Main source of mercury is cinnabar. However, there are at least thirty different minerals in which mercury occurs in more than trace amounts. In chlor-alkali plants, plastics, electrical, electronic industries and in units manufacturing organo-mercurial compounds, mercury finds wide spread usage. Effluents from these industries and the subsequent use, abuse and refuse of their products constitute an important source of mercury in the environment.

Another source of mercury pollution is the combustion of fossil fuels. Coal on an average contains unto 0.5 ppm of mercury while in fuel oils mercury levels range between 0.1 – 0.35 ppm. It has been estimated that on global scale about 5000 tons of mercury are released from the combustion of fossil fuels alone.

Elemental mercury and some of its organic derivatives are regularly released from earth’s crust into the atmosphere – a process often referred to as ‘natural de-gasing’ of earth’s crust. It has been estimated that about 25,000 to 150,000 tons of mercury are discharged by this process while manmade sources contribute only 8,000 to 10,000 tons of mercury into the environment.

Based on toxicological characteristics there are three important forms of mercury: elemental mercury, inorganic and organic mercury. Certain anaerobic bacteria in bottom sediments of water bodies convert inorganic mercury to more toxic organo-mercury compounds.


For example Clostridium cochlearum under anaerobic conditions transform mercury to highly toxic methyl mercury while the same is done under aerobic conditions by some bacteria belonging to genus Psuedomonas, and Neurospora crassa which is a fungus. Under alkaline conditions monomethyl mercury could be changed to dimethyl mercury, a volatile compound which can contaminate the atmosphere.

Under acidic conditions dimethyl mercury is converted back to mono-methyl mercury. It is mostly methyl mercury which is absorbed by aquatic biota. Organo-mercurials are converted to inorganic mercury under oxidizing conditions. Ultra-violet light hastens the process.

Reaction with hydrogen sulphide under anaerobic conditions causes the formation of poorly soluble mercuric sulphide which is mobilized to produce mercuric sulphate under aerobic conditions. Natural processes are, therefore, responsible for interconversion of one form of mercury into another (Gavis and Fergusan, 1972, Coldwater, 1972).

Mercury vapours readily diffuse across alveolar membrane and are lipid soluble. Mercury has an affinity for red blood cells and central nervous system. Absorption of metallic mercury from the gastro-intestinal tract (about 0.01%) is not of any toxicological significance.


The absorption of inorganic salts of mercury from intestines has been shown to be about 7% only. Organo-mercurials are, however, efficiently absorbed – almost 90-95% absorption has been recorded. Since the rate of excretion of methyl mercury is considerably slower than the rate of its uptake, it is bio-accumulated and bio-magnified along the food chain.

Kidneys possess largest mercury content following exposure to inorganic forms while organic mercury has a greater affinity for brain. Within a cell mercury may bind to a number of enzyme systems including those of microsomes and mitochondria resulting in general non-specific cell injury or death. Mercury has particular affinity for ligand containing sulph-hydryl groups and in liver cells it forms soluble complexes with cystein and glutathione which are excreted through bile and are reabsorbed form the intestines.

All forms of mercury cross placenta and reach the foetus, which may possess a much higher concentration as compared to the maternal tissues. This is particularly true of alkyl-mercury compounds which attain almost twice as much mercury content as found in maternal tissues. Thus alkyl mercury exposures are very dangerous in case of pregnant females. Although mercury is excreted From the body predominantly through urine and faeces, almost 5% of mercury concentration in blood may appear in maternal milk. Thus nursing may greatly enhance the neo-natal exposures.

Inhalation of mercury vapours produces an acute corrosive bronchitis, interstitial pneumonitis and in higher doses central nervous system may be affected which results in increased excitability, tremours, impaired vision, muscular convulsions, madness and paralysis. Ultimately kidney failure occurs.


Deliberate or accidental ingestion of divalent mercury salts causes corrosive ulceration, bleeding and necrosis of gastro-intestinal tract. Severe abdominal cramps, bloody diarrhoea and suppression of urination follow. If the patient survives the gastro-intestinal damages, kidney failure occurs within twenty four hours owing to necrosis of proximal tubular epithelium.

Mercurous compounds are less damaging in their action than mercuric salts probably because of their low solubility. Possibly the most important form of mercury in terms of toxic effects is methyl mercury. The main site of injury which is of a permanent nature is the central nervous system.

The neurons in focal areas of cerebral cortex undergo degenerative changes and necrosis. This result in tremours, inability to co-ordinate voluntary movements, paralysis, impairment of vision, loss of hearing, speech and coma in severe cases. There is no effective treatment known for alkyl-mercury poisoning Mercury has teratogenic action and is capable of inducing abortions and embryo toxic effects (Goldwater, 1972).

Two major episodes of mercury poisoning have occurred in Japan, in Minamata bay and Naigata as a consequence of industrial discharge of mercury compounds. Mercury was absorbed, bio-accumulated and bio-magnified to high levels. Fishes collected from Minamata bay and Agano River contained as much as 10-12 mg of mercury per kg of their flesh and bones.


The largest epidemic of methyl mercury poisoning, however, took place in 1971-72 in Iraq when scarecity forced people to eat wheat grains treated with methyl mercury based fungicide which were intended to be used as seeds. The average methyl mercury content of these grains was about 4.8 – 14.6 mg per kg. About 6000 people were affected with the poisoning and some 500 deaths occurred (Bakir et al, 1973).

Mothers exposed to sublethal doses showed only slight symptoms of mercury poisoning but gave birth to retarded offsprings and continued to secrete mercury with their milk for long periods of time. We do not have to stretch our imagination too far to visualize the fate of the unfortunate child who is fed mercury contaminated milk straight from mother’s breasts.