Methyl mercury toxicity

Ban M, de Ceaurriz J. 1988. Probenecid-induced protection against acute hexachloro-1,3-butadiene and methyl mercury toxicity to the mouse kidney. Toxicol Lett 40 71-76. 

Trasande, L., Landrigan, P.J., and Schechter, C. (2005) Public health and economic consequences of methyl mercury toxicity to the developing brain. Environmental Health Perspectives 113 590-596. http //www.ehponline.org/members/2005/7743/7743.pdf. Cited 19 January 2009. 

During long-term constant exposure (several months) to methyl mercury in food, there is a linear relationship between daily intake of methyl mercury and the concentration of mercury in blood. The mercury concentration in blood (pg/L) corresponds to the daily intake of methyl mercury (pg/ day) multiplied by 0.5-1. When exposure is continuous, the blood mercury concentration is proportional to the concentration in the brain, the critical organ for methyl mercury toxicity. Because of mercury s short half-life in the blood (2-4 days), evaluation of blood mercury is of limited clinical value if a substantial amount of time has passed since time of exposure [43]. 

Thus, the best approach is prevention. Since young children appear to be the most sensitive to methyl-mercury toxicity, children under 7 years and pregnant or breast-feeding women should limit their consumption of fish that are known to have high levels of methylmercury in their edible tissues. 

Tamashiro H, Arakaki M, Akagi H, et al. 1986. Effects of ethanol on methyl mercury toxicity in rats. J Tox Environ Health 18 595-605. 

Tumer CJ, Bhatnagar MK, Yamashiro S. 1981. Ethanol potentiation of methyl mercury toxicity A preliminary report. J Tox Environ Health 7 665-668. 

Oliveira Ribeiro, C.A., L. Belger, E. Pelletier and C. Rouleau. Histopathological evidence of inorganic mercury and methyl mercury toxicity in the arctic charr (Salvelinus alpinus). Environ. Res. 90 217—225, 2002. 

Welsh, S. O., 1979, The protective effect of vitamin E and N,N-diphenyl-p-phenylcne-dia-mine (DPPD) against methyl mercury toxicity in the rat, J. Nutr. 109 1673. 

Alexander, J., Hostmark, A. T., Forre, 0., and von Kraemer Bryn, M., 1979, The influence of selenium on methyl mercury toxicity in rat hepatoma cells, human embryonic fibroblasts and human lymphocytes in culture, Acta pharmacol. et toxicol. 45 379. 

It has been stated [11] that about 400 tonnes of mercury lie at the bottom of Minamata Bay near the point of discharge of mercury wastes and although further dumping was finally stopped in 1968, this cannot prevent the future possibility of conversion of inorganic to methyl mercury and its accumulation in fish. By 1973, sixty-five people had died from Minamata disease and many more had been crippled, blinded or otherwise affected. It is now known from experimental work with rabbits, that alkyl mercury can readily pass through the placental barrier in mammals [60] (p. 84) and this is borne out by the fact that a number of children were bom with symptoms of methyl mercury toxicity to women at Minamata who were not evidently themselves affected. 

Kendall, M. W. Acute effects of methyl mercury toxicity in channel catfish (Ictalurus punctatus). Bull. Env. Contam. Toxicol. 13, 570 (1975). 

The primary target of methyl mercury toxicity is the central nervous system [43]. 

Thus, there is not a great deal of difference between the three classes in acute toxicity all are highly toxic. However, methyl mercury is more persistent than the other two types, and so has the greater potential to cause chronic toxicity. The latter point is important when considering the possibility of sublethal effects. 

Monteiro, L.R. and Furness, R.W (2001). Kinetics, dose-response, excretion and toxicity of methyl mercury in free living Cory s shearwater chicks. Environmental Toxicology and Chemistry 20, 1816-1824. 

With respect to Cr a distinction should be made between Cr(III), which is the common oxidation state in the soils, being rather immobile and so toxic, and Cr(VI), which is very mobile and very toxic. With respect to Hg, the situation is even more complex, due to the occurrence of mercuric mercury (Hg2+), mercurous mercury (Hg2+), elemental mercury (Hg°) and organic mercury species, such as methyl mercury, (CH3)2Hg (see Section 18.5). Furthermore, volatilization of elemental mercury and organic mercury species is common. A description of these... 

In the environment, metals are common as a chemical species, and as usual the metal-organic species are more toxic. For example, the inorganic lead and mercury species are less toxic for living organisms than the organic ones (methyl mercury, tetraethyl lead). However inorganic arsenic compounds are more toxic than organic... 

The biological half-life in humans for methyl mercury is about 70 days because elimination is slow, irregular, and individualized, there is a considerable risk of an accumulation of mercury to toxic levels. A precise relationship between atmospheric levels of alkyl mercury and concentrations of mercury in blood or urine has not been shown. Clinical observations indicate that concentrations of 50-100pg mercury/lOOml of whole blood may be associated with symptoms of intoxication concentrations around 10-20pg mercury/ 100 ml are not associated with symptoms. In a study of 20 workers engaged in the manufacture of organic mercurials and exposed for 6 years to mercury concentrations in air between 0.01 and O.lmg/m, there was no evidence of physical impairment or clinical laboratory abnormalities. Low levels of methyl mercury in the blood do not seem to affect the results of behavioral performance tests. ... 

Junghans RP A review of the toxicity of methyl mercury compounds with application to occupational exposures associated with laboratory uses. Environ Res 31 1-31, 1983... 

There are several different types of organic mercury, but by far the most important in terms of health effects is methyl mercury. When atmospheric mercury is deposited on the ground or in the water, it is converted to methyl mercury by bacteria. Mercury compounds are very toxic and this is the bacteria s way to detoxify mercury. Small animals then consume the bacteria, along with the methyl mercury and bigger animals in turn consume the smaller animals, thus increasing the concentrations of methyl mercury. Methyl mercury accumulates in the larger carnivorous animals, most important of which are fish such as tuna, pike, and shark. 

It turns out that most of these compounds have similar characteristics that contribute to their toxicity to both humans and other species of plants and animals. First, the compounds are environmentally persistent. Many of the early pesticides, and certainly the metals, do not break down in the environment or do so only very slowly. If persistent chemicals are released continually to the environment, the levels tend to rise ever higher. This means they are available to cause harm to other organisms, often not even the target of the pesticide. Second, the early pesticides were broad acting and toxic to many species, not just the target species. These poisons often killed beneficial insects or plants. Third, many of these compounds would bioaccumulate or concentrate in species as they moved up the food chain. The chlorinated pesticides accumulate in the fat of animals. Animals that consumed other animals accumulated more and more of these pesticides. Most species could not metabolize or break down the compounds. Lead accumulates in bone and methyl mercury in muscle. And finally, because of their persistence in the environment and accumulation in various species, the persistent toxicants spread around the world even to places that never used them. Animals at the top of the food chain, such as polar bears and beluga whales, routinely have fat PCB levels greater that 6 ppm. 

Biotransformation An organism changing one substance into another form often to increase excretion or reduce toxicity Bacteria changing mercury into methyl mercury... 

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