Neurodevelopmental Effects of Prenatal and Postnatal Methylmercury Exposure Among Children in the First Grade in Kinan Region, Japan
Masaaki NakamuraNozomi TatsutaKatsuyuki MurataKunihiko NakaiToyoto IwataTakayuki OtobeMineshi SakamotoMegumi YamamotoMina ItataniYoko MiuraChihaya Koriyama
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The most severe effects of methylmercury (MeHg) exposure to child development are thought to develop through exposure during fetal life and childhood. However, the comparison of neurodevelopmental effects by prenatal and postnatal MeHg exposure (PreMeHg and PostMeHg, respectively) remains unclear. We aimed to investigate the associations between neurodevelopmental indicators and PreMeHg or PostMeHg. The participants were 134 children in the first grade of elementary schools aged 7–8 years from the Kinan region, an area with high consumption of MeHg-rich whales and tunas in Japan. We measured MeHg levels in preserved umbilical cord tissues and total mercury (T-Hg) levels in children’s hair to estimate PreMeHg and PostMeHg levels, respectively. Neuropsychological (intelligence quotient, Boston Naming Test, and reading tests) and neurophysiological (brainstem auditory evoked potential [BAEP], visual evoked potentials [VEP], and color vision) studies were performed to evaluate neurodevelopmental status. Multiple regression analyses were conducted according to sex. The geometric mean MeHg levels in preserved umbilical cord tissues and T-Hg levels in children’s hair were 0.11 µg/g and 2.94 µg/g, respectively. Neither PreMeHg nor PostMeHg was related to neuropsychological indicators. Positive associations between MeHg exposure and neurophysiological results were observed only in boys. PreMeHg was positively associated with N145 latency in VEP (β: 12.01, 95% confidence interval [CI]: 0.648, 23.38). PreMeHg or PostMeHg was significantly associated with the III–V interpeak intervals in BAEP (β [95% CI] = 0.142 [0.041, 0.243] and 0.159 [0.052, 0.265], respectively). After adjusting for PreMeHg, the significant positive correlation between PostMeHg and BAEP latencies disappeared. In conclusion, auditory and visual circuits might be more affected by PreMeHg than by PostMeHg only in boys. Further studies are needed to investigate the balance in the body between MeHg and selenium or docosahexaenoic acid with protective effects against MeHg toxicity during the fetal period or childhood according to sex.Keywords:
Methylmercury
The central nervous system is particularly vulnerable to prenatal exposure to methylmercury. Due to the widespread exposure to methylmercury from fish, several prospective environmental epidemiology studies have been initiated, in which the maternal exposure during the pregnancy is related to the neurobehavioural development of the children. We have studied a Faroese birth cohort prenatally exposed to methylmercury from maternal intake of contaminated pilot whale meat. At seven years of age, clear dose-response relationships were observed for deficits in attention, language, and memory. An increase in blood pressure was also associated with the prenatal exposure level. The exposure limit for mercury has therefore been decreased.
Methylmercury
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MERCURY EXPOSURE
Environmental epidemiology
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The danger of methylmercury poisoning appears to be slight when the environment is not directly contaminated with methylmercury. Sediments rapidly bind mercury and decrease its availability to aquatic organisms. Sediments further have a greater propensity to demethylate than to methylate mercury. In noncontaminated aquatic ecosystems, the concentrations of methylmercury and inorganic mercury are many times lower than those that have been found to cause toxicity, even in the most sensitive organisms. Methylmercury bound to protein is comparatively less toxic than methylmercury salts, and selenium present in this protein appear to be one of the major detoxifying agents for methylmercury. This is particularly important in seafood, where there is an excess of selenium compared to methylmercury.
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The danger of methylmercury poisoning appears to be slight when the environment is not directly contaminated with methylmercury. Sediments rapidly bind mercury and decrease its availability to aquatic organisms. Sediments further have a greater propensity to demethylate than to methylate mercury. In noncontaminated aquatic ecosystems, the concentrations of methylmercury and inorganic mercury are many times lower than those that have been found to cause toxicity, even in the most sensitive organisms. Methylmercury bound to protein is comparatively less toxic than methylmercury salts, and selenium present in this protein appear to be one of the major detoxifying agents for methylmercury. This is particularly important in seafood, where there is an excess of selenium compared to methylmercury.
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Methylmercury distribution and production in the environment are reviewed. As for methylmercury distribution, the proportions of methylmercury to the total mercury in waters, soils, sediments and airs are mainly discussed. The origin of methylmercury in fish is also discussed. Methylation of inorganic mercury in the environment can be roughly divided into two groups ; one is biological and the other is chemical methylation. In this article, chemical methylations are discussed in detail. Effects of environmental factors, such as pH, redox potential and temperature, on the methylmercury production are also mentioned.
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