Lecture on Methylmercury Poisoning in Minamata (MPM)
This chapter outlines the methylmercury poisoning in Minamata (MPM): about the history, symptom pathogenesis, research on the causal agent, and responses of the national and local governments and the responsible company, i.e., Chisso, to the outbreak of MPM. A book written by Nishimura and Okamoto (2001) played an important role to clarify the mechanism of the MPM outbreak. Based on this book and the published data on mercury concentrations of aquatic organisms and newborns’ umbilical cords, how methylmercury generated in the plant, flew into the sea, transferred to aquatic organisms, and was consumed by residents are explained. Victims of MPM, compensation and environmental restructure, and court ruling against this incident are described. Based on lecture notes from a university course, students’ suggestions for avoiding a repeat of the tragedy are also introduced.
KeywordsBioaccumulation Fetus Hunter-Russel syndrome Intoxication Methylmercury Neurological syndrome Poisoning
Thank you for joining my class. In this lecture, I would like to discuss the issues of the so-called Minamata disease, which is a typical pollution-related disease caused by effluents containing mercury from chemical factories. In this class, I will call this disease MPM (an abbreviation of methylmercury poisoning among people living in the Minamata area). The extent and severity of the health damage as well as the destruction of the natural environment caused by such environmental pollution was unprecedented in the human history. Before explaining MPM, I will mention the properties and toxicity of mercury briefly.
2.1 General Information on Mercury
Mercury is a ubiquitous environmental toxicant. It exists in three forms, that is, elemental (Hg0), inorganic (Hg2+), and organic forms. Hg0 takes a liquid form at room temperature but readily evaporates into mercury vapor. Hg2+ occurs naturally in the environment in the form of divalent cationic salts of mercury, such as HgCl2. Among the three forms, organic mercury, primarily methylmercury, is most hazardous. Methylmercury is bioavailable and can be bioaccumulated within food webs. Seafood consumption, especially the consumption of fish, is the main source of humans’ exposure to methylmercury. MPM is the first incident in the world, although there were a few incidents where several persons had suffered from direct exposure of organic mercury in a laboratory or in a factory.
2.2 Outbreak of MPM
In November 1962, a child diagnosed with cerebral paralysis was certified as a congenital (fetal) MPM patient (the first official acknowledgment of a congenital MPM patient). As the investigation into the cause took a long time, the outbreak of MPM continued, and the geographical range of inhabitants affected by MPM expanded along the Shiranui Sea coast (Fig. 2.1a).
2.3 What Is MPM?
I will explain the symptoms of MPM. MPM is a neurological syndrome which was caused by eating fish and shellfish contaminated by methylmercury compounds discharged artificially. The first and second outbreaks of this kind of disease in Japan were caused by effluents discharged from a factory of Shin-Nippon Chisso Hiryo (hereafter, referred to as Chisso) in Minamata, Kumamoto Prefecture, and a factory of Showa Denko in Kanose Town, Niigata Prefecture, respectively (Fig. 2.1c).
Methylmercury is a stable organic mercury compound and is the most toxic form of mercury in the environment not only to humans but also to wildlife (Wolfe et al. 1998, Henriques et al. 2015). Because methylmercury is lipid-soluble, it readily crosses the blood-brain barrier and accumulates in the brain. Methylmercury in the brain causes lysis of cells of the central nervous system, resulting in irreversible, permanent damages of the cells (Rabenstein 1978). Thus, MPM is widely recognized as a disorder in the brain, while Shiraki (1979) suggested that MPM produces lesions not only in the brain but also in the vascular and endocrine systems.
This methylmercury poisoning that occurred in Japan is classified into two types: typical and atypical. The medical condition of the former type was acute and fulminant due to the consumption of a large amount of methylmercury compounds during a short period. In severe cases, such patients fall into a state of madness, lose consciousness, and may even die. The acute type presented most of the following symptoms: (i) ataxia, that is, difficulty coordinating movement of hands and feet; (ii) dysarthria, that is, speech becomes slurred and unclear; (iii) concentric constriction of the visual field, that is, narrowing of the field of vision; (iv) paresthesia, that is, sensory disorders in the distal portion of the four extremities, e.g., loss of sensation in the hands and feet; (v) hearing impairment; (vi) disequilibrium, that is, impairment of faculties for maintaining balance; (vii) tremors, that is, trembling of the hands and feet; and (viii) disorder of the ocular movement, that is, eye movement becomes erratic.
The first organic mercury poisoning occurred at Saint Bartholomew’s Hospital in England in 1865 when two laboratory technicians were poisoned with dimethylmercury during their experiments and ended in death (Iriguchi 2012). They complained of sore gums; salivation; numbness of the feet, hands, and tongue; deafness; and poor vision, which were similar to MPM patients excluding the first two symptoms that are characteristics of mercury vapor poisoning. This incident was first reported in “Saint Bartholomew’s Hospital reports” (Edwards, 1865, 1866), which were the world’s first case reports, and then it was described extensively in the journal Chemical News in 1866. Thereafter, the pathology of this affair was described by Hepp (1887) in detail as a disorder of the central nervous system due to methylmercury poisoning (Iriguchi 2014).
Other than these two incidents that occurred at Saint Bartholomew’s Hospital and the seed factory, poisoning by direct incorporation of methylmercury had occurred in Canada (Hill 1943, Ahlmark 1948) and Sweden (Lundgren and Swensson 1949, Höök et al. 1954) before the outbreak of MPM. Zangger (1930) also reported organic mercury poisoning among workers in the process of acetaldehyde production where inorganic mercury was used as a catalyst similar to the Chisso Minamata factory, suggesting that inorganic mercury had changed to organic mercury compounds in this production process.
In general, the symptoms of the typical MPM were similar to those of the preceding accidental cases of the methylmercury poisoning; however, there were some differences in the combination of symptoms and in the severity of the disease state between them, because the amount of and/or the exposure period to methylmercury were variable among the MPM patients. In relatively mild cases in MPM, the condition is barely distinguishable from other ailments such as headache, chronic fatigue, and a generalized inability to distinguish taste and smell.
Thus, besides the typical type, there was an atypical MPM which exhibited only one or a limited number of the symptoms. Such a type of case was liable to become chronic. For instance, neurological disorders such as a hypoesthesia at the distal parts of the extremities and around the lips, which were considered to be caused by a long-term dietary exposure to methylmercury compounds, were still detected among residents in a fishing village in Goshoura-jima island 10 years after the cessation of methylmercury dispersion from Minamata (Ninomiya et al. 1995). On the other hand, delayed MPM is defined as the latent development of methylmercury poisoning after multiple years of cessation from a long exposure through contaminated food (Miura 2014). Thus, there is a large variability in the type and the degree of symptoms, resulting in difficulties in diagnosis and certification of MPM.
There have been cases of congenital MPM, where fetuses were poisoned by methylmercury compounds via the placenta after their mothers ingested contaminated foods during pregnancy and were born with a condition resembling cerebral palsy. The symptoms of patients were serious including both in mental and physical development due to extensive and intensive lesions of their brains (Takeuchi 1966: Fig. 2.2b). They showed significant impairments in chewing, swallowing, speech, gait, and other coordination and involuntary movement (Ekino et al. 2007). The most severe effects which were found following this high-dose poisoning included cerebral palsy, deafness, blindness, and dysarthria (National Research Council 2000). Shiraki (1979) proved the intrusion of methylmercuric chloride into fetuses after performing intravenous injections on mother rats by the autoradiography. Lipophilic methylmercury is readily transferred to the fetus across the placenta via neutral amino acid carriers and concentrated in the central nervous system of fetuses’ brains (Kajiwara et al. 1996). The blood-brain barrier is not fully developed until after the first year of life, and methyl mercury can cross this incomplete barrier (Rodier 1995). Thus, the developing brain is extremely vulnerable to methylmercury.
What kind of medical treatment is effective for MPM? In the initial stages, causative treatments, involving patients taking medicines to force methylmercury compounds to be excreted from the body, are applied. However, a fundamental cure for MPM has not yet been found. The main treatments involve the temporary relief of symptoms (symptomatic therapies), as well as rehabilitation (physiotherapy and occupational therapy).
2.4 Investigations on the Cause of MPM
Investigations to clarify the cause of this disease started. On May 28, 1956, the Minamata Strange Disease Action Committee (MSDAC) which was established by Minamata Health Center, Minamata City, City Medical Association, Municipal Hospital, and Chisso Hospital was established. On August 14, 1956, MSDAC asked Kumamoto University Medical School (KU) to investigate the cause of the disease. Then, KU formed a Minamata Disease Study Group. On November 3, 1956, KU held an interim report meeting, where MSDAC members and Prefectural Public Health Department staff attended. At this meeting, KU reported that the disease was a kind of heavy metal poisoning and that the causative agent had entered the human body through consumption of fish and shellfish captured in this area. Although this report was “tentative,” these findings show that in only 6 months since the official acknowledgment of MPM, researchers at KU strongly suspected that this disease was caused by seafood poisoning. At that time, this disease could have been avoided by banning all fisheries in Minamata Bay and prohibiting the consumption of local seafood (Tsuda 2014). However, such measures were not adopted. It was the start of a continuing tragedy.
It took 3 years to reveal the causative agent of MPM. At the initial stage of the research, manganese, selenium, and thallium were suspected as the causative agent. BritishneurologistDouglas McAlpine, who examined 15 patients admitted into the KU hospital in 1956, published a paper in collaboration with Shukuro Araki of KU, suggesting that MPM symptoms resembled those of methylmercury poisoning which showed ataxia, dysarthria, and constriction of the visual fields (McAlpine and Araki 1958). They also suggested that this disease was caused by eating fish captured in Minamata Bay which were contaminated by “an inorganic chemical compound contained in the effluent which flowed into Minamata Bay from a nearby fertilizer factory.” At that time, there was no fertilizer factory other than the Chisso Minamata factory. On September 26, 1958, Professor Tadao Takeuchi of KU also announced at the meeting of the study group “Pathological findings coincided completely with the Hunter-Russell syndrome.” Investigations regarding the epidemiology, pathology, and etiology of MPM advanced further by KU, and the results were published mainly in domestic journals quickly and sequentially as follows.
2.4.1 Epidemiological Examinations
Kitamura et al. (1957a) confirmed 52 patients had MPM during the period from 1953 to 1956. They found that (1) the fatality rate in these patients was 33%; (2) the onset area was fishing and agrarian villages around Hyakken Port in Minamata City; (3) fishermen and their families comprised a high proportion of the total patients; and (4) cats inhabiting the same area also showed similar symptoms, and shortly after, the majority died. These findings suggested that exposure to an agent which was common to residents and cats caused this disease and that fish and shellfish inhabiting the Minamata Bay area were contaminated and these seafood contained the causative agent. This conclusion was supported by observations that migratory fish became poisonous during a short stay in Minamata Bay (Kitamura et al. 1957b). Further epidemiological observations showed that (1) in 1957, no new patients were diagnosed as seafood in this area was temporarily not consumed (Kitamura et al. 1957b); (2) in 1958, MPM patients occurred again as a result that residents restarted eating seafood (Kitamura et al. 1959); and (3) since 1959, the onset area expanded to northern and southern areas of Minamata City, associated with the shift of the wastewater outlet from Hyakken Port in Minamata Bay to the mouth of Minamata River (Kitamura et al. 1960a). Kitamura et al. (1960b) found high concentrations of mercury in organs, hair, and urine of MPM patients as well as in organs of cats that showed similar symptoms to MPM, suggesting mercury in wastewater from the factory as a potential causative agent.
2.4.2 Finding of the Congenital MPM
Kitamura et al. (1959) found nine infants having cerebral palsy around Minamata Bay, accounting for >10% of the total newborns in the MPM-prone area in 1956. They suspected that intoxicating substance moved to the infants through the placenta or mother’s milk, even if their mothers showed no obvious symptoms of MPM. Nagano et al. (1960) also reported similar 15 cases of infants who were born during the period of 1955–1958. The study group of KU, however, hesitated to conclude that such cases were caused by the congenital MPM, because similar cases had not been reported from the world. At the Kumamoto medical conference held on November 25, 1962, Dr. Tadao Takeuchi of the study group did a presentation about the anatomy of two congenital patients’ brains (Takeuchi et al. 1964), while Dr. Masazumi Harada did a presentation about a clinical manifestation of a congenital patient whose brain was served for the dissection (Harada 1972). These presentations concluded that methylmercury consumed by mothers had impaired fetuses’ brains (Fig. 2.2b). Thus, they revealed evidence of congenital MPM.
2.4.3 Feeding Experiments on Animals
Ito (1957) fed fish and shellfish collected from Minamata Bay to five cats, and he confirmed that symptoms of MPM appeared 7–47 days after, showing a lesion in the central nervous system. Thereafter, several animal experiments to feed cats, rats, or mice on fish and/or shellfish were conducted, indicating that coastal animals collected from the Minamata area contained the substance causing MPM (e.g., Takeuchi et al. 1957c, Shiraishi et al. 1959, Kojima 1960).
2.4.4 Pathological Examinations
Takeuchi et al. (1957a, b) dissected diseased cats and birds which were collected from the coastal area in Minamata City for pathological examinations and found that these animals were suffering from an intoxicated encephalopathy which was the same disease as residents. Takeuchi et al. (1959a, b) pointed out that the histopathological diagnoses on brains of acute and chronic MPM patients and the symptom of MPM such as ataxia, constriction of the visual field, and dysarthria closely resembled those of organic mercury poisoning known as the “Hunter-Russel syndrome.” Tokuomi (1960) and Tokuomi et al. (1960) pointed out that (1) symptoms of MPM corresponded completely to those of organic mercury poisoning; (2) the concentration of mercury in the urine of patients was significantly high; (3) same symptoms and same lesions were found between MPM patients and experimental animals that were given methylmercury, and they concluded that MPM was food poisoning caused by the consumption of organic mercury. Takeuchi et al. (1960a) and Takeuchi and Morikawa (1960) also reached the same conclusion based on results on necropsies of patients, examinations of the clinical and pathological observations in stray cats and wild fish, and feeding experiments using cats and rats.
2.4.5 Field Surveys to Search for the Causative Agent
As a result of these patient and steady researches, the study group of KU reached a conclusion. On July 22, 1959, KU made an announcement, saying that “MPM is a disease of the nervous system which is caused by eating fish and shellfish captured from Minamata Bay. Mercury has come to our attention as a likely cause of pollution of fish and shellfish.” After this announcement, the study group of KU continued the research to reveal the causative agent of MPM. On September 29, 1960, Makio Uchida of KU announced that “We extracted an organic mercury compound from shellfish in Minamata Bay.”
2.4.6 Feeding Experiments of Organic Mercury on Animals
Takeuchi and Morikawa (1960) and Takeuchi et al. (1962) fed methylmercury compounds on cats, and they confirmed the development of MPM. Other members of KU also showed that experimental animals orally dosed with certain amounts (~20 mg Hg kg−1 for cats, rabbits, and dogs, after Irukayama et al. (1964a)) of alkyl mercury compounds having CH3, C2H5, and C3H7 induce symptoms consistent with MPM within 5 days to approximately 2 months (Tokuomi et al. 1960, Sebe et al. 1961, Takaba 1962, Irukayama et al. 1963, Takeshita and Uchida 1963). Morikawa (1961) confirmed that a kitten born from a mother cat which was dosed with bisethylmercuric sulfide had symptoms similar to congenital MPM.
2.4.7 Extraction of Organic Mercury from Aquatic Organisms
Uchida et al. (1961a, b), Hirakawa (1962), and Inoue (1962) extracted crystals from tissues of the mussel, H. mutabilis, collected from Minamata Bay and identified them as methyl methylmercuric sulfide (CH3HgSCH3) (Irukayama et al. (1964a) described that this organic mercury should be identified as (CH3Hg)2S). Irukayama et al. (1962a) extracted organic mercury from the mussel, H. mutabilis, and the scarbreast tuskfin, Choerodon azurio, collected from Minamata Bay. This organic mercury contained in H. mutabilis as well as in the Japanese littleneck, Ruditapes philippinarum, was identified as methylmercuric chloride (CH3HgCl) (Irukayama et al. 1964a).
2.4.8 Experiments on Bioaccumulation by Aquatic Organisms
Irukayama et al. (1962b) showed that R. philippinarum accumulated 40–129 ppm (dry weight basis) of Hg during 4–14 days of culture in seawater containing 0.2–0.3 ppm of alkyl mercury and that this clam accumulated 22.5 ppm within 5 days of culture in water containing mercury sludge discharged from Chisso Minamata factory.
2.4.9 Extraction of Organic Mercury from the Factory
CH3HgCl was extracted from mercury sludge (mixture of inorganic mercury and activated charcoal which was used as the catalyst) in the acetaldehyde plant (Irukayama et al. 1962c) and from sediments in the drainage close to Hyakken Port (Irukayama et al. 1962d). Irukayama et al. (1964a) concluded that the causative agent of MPM was CH3HgCl and that the functional group is methylmercury (CH3Hg-).
Finally, the study group of KU concluded that (1) a variety of coastal animals contained large enough amount of methylmercury to cause MPM; (2) methylmercury occurred in wastewater and sludge in Chisso Minamata factory; and (3) methylmercury in coastal animals originated from Chisso Minamata factory. On February 20, 1963, KU made a formal announcement stating that “MPM is a disease of the central nervous system caused by eating fish and shellfish from Minamata Bay. The causative agent of poisoning is methylmercury compounds found in shellfish as well as in the sludge of the Chisso Minamata factory.” Later, the study group summarized their results in a book (Minamata Disease Study Group 1966). Such a process shows that the researchers of KU accumulated scientific evidences sincerely and steadily. In those days, there was an atmosphere that researchers should avoid studies which might result in the conflict of becoming political issues. The researchers were at risk for suffering from the mercury poisoning themselves in the process of the extraction and synthesis of methylmercury during their experiments. They finally reached the truth; however, 7 years had passed after the official acknowledgment. During this period, the Chisso Minamata factory continued to drain wastewater containing organic mercury, and the number of MPM patients steadily increased.
2.5 Initial Responses of the National and Local Governments to the Outbreak of MPM
Let’s look back to the national and local governments’ responses. In November 1956, a research team of the Ministry of Health and Welfare (MHW) started an epidemiological survey. In March 1957, they suspected fishery products collected from Minamata Bay as a cause of the disease and recommended to investigate the relationship between wastewater discharged from the plant and fish in Minamata Bay. In addition to this, KU also suggested to the Kumamoto prefectural government (KP) to ban the fisheries in Minamata Bay on February 26, 1957. In March 1957, therefore, KP made enquiries to the Shizuoka prefectural government (SP) about the poisoning of Japanese littleneck R. philippinarum which had occurred in Hamana-ko lagoon, because SP used to stop the fishery and selling the clam and to prevent the occurrence of food poisoning by applying the Food Sanitation Act (FSA) (Fukai 1999). On August 16, 1957, KP made inquiries to MHW, on the possible implementation of FSA. On September 11, 1957, MHW replied, “Fish and shellfish collected from Minamata Bay may cause the disease, however, as there is no clear evidence that all fish and shellfish in Minamata Bay are contaminated, FSA should not be applied.” KP followed this recommendation and did not implement the FSA. Nobuo Miyazawa who devoted his life to the clarification of the Minamata incident in favor of the patients after his assignment in Kumamoto as a broadcaster of NHK, however, revealed underlying facts by his thorough coverage (Miyazawa 1996). The vice-governor of KU, Chokichi Mizukami, who had been a government bureaucrat, requested MHW not to recommend the enforcement of FSA. Mayor of Minamata City, Hikoshichi Hashimoto, who designed the acetaldehyde plant of the Chisso Minamata factory and served as a director of the factory later, also opposed to be subject of FSA. The two persons might fear of paying the compensation money for fishery banning by Chisso.
On the other hand, the Fisheries Experimental Station of KP showed that the coastal waters were seriously affected based on a survey of the oyster (species belonging to Ostreidae) distributed along the shore in the Minamata area in summer, 1957 (Fig. 2.3). The mortality rate of the oyster distributed in Minamata Bay was very high, attaining to 60–100%. Even in Tsunagi which is located ~10 km north from Minamata, a mortality of 30% was found. The results were reported to the Fisheries Division of KP immediately; however, the findings were not reflected in an administrative measure.
The main symptoms of this disease, which are ataxia, concentric constriction of the visual field, and paresthesia, as well as observations of the pathologic autopsy closely agreed with those of organic mercury poisoning.
Concentrations of mercury in the urine of patients were high in comparison with reference values.
Large amounts of mercury were found in the brain, liver, and kidney of patients in comparison with reference values.
Extremely large amounts of mercury were found in sediments in Minamata Bay in comparison with other regions.
Large amounts of mercury were found in mussels in Minamata Bay in comparison with other regions, and cats which ate these mussels developed similar symptoms and tissue abnormalities.
Large amounts of mercury were found in organs, especially in the brain, of cats which developed the disease experimentally or spontaneously.
Animals which were administered with organic mercury developed similar symptoms and tissue abnormalities.
Thus, the committee reached an exact conclusion that MPM was food poisoning caused by organic mercury. However, this report was not approved by the cabinet meeting due to an opposite opinion offered by the minister of the International Trade and Industry, Hayato Ikeda, who later became the prime minister in 1960 and promoted Japan’s rapid economic growth in the 1960s (Masano 2013, Takamine 2016). This committee was dissolved on the following day, and MHW was unable to implement any appropriate measures.
As described in the next section, Chisso made a contract regarding the compensation with a patient group through the mediation of KP and Minamata City. At that time the local governments established a patient certification program for specifying persons who had suffered from MPM. This system continued after an establishment of the Act on Special Measures Concerning Relief for Health Damage by Pollution that was enforced in December 1969. For this purpose certification councils had been established; however, the certification criteria were too strict to cover all patients resulting in many lawsuits to claim for the compensation.
2.6 Initial Responses of Chisso to the Doubt that Its Own Wastewater Caused MPM
Now, I will focus on the responsible company that caused MPM, Chisso. This company first opened a chemical factory in Minamata in 1908. The factory initially produced fertilizer and then followed the nationwide expansion of Japan’s chemical industry, branching out into the production of acetylene, acetaldehyde, acetic acid, vinyl chloride, and octanol. The Chisso Minamata factory first started the production of acetaldehyde, a material used for production of plastics and other plasticizers, in 1932.
How did this company take countermeasures against the outbreak of MPM? In September 1958, Chisso changed the discharge system for plant effluents from the acetaldehyde manufacturing process. Before this change, effluents were discharged directly into the Hyakken Port in Minamata Bay (Fig. 2.1b). In this system, effluents were stored in the Hachiman Pool prior to discharge of the supernatant to the mouth of Minamata River. However, this new system resulted in the expansion of the onset area of MPM to the north of the river mouth in March 1959 and thereafter. In October 1959, the Ministry of International Trade and Industry (MITI) instructed the factory to remove the new drainage channel, and then in the next month discharging from the Hachiman Pool to the mouth of Minamata River stopped. Instead of this, the factory constructed a “wastewater purifying facility” in December 1959; thereafter wastewater was channeled into the Hyakken Port again after the treatment by this facility. This apparatus in this facility, however, has a function to neutralize acids and to remove suspended solids, but has no function to remove organic mercury compounds. Chisso publicized this as “complete purification of wastewater,” and then many organizations including the research members of KU accepted this claim as true, resulting in the ending of investigations. Residents resumed eating fish again.
Later, the director of the Chisso Minamata factory, Eiichi Nishida, testified that the change of the discharge system aimed to dilute the wastewater by seawater in Shiranui Sea and that regarding this matter they continued to communicate with MITI (Miyazawa 1997). This evidence indicates that not only Chisso but also MITI recognized the toxicity of the wastewater discharged from the factory.
Kanji Irie, a managing director of Chisso, recorded a note regarding interviews with Hajime Hosokawa, a director of Chisso Hospital, which was confiscated by public prosecutors and later used for the criminal trial of the events leading to MPM (Miyazawa 2011). According to this, Dr. Hosokawa noticed that consumption of local fish by residents caused MPM by summer 1957. He suspected wastewater discharged from the plant as the cause of MPM; therefore, he proposed to the factory director to examine the relationship between the disease and wastewater. On July 21, 1959, Hosokawa started an experiment to give wastewater to two cats from his own will, and then he found that one of the cats (called as No. 400 cat) developed the symptoms on October 6. He reported this result to managers of Chisso Minamata factory and insisted to continue this experiment; however, they ordered to stop the experiment. Hosokawa resumed the experiment after August 1960 and then confirmed the development of the symptoms on cats again. On the other hand, in 1961, an engineer of the factory, Shun’ichi Ishihara, detected methylmercury from a drain in the plant and reported it to the managers; however, they did not reveal these results to the public.
In August 1959, Chisso asserted that as “The organic mercury theory of KU is speculation without definitive proof, and it is irrational in view of chemistry common sense” at a Special MPM Committee meeting of the Kumamoto prefectural assembly. In addition to this, Chisso introduced other hypotheses proposed by Takeji Oshima of the Japan Chemical Industry Association, Raisaku Kiyoura of Tokyo Institute of Technology, and Kikuji Tokita of Toho University who insisted the consumption of fish polluted by abandoned explosive or decayed fish as the cause of the disease without significant data. As shown by these events, a hostility developed between KU and Chisso resulting in lack of trust and integrity. The noncooperative attitude of the Chisso managers delayed the conclusion of the causative agent by the researchers of KU by 1962.
On November 25, 1959, the mutual aid society of patients (MAS) demanded compensation from Chisso. At the beginning, Chisso neglected the request, asserting as “There is no clear link between the mercury contamination and the factory wastewater.” In December 1959, with mediation by the Kumamoto Prefecture governor and Minamata City mayor, MAS was persuaded to sign the “Mimai-kin (consolatory present of money)” agreements, in which Chisso paid lump sum compensation of ¥300,000 ($833 at that time) for each dead patient and an annual stipend for surviving patient (¥100,000 for an adult and ¥30,000 for a child). Even in contemporary terms, the sums awarded were extremely low. The agreements included the sentence “Even if it shall be revealed in the future that wastewater discharged from the factory causes MPM, no further demands for compensation will be made.”
From these results, I must say that Chisso was trying to hide the truth and to reduce compensation to victims as much as possible and that they continued to produce acetaldehyde accompanied by wastewater containing methylmercury until 1968 when a new plant of the acetaldehyde production without using mercury started to produce at another factory of Chisso, even though they knew the fact that their own wastewater had caused MPM.
2.7 Counterclaims of Chisso
Although we continue to use mercury as a catalyst in the plant for acetaldehyde production since 1932, why did an important number of MPM patients first occur in 1954?
There are many factories producing acetaldehyde not only in Japan but also all over the world; nevertheless, why did only Minamata factory cause MPM?
We are using inorganic mercury. There is no information that inorganic mercury changes to organic mercury compounds in plants as well as in natural conditions.
I will explain why these counterclaims by Chisso were wrong in the latter half of this lecture.
2.8 A Book Written by Nishimura and Okamoto (2001)
During the preparation for the lectures in Kyoto University, I came across a book written by Nishimura and Okamoto (2001). The first author, Hajime Nishimura, covers broad areas including not only his major, industrial chemistry and process engineering, but also gene technology, environmental sciences, and social sciences. The second author of that book, Tatsuaki Okamoto, was familiar with the circumstances of Chisso from 1957 to 1990 as an employee of Chisso. He described his opinion in the book, “I could not stand on the side of managers of Chisso who care nothing for anybody. I have chosen to voice my concerns as a member of the labor union of Chisso together with the patients of MPM.”
That book attempted to answer the question why did MPM occur by examining the flow of the causative agent, methylmercury, quantitatively in the process from the acetaldehyde production in the factory through coastal environments including water, sediment, and marine organisms and finally to residents throughout the period of the disease outbreak. At that time, quantitative information on methylmercury in the production processes and in the coastal ecosystem was limited. Under such circumstances, the book showed several hypotheses. Some predictable expressions may be used, but it should be permitted in such a general book, whereas a few researchers have criticized this book severely by saying that this book includes some erroneous hypotheses (Suzuki 2007, Miyazawa 2010). However, I considered that this book played an important role in clarifying the underlying causes of MPM even if some hypotheses in light of new findings need revision; therefore, I decided to introduce this book in my lecture.
I will explain how methylmercury was produced in the acetaldehyde production plant of the factory and in coastal waters and how the local residents suffered from MPM mainly based on this book.
2.9 Chemical Reaction in Acetaldehyde Production Process
2.10 Relationship Between the Methylmercury Emission and the MPM Outbreak
After World War II, the demand for octanol had increased, because this was one of the basic materials used in the chemical industry. At that time, octanol produced by Chisso accounted for 85% of the market share in Japan. Acetaldehyde was a fundamental material for producing octanol. After the commencement of acetaldehyde production by Chisso Minamata factory in 1932, the production of acetaldehyde increased rapidly after the mid-1950s and attained the maximum production of 45,245 tons in 1960. In 1962, the production decreased to 26,500 tons due to labor troubles; however, in 1963, the production increased again to 38,500 tons. After 1964, the production decreased. In May 1968, the production was finished, because another factory of Chisso began to produce acetaldehyde using a different method.
Nishimura and Okamoto (2001) estimated the amounts of methylmercury emission and inflow into the coastal sea from the Chisso Minamata factory in each year using the techniques of chemical process engineering. There was a time lag in increasing and decreasing patterns between the acetaldehyde production and methylmercury emission (Fig. 2.5). In 1951, the methylmercury emission increased abruptly from 4.5 kg in the preceding year to 23.3 kg, all of which were considered to flow into the sea, in spite of the lack of a rapid increase in the acetaldehyde production. Nishimura and Okamoto (2001) pointed out three reasons for this rapid increase.
Irukayama et al. (1967a) introduced data of wastewater discharged from the acetaldehyde production plant as (1) the amount of wastewater, which contained 10–20 ppm of mercury, increased from 2 m3 h−1 in 1952 to 6 m3 h−1 in 1959 (Fig. 2.6); and (2) when the plant was cleaned four times a year, 30 m3 h−1 of washing water was discharged. The data were provided by the Minamata plant in 1959, indicating that they had recognized the discharge of a large amount of mercury from their own factory.
The estimated annual methylmercury emission peaked in 1959, accounting for 114 kg (Fig. 2.5). In this year, the factory did not discharge wastewater for 2 months; therefore, the outflow of methylmercury was estimated to be 95 kg. In 1960, the factory constructed a circulation system in the rectifying column drain to avoid discharging mercury to the sea. This construction was considered to reduce 75% of methylmercury outflow, contributing to the rapid decrease in the outflow, and then finally the outflow was finished in May 1968. The total amount of methylmercury that flowed into the sea from the factory was estimated to be approximately 640 kg. On the other hand, the total amount of mercury that flowed into the sea was estimated to be approximately 82 tons (Silver et al. 1994).
The exact number of MPM patients is unclear; however, we can trace the trend of this disease based on the number of the three kinds of patients in each year. One is the typical type of MPM patients which had been certified by the local governments by July 1970 as having most of the characteristic symptoms (i.e., paresthesia, visual field constriction, ataxia, impaired hearing and speech impairment, etc.). The second is the atypical MPM patients who had been recognized by the KU medical team, as having a limited number of the characteristic symptoms, at the time of mass examinations conducted in 1971 and 1972. The third is the congenital MPM patients who were certified by 2000. A patient of the typical MPM was recognized first in 1953.
2.11 Analysis of Umbilical Cords as an Indicator of Methylmercury Effects
Japanese people have a custom to preserve dried umbilical cords of newborns as a birth commemoration. Nishigaki and Harada (1975) and Harada et al. (1977, 1999) analyzed methylmercury concentrations in umbilical cords of babies who were born in the Minamata area (mainly Minamata City, Izumi City, and Tsunagi Town) during the period from 1935 to 1971 and found that (1) methylmercury concentrations in umbilical cords of babies born in the MPM-prone area were significantly higher than the value obtained from a reference cite (Tokyo, 0.11 ± 0.03 ppm); (2) methylmercury concentrations in umbilical cords of congenital MPM patients (1.6 ± 1.0 ppm) were significantly higher in comparison with those of acquired MPM patients (0.72 ± 0.65 ppm), mental retardation (0.74 ± 0.64 ppm), other diseases (0.22 ± 0.15 ppm), and no symptoms (0.28 ± 0.20 ppm); and (3) methylmercury concentrations attained the highest levels during the period from 1954 to 1964 when a large amount of acetaldehyde was produced. Akagi et al. (1998) estimated a daily mercury intake by mothers who gave birth to congenital MPM babies to be 225 μg which was 4–5 times higher than the current limit of mercury exposure. They also estimated methylmercury concentrations in cord blood and maternal hair of fully developed congenital or infantile MPM patients to be 20–699 μg L−1 (median, 216 μg L−1) and 3.8–133 μg g−1 (median, 41 μg g−1), respectively.
2.12 Concentrations of Mercury in Aquatic Organisms
I estimated the relationship between the production and inflow of methylmercury and the outbreak of MPM in the Minamata area. These two components can be explained thoroughly by revealing the bioaccumulation of methylmercury in aquatic organisms.
Since 1958, intensive surveys had been carried out to determine mercury concentrations in marine organisms collected from Minamata Bay and the Shiranui Sea (Fishery Research Institute 1960, Kitamura et al. 1960b, Chisso Co. 1961, Kumamoto University 1961, Seikai Regional Fisheries Research Laboratory 1964, Irukayama et al. 1967b, 1972). When evaluating the effects of mercury on the environments, we should analyze methylmercury compounds as target toxic substances. In the 1950s and early 1960s, however, the method to analyze methylmercury had not been established yet. At the early stage of the investigation, the arc light emission line spectrum analysis was used for the detection of total mercury. In this method, concentrations were estimated by the strength of the emission line. Thereafter, the colorimetric method using dithizone was used for the quantification of organic and total mercury. Presently, gas chromatography (GC) with detection by electron capture detector (ECD) is the most widely used technique for the determination of organic mercury species.
Jernelöv and Lann (1973) showed approximate proportions of methylmercury to total mercury of components of freshwater and estuarine ecosystems as <1% for water, 1–10% for sediments, and 90–99% for biota. Kannan et al. (1998) found <0.003–52% for water, 0.77% for sediments, and 83% for fish muscle in estuarine waters in the Florida peninsula. It has been also reported that methylmercury accounts for the majority of total mercury in fish, regardless of the level of contamination found within the environment (Silver et al. 1994, Mason et al. 2000, Bowles et al. 2001, Ikingura and Akagi 2003, Maršálek et al. 2006, Amlund et al. 2007, Magalhães et al. 2007), implying that we can evaluate the toxicity of marine animals using values of total mercury. Inorganic divalent mercury and organic mercury compounds are absorbed through gills, intestine, or skin, distributed through bloodstreams and accumulated in the liver; thereafter, the former is excreted through the kidney, and organs like muscles and brain are only affected to a small extent, whereas the latter is not rapidly excreted and subsequently it accumulates in muscle and brain (Jernelöv and Lann 1971). The lipophilic nature, affinity for the sulfhydryl groups of certain proteins, and long biological half-life (e.g., 2 years in fish) of methylmercury lead to a rapid accumulation in organisms (Jernelöv and Lann 1971, Magalhães et al. 2007).
Regarding benthic/sedentary species that live in/on seabed or in bottom layers, extremely high levels of mercury were found in benthic/sedentary three species, Acanthopagrus schlegelii (Japanese name, Kurodai; maximum value, 117.5 ppm; sampling site, off Hachiman, data source, Irukayama et al. 1972), Hormomya mutabilis (Hibarigaimodoki, 111 ppm, unpublished data of Chisso Co., after Nishimura and Okamoto 2001), and Ruditapes philippinarum (Asari, 100 ppm, the mouth of Minamata River, Kitamura et al. 1960b). The former species, the black seabream, is a sedentary carnivorous fish. Relatively high levels of mercury were found also in other sedentary carnivorous fish, Terapon jarbua (Kotohiki, 64.3 ppm, Minamata Bay; Chisso Co. 1961), Pennahia argentata (Shiroguchi, 59.2 ppm, the Shiranui Sea, Kitamura et al. 1960b), Apogon sp. (Tenjikudai, 47.5 ppm, mouth of Minamata River, Kitamura et al. 1960b), and Lateolabrax japonicus (Suzuki, 41.5 ppm, mouth of Minamata River, Kitamura et al. 1960b). Such high levels of mercury are estimated to have resulted from the bioaccumulation through food chains.
Among the three species showing extremely high concentrations of mercury, H. mutabilis and R. philippinarum are suspension feeding bivalves, which consume phytoplankton, indicating intense bioaccumulation occurred even in animals belonging to the trophic level 2 (primary consumers, see Fig. 2.11). These findings mean that intense bioaccumulation occurred between water and phytoplankton or that mercury was directly incorporated into bivalve tissues. The mercury concentration in plankton at that time is unclear, excepting for two case studies. Kitamura et al. (1960b) noted 5–6 ppm (wet weight basis) in the inner part of Minamata Bay. The other case was conducted by Fisheries Research Institute (1960), indicating that 289 ppm of mercury was accumulated in the green alga Dunaliella sp. during 12 days of culture in water containing 0.1 ppm mercury. These results suggest that phytoplankton has a large ability to accumulate mercury into cells or to adsorb mercury onto the surface of cells even if mercury concentrations are extremely low.
Regarding the mercury concentrations of pelagic animals that live in the middle and/or surface layers, piscivorous fish, Sphyraena sp. (Kamasu), showed a high value, 58.3 ppm (Kumamoto University 1961: Fig. 2.11). Such piscivorous fish, which belong to the trophic level 4 (tertiary consumers), feed on other fish belonging to the trophic level 2 or 3, probably resulting in high levels of the mercury concentration through the food chain. Planktivorous suspension feeder, Engraulis japonicus (Katakuchi-iwashi), which constitutes one of key fish species in the food web in Japanese coastal waters, is also distributed densely in the Minamata area. Most cats living in fishing villages along the coasts of Shiranui Sea became MPM probably due to eating this species extensively. A maximum concentration of mercury for this species was 21.9 ppm (Chisso Co. 1961), which was similar to the values obtained for Scomberomorus niphonius (Sawara, 21.8 ppm, the mouth of the Minamata River, Kitamura et al. 1960b) and Trichiurus lepturus (Tachiuwo, 18.8 ppm, Tsunagi, Kitamura et al. 1960b). Considering that these species have a pelagic life and large moving ability, these fish contaminated by mercury potentially played a large role in the dispersal of the mercury pollution.
2.13 Bioindicators of Mercury Pollution
On the other hand, P. argentata collected from the area close to Amakusa Islands (Fig. 2.1) accumulated higher concentrations of mercury (Fig. 2.14) irrespective of the low levels of mercury in the sediment and of being distant from the pollution source, that is, Chisso Minamata factory, suggesting that the fish incorporated methylmercury from seawater directly or from food items, i.e., plankton that had accumulated and/or adsorbed methylmercury from seawater (Nishimura and Okamoto 2001).
2.14 Accumulation Pathways of Methylmercury in Aquatic Organisms
There are arguments about the pathways by which methylmercury is accumulated in aquatic organisms, that is, whether the animals incorporate methylmercury directly from water through the gills or from components of the food chain. Higher concentrations of mercury with increasing trophic level have often been found, suggesting that the bioaccumulation of methylmercury occurs through food chains (Mason et al. 2000, Bowles et al. 2001, Ikingura and Akagi 2003, Magalhães et al. 2007). Several dietary exposure studies also have shown that fish readily accumulate methylmercury, mainly in the muscle (Amlund et al. 2007). Hall et al. (1997) indicated that the freshwater fish (Phoxinus neogaeus) concentrated methylmercury mainly through the diet, while water contributed, at most, 15% of the mercury to fish at natural levels of methylmercury. Lawson and Mason (1998) confirmed the transfer of methylmercury from seawater to an experimental food chain which constituted of phytoplankton (Thalassiosira weissflogii), copepod (Eurytemora affinis), and sheepshead minnow (Cyprinodon variegatus). They also showed that a benthic amphipod Hyalella azteca was able to incorporate methylmercury from decayed phytoplankton. Bowles et al. (2001) showed that the greatest bioaccumulation of methylmercury occurred between seston (plankton) and the water column (bioaccumulation = 105.36) in a tropical lake; then methylmercury was biomagnified through a plankton-based food chain comprising of four trophic levels (phytoplankton, zooplankton, planktivore, piscivore). Bioenergetic models for methylmercury accumulation in walleye and yellow perch also suggested that food is the overwhelming (99%) uptake pathway at a water methylmercury concentration of 0.05 μg m−3; however, as the water methylmercury concentration increased to 0.3 μg m−3, the food pathway decreased to 90% (Harris and Snodgrass 1993). Wang and Wong (2003) showed that 56–95% of methylmercury in ingested prey was retained in a marine predatory fish 1 day after digesting. These studies indicated that methylmercury is assimilated and retained by fish from dietary sources.
On the other hand, there are several studies which suggested the importance of direct uptake from water through the gills. Jernelöv and Lann (1971) suggested that for bottom-feeding freshwater fish, >75% of methylmercury, and even in predatory fish (pike), 60% of methylmercury was taken up directly through the gills. Rodgers and Beamish (1981) found that the methylmercury uptake rate of rainbow trout was positively correlated with both oxygen consumption and methylmercury concentration and that the percent utilization of methylmercury from water was ~8%, assuming an oxygen percent utilization of 33%. A similar value (10%) was found also by Phillips and Buhler (1978). At the same time, they showed 68% of methylmercury ingested was assimilated by rainbow trout as well, suggesting that food and water both are important pathways of methylmercury accumulation.
Laboratory rearing experiments of Japanese littleneck, Ruditapes philippinarum, showed that the clams accumulated organic mercury from water containing alkyl mercury (0.2–0.3 ppm) into their bodies (40–129 ppm dry wt basis) during 4–14 days (Irukayama et al. 1962b), suggesting that the clams incorporated organic mercury directly from water. Chloride ions may enhance uptake of methylmercury from water by forming membrane permeable methylmercury complexes (Boudou et al. 1983).
Uptake rate of methylmercury by fish = 1260 mg O2 kg−1 h−1 × (10 ng L−1/10 mg L−1),
where 1260 mg O2 kg−1 h−1 is the oxygen uptake rate by fish, 10 ng L−1 is the concentration of methylmercury in seawater, and 10 mg L−1 is the concentration of oxygen in seawater.
Values obtained from stations close to Amakusa Islands in the Shiranui Sea showed relatively high mercury concentrations, suggesting the expansion of methylmercury over a large area. It is considered that methylmercury was incorporated into anchovy, which were preyed on by carnivorous fish through the predator-prey relationship, and then methylmercury settled onto the seabed after the death of fish. Considering the results in the previous studies and the temporal and spatial pattern of the methylmercury concentrations in fish found in the MPM-prone area, direct uptake by fish in this area was possible. There are no practical observations which show the direct incorporation of methylmercury from water by Japanese anchovies under the condition of the methylmercury uptake rate that is the same as or similar to the oxygen uptake rate. Due to the lack of evidence, the hypothesis of the direct methylmercury incorporation presented by Nishimura and Okamoto (2001) has been criticized severely by a few researchers (Suzuki 2007; Miyazawa 2010). Further studies should be conducted to prove this hypothesis.
I summarize the flow of mercury from the Chisso Minamata factory to the coastal waters and then finally to residents mainly based on findings obtained so far (Fig. 2.17). Methylmercury compounds produced as by-products in the acetaldehyde production plant were discharged into coastal waters. Part of methylmercury might be incorporated into pelagic fish through the gills. Such fish were fed on by carnivorous fish. Part of methylmercury was incorporated into phytoplankton and might have been bioaccumulated through food chains. After the death of plankton and aquatic organisms, they settled onto the bottom, and then they were incorporated into benthic animals. Part of methylmercury might have been deposited directly to the seabed. Inorganic mercury flowing into coastal areas was accumulated in sediments and was transformed to methylmercury due to bacterial activities, a process which might be accelerated under organic pollution. Methylmercury was incorporated into benthic animals and then moved to demersal fish. By eating these polluted fishery products, people became MPM.
2.15 Disapproval of Chisso’s Counterclaims
As described earlier, Chisso had repeated claims that they were not responsible based on three viewpoints.
Chisso changed the promoter from manganese dioxide to iron sulfate and nitric acid in 1951. As a result, the production of methylmercury had increased rapidly.
Chisso added seawater to industrial water since 1955, resulting in high concentrations of chloride ions in the reaction vessel, which promoted evaporation and accumulation of methylmercury in a drain of the rectifying column.
Chisso used pyrite cinders as an alternative to iron sulfate to reduce costs since 1951, which disturbed the continuous running of the system, resulting in the discharge of a large amount of mother liquor, which contained methylmercury.
Chisso discharged a large amount of effluents into the sea.
MPM first occurred in 1941.
Showa Denko also caused methylmercury poisoning in Niigata Prefecture.
Methylmercury poisoning occurred in other localities in the world (e.g., China in the 1970s, the Amazon basin in the 1990s, Ontario in Canada, Mindanao in the Philippines).
Industrial water in Chisso Minamata factory included a lot of chloride ions due to poor management of wastewater.
It was widely known that methylmercury was generated in acetaldehyde production plants using acetylene and inorganic mercury as the material and catalyst, respectively. According to Iriguchi (2012, 2014) and Ishihara (2014), the generation of organic mercury in this process had been suggested by Hofmann and Sand (1900), Nieuwland and Maguire (1906), Whitmore (1921), and Vogt and Nieuwland (1921) repeatedly. For example, Vogt and Nieuwland (1921) showed chemical formulae in the acetaldehyde production which had been employed commercially (Fig. 2.16). Nishimura and Okamoto (2001) pointed out that these formulae contained wrong intermediates; however, it is notable that Vogt and Nieuwland (1921) had suggested the generation of methylmercury before the start of acetaldehyde production in Minamata. The abstracts of Nieuwland and Maguire (1906) and Vogt and Nieuwland (1921) were introduced in the journals Tokyo Kagaku Kaishi (later, Nippon Kagaku Kaishi) in 1906 and The Journal of the Society of Chemical Industry, Japan, in 1922, respectively, in Japanese. Ochi and Onozawa (1920) also reported the same chemical reaction in 1920. A chemical company in Germany, Wacker Chemie/Consortium, started the production of acetaldehyde using acetylene as raw material and mercury as a catalyst in 1916 for the first time in the world. Within the same year, workers who came into contact with the sludge discharged from the plant developed central nervous system disorders. According to the suggestion of Professor Heinrich Zangger of the University of Zürich, the factory disposed the sludge and wastewater underground avoiding underground aquifers, thereby limiting exposures to mercury and development of nervous system disorders. Later, Zangger (1930) concluded that this disorder was caused by organic mercury poisoning in a result of reference to Edwards (1865, 1866), Hepp (1887), Hofmann and Sand (1900), Nieuwland and Maguire (1906), and Whitmore (1921) (after Iriguchi, 2014). In addition to this, by 1932 when Chisso started to produce acetaldehyde, it was in the public domain that methylmercury was able to cause the serious poisoning to the central nervous system of human beings as shown by the accident which occurred in 1865 at Saint Bartholomew’s Hospital. This information had been introduced to Japan through a paper written by Hepp (1887) and the journal Chemical News at least by 1927.
It had been proved that methylmercury could be generated from inorganic mercury in natural environments.
Chisso obtained the information that methylmercury had been detected from a drain in the plant in 1961.
2.16 Government’s Consensus Opinion
While effective measures by the national and local governments were not taken, methylmercury spread to another locality. On May 31, 1965, Niigata University reported to the Niigata Prefectural Public Health Department that “There have been sporadic cases of mercury poisoning from an unknown source in the lower Agano river.” In June 1967, patients in Niigata Prefecture sued Showa Denko as the pollution source of Niigata MPM and sought a compensation claim in the Niigata District Court.
On September 26, 1968, the MHW and the Science and Technology Agency announced the consensus opinion of the government that “Minamata disease” in Kumamoto Prefecture was caused by a methylmercury compound generated by the acetaldehyde and acetic acid manufacturing facilities at the Chisso Minamata factory (Ministry of the Environment, Japan 2013). Niigata methylmercury poisoning was recognized at the same time. Twelve years had passed since the official acknowledgment in 1956. How should we interpret these environmental perturbations?
The number of the patients who had been recognized officially before January 1970 was 121, among which 98 patients comprised of adults and children who had eaten fish and shellfish polluted by methylmercury, while 23 were congenital MPM patients (Harada 1972). However, these patients were included in the typical type of MPM, and this was only the tip of the iceberg in the total number of MPM patients.
The exact total number of the dead caused by methylmercury poisoning is not clear. On August 29, 1956, Dr. Hosokawa of Chisso Hospital reported to the Ministry of Health and Welfare that 11 persons had died among 30 patients within a month (Harada 1972). It was also reported that this disease caused death of 17 of 54 patients during the period of the initial stage of the outbreak (December 1953 to December 1956) (Minamata City 2007). These results indicate that the mortality rate was high, attaining ~30%. Harada and Tajiri (2009) reported that 17 of 188 newborns in the disease-prone area in Minamata City during the period from 1955 to 1958 were diagnosed as having congenital MPM.
The number of certified patients recognized by the “Law Concerning Compensation and Prevention of Pollution-Related Health Damage” by January/February 2016 was 3017 including 1787 in Kumamoto Prefecture, 493 in Kagoshima Prefecture, and 704 in Niigata Prefecture (Takamine 2016). Figure 2.1 shows residential areas of the certified patients, extending over a 60 km-long and 25 km-wide area surrounding Shiranui Sea in Kumamoto and Kagoshima Prefectures and over a 50 km-long area along the Agano River in Niigata Prefecture. Among the certified patients, ~70 persons were born having congenital MPM (Harada and Yorifuji 2009) in Kumamoto and Kagoshima prefectures. In Niigata Prefecture, only one person was born as having congenital methylmercury poisoning. At that time, most of pregnant women aborted, or birth control was recommended by the local government to women of childbearing age who lived in the polluted area and who had hair mercury concentrations of 50 ppm or higher.
In the 1950s, fisheries were one of the major industries in coastal areas around the Shiranui Bay. However, due to the outbreak of MPM, fishermen had been compelled to stop fisheries. The Fishermen’s Cooperative in Minamata City (FCM) placed self-imposed restrictions on harvests in Minamata Bay since August 1957. In July 1959, the Minamata City Fresh Seafood Retailers Union determined not to buy any fish and shellfish captured from the coastal area around Minamata.
It was recognized that the outbreak of MPM drew to a close after 1960 owing to FCM’s self-imposed restrictions on fishing and to the construction of a sedimentary pool and effluent-treatment device. In April 1962, FCM lifted the voluntary restrictions on fishing partially, and in May 1964, FCM completely abolished all restrictions. In May 1973, however, they enforced restrictions again according to the announcement by KU, “The fish and shellfish of Minamata Bay and surrounding areas are still unsafe.” The FCM did not carry out harvesting operations in the bay from 1975 to 1992.
2.18 Compensation and Environmental Restructure
The damage caused by methylmercury discharged from the responsible companies includes (i) health damage to individual persons, (ii) environmental pollution including the toxification of fish/shellfish, and (iii) psychological distress in the local community due to discrimination of the victims and conflicts among local residents (Ministry of the Environment, Japan 2013).
In the late 1950s, residents who suffered from methylmercury poisoning established the mutual aid society of patients (MAS), and then MAS started to negotiate for compensation with Chisso. In April 1969, MAS split into two groups, those who would lodge the pledge and request mediation by the government in settling the matter (the mediation faction) and those who would negotiate directly with Chisso but later took their claims to court (later referred to as the litigation faction).
Based on the newly established law, the “Law Concerning Special Measures for the Relief of Pollution-Related Health Damage,” the certification system started in December 1969. In this system, applicants who wanted to be certified as a methylmercury poisoning patient were subject to medical examination by the prefecture, followed by medical review by the certification council; then the prefectural governor determined whether or not a person suffers from methylmercury poisoning. Among the applicants, however, only a limited number of persons have been certified. Persons who were not certified as methylmercury poisoning patients or belonged to the litigation faction sued responsible companies and national and local governments successively mainly between the late 1960s and the 1990s. These suits had been reported widely by the mass media, making it a subject of social concern. The national government decided to settle the problems politically in 1995, and 11,152 persons accepted compensation, while in 2009 the “Act on Special Measures Concerning Relief for Victims of Minamata disease and Solution to the Problem of Minamata disease” was enacted; then based on this law, 32,244 persons accepted compensation. It is said that more than 100,000 people, approximately half of the population in the Minamata area, had health issues due to methylmercury discharged from Chisso; however, these persons have not been granted compensation yet.
In 1959, fishermen in Minamata City and in the coastal area of the Shiranui Sea who had not been able to continue fisheries demanded to Chisso for (i) compensation to the fishing industry, (ii) complete removal of sedimentary sludge, and (iii) installation of an effluent-processing device. After the first and second fishermen’s disputes (large-scale demonstrations associated with violence), fishermen won the compensation from Chisso. Chisso also paid compensation money to the fishermen’s cooperative association, because the fishermen were compelled to stop fisheries by 1997.
Even though the discharge of the methylmercury compound was stopped in May 1968 by the Chisso Minamata factory and in May 1965 for the Kanose factory of Showa Denko, it was necessary to remove the polluted sediments close to the discharge point. From 1977 to 1990, Kumamoto prefectural government (KP) reclaimed 58 ha of the inner part of Minamata Bay where the seabed was heavily contaminated by mercury using sediments (1.5 × 106 m3) dredged from the outside of this area (151 ha) where the mercury concentrations were above the provisional reference value for removal (25 ppm). The cost was paid by Chisso, the national government, and KP. Nowadays the reclaimed land is maintained as a park. In Niigata Prefecture, in 1976, Showa Denko paid the costs of dredging mercury-containing sediments from locations near the factory wastewater drain outlet.
In 1974, KP installed dividing nets to contain polluted fish inside Minamata Bay. In 1997, the governor of KP declared that fishery products collected from Minamata Bay were safe based on the fact that the mercury levels for seven species of fish were below the provisional control values (mercury <0.4 ppm, methylmercury <0.3 ppm) for three consecutive years, and then the dividing nets were removed.
2.19 Court Ruling
When chemical factories drain wastewater, they have to carry out detailed surveys in order to evaluate whether wastewater contains substances that are possible to endanger lives and health of humans and animals or not. Regarding discharge of effluents, the factories must use highest levels of information, technology, literature surveys, environmental monitoring, and safety verification.
If wastewater is revealed to contain harmful substances or if there is any suspicion about it, chemical factories have to prevent pollution beforehand as possible as they can, using measures such as halting the operation of the plant immediately. Especially, chemical factories have a duty to protect from harm the life and health of local residents beforehand.
If Chisso discharged their duty, they could predict the risk of wastewater to humans successfully and never triggered MPM or expanded this disease over wide areas. Chisso, however, did not perform appropriate countermeasures in all aspects including environmental monitoring, fishery compensation, investigation on the cause of MPM, and treatment of wastewater.
The “Mimai-kin agreements” should be avoided. The agreements took advantage of the victims’ ignorance and poverty to deprive them of a legitimate right to claim further damages in exchange for a low amount of compensation. The agreements should be deemed invalid, because these are offensive to public order and morals.
Pollution disasters are usually caused by companies irrespective of residents’ will.
Residents scarcely escape from pollution disasters, and in most cases, no blame is imputable to them.
Pollution disasters often have an influence on an unspecified large number of residents inhabiting over a large area, resulting in having serious adverse impacts on the society.
Residents living in the same environment suffer similar damage although to varying degrees. Within a family, it is not rare that all or most of the members are affected, resulting in ruin on the entire family.
Companies aim to make profit by manufacturing activities which may produce pollution, whereas such activities never bring benefits to residents directly.
On February 29, 1988, the Supreme Court sentenced the former president of Chisso, Kiichi Yoshioka, and the former director of Minamata factory, Eiichi Nishida, of being guilty, that is, 2 years of imprisonment but with probation of 3 years for their crimes as causing death or injury through negligence in the pursuit of social activities. These were the criminal penalty to Chisso. It can be said that Chisso succeeded in lessening charges which they deserved.
On October 15, 2004, the Supreme Court handed down its ruling on the lawsuit which had been brought by patients who had moved from the Minamata area to the Kansai district. The ruling found the national government and KP jointly liable for the payment of the compensation in view of their failure to prevent the outbreak and spread of MPM. However, nobody was accused of any criminal charges.
2.20 Assignment to Students
- 1.Lack of information/experience
Unknown cause of the disease at the initial stage of the outbreak
- 2.Physical and biological aspects
Migration of contaminated marine organisms and movement of polluted water by current
Polluted water and bioaccumulation in aquatic products
- 3.Lacking responsibility of the causative company, Chisso
Facts being hidden by Chisso
Chisso’s dishonest initial reaction and long period (12 years) to admit responsibility
Ethical misconduct by Chisso
Change of the promoter, rapid increase of the acetaldehyde production, change of the discharge point, and insufficient purification apparatus constructed by Chisso
- 4.Neglecting obligations by the governments
Slow response to the pollution, neglect in preventing the disease, and the failure to institute a compulsory ban on fishing
- 5.Social background
Pursuit of economic interests by the enterprises, government, and individuals
Ordinary citizens’ reaction: consideration for the economically “contributing” company, Chisso, and treating the patients like nuisances
In addition to these reasons, there was no organization to research MPM except Kumamoto University Medical School (KU). They were not always familiar with industrial chemistry, marine ecology, and environmental sciences. Chisso not only diffused to inform the production process as well as to provide materials for clarifying the disease cause to KU but also disrupt their research works. Researchers in other faculties like the engineering in KU were not included in the members of the study group of KU. Thus, they were ridden with limited information and resources.
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