Man-Made Disaster: Mercury Poisoning in Japan

Man-Made Disaster: Mercury Poisoning in Japan

Mercury poisoning in Japan resulted to a disease named “Minamata Disease”. The disease whose name was derived from its place of occurrence, Minamata, reportedly originated between the years 1932 and 1968 (Boston University, 2019). The disease is believed to have mostly affected the residents of Minamata City, 3000 of whom have been certified as victims of the poisoning (Funakoshi & Kim, 2017).

The poisoning observed in Minamata was primarily caused by the ingestion of fish contaminated with methylmercury. This mode of poisoning is considered the chief mechanism as “the primary source of dietary ingestion is the consumption of contaminated fish” (Posin & Sharma, 2020, p. 25). Fetuses and children are more susceptible to mercury poisoning. As such, pregnant women are advised to avoid the consumption of fish especially known to contain toxic levels of methylmercury (Posin & Sharma, 2020). These kinds of fish include tuna, swordfish, tilefish, king mackerel, and shark (Posin & Sharma, 2020). Additionally, muskellunge and pike are some of the freshwater fish known to be heavily contaminated with mercury (Posin & Sharma, 2020). A cause more particular to the Minamata City case is the release of methylmercury in wastewater by the Japanese fertilizer company The Chisso Corporation. Methylmercury and other toxic compounds of mercury were ‘discharged directly into Minamata Bay’ by the company between the years mentioned above (Balogh et al., 2015, p. 5400).

A study conducted by Balogh et al. (2015) among residents of Minamata identified thousands of individuals as having been affected by the consumption of shellfish and tainted fish from the contaminated water body (Balogh et al., 2015). Moreover, mercury isotope studies conducted on sediments from the Yatsushiro Sea and Minamata Bay between 1978 and 2013 confirmed that the latter contained more methylmercury (Balogh et al., 2015).

Mercury poisoning in Minamata has been associated with several effects especially on the inhabitants of the City. Interestingly, the effects of mercury poisoning are more dependent on the period of retention of the compound in the body than a mere deposition. Firstly, mercury poisoning is associated with an increased risk for the development of psychiatric illnesses. For example, according to a study by Yorifuji et al. (2011) the even individuals in the general population exposed to mercury in Minamata exhibited heightened risk for behavioral dysfunction and intellectual impairment. Secondly, mercury poisoning in utero is associated with cerebral palsy-like symptoms such as “neurodevelopmental delays and cognitive deficits” (Bernhoft, 2012). Additionally, postnatal exposure is linked to an array of symptoms including extrapyramidal, auditory, and visual impairments, ataxia, and paraesthesia (Bernhoft, 2012). Exposure to larger doses of toxic chemicals like in Minamata is characterized by clonic seizures (Bernhoft, 2012). Another effect that is not directly linked to humans is the marked reduction in catches following environmental pollution. For instance, this effect as observed in Minamata led to the establishment of compensation agreements between fishery cooperatives and Chisso in the years 1926 and 1943 (Boston University, 2019).

One of the lessons learned from the Minamata City incident is the need for rigorous pilot tests before the production mechanism or processing of any chemical compound is started. For instance, in this scenario, the substantial mercury poisoning observed especially in 1932 is arguably attributable to the production of acetaldehyde (Boston University, 2019). The Chisso Minamata Corporation reportedly produced an estimated 210 tons of acetaldehyde per annum during the initial stages (Boston University, 2019). The production of the compound relied on the use of mercury sulfate as a catalyst, something that led to the release of methylmercury as a byproduct of the catalytic reaction. This toxic product was released into the Minamata City waterways until 1968 when a realization of its toxicity was made (Boston University, 2019). As such, an initial pre-production chemical test and analysis regarding the production method would have saved the City this form of pollution and consequently the disease. Another lesson learned from the case is the need for the government to ensure adequate allocation of resources to medical research and intervention. This move would ensure timely diagnosis of conditions followed by prompt appropriate treatment mechanisms that are evidence-based. For instance, the Minamata Disease was diagnosed after several cases, something that would have possibly been averted should the government have invested sufficiently in the needed resources. For instance, it was only until around 1956 that the Strange Disease Countermeasures Committee was initiated by the city government to carry out further investigations into the illness of the first group of patients (Boston University, 2019). This move was initiated after the disease “was suspected to be contagious and as a precaution patients were isolated and their homes disinfected” (Boston University, 2019). Another lesson that especially concerns the company is the need to reinforce investigation agencies that ensure the audit of industries that release waste products into the waterways. Such agencies, for instance, would have come in handy in the Minamata case should a thorough evaluation of the byproducts have been carried out.

References
Balogh, S. J., Tsui, M. T.-K., Blum, J. D., Matsuyama, A., Woerndle, G. E., Yano, S., & Tada, A. (2015). Tracking the fate of mercury in the fish and bottom sediments of Minamata Bay, Japan, using stable mercury isotopes. Environ. Sci. Technol., 49(9), 5399-5406. https://doi.org/10.1021/acs.est.5b00631.
Bernhoft, R. A. (2012). Mercury Toxicity and Treatment: A Review of the Literature. Journal of Environmental and Public Health, 460508. doi: 10.1155/2012/460508.
Boston University. (2019, December 14). Minamata Disease. Retrieved from Boston University: http://www.bu.edu/sustainability/minamata-disease/
Funakoshi, M., & Kim, K. H. (2017, September 21). More than 60 years on, Japan’s mercury-poison victims fight to be heard. Retrieved from Reuters: https://www.reuters.com/article/us-japan-minamata-victims/more-than-60-years-on-japans-mercury-poison-victims-fight-to-be-heard-idUSKCN1BV326
Posin, S. L., & Sharma, S. (2020). Mercury toxicity. Treasure Island (FL): StatPearls Publishing. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499935/
Yorifuji, T., Tsuda, T., Inoue, S., Takao, S. & Harada, M. (2011). Long-term exposure to methylmercury and psychiatric symptoms in residents of Minamata, Japan. Environ Int, 37(5), 907-913. doi:10.1016/j.envint.2011.03.008.



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