Power point presentation APA Format 9-11 Slides on hazardous waste incidnet such as Minimata Bay

Trace Elements and Electrolytes, Vol. 31 - No. 2/2014 - Letter to the editor 86

Letter ©2014 Dustri-Verlag Dr. K. Feistle

ISSN 0946-2104

DO110.5414n"EX01331 e-pub: January 22. 2014

Reconsideration of Minamata disease

Nobuo Ishihara

The Kanagawa Health Sen/ice Association Naka-Ku, Yokotiama, Japan

First report of methylmercury intoxication

Sir, - Since 1958 it has been widely be- lieved in Japan that the first report of methyl- mercury intoxication was the report of Hunter et al. [1]. This understanding is based on the announcement issued in 1958 by the study group for Minamata disease at Kumamoto University. The study group summarized the symptoms under the name of Humter-Russel syndrome. The announcement indicated that the report of Hunter et al. [1] was the first report of methylmercury intoxication. To our regret, this announcement was incorrect.

In the report of Hunter et al. [1] they in- troduced clearly the reports of Edwards [2, 3], in which two lethal cases of occupational methylmercury intoxication occurred in 1864 in the laboratory of St. Bartholomew's Hospital in London. As the sequences of symptoms indicated the altogether excep- tionally poisonous nature of methylmercury. Dr. Phipson [4,5] introduced these two cases in ajournai named "Chemical News". These two lethal cases were also quoted precisely by Hepp [6] in his review about the toxic properties of mercury and mercurial's. These important reports [1, 4, 5, 6] were already referable in Japan far before the start of ac- etaldehyde production in Minamata plant (1932). Except the report of Hunter et al. [1] other reports have been ignored by scientists in Japan.

The reason why the study group in Ku- mamoto University decided the report of Hunter et al. [ 1 ] to be the first report of meth- ylmercury intoxication still remains unclear. It is possible that the study group examined only the citation of Hunter's report in a cer- tain monograph, and did not examine the original. Another consideration was pre- sented by Iriguchi [7]. The decision by the study group at Kumamoto University was

very convenient for the authorities (Ministry of Health and Welfare (MHW), Kumamoto Prefecture, Minamata city, the plant) and physicians patronized by stakeholders. They could point out that the start of acetaldehyde production in Minamata and the dumping of methylmercury into Minamata Bay was 8 years prior to the publication of the report of Hunter et al. [1], and they could make an excuse that Minamata disease was a new disease unknown in the medical world. This consideration is very thoughtful, and might be correct.

The misunderstanding about the first re- port of methylmercury intoxication should be corrected completely in textbooks and medical dictionaries as soon as possible.

Another doubt about the naming "Hunter- Russel Syndrome" is the number of authors. If the naming "Hunter-Russel Syndrome" was based on the report of Hunter et al. [1], the correct name should be "Hunter-Bomford- Russel Syndrome". But, this was not the case. This fact also indicates that the study group of the Kumamoto University made decision without examining the original of the report of Hunter et al. [1].

Organic mercury formation in the acetaldehyde production

In 1881, Kutscheroff [8] invented the procedure of acetaldehyde production from acetylene with inorganic mercury as cata- lyst in sulfuric acid solution. In 1900, Hoff- man and Sand [9] analyzed this reaction, and reported that inorganic mercury added as catalyst should be converted to organic mercury. Nieuwland and Maguire [10] also concluded the formation of organic mercxuy. The summary of this report was introduced in a Japanese journal in Japanese [II]. In 1916, Wacker-Chemie started acetaldehyde produc- tion from acetylene using inorganic mercury as catalyst in Burghausen (Germany) at large scale. In the end of the same year, intoxica- tion due to organic mercury occurred among workers in the factory [12, 13]. The formation of organic mercuiy from inorganic mercury added as catalyst became to be clear In 1921, Ochi and Onozawa [14] reported a similar re- sult. In 1921 it was reported that mercury did not remain long in the form of inorganic mer-

Trace Elements and Electrolytes, Vol. 31 - No. 2/2014 - Letters to the editor 87

cury, but was converted to an organic com- pound, and that this organic compound acted as catalyst [15, 16, 17].

These reports [9, 10, 11, 14, 15, 16, 17] were referable in Japan prior to the start of acetaldehyde production in the Minarnata plant and indicated clearly that the dangers were already common knowledge among professionals in the manufacturing of acet- aldehyde.

It should have been possible to warn or inform the authorities (governments, plant) prior to the start of the acetaldehyde produc- tion in 1932 in the Minamata plant. But this did not happen. Far before the outbreak of Minamata disease, the formation of organic mercury in the production of acetaldehyde and the toxic properties of organic mercury (methylmercury) were common knowledge and referable to physicians. But nobody was interested in such subjects.

This important information [5, 6, 9, 10, 11, 14, 15, 16, 17] has been neglected by scientists engaged in the study of Minamata disease. Most physicians did not know the process of acetaldehyde production. At the outbreak of Minamata disease most physi- cians were not interested in getting insight into the plant or learning about procedures of acetaldehyde production. These important reports, therefore, have been neglected.

It is clear that the indifference of physi- cians to his important information resulted in the allowance for the damping of wastes into the sea of Minarnata, and accelerated the out- break of Minamata disease. The responsibility of scientists and physicians for the outbreak of Minamata disease, therefore, is clear. Of course, the responsibility of authorities (MHW, Kumamoto Pref., Minamata City) is clear. In addition, several scientists under the patronage of stakeholders were busily engaged to deny the methylmercury theory. Their responsibility should be cross-examined.

Consideration of Minamata disease as food poisoning [18]

This consideration is still minor in Japan. Soon after the outbreak of Minamata disease, the uptake of polluted sea food was strongly suspected by Kitamura et al. [19] and Me Alp- ine and Araki [20]. At this point, the local gov-

ernment of Kumamoto Prefecture considered to apply the Food Sanitation Act. The local government had the authority to decide the application of this Act. The local government of Kumamoto Prefecture, however, asked the opinion of the MHW for the application of the Food Sanitation Act. The chief of the Public- Health Bureau of MHW replied in 1957 that it was impossible to apply the Act. The reason of this decision was that there was no clear evidence that all seafood in the area was poi- soned. In 1950 a serious food poisoning due to shellfish occurred in Hmanako Lake area (Shizuoka Prefecture). In this case, the local government of Shizuoka Prefecture decided quickly to apply the Food Sanitation Act with- out consulting the MHW. The reason for the local government of Kumamoto Prefecture might be the anxiety to commit the compen- sation process. Of course, the major (Kuma- moto city) was a former important member of the Chisso plant as one the main staffs.

This decision of Kumamoto Prefecture ac- celerated the environmental pollution by methylmercury and the occurrence of Mina- mata disease. It is clear that the authorities were not interested in the environmental pol- lution and its health effects. Many physicians and scientists engaged in chemical plants were not interested in the environmental pol- lution and its health effects.

As Minamata disease was evoked by the consumption of polluted seafood, physicians had to inform soon after the examination of patients. In Japan, a physician is requested to notify the case of food poisoning to the local government. In the case of Minamata disease, however, few physicians informed the local government about patients suffering fi-om Minamata disease due to food poisoning.

As pointed out by Iriguchi [21], we have to keep in mind that Minamata disease was not evoked by the Minamata area. The envi- ronmental pollution by methylmercury ñ̂ om the plant is the cause of Minamata disease.

Acknowledgment

The author is indebted to Professor Norio Iriguchi (Kumamoto University), Yoshihide Tsuda (Okayama University), and Jun'ichi Mizumoto (Kumamoto) for their valuable helps in collecting literatures.

Trace Elements and Electrolytes, Vol. 31 - No. 2/2014 - Letters to the editor

Reference

[ 1 ] Hunter D, Bomford RR, Rüssel DS. Poisoning by methylmercury compounds. Q J Med. 1940; 9: 193-213.

[2] Edwards GN. Two cases of poisoning by mercuric methide (= methylmercury). Saint Bartholomew's HospRep. 1865; / ; 141-144.

[3] Edwards GN. Note on the termination of the sec- ond case of poisoning by mercuric methide. Saint Bartholomew's Hop Rep. 1866; 2: 211-213.

[4] Phipson TL. The "Cosmos" and the poisoning by mercuric methide. Chemical News. 1865; 12: 289-290.

[5] Phispon TL. On the toxic properties of mercuric methide. Chemical News. 1866; 13: 47.

[6] Hepp P. Ueber Quecksilberaethylverbindungen und ueber das Verhaeltniss der Quecksilberaethyl- zur Quecksilbervergiftung. Archive fuer experi- mentelle Pathologie und Pharmakologie. 1887; 2i. 91-128.

[7] Iriguchi N. Minamata Bay 1932. Tokyo: Nippon Hyouronsha, 2012. p.l65.

[8] Kutscherojf M. Ueber eine neue Methode direkter Addition von Wasser (Hydratation) an die Koh- lenwasserstofFe der Acetylenereihe. Berichte der deutschen chemischen Gesellschaft. 1881; 14: 1540-1542.

[9] Hofmann KA, Sand J. Ueber das Verhalten von Mercurisalzen gegen Olefine. Berichte der deut- schen chemischen Gesellschaft. 1900; 33: 1340- 1353.

[10] Nieiiwland JA, Magiiire JA. Reaction of acetylene with acidified solution of mercury and silver salts. JAmChemSoc. 1906; 2«; 1025-1031.

[11] Iwasaki. Reaction of acetylene with acidified so- lution of mercury and silver salts, (summary of 11 in Japanese). Tokyo Kagaku Kaishi. 1906; 27: 1232-1233.

[12] Zangger H. Erfahrungen ueber Quecksilberver- giftungen. Gewerbepathol Gewerbehyg. 1930; 1: 539-560.

[13] Koelsch F. Gesundheitsschaedigungen durch or- ganische Quecksilberverbindungen. Gewerbapath Gewerbehyg. 1937; AV 113-116.

[14] Ochi S, Onozawa Y. On the acetylene production from acetylene [in Japanese]. Kogyo Kagaku Zasshi. 1920; 25.-935-954.

[15] Vogt R, Nieuwland JA. The role of mercury salts in the catalytic transformation of acetylene into acetoaldehyde, and a new commercial process for the manufacture of paraldehyde. J Am Chem Soc. 1921; 45. 2071-2081.

[16] Iki. The role of mercury salts in the catalytic trans- formation of acetylene into acetoaldehyde, and a new commercial process for the manufacture of paraldehyde. (summary of 15 in Japanese). Kou- gyou Kagaku Zasshi. 1922; 25: 980-981.

[17] Whitemore PC. Organic compounds of mercury. Am Chem Soc Monograph Series. New York: Chemical Catalogue Company, 1921. p. 26-37.

[18] Yorifuji T, Tsuda T, Harada M. Minamata disease: catastrophic food poisoning by methylmercury and challenges for the democracy and justis. In: Late Lessons from early warnings: science, pre- caution, innovation, ed by EEA, (European Envi- ronment Agency), Chapter 5, EU, Luxemburg, 2013

[ 19] Kitamiira S, Miyata C. Tomita M, Date S. Ueda K, Misumi H, Kojima T, Minamoto H, Kurimoto S, Noguchi Y, Nakagawa R. Results of epidemio- logical investigation on unknown disease affected central Nervous system, which ocured in Mina- mata area, [in Japanese]. Kumamoto Igaku Zasshi. 1957; 31 (Suppl 1): 1-9.

[20] McAlpine D, Araki S. Minamata disease: an un- usual neurological disorder caused by contami- nated fish. Lancet. 1958; 2: 629-631.

[21] Iriguchi N. Minamata Bay, 1932. Tokyo: Nihon Hyouronsha, 2012. pi72.

Correspondence to Nobuo Ishihara, MD, PhD 60-1-1405 Yamashita-cho, Nakaku, Yokohama 231-0023, Japan Tel./Fax:+81-45-212-3050

Copyright of Trace Elements & Electrolytes is the property of Dustri-Verlag Dr. Karl Feistle GmbH & Co., KG and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.