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Gunnar Nordberg

Inorganic Mercury

Mercury combines readily with sulphur and halogens at ordinary temperatures and forms amalgams with all metals except iron, nickel, cadmium, aluminium, cobalt and platinum. It reacts exothermically (generates heat) with alkaline metals, is attacked by nitric acid but not by hydrochloric acid and, when hot, will combine with sulphuric acid.

Inorganic mercury is found in nature in the form of the sulphide (HgS) as cinnabar ore, which has an average mercury content of 0.1 to 4%. It is also encountered in the earth’s crust in the form of geodes of liquid mercury (in Almadén) and as impregnated schist or slate (e.g., in India and Yugoslavia).

Extraction. Mercury ore is extracted by underground mining, and mercury metal is separated from the ore by roasting in a rotary kiln or shaft furnace, or by reduction with iron or calcium oxide. The vapour is carried off in the combustion gases and is condensed in vertical tubes.

The most important uses of metallic mercury and its inorganic compounds have included the treatment of gold and silver ores; the manufacture of amalgams; the manufacture and repair of measurement or laboratory apparatus; the manufacture of incandescent electric bulbs, mercury vapour tubes, radio valves, x-ray tubes, switches, batteries, rectifiers, etc.; as a catalyst for the production of chlorine and alkali and the production of acetic acid and acetaldehyde from acetylene; chemical, physical and biological laboratory research; gold, silver, bronze and tin plating; tanning and currying; feltmaking; taxidermy; textile manufacture; photography and photogravure; mercury-based paints and pigments; and the manufacture of artificial silk. Some of these uses have been discontinued because of the toxic effects that the mercury exposure exerted upon workers.

Organic Mercury Compounds

Organic compounds of mercury may be considered as the organic compounds in which the mercury is chemically linked directly to a carbon atom. Carbon-mercury bonds have a wide range of stability; in general, the carbon-to-mercury bond in aliphatic compounds is more stable than that in aromatic compounds. According to one reliable estimate, more than 400 phenyl mercurials and at least that number of alkyl mercury compounds have been synthesized. The three most important groups in common usage are the alkyls, the aromatic hydrocarbons or aryls and the alkoxyalkyls. Examples of aryl mercury compounds are phenylmercuric acetate (PMA), nitrate, oleate, propionate and benzoate. Most available information is about PMA.

Uses. All the important uses of the organic mercury compounds depend on the biological activity of these substances. In medical practice organic mercury compounds are used as antiseptics, germicides, diuretics and contraceptives. In the field of pesticides they serve as algicides, fungicides, herbicides, slimacides and as preservatives in paints, waxes and pastes; they are used for mildew suppression, in antifouling paints, in latex paints and in the fungus-proofing of fabrics, paper, cork, rubber and wood for use in humid climates. In the chemical industry they act as catalysts in a number of reactions and the mercury alkyls are used as alkylating agents in organic syntheses.


Absorption and effects: Inorganic and metallic mercury

Vapour inhalation is the main route for the entry of metallic mercury into the body. Around 80% of inhaled mercury vapour is absorbed in the lung (alveoli). Digestive absorption of metallic mercury is negligible (lower than 0.01% of the administered dose). Subcutaneous penetration of metallic mercury as the result of an accident (e.g. the breakage of a thermometer) is also possible.

The main routes of entry of inorganic mercury compounds (mercury salts) are the lungs (atomization of mercury salts) and the gastrointestinal tract. In the latter case, absorption is often the result of accidental or voluntary ingestion. It is estimated that 2 to 10% of ingested mercury salts are absorbed through the intestinal tract.

Skin absorption of metallic mercury and certain of its compounds is possible, although the rate of absorption is low. After entry into the body, metallic mercury continues to exist for a short time in metallic form, which explains its penetration of the blood-brain barrier. In blood and tissues metallic mercury is rapidly oxidized to Hg2+ mercury ion, which fixes to proteins. In the blood, inorganic mercury is also distributed between plasma and red blood cells.

The kidney and brain are the sites of deposition following exposure to metallic mercury vapours, and the kidney following exposure to inorganic mercury salts.

Acute poisoning

The symptoms of acute poisoning include pulmonary irritation (chemical pneumonia), perhaps leading to acute pulmonary oedema. Renal involvement is also possible. Acute poisoning is more often the result of accidental or voluntary ingestion of a mercury salt. This leads to severe inflammation of the gastrointestinal tract followed rapidly by renal insufficiency due to necrosis of the proximal convoluted tubules.

The severe chronic form of mercury poisoning encountered in places like Almadén up until the early 20th century, and which presented spectacular renal, digestive, mental and nervous disorders and terminated in cachexia, was eliminated by means of preventive measures. However, a chronic, “intermittent” poisoning in which periods of active intoxication are interspersed between periods of latent intoxication can still be detected among mercury miners. In the latent periods, symptoms remit to such a degree that they are visible only on close search; only the neurological manifestations persist in the form of profuse sweating, dermographia and, to some extent, emotional instability.

A condition of “micromercurialism” characterized by functional neurosis (frequent hysteria, neurasthenia, and mixed forms), cardiovascular lability and secretory neurosis of the stomach has also been described.

Digestive system. Gingivitis is the most common gastrointestinal disorder encountered in mercury poisoning. It is favoured by poor oral hygiene and is accompanied by an unpleasant, metallic or bitter taste in the mouth. Ulceromembranous stomatitis is much less common and is normally found in persons already suffering from gingivitis who have accidentally inhaled mercury vapours. This stomatitis commences with the subjective symptoms of gingivitis with increased salivation (mercurial ptyalism) and coating of the tongue. Eating and drinking produce a burning sensation and discomfort in the mouth, the gums become increasingly inflamed and swollen, ulcers appear and there is spontaneous bleeding. In acute cases, there is high fever, inflammation of the submaxillary ganglions and extremely fetid breath. Alveolodental periostitis has also been observed.

There may be a bluish line on the tooth edge of the gums, in particular in the vicinity of infected areas; this line is, however, never encountered in persons without teeth. Slate-grey punctiform pigmentation of the oral mucosae—the vestibular side of the gums (usually those of the lower jaw), the palate, and even the inside of the cheeks—has also been observed.

Recurrent gingivitis affects the supporting tissues of the teeth, and in many cases the teeth have to be extracted or merely fall out. Other gastrointestinal disorders encountered in mercury poisoning include gastritis and gastroduodenitis.

Non-specific pharyngitis is relatively common. A rarer manifestation is that of Kussmaul’s pharyngitis which presents as a bright-red coloration of the pharynx, tonsils and soft palate with fine arborisation.

Nervous system involvement may occur with or without gastrointestinal symptoms and may evolve in line with two main clinical pictures: (a) fine-intention tremor reminiscent of that encountered in persons suffering from multiple sclerosis; and (b) Parkinsonism with tremor at rest and reduced motor function. Usually one of these two conditions is dominant in the over-all clinical picture which may be further complicated by morbid irritability and pronounced mental hyperactivity (mercurial erethism).

Mercurial Parkinsonism presents a picture of unsteady and staggering gait, absence of balance-recovery reflexes and hypotonia; vegetative symptoms are slight with mask-like facies, sialorrhea, etc. However, Parkinsonism is usually encountered in milder forms, in particular as micro-Parkinsonism.

The most frequently encountered symptoms resemble those presented by persons with multiple sclerosis, except that there is no nystagmus and the two conditions have a different serology and different clinical courses. The most striking feature is tremor which is usually a late symptom but may develop prior to stomatitis.

Tremor usually disappears during sleep, although sudden generalized cramps or contractions may occur; however, it always increases under emotional stress and this is such a characteristic feature that it provides firm grounds for a diagnosis of mercury poisoning. Tremor is particularly pronounced in situations where the patient feels embarrassed or ashamed; often he or she will have to eat in solitude since otherwise he would be incapable of raising food to his lips. In its most acute form, the tremor may invade all the voluntary muscles and be continuous. Cases still occur in which the patient has to be strapped down to prevent him falling out of bed; such cases also present massive, choreiform movements sufficient to wake the patient from his sleep.

The patient tends to utter his words in staccato fashion, so that his sentences are difficult to follow (psellismus mercurialis); when a spasm ceases, the words come out too fast. In cases more reminiscent of parkinsonism, speech is slow and monotonous and the voice may be low or completely absent; spasmodic utterence is, however, more common.

A highly characteristic symptom is a desire for sleep, and the patient often sleeps for long periods although lightly and is frequently disturbed by cramps and spasms. However, insomnia may occur in some cases.

Loss of memory is an early and dementia a terminal symptom. Dermographia and profuse sweating (for no obvious reason) are frequently encountered. In chronic mercury poisoning, the eyes may show the picture of “mercurialentis” characterized by a light-grey to dark, reddish-grey discoloration of the anterior capsule of the crystalline lens due to the deposition of finely divided particles of mercury. Mercurialentis can be detected by examination with a slit-lamp microscope and is bilateral and symmetrical; it usually appears some considerable time before the onset of general signs of mercury poisoning.

Chronic exposure

Chronic mercury poisoning usually starts insidiously, which makes the early detection of incipient poisoning difficult. The main target organ is the nervous system. Initially, suitable tests can be used to detect psychomotor and neuro-muscular changes and slight tremor. Slight renal involvement (proteinuria, albuminuria, enzymuria) may be detectable earlier than neurological involvement.

If excessive exposure is not corrected, neurological and other manifestations (e.g., tremor, sweating, dermatography) become more pronounced, associated with changes in behaviour and personality disorders and, perhaps, digestive disorders (stomatitis, diarrhoea) and a deterioration in general status (anorexia, weight loss). Once this stage has been reached, termination of exposure may not lead to total recovery.

In chronic mercury poisoning, digestive and nervous symptoms predominate and, although the former are of earlier onset, the latter are more obvious; other significant but less intense symptoms may be present. The duration of the period of mercury absorption preceding the appearance of clinical symptoms depends on the level of absorption and individual factors. The main early signs include slight digestive disorders, in particular, loss of appetite; intermittent tremor, sometimes in specific muscle groups; and neurotic disorders varying in intensity. The course of intoxication may vary considerably from case to case. If exposure is terminated immediately upon the appearance of the first symptoms, full recovery usually occurs; however, if exposure is not terminated and the intoxication becomes firmly established, no more than an alleviation of symptoms can be expected in the majority of cases.

Kidney. There have been studies over the years on the relationships between renal function and urinary mercury levels. The effects of low-level exposures are still not well documented or understood. At higher levels (above 50 μg/g (micrograms per gram) abnormal renal function (as evidenced by N-acetyl-B-D-glucosaminidase (NAG), which is a sensitive indicator of damage to the kidneys) have been observed. The NAG levels were correlated with both the urinary mercury levels and the results of neurological and behavioural testing.

Nervous system. Recent years have seen the development of more data on low levels of mercury, which are discussed in more detail in the chapter Nervous system in this Encyclopaedia.

Blood. Chronic poisoning is accompanied by mild anaemia sometimes preceded by polycythaemia resulting from bone marrow irritation. Lymphocytosis and eosinophilia have also been observed.

Organic Mercury Compounds

Phenylmercuric acetate (PMA). Absorption may occur through inhalation of aerosols containing PMA, through skin absorption or by ingestion. The solubility of the mercurial and the particle size of the aerosols are determining factors for the extent of absorption. PMA is more efficiently absorbed by ingestion than are inorganic mercuric salts. Phenylmercury is transported mainly in blood and distributed in the blood cells (90%), accumulates in the liver and is there decomposed into inorganic mercury. Some phenylmercury is excreted in the bile. The main portion absorbed in the body is distributed in the tissues as inorganic mercury and accumulated in the kidney. On chronic exposure, mercury distribution and excretion follow the pattern seen on exposure to inorganic mercury.

Occupational exposure to phenylmercury compounds occurs in the manufacture and handling of products treated with fungicides containing phenylmercury compounds. Acute inhalation of large amounts may cause lung damage. Exposure of the skin to a concentrated solution of phenylmercury compounds may cause chemical burns with blistering. Sensitization to phenylmercury compounds may occur. Ingestion of large amounts of phenylmercury may cause renal and liver damage. Chronic poisoning gives rise to renal damage due to accumulation of inorganic mercury in the renal tubules.

Available clinical data do not permit extensive conclusions about dose-response relationships. They suggest, however, that phenylmercury compounds are less toxic than inorganic mercury compounds or long-term exposure. There is some evidence of mild adverse effects on the blood.

Alkyl mercury compounds. From a practical point of view, the short-chained alkyl mercury compounds, like methylmercury and ethylmercury, are the most important, although some exotic mercury compounds, generally used in laboratory research, have led to spectacular rapid deaths from acute poisoning. These compounds have been extensively used in seed treatment where they have been responsible for a number of fatalities. Methylmercuric chloride forms white crystals with a characteristic odour, while ethylmercury chloride; (chloroethylmercury) forms white flakes. Volatile methylmercury compounds, like methylmercury chloride, are absorbed to about 80% upon inhalation of vapour. More than 95% of short-chained alkyl mercury compounds is absorbed by ingestion, although the absorption of methylmercury compounds by the skin can be efficient, depending on their solubility and concentration and the condition of the skin.

Transport, distribution and excretion. Methylmercury is transported in the red blood cells ( 95%), and a small fraction is bound to plasma proteins. The distribution to the different tissues of the body is rather slow and it takes about four days before equilibrium is obtained. Methylmercury is concentrated in the central nervous system and especially in grey matter. About 10% of the body burden of mercury is found in the brain. The highest concentration is found in the occipital cortex and the cerebellum. In pregnant women methylmercury is transferred in the placenta to the foetus and especially accumulated in the foetal brain.

Hazards of organic mercury

Poisoning by alkyl mercury may occur on inhalation of vapour and dust containing alkyl mercury and in the manufacture of the mercurial or in handling the final material. Skin contact with concentrated solutions results in chemical burns and blistering. In small agricultural operations there is a risk of exchange between treated seed and products intended for food, followed by involuntary intake of large amounts of alkyl mercury. On acute exposure the signs and symptoms of poisoning have an insidious onset and appear with a latency period which may vary from one to several weeks. The latency period is dependent on the size of the dose—the larger the dose, the shorter the period.

On chronic exposure the onset is more insidious, but the symptoms and signs are essentially the same, due to the accumulation of mercury in the central nervous system, causing neuron damage in the sensory cortex, such as visual cortex, auditory cortex and the pre- and post-central areas. The signs are characterized by sensory disturbances with paresthaesia in the distal extremities, in the tongue and around the lips. With more severe intoxications ataxia, concentric constrictions of the visual fields, impairment of hearing and extrapyramidal symptoms may appear. In severe cases chronic seizures occur.

The period in life most sensitive to methylmercury poisoning is the time in utero; the foetus seems to be between 2 and 5 times more sensitive than the adult. Exposure in utero results in cerebral palsy, partly due to inhibition of the migration of neurons from central parts to the peripheral cortical areas. In less severe cases retardation in the psychomotor development has been observed.

Alkoxyalkyl mercury compounds. The most common alkoxyalkyl compounds used are methoxyethyl mercury salts (e.g., methoxyethylmercury acetate), which have replaced the short-chain alkyl compounds in seed treatment in many industrial countries, in which the alkyl compounds have been banned due to their hazardousness.

The available information is very limited. Alkoxyalkyl compounds are absorbed by inhalation and by ingestion more efficiently than inorganic mercury salts. The distribution and excretion patterns of absorbed mercury follow those of inorganic mercury salts. Excretion occurs through the intestinal tract and the kidney. To what extent unchanged alkoxyalkyl mercury is excreted in humans is unknown. Exposure to alkoxyalkyl mercury compounds can occur in the manufacture of the compound and in handling the final product(s) treated with the mercurial. Methoxyethyl mercury acetate is a vesicant when applied in concentrated solutions to the skin. Inhalation of methoxyethyl mercury salt dust may cause lung damage, and chronic poisoning due to long-term exposure may give rise to renal damage.

Safety and Health Measures

Efforts should be made to replace mercury with less hazardous substances. For example, the felt industry may employ non-mercurial compounds. In mining, wet drilling techniques should be used. Ventilation is the main safety measure and if it is inadequate, the workers should be provided with respiratory protective equipment.

In industry, wherever possible, mercury should be handled in hermetically sealed systems and extremely strict hygiene rules should be applied at the workplace. When mercury is spilt, it very easily infiltrates into crevices, gaps in the floor and workbenches. Due to its vapour pressure, a high atmospheric concentration may occur even following seemingly negligible contamination. It is therefore important to avoid the slightest soiling of work surfaces; these should be smooth, non-absorbent and slightly tilted towards a collector or, failing this, have a metal grill over a gutter filled with water to collect any drops of spilt mercury which fall through the grill. Working surfaces should be cleaned regularly and, in the event of accidental contamination, any drops of mercury collected in a water trap should be drawn off as rapidly as possible.

Where there is a danger of mercury volatilizing, local exhaust ventilation (LEV) systems should be installed. Admittedly, this is a solution which is not always applicable, as is the case in premises producing chlorine by the mercury cell process, in view of the enormous vaporization surface.

Work posts should be planned in such a way as to minimize the number of persons exposed to mercury.

Most exposure to organic mercury compounds involves mixed exposure to mercury vapour and the organic compound, as the organic mercury compounds decompose and release mercury vapour. All technical measures pertaining to exposure to mercury vapour should be applied for exposure to organic mercury compounds. Thus, contamination of clothes and/or parts of the body should be avoided, as it may be a dangerous source of mercury vapour close to the breathing zone. Special protective work clothes should be used and changed after the workshift. Spray painting with paint containing mercurials requires respiratory protective equipment and adequate ventilation. The short-chained alkyl mercury compounds should be eliminated and replaced whenever possible. If handling cannot be avoided, an enclosed system should be used, combined with adequate ventilation, to limit exposure to a minimum.

Great care must be exercised in preventing the contamination of water sources with mercury effluent since the mercury can be incorporated into the food chain, leading to disasters such as that which occurred in Minamata, Japan.



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Part I. The Body
Part II. Health Care
Part III. Management & Policy
Part IV. Tools and Approaches
Part V. Psychosocial and Organizational Factors
Part VI. General Hazards
Part VII. The Environment
Part VIII. Accidents and Safety Management
Part IX. Chemicals
Using, Storing and Transporting Chemicals
Minerals and Agricultural Chemicals
Metals: Chemical Properties and Toxicity
Part X. Industries Based on Biological Resources
Part XI. Industries Based on Natural Resources
Part XII. Chemical Industries
Part XIII. Manufacturing Industries
Part XIV. Textile and Apparel Industries
Part XV. Transport Industries
Part XVI. Construction
Part XVII. Services and Trade
Part XVIII. Guides

Metals: Chemical Properties and Toxicity References

Agency for Toxic Substances and Disease Registry (ATSDR). 1995. Case Studies in Environmental Medicine: Lead Toxicity. Atlanta: ATSDR.

Brief, RS, JW Blanchard, RA Scala, and JH Blacker. 1971. Metal carbonyls in the petroleum industry. Arch Environ Health 23:373–384.

International Agency for Research on Cancer (IARC). 1990. Chromium, Nickel and Welding. Lyon: IARC.

National Institute for Occupational Safety and Health (NIOSH). 1994. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 94-116. Cincinnati, OH: NIOSH.

Rendall, REG, JI Phillips and KA Renton. 1994. Death following exposure to fine particulate nickel from a metal arc process. Ann Occup Hyg 38:921–930.

Sunderman, FW, Jr., and A Oskarsson,. 1991. Nickel. In Metals and their compounds in the environment, edited by E Merian, Weinheim, Germany: VCH Verlag.

Sunderman, FW, Jr., A Aitio, LO Morgan, and T Norseth. 1986. Biological monitoring of nickel. Tox Ind Health 2:17–78.

United Nations Committee of Experts on the Transport of Dangerous Goods. 1995. Recommendations on the Transport of Dangerous Goods, 9th edition. New York: United Nations.