Prenatal and postnatal methyl mercury exposure in Niigata, Japan: adult outcomes

• Published in: NeuroToxicology Vol. 81; pp. 364 - 372
• Main Authors: Saito, Hisashi, Sekikawa, Tomoko, Taguchi, Jun, Shozawa, Tetsu, Kinoshita, Yasuko, Matsumura, Kouko, Yanagihara, Kiyoko, Nikaido, Kazue, Urasaki, Sadako, Imaizumi, Haruyuki, Hatano, Hideto
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.12.2020; Elsevier BV
• Subjects: adult outcomes; Animals; child development; Female; fish; Fishes; Food Contamination; Hair; Hair - chemistry; Humans; industrial pollution; Japan; Japan - epidemiology; Mercury; Mercury - analysis; Mercury Poisoning, Nervous System; Mercury Poisoning, Nervous System - diagnosis; Mercury Poisoning, Nervous System - epidemiology; methyl mercury; Methylmercury Compounds; Methylmercury Compounds - analysis; Methylmercury Compounds - toxicity; Niigata; poisoning; postnatal exposure; Pregnancy; prenatal exposure; Prenatal Exposure Delayed Effects; Japan; prenatal exposure; poisoning; fish; child development; postnatal exposure; methyl mercury; industrial pollution; adult outcomes; Niigata
• DOI: 10.1016/j.neuro.2020.09.031
• ISSN: 0161-813X; 1872-9711

Methyl mercury (MeHg) poisoning or Minamata disease (MD) from fish consumption is a public health concern throughout the world because all fish contain small amounts. The lowest exposure level needed to impair children's development is controversial. Actual poisoning with MeHg from fish consumption has been reliably reported only two times. It occurred in Minamata, Japan in the 1950s and then in Niigata, Japan in the 1960s. On each occasion, massive industrial pollution led to local fish having mercury levels as high as 40ppm. In Niigata the pollution was on the Agano River and there were over 2000 commercial fishermen active at that time. We studied adult subjects who had been exposed perinatally to MeHg from fish consumption during the Niigata poisoning to determine the long-term impact of exposure. We identified mothers with elevated levels of exposure during the epidemic and those diagnosed with MeHg poisoning. The subjects of the study were their adult children, born during the epidemic. The evaluation consisted of a questionnaire (administered by interview) focusing on development, symptoms, and current function and a standard medical and neurological examination. The subjects were divided into four groups based upon prenatal levels of mercury in maternal hair or the presence of MD. For Group A the hair mercury levels were 50ppm or more, for Group B the mercury levels were 25-49ppm, and for Group C 10-24ppm. The subjects in Group D were born to mothers diagnosed with MD, but their mercury levels were not measured. Exposure was predominantly prenatal, but some mothers also breast fed their infants. Group A included 13 subjects among whom two were diagnosed with congenital MeHg poisoning and in two others it was suspected. Group B included 10 subjects, of whom three had symptoms compatible with MeHg poisoning. Group C had nine subjects including one with intellectual deficit and another with hearing loss. Group D had eight subjects of whom four had symptoms compatible with MeHg exposure, but only one had abnormal neurological findings. Among the subjects thought to have congenital or childhood MeHg poisoning, intelligence did not appear to have declined over time. More children were affected by prenatal and postnatal MeHg exposure at Niigata than was previously reported.