Abstract
Large-scale MeHg poisoning occurred in Niigata, Japan in the 1960s. Hair mercury levels were measured early in the epidemic of MeHg poisoning. The severe prenatal exposure cases with conditions resembling cerebral palsy, i.e., congenital Minamata disease are well-known, although severe prenatal and postnatal MeHg exposure cases who did not develop such severe symptoms are not well-known. We conducted follow-up neurologic examinations and interviews of four participants with a history of prenatal and postnatal MeHg exposure who had-along with their mothers undergone hair mercury measurement in June 1965. We describe their development and subjective symptoms in childhood and neurologic signs in adulthood. The hair mercury levels of the four participants ranged from 63.0 to 111.0 ppm in 1965, and maternal levels ranged from 58.0 to 275.0 ppm. Although the four participants had high prenatal and postnatal MeHg exposures, they did not develop severe symptoms resembling cerebral palsy. They had symptoms such as poor concentration and poor memory which are thought to be neuropsychological dysfunction, as well as MeHg poisoning in childhood. One was intellectually impaired (Total IQ, 79). Nearly 50 years after prenatal and postnatal MeHg exposure, they had neurologic signs such as sensory disturbances of the bilateral distal extremities and blurred vision. There are several limitations such as a possibility of selection bias, etc. in the present study. 4 cases had various signs and symptoms possibly due to prenatal and postnatal MeHg exposure such as neurologic signs and neuropsychological dysfunction during lifetime.
Highlights
Large-scale methylmercury (MeHg) poisoning from fish consumption occurred in Japan at Minamata (Minamata disease), in the 1950s, and at Niigata, in the 1960s (Figure 1) [1,2,3,4,5,6]
Total hair mercury levels were measured in the four participants in June 1965 early in the epidemic of MeHg poisoning in Niigata
Their ages ranged from 2 months to 10 years, and their hair mercury levels ranged from 63.0 to 111.0 ppm, while their maternal levels ranged from 58.0 to 275.0 ppm
Summary
Large-scale methylmercury (MeHg) poisoning from fish consumption occurred in Japan at Minamata (Minamata disease), in the 1950s, and at Niigata, in the 1960s (Figure 1) [1,2,3,4,5,6]. The MeHg poisoning in Niigata is less well known internationally than the event in Minamata [7]. Data on MeHg exposure in Minamata are very limited. Since at Niigata the cause was recognized early in the epidemic of MeHg poisoning, MeHg exposure could be examined by hair mercury levels [7,8]. Before the epidemic of MeHg poisoning in Niigata, residents in the Agano River basin consumed fish and shellfish from the river for their daily meals. Fishing was part of the livelihood of most residents, and fish and shellfish from the river were an essential source of protein [9,10]
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