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Manganese

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Gunnar Nordberg

Occurrence and Uses

Manganese (Mn) is one of the most abundant elements in the earth’s crust. It is found in soils, sediments, rocks, water and biological materials. At least a hundred minerals contain manganese. Oxides, carbonates and silicates are the most important among manganese-containing minerals. Manganese can exist in eight oxidation states, the most important being +2, +3, and +7. Manganese dioxide (MnO2) is the most stable oxide. Manganese forms various organometallic compounds. Of major practical interest is methylcyclopentadienyl manganese tricarbonyl CH3C5H4Mn(CO)3, often referred to as MMT.

The most important commercial source of manganese is manganese dioxide (MnO2), which is found naturally in sedimentary deposits as pyrolusite. Two other types of deposit can be distinguished: carbonate accumulations, which are usually composed mainly of rhodocrosite (MnCO3), and stratiform deposits. However, only the sedimentary deposits are significant, and those are usually worked by opencast techniques. Sometimes underground mining is necessary, and room and pillar extraction is carried out; seldom is there any call for the techniques used in deep metal mining.

Manganese is used in the production of steel as a reagent to reduce oxygen and sulphur and as an alloying agent for special steels, aluminium and copper. It is used in the chemical industry as an oxidizing agent and for the production of potassium permanganate and other manganese chemicals. Manganese is used for electrode coating in welding rods and for rock crushers, railway points and crossings. It also finds use in the ceramics, match, glass and dyestuff industries.

Several manganese salts are used in fertilizers and as driers for linseed oil. They are also utilized for glass and textile bleaching and for leather tanning. MMT has been used as a fuel-oil additive, a smoke inhibitor, and as an antiknock gasoline additive.

Hazards

Absorption, distribution and excretion

In occupational situations manganese is primarily absorbed by inhalation. Manganese dioxide and other manganese compounds which occur as volatile by-products of metal refining are practically insoluble in water. Thus, only particles small enough to reach the alveoli are eventually absorbed into the blood. Large inhaled particles may be cleared from the respiratory tract and swallowed. Manganese may also enter the gastrointestinal tract with contaminated food and water. The rate of absorption can be influenced by a dietary level of manganese and iron, the type of manganese compound, iron deficiency and age. However, the risk of intoxication by this route is not great. Absorption of manganese through the skin is negligible.

After inhalation, or after parenteral and oral exposure, the absorbed manganese is rapidly eliminated from the blood and distributed mainly to the liver. The kinetic patterns for blood clearance and liver uptake of manganese are similar, indicating that these two manganese pools rapidly enter equilibrium. Excess metal may be distributed to other tissues such as kidneys, small intestine, endocrine glands and bones. Manganese preferentially accumulates in tissues rich in mitochondria. It also penetrates the blood-brain barrier and the placenta. Higher concentrations of manganese are also associated with pigmented portions of the body, including the retina, pigmented conjunctiva and dark skin. Dark hair also accumulates manganese. It is estimated that the total body burden for manganese is between 10 and 20 mg for a 70 kg male. The biological half-life for manganese is between 36 and 41 days, but for manganese sequestered in the brain, the half-life is considerably longer. In the blood, manganese is bound to proteins.

The organic compound MMT is rapidly metabolized in the body. The distribution seems to be similar to that seen after exposure to inorganic manganese.

Bile flow is the main route of excretion of manganese. Consequently, it is eliminated almost entirely with faeces, and only 0.1 to 1.3% of daily intake with urine. It seems that biliary excretion is the main regulatory mechanism in the homeostatic control of manganese in the body, accounting for a relative stability of manganese content in tissues. After exposure to the organic compound MMT, excretion of manganese goes to a large extent with urine. This has been explained as a result of biotransformation of the organic compound in the kidney. As a metalloprotein compound of some enzymes, manganese is an essential element for humans.

Exposure

Intoxication by manganese is reported in mining and processing of manganese ores, in the production of manganese alloys, dry-cell batteries, welding electrodes, varnishes and ceramic tiles. Mining of ore can still present important occupational hazards, and the ferromanganese industry is the next most important source of risk. The operations that produce the highest concentrations of manganese dioxide dust are those of drilling and shotfiring. Consequently, the most dangerous job is high-speed drilling.

Considering the dependence of deposition sites and solubility rate of particle size, the dangerous effect of exposure is closely related to the particle size composition of manganese aerosol. There is also evidence that aerosols formed by condensation may be more harmful than those formed by disintegration, which can be connected again with the difference in particle size distribution. The toxicity of different manganese compounds appears to depend on the type of manganese ion present and on the oxidation state of manganese. The less oxidized the compound, the higher the toxicity.

Chronic manganese poisoning (manganism)

Chronic manganese poisoning can take either a nervous or pulmonary form. If the nervous system is attacked, three phases can be distinguished. During the initial period, diagnosis may be difficult. Early diagnosis, however, is critical because cessation of exposure appears to be effective in arresting the course of the disease. Symptoms include indifference and apathy, sleepiness, loss of appetite, headache, dizziness and asthenia. There may be bouts of excitablity, difficulty in walking and coordination, and cramps and pains in the back. These symptoms can be present in varying degrees and appear either together or in isolation. They mark the onset of the disease.

The intermediate stage is marked by the appearance of objective symptoms. First the voice become monotonous and sinks to a whisper, and speech is slow and irregular, perhaps with a stammer. There is fixed and hilarious or dazed and vacant facies, which may be attributable to an increase in the tonus of the facial muscles. The patient may abruptly burst into laughter or (more rarely) into tears. Although the faculties are much decayed, the victim appears to be in a perpetual state of euphoria. Gestures are slow and awkward, gait is normal but there may be a waving movement of the arms. The patient is unable to run and can walk backwards only with difficulty, sometimes with retropulsion. Inability to perform rapid alternating movements (adiadochokinesia) may develop, but neurological examination displays no changes except, in certain cases, exaggeration of the patellar reflexes.

Within a few months, the patient’s condition deteriorates noticeably and the various disorders, especially those affecting the gait, grow steadily more pronounced. The earliest and most obvious symptom during this phase is muscular rigidity, constant but varying in degree, which results in a very characteristic gait (slow, spasmodic and unsteady), the patient putting his or her weight on the metatarsus and producing a movement variously described as “cock-walk” or “hen’s gait”. The victim is totally incapable of walking backwards and, should he or she try to do so, falls; balance can hardly be preserved, even when trying to stand with both feet together. A sufferer can turn round only slowly. There may be tremor, frequently in the lower limbs, even generalized.

The tendinous reflexes, rarely normal, become exaggerated. Sometimes there are vasomotor disorders with sudden sweating, pallor or blushing; on occasion there is cyanosis of the extremities. The sensory functions remain intact. The patient’s mind may work only slowly; writing becomes irregular, some words being illegible. There may be changes in the pulse rate. This is the stage at which the disease becomes progressive and irreversible.

Pulmonary form. Reports of “manganese pneumoconiosis” have been contested in view of the high silica content of the rock at the site of exposure; manganese pneumonia has also been described. There is also controversy over the correlation between pneumonia and manganese exposure unless manganese acts as an aggravating factor. In view of its epidemic character and severity, the disease may be a non-typical viral pneumopathy. These manganic pneumonias respond well to antibiotics.

Pathology. Some authors maintain that there are widespread lesions to the corpus striatum, then to the cerebral cortex, the hippocampus and corpora quadrigemina (in the posterior corpora). However, others are of the opinion that the lesions to the frontal lobes provide a better explanation for all the symptoms observed than do those observed in the basal ganglia; this would be confirmed by electroencephalography. The lesions are always bilateral and more or less symmetrical.

Course. Manganese poisoning ultimately becomes chronic. However, if the disease is diagnosed while still at the early stages and the patient is removed from exposure, the course may be reversed. Once well established, it becomes progressive and irreversible, even when exposure is terminated. The nervous disorders show no tendency to regress and may be followed by deformation of the joints. Although the severity of certain symptoms may be reduced, gait remains permanently affected. The patient’s general condition remains good, and he or she may live a long time, eventually dying from an intercurrent ailment.

Diagnosis. This is based primarily on the patient’s personal and occupational history (job, length of exposure and so on). However, the subjective nature of the initial symptoms makes early diagnosis difficult; consequently, at this stage, questioning must be supplemented by information supplied by friends, colleagues and relatives. During the intermediate and full-blown stages of the intoxication, occupational history and objective symptoms facilitate diagnosis; laboratory examinations can provide information for supplementing the diagnosis.

Haematological changes are variable; on the one hand, there may be no changes at all, whereas, on the other, there may be leucopenia, lymphocytosis and inversion of leucocyte formula in 50% of cases, or increase in haemoglobin count (considered as the first sign of poisoning) and slight polycythaemia.

There is diminished urinary excretion of 17-ketosteroids, and it may be assumed that the adrenal function is affected. Albumin level in the cerebrospinal fluid is increased, often to a marked degree (40 to 55 and even 75 mg per cent). Digestive and hepatic symptoms are non-indicative; there is no sign of hepatomegalia or splenomegalia; however, accumulation of manganese in the liver may result in metabolic lesions which seem to be related to the patient’s endocrinological condition and may be influenced by the existence of neurological lesions.

Differential diagnosis. There may be difficulty in distinguishing between manganese poisoning and the following diseases: nerve syphilis, Parkinson’s disease, disseminated sclerosis, Wilson’s disease, hepatic cirrhosis and Westphal-Strümpell’s disease (pseudo-sclerosis).

Safety and Health Measures

The prevention of manganese poisoning is primarily a question of suppression of manganese dusts and fumes. In mines, dry drilling should always be replaced by wet drilling. Shotfiring should be carried out after the shift so that the heading can be well ventilated before the next shift starts up. Good general ventilation at source is also essential. Airline respiratory protection equipment as well as independent respirators have to be used in specific situations to avoid excessive short-term exposures.

A high standard of personal hygiene is essential, and personal cleanliness and adequate sanitary facilities, clothing and time must be provided so that compulsory showering after work, a change of clothes and a ban on eating at the workplace can be effected. Smoking at work should be prohibited as well.

Periodic measurements of exposure levels should be performed, and attention should be given to the size distribution of airborne manganese. Contamination of drinking water and food as well as workers’ dietary habits ought to be considered as a potential additional source of exposure.

It is inadvisable for workers with psychological or neurological disorders to be employed in work associated with exposure to manganese. Nutritional deficiency states may predispose to anaemia and thus increase susceptibility to manganese. Therefore workers suffering from such deficiencies have to be kept under strict surveillance. During the anaemic state, subjects should avoid exposure to manganese. The same relates to those suffering from lesions of the excretory organs, or from chronic obstructive lung disease. A study has suggested that long-term manganese exposure may contribute to the development of chronic obstructive lung disease, particularly if the exposure is combined with smoking. On the other hand impaired lungs may be more susceptible to the potential acute effect of manganese aerosols.

During the periodic medical examinations the worker should be screened for symptoms which might be connected with the subclinical stage of manganese poisoning. In addition, the worker should be examined clinically, particularly with a view to detecting early psychomotor changes and neurological signs. Subjective symptoms and abnormal behaviour may often constitute the only early indications of health impairment. Manganese can be measured in blood, urine, stools and hair. Estimation of the extent of manganese exposure by means of manganese concentration in urine and blood did not prove to be of great value.

The average manganese blood level in exposed workers seems to be of the same order as that in non-exposed persons. Contamination during sampling and analytical procedures may at least partly explain a rather wide range found in literature particularly for blood. The use of heparin as an anticoagulant is still quite common although the manganese content in heparin may exceed that in blood. The mean concentration of manganese in urine of non-exposed people is usually estimated to be between 1 and 8 mg/l, but values up to 21 mg/l have been reported. Daily manganese intake from human diets varies greatly with the amount of unrefined cereals, nuts, leafy vegetables and tea consumed, owing to their relatively high content of manganese, and thus affects the results of normal manganese content in biological media.

A manganese concentration of 60 mg/kg of faeces and higher has been suggested as indicative of occupational exposure to manganese. Manganese content in hair is normally below 4 mg/kg. As the determination of manganese in urine, which is often used in practice, has not yet been validated enough for assessment of individual exposure, it can be used only as a group indicator of the mean level of exposure. Collection of the stool and the analysis of manganese content is not easy to perform. Our present knowledge does not include any other reliable biological parameter which might be used as an indicator of individual exposure to manganese. Thus the assessment of workers’ exposure to manganese still has to rely on manganese air levels. There is also very little reliable information about the correlation between the manganese content in the blood and urine and the findings of neurological symptoms and signs.

Persons with the signs of manganese intoxication should be removed from exposure. If the worker is removed from exposure shortly after the onset of symptoms and signs (before the fully developed stage of manganism) many of the symptoms and signs will disappear. There may be some residual disturbances, however, particularly in speech and gait.

 

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Contents

Preface
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
Metals: Chemical Properties and Toxicity
Resources
Minerals and Agricultural Chemicals
Using, Storing and Transporting Chemicals
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 Additional Resources

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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.