Methylmercury level in umbilical cords from patients with congenital Minamata disease

Abstract

A total of 151 umbilical cords during the period from 1950 to 1969 were collected from the residents of the Minamata area (including 25 patients with congenital Minamata disease) for methylmercury (MeHg) analysis. When the MeHg discharge from the Chisso Company’s Minamata factory into the Minamata Bay is compared with the incidence of congenital Minamata disease, the abrupt increase of the former in 1952 [Nishimura H. Chem. Today 1998;323:60–66] was found to precede that of the latter by approximately 2 years, thereby indicating that MeHg is the cause of the disaster. This was confirmed by the elevated levels of MeHg in the umbilical cords from residents of the Minamata area [from 0.35±0.30 (S.D.) ppm in 1952 to 0.96±0.75 ppm in 1955], the MeHg levels (1.60±1.00 ppm) in the cords from patients with congenital Minamata disease showing the highest values [P<0.01 vs. acquired Minamata disease (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), respectively]. Thus, in order to fill a gap, which extends over a long period of time, in studies on environmental Hg pollution, umbilical cord samples were considered to be a useful tool.

Introduction

In 1932 Chisso Company’s Minamata factory, Kumamoto Prefecture, Japan, began production of acetaldehyde using inorganic mercury as a catalyst. Waste water from the Chisso factory had since been discharged into and spreading throughout the Shiranui Sea till 1966. The resulting methylmercury (MeHg) poisoning is now known as Minamata disease (Harada, 1995, Harada, 1997). Minamata disease was first noticed in 1956 and its cause was identified in 1959. In approximately 1953, however, cats had begun to go mad and to die inexplicably. Moreover, fish were found floating on the sea and some birds fell into the sea while flying. Also, it was disclosed that there were many children with congenital cerebral palsy in the area. These children were not officially recognized as having Minamata disease until 1962 because they had not eaten any of contaminated fish or shellfish (Harada, 1978). In 1968 the Chisso factory discontinued production of acetaldehyde, and then through hardships and privations Minamata disease was socially and politically settled in 1997 with a plausible explanation for the cause and the disaster.

Unbelievably, however, the cause, particularly the discharge of MeHg, has never been proved even in court because no data of MeHg was available either on the waste water or on the seawater owing to lack of methods of analysis in those days. Thus the explanation without any evidence has produced the following puzzling question about the case: Why did the Chisso factory suddenly become rampant and cause the outbreak in 1953 in spite of a successive operation of 20 years since 1932?

Quite recently, Nishimura (1998) has succeeded in providing an accurate answer to this question by extensively investigating both the chemical reaction system and the ecological system, that is, the change of co-catalyst in the mother liquid of a gas–liquid reactor from manganese dioxide to ferric ion in 1951 increased the amount of the MeHg discharge by approximately six times, thereafter leading to the outbreak in 1953.

In our previous study we revealed that the umbilical cords of the residents of Minamata reflected a chronological transition in MeHg pollution (Nishigaki and Harada, 1975). We report here that the umbilical cords of patients with congenital Minamata disease also seem to reflect the chronological transition.