Seafood, mercury

U.S. Food and Drug Administration, Center for Food Safety and Applied Nutrition, Office of Seafood, Mercury Levels in Seafood Species, May 2001 http // www.cfsan.fda.gov/ frf/sea-mehg.htlm (Accessed 29 July, 2003). 

INTEGRATED STUDIES Adriatic Sea mercury-contaminated area vs. reference site various seafood products of commerce edible portions ... 

Proposed mercury criteria for the protection of sensitive aquatic organisms, birds, and mammals, as well as human health, are shown in Table 5.11. In almost every instance, these criteria are listed as concentrations of total mercury, with most, if not all, the mercury present as an organomercury species. In some cases the recommended criteria are routinely exceeded, as is the case for brown bears (Ursus arctos) in the Slovak Republic (Zilincar et al. 1992), and in Italian seafood products recommended for human consumption (Barghigiani and De Ranieri 1992). 

Cappon, C.J. and J.C. Smith. 1982. Chemical form and distribution of mercury and selenium in edible seafood. Jour. Anal. Toxicol. 6 10-21. 

Schumacher, M., J. Batiste, M.A. Bosque, J.L. Domingo, and J. Corbella. 1994. Mercury concentrations in marine species from the coastal area of Tarrgona Province, Spain. Dietary intake of mercury through fish and seafood consumption. Sci. Total Environ. 156 269-273. 

Arsenic is an ancient and well-known hazard and, along with lead and mercury, is an important environmental contaminant. The inorganic form is far more toxic than organic arsenic, which is commonly found in seafood. Arsenic-contaminated drinking water is a worldwide problem that affects millions of people. Human exposure also occurs from arsenic-treated lumber. 

Carlson, L., B. Holmquist, R. Ladd, et al. 1996. Immunoassay for mercury in seafood and animal tissues. In R.C. Beier and L.H. Stanker (eds), Immunoassays for Residue Analysis, pp. 388-394. Oxford Oxford University Press. 

The most notorious incident of widespread mercury poisoning in modem times occurred in the Minimata Bay region of Japan during the period of 1953 to 1960. Mercury waste from a chemical plant draining into the bay contaminated seafood consumed regularly by people in the area. Overall, 111 cases of poisoning with 43 deaths and 19 congenital birth defects were documented. The seafood was found to contain 5 to 20 ppm of mercury. 

Species of Fish/Seafood Tissue Type Mercury Concentrations... 

TABLE 22.4. Mercury Levels for Different Seafood Species [74]... 

NST, Determination of mercury and organic mercury content in local seafood, NST Quarterly, January 1996, www.mint.gov.my/papers/NST/1996/Nstl 96.htm (accessed 27 April 2004). 

L. N. Liang, G. B. Jiang, J. G. Liu, J. T. Hu, Speciation analysis of mercury in seafood by using high-performance liquid chromatography on-line coupled with cold-vapor atomic fluorescence spectrometry via a post column microwave digestion, Anal. Chim. Acta, Ml (2003), 131-137. 

Example Mercury is a known contaminant of seafood, and regulatory bodies such as the US Food and Drug Administration (FDA) recommend consumption of certain fish on the basis of their ppm levels of methylmercury substances, with a set action level for mercury in seafood of 1 ppm. The US EPA has also set an official reference dose (RfD) for mercury at 0.1 p,gkg per day in humans (corresponding to a blood mercury level of 5.8 p.g 1 or 5.8ppb), which is defined as the amount of mercury an individual (including sensitive subpopulations) can be exposed to on a daily basis over their lifetime without appreciable risk of effects. 

Plessi, M., Bertelli, D., Monzani, A. Mercury and selenium content in selected seafood. J. Food Compos. Anal. 14, 461 67 (2001)... 

The Japanese diet contains a lot of fish, and the local fishermen and their families would eat more fish than most. The fishermen were catching fish and seafood in the waters of Minamata Bay, waters which proved to be heavily contaminated with methyl mercury. In 1956 the first case of what became known as Minamata disease was reported and then other people started to present themselves to doctors and at hospitals with various symptoms such as muscular incoordination and difficulties in speech. Their pet cats, which were also eating the fish, suffered similar symptoms. 

Dr Hosokawa, director of the Minamata City hospital was conducting his own experiments based on the theory from the university He fed cats waste effluent from the factory that was producing acetaldehyde and was able to produce similar symptoms in them, and he detected other changes by pathological examination at autopsy The company that owned the factory, the Chisso Minamata Chemical Company, was aware of his work and by 1959 knew that it was likely that Minamata disease was caused by the effluent from their factory In i960 methyl mercury was detected in seafood and in 1961 it was detected in sediments derived from the factory. In 1966 the factory installed a water circulation system which removed the mercury pollution. The factory eventually stopped the process in 1968 and in the same year the Japanese government announced its opinion that the disease was due to consumption of methyl mercury in contaminated fish and seafood. 

One of the particularly tragic aspects of the Minamata disaster was the effect methyl mercury exposure had on unborn children. Some of the mothers exposed to methyl mercury from the fish and seafood gave birth to babies who were severely affected with a disorder similar to infantile paralysis, suffering cerebral palsy and mental retardation. This occurred even in mothers who showed no symptoms themselves, a classic characteristic of a teratogen. Some babies were born completely paralysed. 

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