After reading this article you will learn about:- 1. Biochemical Effects of Mercury 2. Toxic Effects of Mercury 3. Remedial Measures.
Biochemical Effects of Mercury:
Mercury (Hg) is a well-known toxic metal which came to the limelight after the incidence of “Minamata disease” in 1953-60 in Japan. A total of 111 cases of mercury-poisoning were reported among people who had eaten mercury-contaminated fish from Minamata Bay. Among them, about 45 people died.
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Genetic defects were observed in 20 babies whose mothers had consumed seafood from the bay. The sea fish in the Bay were found to have 27-102 PPm of mercury in the form of methyl mercury. This mercury source was the effluent from a vinyl chloride plant, Minamata Chemical Company, which used to discharge into the bay.
This was followed by a more tragic report of mercury poisoning from Iraq, in 1972, where 450 villagers died after eating wheat which had been dusted with a mercury-containing pesticide. These two tragic events boosted the awareness of Hg as a pollutant, resulting in its being studied more extensively than any other trace element.
In nature, Hg occurs as a trace component of many minerals, continental rocks containing an average of about 80 parts per billion of Hg. The principal ore is Cinnabar, HgS. Fossil fuels, coal and lignite contain about 100 parts per billion of Hg. The natural abundance in soil is 0.1 parts per million.
Hg finds a wide variety of applications. The largest consumer is the chlor-alkali industry which manufactures Cl2 and NaOH by an electrolytic process using Hg electrodes. The second largest consumption of Hg is in the production of electrical apparatus, e.g. Hg vapour lamp, electrical switches, Hg batteries etc. The third largest consumer is the agricultural industry using a large number of fungicides for seed dressings.
Some typical compounds of this category are:
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The impact of seed dressing is enormous since it is applied to a large volume of seed, which is subsequently sowed over millions of acres, thereby causing a widespread dispersal of Hg compounds. Furthermore, Hg undergoes translocation in plants and animals and then finds its way into the human food chain.
Hg enters the environment mainly through human activities, as above. Sewage effluent sometimes contains up to 10 times the level of Hg in natural water (0.001-0.0001 ppm).
Once Hg is absorbed on sediments of water bodies and streams, it is slowly released into the water and constitutes a reservoir which is likely to cause chronic pollution long after the original source of Hg is removed. Current rate of natural addition of Hg to the oceans is about 5,000 tons per annum and a further 5.000 tons is added via human activities.
Toxic Effects of Mercury:
The toxicity of Hg depends on its chemical species as shown in Table 25.9:
Elemental Hg is fairly inert and non-toxic. If swallowed, it is excreted without serious damage. It has a fairly high vapour pressure and so the vapour, if inhaled, is quite toxic. Hence, Hg should be handled only in well-ventilated areas and spills should be cleaned up as quickly as possible. Hg vapour, when inhaled, enters the brain through the blood stream, leading to severe damage of the central nervous system.
Hg2/2 +forms an insoluble chloride with chloride ions. As our stomachs contain a fairly high concentration of chloride, Hg2/2 +is not toxic. Hg2+ (mercuric ion), however, is fairly toxic.
Because of its high affinity for sulphur atoms, it easily attaches itself to the sulphur-containing amino acids of proteins It also forms bonds with haemoglobin and serum albumin, both of which contain sulphydryl groups This ion however, does not travel across biological membranes and, hence, does not get access into biological cells.
The most toxic species are the organomercurials, particularly CH3Hg+ (methyl mercury), which are soluble in fat, the lipid fraction of membranes and brain tissue. The covalent Hg-C bond is not easily disrupted and the alkyl mercury is retained in cells for prolonged periods of time. The most dangerous aspect is the ability of RHg+ to move through the placental barrier and enter fetal tissues.
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Attachment of Hg to cell membranes is likely to inhibit active transport of sugars across the membrane and allow the passage of K to the membrane. In case of brain cells, this will result in energy deficiency in the cell and disorders in the transmission of nerve impulses.
This will explain why babies born to mothers subjected to methyl mercury poisoning suffer from irreversible damage to the central nervous system including cerebral palsy, mental retardation and convulsions. Methyl mercury poisoning also leads to segregation of chromosomes, chromosome breakage in cells and inhibited cell division. All the symptoms of mercury poisoning set in at blood levels of 0.5 ppm of CH2Hg+.
Biological Methylation: Amplification in Food Chain:
The Minamata Chemical Company discharged Hg into Minamata Bay, but the fish in the Bay were found to contain CH3Hg+. This missing link was filled up by subsequent research. Hg or its salts can be converted to methyl mercury by anaerobic methane-synthesizing bacteria in water.
This conversion is facilitated by Co(III)-containing vitamin B12 con-enzyme. A CH3-group bonded to Co (III) on the coenzyme is transferred enzymatically by methyl cobalamin to Hg2+, yielding CH3Hg+ or (CH3)2Hg:
An acidic medium promotes the conversion of dimethyl mercury to methyl mercury which is soluble in water. It is methyl mercury which enters the food chain through plankton and is concentrated by fish by a factor of 10 or more as it passes up the food chain, as shown in Fig. 25.6.
The Hg concentration builds up at each level of the food chain. This is valid even in uncontaminated waters. Hg has always been part of our environment and Hg cycles existed long before any industry developed. Large fish of ancient ages, preserved in some museums, have been found to contain significant level of Hg. However, Hg pollution considerably enhances the Hg concentration in each level of the food chain.
Soon after the Minamata disaster, it was reported that freshwater fish from Lake Erie and the St Clair River showed high levels of Hg (0.1-3.5ppm), in the form of methyl mercury in their living tissues. As a result, important commercial fisheries in those areas were closed down.
Minamata Disease:
In the early 1950s, people in the small coastal village of Minamata, Japan, noticed strange behavior that they called dancing cats. Inexplicably, cats would begin twitching, stumbling, and jerking about as if they were drunk. Many became “suicidal” and staggered off docks into the ocean.
The residents did not realize it at the time, but they were witnessing an ominous warning of an environmental health crisis that would make the name of their village synonymous with a deadly disease. Their cats were suffering from brain damage that we now know was caused by methyl mercury poisoning.
In 1956, the first human case of neurological damage was reported. A five-year-old girl who had suddenly lapsed into a convulsive delirium was brought into the local clinic. Within a few weeks there seemed to be an epidemic of nervous problems in the village, including numbness, tingling sensations, headaches, blurred vision, slurred speech, and loss of muscle control.
For an unlucky few, these milder symptoms were followed by violent trembling, paralysis, and even death. An abnormally high rate of birth-defects also occurred. Children were born with tragic deformities, paralysis, and permanent mental retardation. Lengthy investigations showed that these symptoms were caused by mercury from fish and seafood that formed a major part of the diet of both humans and their cats.
For years the Chisso Chemical Plant had been releasing residues containing mercury into Minamata Bay. Since elemental mercury is not water soluble, it was assumed that it would sink into the bottom sediments and remain inert.
Scientists discovered, however, that bacteria living in the sediments were able to convert metallic mercury into soluble methyl mercury, which was absorbed from the water and concentrated in the tissues of aquatic organisms.
People who ate fish and shellfish from the bay were exposed to dangerously high levels of this toxic chemical. Altogether, more than 3.500 people were affected and about 50 died of what became known as Minamata Disease. After nearly twenty years of rancorous protests and litigation, the Chisso Company finally admitted that it was guilty of dumping the mercury and agreed to pay reparations to the victims.
Dumping of mercury into Minimata Bay was stopped twenty years ago. Mud containing mercury was dredged up and buried elsewhere so the bay is now considered safe for fishing. The minds and bodies of those people who ate the mercury-poisoned fish, however, can never be repaired. Have we learned from this tragedy how to anticipate and prevent future environmental disasters?
Remedial Measures of Mercury:
Further environmental pollution by Hg can be prevented by adopting the following measures, as recommended by the Environmental Protection Agencies of USA and Sweden:
1. All chlor-alkali plants must stop using Hg electrodes and switch to new technology.
2. All alkyl mercury pesticides must be banned.
3. All other mercurial pesticides must be restricted to some selected areas.
It should be noted that the already contaminated sediments of rivers and lakes will continue to yield highly toxic CH2Hg+ into the waters for many years to come. In Sweden, pilot experiments were undertaken for decontamination of sediments by covering the bottom sediments with fresh, finely divided materials having high adsorption capabilities and, alternatively, by burying the sediments under inorganic inert materials.