The extreme toxicity of Mercury (Hg), those suspected some centuries back, was fully appreciated in the year 1953, when 52% person living in the fishing village along Minamata Bay, Japan, Died of a Mysterious disease. Investigations revealed that the victims had eaten shell-fish contaminated with Hg-containing effluent from a nearby plastic factory operating since 1949. The unit was producing vinyl chloride & acetaldehyde by catalytic conversion of acetylene using HgCl2 as the catalyst. The ailment becomes known as “Minamata Diseases”. Minamata Diseases are a methylmercury poisoning disease of the central nervous system. There have been cases of fetal-type Minamata Disease which were caused when the mothers had been exposed to the methylmercury during pregnancy.
Mercury is a heavy metal of known toxicity.The clinical impact of smaller mercury exposures remains controversial. It exists in several forms: Inorganic Mercury, which includes metallic mercury and mercury vapor (Hg0) and mercurous (Hg+) or mercuric (Hg++) salts; and organic mercury, which includes compounds in which mercury is bonded to a structure containing carbon atoms (methyl, ethyl, phenyl or similar groups).
Epidemiological Features: The epidemiological features of Minamata disease were found to be:
- People who ate a great deal of fish and shellfish succumbed to this Disease
- Both men and women, in each age bracket (except infants), contracted this Disease and
- Cats kept by patients showed similar symptoms. Deducing from these facts, food poisoning caused by fish and shellfish, specifically bacterial cerebritis, was suspected.
Treatment of Mercury Poisoning & Minamata Disease :
Notify state and regional health officials to make clear the functional mechanism of exposure as well as to organization desirable decontamination measures, must these be needed.
Once the neurologic outcomes of Minamata ailment became visible, they are, unluckily, irreversible. The aim of medical management in Minamata ailment is to decrease the total body problem of mercury and lessen furthermore damage.
Pre-hospital treatment involves accumulating information on the time, type, and way of mercury exposure, in addition to the following :
• Initial investigation – Airway, breathing, and circulation ( ABCs )
• Intravenous ( IV ) admittance
• Removal from the infected area
Surgery does not have a function in the remedy for Minamata ailment; nevertheless, in some other type of mercury exposure, surgical treatment may well be needed. Surgical treatment sometimes has been utilized to eliminate ingested mercury which has become deposited in the intestine or colon.
Chelating agents that contain thiol groups can bind to mercury very effectively. For severe, inorganic toxicity, dimercaprol ( British antilewisite BAL ) has normally been suggested, but oral agents are achieving importance. Chelation with 2,3-dimercaptosuccinic acid ( DMSA or succimer) has been found to induce enhanced mercury excretion, compared with N -acetyl-D, L-penicillamine, in adults with severe mercury vapor exposure. DMSA is usually efficiently tolerated and has also shown efficiency in kids and children exposed to mercury. Chelation therapy can be prescribed in the outpatient setting with an oral chelator, such as DMSA.
Seafood rich in organic mercury should, of course, be avoided. Predators such as sharks and tuna typically have increased mercury concentrations compared with herbivorous fishes.
Deterrence and Prevention
Workplace hygiene and careful monitoring and disposal of industrial waste are equally important in the prevention of mercury poisoning. Minamata disease can be prevented by reducing or eliminating one’s consumption of fish caught from bodies of water that are contaminated with high concentrations of mercury.
Md Shahinur Islam
Dept. of Chemistry
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