iFinancialAdviser
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 Posted: Fri Nov 02, 2007 4:37 am Post subject: |
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Mercury and most of its compounds are extremely toxic and are generally handled with care; in cases of spills involving mercury (such as from certain thermometers or fluorescent light bulbs) specific cleaning instructions should be used to avoid toxic exposure. It can be inhaled and absorbed through the skin and mucous membrane, so containers of mercury are securely sealed to avoid spills and evaporation. Heating of mercury, or compounds of mercury that may decompose when heated, should always be carried out with adequate ventilation in order to avoid exposure to mercury vapor. The most toxic forms of mercury are its organic compounds, such as methylmercury.
Occupational exposure
Due to the health effects of mercury exposure, industrial and commercial uses are regulated in many countries. The World Health Organization, OSHA, and NIOSH all treat mercury as an occupational hazard, and have established specific occupational exposure limits. Environmental releases and disposal of mercury are regulated in the U.S. primarily by the United States Environmental Protection Agency.
A study has shown that acute exposure (4-8 hours) to calculated elemental mercury levels of 1.1 to 44 mg/m3 resulted in chest pain, dyspnea, cough, hemoptysis, impairment of pulmonary function, and evidence of interstitial pneumonitis.
Acute exposure to mercury vapor has been shown to result in profound central nervous system effects, including psychotic reactions characterized by delirium, hallucinations, and suicidal tendency. Occupational exposure has resulted in broad-ranging functional disturbance, including erethism, irritability, excitability, excessive shyness, and insomnia. With continuing exposure, a fine tremor develops and may escalate to violent muscular spasms. Tremor initially involves the hands and later spreads to the eyelids, lips, and tongue. Long-term, low-level exposure has been associated with more subtle symptoms of erethism, including fatigue, irritability, loss of memory, vivid dreams, and depression.
Treatment
Research on the treatment of mercury poisoning is limited. Currently available drugs for acute mercurial poisoning include chelators N-acetyl-D,L-penicillamine (NAP), British Anti-Lewisite (BAL), 2,3-dimercapto-1-propanesulfonic acid (DMPS), and dimercaptosuccinic acid (DMSA). In one small study including 11 construction workers exposed to elemental mercury, patients were treated with DMSA and NAP.[26] Chelation therapy with both drugs resulted in the mobilization of a small fraction of the total estimated body mercury. DMSA was able to increase the excretion of mercury to a greater extent than NAP.
Mercury in fish
Fish and shellfish have a natural tendency to concentrate mercury in their bodies, often in the form of methylmercury, a highly toxic organic compound of mercury. Species of fish that are high on the food chain, such as shark, swordfish, king mackerel, albacore tuna, and tilefish contain higher concentrations of mercury than others. This is because mercury is stored in the muscle tissues of fish, and when a predatory fish eats another fish, it assumes the entire body burden of mercury in the consumed fish. Since fish are less efficient at depurating than accumulating methylmercury, fish-tissue concentrations increase over time. Thus species that are high on the food chain amass body burdens of mercury that can be ten times higher, or more, than the species they consume. This process is called biomagnification. The first occurrence of widespread mercury poisoning in humans occurred this way in Minamata, Japan, now called Minamata disease.
The complexities associated with mercury fate and transport are relatively succinctly described by USEPA in their 1997 Mercury Study Report to Congress. Because methylmercury and high levels of elemental mercury can be particularly toxic to unborn or young children, organizations such as the U.S. EPA and FDA recommend that women who are pregnant or plan to become pregnant within the next one or two years, as well as young children avoid eating more than 6 ounces (one average meal) of fish per week. In the United States the FDA has an action level for methyl mercury in commercial marine and freshwater fish that is 1.0 parts per million (ppm), and in Canada the limit for the total of mercury content is 0.5 ppm.
Species with characteristically low levels of mercury include shrimp, tilapia, salmon, pollock, and catfish (FDA March 2004). The FDA characterizes shrimp, catfish, pollock, salmon, and canned light tuna as low-mercury seafood, although recent tests have indicated that up to 6 percent of canned light tuna may contain high levels.
Mercury and aluminium
Mercury readily combines with aluminium to form a mercury-aluminum amalgam when the two pure metals come into contact. However, when the amalgam is exposed to air, the aluminium oxidizes, leaving behind mercury. The oxide flakes away, exposing more mercury amalgam, which repeats the process. This process continues until the supply of amalgam is exhausted, and since it releases mercury, a small amount of mercury can “eat through” a large amount of aluminium over time, by progressively forming amalgam and relinquishing the aluminium as oxide.
Aluminium in air is ordinarily protected by a molecule-thin layer of its own oxide, which is not porous to oxygen. Mercury coming into contact with this oxide does no harm. However, if any elemental aluminium is exposed (even by a recent scratch), the mercury may combine with it, starting the process described above, and potentially damaging a large part of the aluminium before it finally ends (Ornitz 1998).
For this reason, restrictions are placed on the use and handling of mercury in proximity with aluminium. In particular, mercury is not allowed aboard aircraft under most circumstances because of the risk of it forming amalgam with exposed aluminium parts in the aircraft.
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http://en.wikipedia.org/wiki/Mercury_(element)#Safety
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