1966), and again in Iraq in 1970–1971 (Bakir et al. Countermeasures against chemical terrorism in Japan, Toward the next generation of air quality monitoring: Mercury, The Minamata Convention on Mercury: A First Step toward Protecting Future Generations, Neonatal exposure to Thimerosal from vaccines and child development in the first 3years of life, Effects of methylmercury exposure on neuronal differentiation of mouse and human embryonic stem cells. Environ Sci Technol.
Methylmercury was eventually acknowledged by governmental authorities in 1968 to be the cause of Minamata disease (Social Scientific Study Group on Minamata Disease 1999). On day 5, EB were plated on laminin-coated dishes and kept in medium containing 10% serum.
Cluster H genes were low expressed on days 0 and 3 and highly increased on days 5, 6 and most on day 7. The effects of methylmercury on human pregnancy have been documented by several events that occurred many years ago in Japan and Iraq. In the enriched neuron differentiation GO term, many markers known to play a critical role in neuronal development were highly (FR > 16) induced, such as Pax6, Tubb3, and Nefl (Liu et al., 2007; Moskowitz and Oblinger, 1995). A transcriptomics study was performed to examine whole-genome expression changes during the first 7 days of the cell differentiation protocol. 2003, 2004). (1957) reported that 50 of 61 cats bred by families of Minamata disease patients died in 1953–1956. On day 3, the EB were transferred to suspension medium supplemented with 0.5μM all-trans-RA. 1959, 1960). Methylmercury, one organic form of mercury, can accumulate up the aquatic food chain and lead to high concentrations in predatory fish. *T > 3.5 and E > 0.05. 2016;41(6):757-763. doi: 10.2131/jts.41.757. Although any error or bias in the research reports is difficult to determine today, one can assume that methylmercury toxicity was unlikely to have been exaggerated. Single cells formed EB. For full access to this pdf, sign in to an existing account, or purchase an annual subscription. (2012) summarized the complexities of providing clear and uniform fish consumption advice to reduce MeHg exposure while … We previously developed a dynamic in vitro model for screening effects of possible neurodevelopmental toxicants, using neural cell differentiation of pluripotent murine embryonic stem cells. The first international report on methylmercury as a likely cause of Minamata disease was published soon thereafter (Kurland et al. RNA quantity was determined using the NanoDrop Spectrophotometer (Isogen Lifescience, de Meern, The Netherlands). The common feature was an ascending paralysis accompanied by movement difficulties, tremors, blindness, disturbance in hearing, and irascibility in the animals (Hepp 1887; Hunter and Russell 1954).
Although the toxicology and environmental epidemiology of methylmercury have been recently outlined [Clarkson and Magos 2006; Grandjean et al. A turn in the debate occurred in 1964, when unused seed grain treated with methylmercury had been used as chicken feed in Sweden (Tejning and Vesterberg 1964).
At that level, an adult weighing 70 kg could eat 200 g of fish per week at a mercury concentration of 1 μg/g. The European Union and the United States have already decided on a ban on mercury exports, and mercury is being phased out in thermometers and scientific instruments (European Union 2007). Most of the patients were fishermen and their families who resided near the coast. 2A and 2B). Eight gene clusters (A–H) were defined by hierarchical clustering (Euclidean distance, ward linkage) on the basis of expression dynamics over time (Figs. This concentration of MeHg did not affect cell viability in the model. The total number of advisories for mercury has been increasing and, by 2008, it exceeded 4,000. After 24 h treatment, 490 genes were significantly regulated, after 48 h treatment, 6 genes, after 72 h, 29 genes, and after 96 h, 97 genes were significantly regulated. 2008).
2018;73(3):258-264. doi: 10.1265/jjh.73.258.
Developmental neurotoxicity was first reported in 1952, but despite accumulating evidence, the vulnerability of the developing nervous system was not taken into account in risk assessment internationally until approximately 50 years later. When consumed by humans, contaminated fish represent a public health risk. In contrast, largely nonpositive findings were initially reported in children from a similar study in the Seychelles (Myers et al. However, no assessment of the associated health risks was produced on this occasion, and no advice was offered to the public. Crows were reported to be becoming sick and dying in the area. However, thin-layer chromatography identification of methylmercury was not successful until 1962, when the substance was identified in sludge from the acetaldehyde plant and the bottom sediment of the effluent channel (Irukayama et al. The sponsor was not involved in analysis or interpretation of the data. 2C) and showed clear germline specificity for induction of neurodevelopmental pathways. eBook files are now available for a large number of reports on the NAP.edu website. Similar problems occurred elsewhere. Cluster D was increased on days 4 and 5. Treatment and morphological scoring for effects on neural outgrowth. Mercury is widespread in our environment.
2004).