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Mercury

Prolonged exposures to relatively high concentrations of mercury in the air produces damage to the nervous system and kidney, but rarely produce a fatal injury. However, accidental oral exposures have caused death (WHO, 1990; ATSDR ,1993c). The presence of mercury in the environment at lower levels also produces potential for human exposure directly through breathing mercury and indirectly through ingestion of fish contaminated with methyl mercury. Methyl mercury is about five times more dangerous than the inorganic and metallic forms of mercury (Casarett and Doull, 1990). Toxic actions of methyl mercury and mercury are different and should be considered separately.

I Elemental mercury. Inhalation of moderate levels of mercury for prolonged periods of time produces unique effects on the central nervous system and the kidney. The chemical form of mercury is important in the determination of the actual toxic effect (Casarett and Doull, 1990; ATSDR, 1993c). For example, elemental mercury is highly charged and does not readily pass through the blood brain barrier but directly reaches the kidney. Therefore, elemental mercury is more toxic to the kidney than the brain. Metallic mercury and organic forms of mercury pass easily through the protective blood brain barrier and may cause brain damage as well as kidney damage (ATSDR, 1993c). Once mercury enters the body it is retained in the kidney, brain, liver and the fetus. It may stay in the body for several months. When mercury is eliminated from the body it appears in the breath, urine, feces, milk and hair. Different organs accumulate and retain mercury at different rates, with the brain and the kidney retaining mercury for periods of months to years. Enzymatic processes in the body transform mercury to the inorganic or metallic form.

Toxic effects of mercury are found in the brain, kidney, skin and liver. At low exposures the toxic effects of mercury are found mainly in the brain. The effects are much more serious in the infant and the fetus because of interference with development of the motor and cognitive functions (ATSDR, 1993c; Casarett and Doull, 1990). There is a latent period between the exposures to mercury and the onset of effects of the poisoning. This delay complicates the diagnosis of the damage and the implementation of the treatment (Clarkson,1992).

At first, low concentrations of mercury seem to have no health effects but signs of toxicity become noticeable with continued exposures (ATSDR 1993c). Toxic signs include loss of feeling or burning sensations in the legs, paralysis, congenital malformations, kidney toxicity and, on rare occasions, death.

Environmental exposures do not produce the more severe effects but subtle toxic effects are possible, especially in the fetus. These changes would not be apparent in the newborn but would become apparent after later development of motor functions such as walking (Casarett and Doull 1990). Unsteadiness and tremors may develop after long periods of exposure. Psychological effects such as insomnia, loss of appetite, shyness, emotional instability and memory loss are also reported in the literature. These actions are partially reversible with termination of exposures to mercury. Cancer is not a significant component of mercury toxicity (ATSDR, 1993c).

While the toxicity of mercury itself is an important concern, the toxic effects of methyl mercury are dangerous because of the higher potency of methyl mercury and its effects on development of the fetal brain.

The occupational safety and health Administration has set a limit of 50 ug/m 3 for metallic mercury in the work place. EPA has set limits for inorganic mercury in drinking water and surface water.

II. Methyl mercury. Human health effects of methyl mercury nearly all involve the ingestion of methyl mercury in fish, or, in one case in grain (Spyker Cranmer J., 1996). Methyl mercury in food is nearly all absorbed into the body and distributed throughout the body to the brain and fetus. Mercury absorbed into the blood stream may be metabolized to the inorganic forms in the liver and removed from the body or reabsorbed from the intestine.

Methyl mercury in the brain and the fetus can be transformed and concentrated. Thus, when the blood levels are decreasing overall the mercury in the brain and fetus may remain high or even increase. Mercury is transferred to hair where its measurement provides a historical indication of past exposures. Equally if not more important, methyl mercury is also excreted into the mother's milk where it is transferred to the nursing infant. Damage has been found in infants and in the fetus even when the mother has shown no toxic effects of mercury exposure.

There is a large body of information on the toxic effects of the chronic ingestion of fish containing methyl mercury by different populations starting before Minimata in Japan in the 1950s to present day exposures in the Amazon river basin. Relatively widespread human poisonings have been documented from these episodes. The actual levels of exposures at which injury begins to occur in the fetus, infants and children remains controversial. The findings from chronic exposures have been used to identify reference doses for estimating the human health hazards ( Sea Food Safety, 1991). The reference doses from these different studies and exposures have converged on values in the 1 to 5 ug/m 3 range. Because of uncertainties in the conditions of the different exposures and in the potential for exposure from eating fish, there is a tendency to rely more on the lower end of the risk of 1 ug/kg/day in fish consumption advisories.

Over 39 states have issued fish consumption advisories to reduce the potential hazards of sport fish high in methyl mercury. It is not certain what the actual hazard is from periodic ingestion of fish which have high levels of methyl mercury, therefore public health agencies have adopted a risk reduction strategy to limit potential exposures to mercury in the more sensitive members of the population.

Deposition of mercury into lakes, streams and watersheds is the first step in contamination of fish (EPA, 1996). However the ultimate level of methyl mercury found in the fish is determined by several factors related to the age and type of fish and the nature of other biota in the water. Bioaccumulation appears to increase as the ecological food webs of the water body become more complex. Thus some ponds and lakes and rivers that appear to be pristine often have surprisingly high levels of mercury in the fish. Other lake which have become acidified also can have fish with high levels of mercury.

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Last Updated: 1/31/03

 

   
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