ES&T
LETTERS Minamata disease Dear Sir: I noted with interest the correspondence in your October issue between Messrs. Kurzel and Cetrulo and Mr. Laubusch concerning the potential teratogenic effects of mercury. While I do not wish to become involved in the main argument, some of the statements made by Kurzel and Cetrulo about the cause of Minamata disease shouldn't be allowed to go unchallenged. It is now firmly established that the initial outbreak of Minamata disease in Japan in 1956 was caused by the consumption of fish and shellfish containing substantial quantities of organic mercury compounds. Minamata Bay received effluent discharges containing both inorganic and organic mercury compounds; however, the evidence suggests that the transformation of inorganic mercury to organic mercury in the environment did not make a significant contribution to the concentration of organic mercury in the fish and shellfish. The Chisso production plant at Minamata City manufactured fertilizers, plastics, fibers, and a range of general chemicals such as acetic and nitric acids. Mercury was used as a catalyst in two processes: for the manufacture of acetaldehyde from 1932-1968 and for the production of vinyl chloride from 1941-1971. Irukayama et al. (/) report estimates by the factory management that the total losses of mercury to the aquatic environment from these operations were 81.3 tons and 0.2 tons respectively. Organic mercury compounds were formed as byproducts in both plants. It is difficult to assess accurately how much of the mercury was discharged in an organic form since the first measurements of organic mercury in the works effluent were not made until 1962 (Irukayama et al. (2)). However, the data obtained between 1966-1969 (Irukayama et al. (3)) indicates that about 20-40% of the mercury discharged was probably in an organic form, i.e., Minamata Bay would have received about 30 tons of organic mercury by direct discharge.
According to Jernelov (Lindberg et al. (4)) sedimentary transformation of inorganic to organic mercury occurs at annual rates of 0.01-10%. The rate of transformation in the sediments of Minamata Bay is not known. However, it must be considerably less than 10% since according to Fujiki and Tajima (5) the total mercury content of the bay sediments did not change significantly between 1963 and 1971. In addition, there is evidence from prolonged laboratory experiments to show that organic mercury could not be produced in detectable amounts from the bay sediments (Irukayama et al. (6)). Even if 10% of the inorganic mercury discharged was transformed in the environment, about 86% of the organic mercury present in the fish and shellfish would still be accounted for by the direct effluent discharge. Data on the mercury content of fish in Minamata Bay (Fujiki and Tajima (5)) provides further confirmation of the view that environmental transformation was insignificant in this situation. In 1966, the Chisso factory ceased the discharge of effluents from their acetaldehyde plant into Minamata Bay. Prior to this date the organic mercury content of fish in the bay was in the range of 10-20 mg/Kg. Since the total mercury content of the sediments, and presumably the environmental transformation rate, did not change, the only explanation for this reduction is that the high levels of organic mercury in fish were the direct result of the organic mercury content of the effluent discharge. In addition, the Japanese Ministry of Public Health and Welfare announced officially on Sept. 26, 1968, that the causative agent of Minamata disease was the methyl mercury compound contained in the waste from the acetaldehyde plant of the Minamata factory. Kurzel and Cetrulo also quote the work of Uchida et al. (7), which identified the toxic compound in the shellfish in Minamata Bay as methyl mercuric sulfide (CHs^HgS. However, this identification was shown in
1964 by Kondo (8) to be incorrect and it is now generally agreed (Irukayama et al. (/ )) that the toxic compound was a lower alkyl mercury halide of the form RHg X (R = CH 3 or C 2 H 5 ; X = CI, I, Br). I have not been able to check the statements with respect to the speciation of mercury in the water of Minamata Bay since neither of the references cited by the authors refers to this work. In conclusion, and at a variance with the statements made by Kurzel and Cetrulo, all the evidence now available points to the direct discharge of alkyl mercury halides from the Chisso factory being the causative agent of Minamata disease. D. Taylor Imperial Chemical Industries, Ltd. Brixham Laboratory Freshwater Quarry Overgang Brixham Devon TQ5 8BA U.K. References (1) Irukayama, K. et al. In "Minamata Disease"; Elsevier: New York, 1977; pp. 1-56. (2) Irukayama, K. et al. Jpn. J. Hyg. 1966, 22, 1258. (3) Irukayama, K. et al. Kumamoto IgK. Z. 1969, 43, 946. (4) Lindberg, S. E. et al. Estuarine Res. 1975, / , 64-108. (5) Fujiki, M.; Tajima, S. New Methods Environ. Chem. Toxicol. 1973, 217-229. (6) Irukayama, K. et al. Kumamoto IgK. Z. 1960, 34, 605. (7) Uchida, M. et al. Kumamoto Med. J. 1961, 14, 181-187. (8) Kondo, T. Yakugaku Zasshi, 1964, 84, 137.
Analytical method validation study Volunteer (unpaid) and subcontracting (paid) participants are needed to perform GC/MS analyses on priority pollutants as part of a validation study on EPA Methods 624 and 625. Method 624 is for 32 purgeable, organic priority pollutants; Method 625 is for 82 acid and base neutral organic priority pollutants. Interested parties should contact Mr. J. E. Henderson or Mr. D. H. Rodgers, Radian Corporation, P.O. Box 9948, Austin, Tex. 78766, (512) 454-4797, ext. 5402 or 5251. Environ. Sci. Technol., Vol. 16, No. 2, 1982
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