation (even for those who do not meet the 52-year judgment conditions, certain remedies have been implemented under the “Act on Special Measures Concerning the Relief of Victims of Minamata Disease and the Solution of the Minamata Disease Problem”). The State maintains the position that persons who do not meet the 52-year judgment conditions cannot be treated as patients with Minamata disease.
The question here is what to consider as “Minamata disease” and what to consider as damage.
When a victim of Minamata Disease pollution claims compensation for damages, the victim does not necessarily complain of suffering from “Minamata Disease” as the national government says. Some people are seeking compensation for damages because they are unable to obtain a salary because of ataxia and narrowing of the visual field due to oral intake of methylmercury and are unable to work.
If Minamata’s disease is interpreted as “methylmercury poisoning” as originally defined, the symptoms that occur in humans will differ. This can also be explained by the following:
The Government of Japan asserts the theory of the “Threshold Organization” in Minamata Disease Litigation. The “threshold mechanism” theory here is the claim that Minamata disease does not develop unless the body ingests more than a certain amount of methylmercury.
However, it can be said that this theory of “threshold mechanism” also presupposes that a condition that satisfies the 52-year judgment condition is defined as “Minamata disease”.
This is because the relationship between the amount of methylmercury intake and the degree of onset of each symptom varies from symptom to symptom (Kumagaya, et al., Science of Toxicology, pp. 4-6, University of Tokyo Press, 2014), and ultimately, the threshold value varies depending on the endpoint of what symptoms should be considered to have resulted in the onset of Minamata disease.
Therefore, it seems unlikely that it would be an objection to the plaintiff who filed a claim for compensation for damages (including a claim based on the State Compensation Act against the State and Kumamoto Prefectures) on the ground that ataxia and visual field stenosis occurred and that work could not be done, rather than on the ground that the plaintiff had suffered from “Minamata Disease” which satisfied the 52-year judgment conditions, because the assumption was different and the “threshold mechanism” of the plaintiff who satisfied the 52-year judgment conditions would be argued. However, in reality, apart from whether or not the 52-year judgment condition is adopted, an abstract specific type of Minamata disease image is decided, and whether or not the disease image agrees with the decided disease image is decided. If this is not the case, the request will be dismissed.
In this way, it can be said that there is a difference between the plaintiff’s claim, the state’s claim against it, and the court’s judgment in filing a claim for damages for Minamata disease.
In the case of Minamata’s disease, if there are no specific symptoms of pollution caused by chemical substances and there are several non-specific symptoms, the lawsuit may consider clarifying what is to be damaged (not simply “claim for compensation for suffering from pollution diseases”), and avoiding the typing of pollution diseases in lawsuits.