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Mercury,
a silvery liquid metal at room temperature was first identified as a human
toxin in 1866 when two laboratory technicians who worked with the metal
died of dimethyl mercury posioning after short exposure periods. It
was not until 1954-1956 after a methyl mercury posioning occurred in Minamata
Bay in Kyushu, Japan occurred that mercury was widely recognized as a dangerous
toxin. Victims had consumed contaminated fish and shellfish. The
source of mercury contamination was from a chemical manufacturing company,
Chisso, who used mercury as a catalyst int he production of acetylaldehyde.
The bay had become contaminated with effluent produced by Chisso and
mercury concentration became biomagnified while ascending through the food
chain. Victims experienced abnormal gait, ataxia, loss of hearing, constriction of visual field, and mental confusion. They were prone to shouting and often coma or death (1). Mercury posioning is the most harmful to the fetus in utero. Methyl mercury readily crosses the placental barrier and causes a high incidence of mental retardation, sensory disturbance, hearing impairment, constriction of the visual field, seizure and cerebral palsy-like symptoms in children with fetal exposure. 
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| Earlier recognition
of mercury as a neurotoxin could have lead to the avoidance of two other
widespread epidemics. In addition to over 1000 people who are estimated
to have died from mercury posioning in Minamata Bay, people were posioned
in Niigata, Japan by eating contaminated seafood (1), and Iraqis who consumed
seed grain (mainly wheat) that had been treated with a methyl mercury fungicide
(2). The photo to the right shows the Minamata Monument which commemorates
victims of the Minamata mercury posioning epidemic. Mercury in the Environment Not only is mercury a hazzard to human health, it is also detrimental to microorganisms, plants and animals. |
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Microorganisms Wood (1984) described tolerance mechanisms by which microorganisms survive mercury toxicity. These mechanisms include: 1) efflux pumps removing Hg ions, 2) Enzymatic reduction of ionic Hg to elemental Hg(0), 3) chelation by molecules such as metallothioneins, 4) binding of Hg to cell surfaces, 5) precipitation of insoluble mercury sulfides and oxides, and 6) biomethylation and subsequent diffusion out of the cell membrane. In contaminated waters, mercury is encountered by methanogenic bacteria (2), which methylate Hg. The reson for methylation is suspected to be a means of elimation of the toxic element from the bacterium. While ionic mercury is retained in the bacterium, methyl mercury can diffuse out of the organism, effectively providing a means of elimination. To other organisms, however, methyl mercury is very toxic. Researchers have documented toxicity in species ranging from other microorganisms to marine invertebrates and vertebrates, to avians and mammals and plants. |
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Aquatic Invertebrates and Vertebrates Mercury accumulates in soft edible tissues of these organisms. Accumulation is dependent on factors such as water salinity, hardness, acidity and temperature. The larval stages of invertebrates are most sensitive to mercury toxicity. Higher accumulation is usually seen in older vertebrates due to longer mercury exposure |
Avians Birds tend to accumulate mercury in the liver and kidneys. Methylmercury is more readily absorbed and accumulated when compared to ionic mercury. Hg is also concentrated in eggs. Methyl mercury partitions into albumin and elemental mercury accumulates in the yolk (3). |
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Mammals During the Minimata epidemic, samples of hair from women exposed to contaminated seafood were measured to determine mercury levels in their bodies. Women of child bearing age with 50 ppm or higher body Hg content were advised not to have children and to use birth control (abortion) if necessary to prevent the birth of an affected child (1). The FDA has established an "action" level of 1.0 ppm mercury in commercial fish. Canned tuna, the number one consumed fish in America contains an average of 0.2 ppm per serving. However, the EPA would like to lower the level to 0.1 micrograms/kg of fish bodyweight. With occasion fish consumption (approximately once a week) this action level provided by the FDA should provide "safe" intake levels of mercury (2). |
Plants Plants notably accumulate higher levels of mercury with increasing soil or water are usually highest in the roots with slow translocation to the shoots. However, some plants take up atmospheric Hg (0) and accumulate it in shoot tissues such as leaves. In fact, vegetation upwind from a mercury-contaminated mining site in Spain was found to contain approximately ten times the level of mercury when compared to plants downwind of the mine (3). Soil type plays an important role in bioavailibility of mercury to plants for uptake. Clay-like soils or soils containing a high amount of organic matter tend to bind mercury causing it to be less bioavilable to the plant (3). Mosses have been reported to accumulate higher amounts of mercury compared to herbaceous species. However, mosses are not high biomass plants. Studies of spruce seedlings exposed to ionic mercury and methyl mercury may give clues to the mechanism of mercury toxicity. Seedlings exposed to both types of mercury resulted in a loss of K+, Mn, Mg at the root tip along with accumulation of iron. The loss of K+ at the root tip suggests that mercury causes changes in root tip cell membrane integrity, while methyl mercury may affect organelle metabolism which subsequently affects cell membrane integrity(3). Research is being conducted on plants that have bacterial genes inserted into them that encode for enzymes that reduce highly toxic methyl mercury to less toxic elemental mercury Hg (0) vapor. The intention of this research is to develop plants that can clean excess methyl mercury from the environment through phytovolatilization (3). |
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