Hazardous Chemical Information System (HCIS)

Manganese

No standard should be applied without reference to Guidance on the interpretation of Workplace exposure standards for airborne contaminants.

1. IDENTITY

2. CHEMICAL AND PHYSICAL PROPERTIES

Manganese is very similar to iron in its physical and chemical properties, the chief difference being that manganese is harder and more brittle but less refractory. The metal readily dissolves in dilute, non-oxidising acids and reacts vigorously with many non-metals at elevated temperatures. Finely divided manganese can combine explosively with a number of materials ⁽³⁾ .

Given below are some of its elemental properties:

Manganese forms a number of oxidation states (VII⁺, VI⁺, III⁺ and II⁺), the more commonly occurring being the most stable Mn(II) and the powerfully oxidising Mn(VII). A more complete review of manganese chemistry can be found in Cotton and Wilkinson ⁽⁴⁾ .

3. MAJOR INDUSTRIAL USES

Manganese is widely used as a component of ferrous alloys in steelmaking (predominantly as ferromanganese and silicomanganese), in a number of non-ferrous alloys; especially with copper and zinc, as manganese dioxide in dry cell batteries, as an oxidising agent in dyes and chemicals, as a catalyst and as manganates and permanganates for disinfecting and bleaching ⁽⁵⁾ .

Exposure to manganese and its compounds can occur during:

(a) mining and processing of the ore;

(b) manganese smelting;

(c) ferrous and non-ferrous alloying;

(d) welding/brazing processes (either from electrodes/rods or parent material);

(e) dry-cell battery manufacture; and

(f) production and use of manganese chemicals and fertilisers.

4. ABSORPTION AND METABOLISM

Manganese is an essential trace element in all living organisms, including plants and bacteria, and is found in all human tissues. Unlike other metals such as lead and cadmium, the concentration of manganese in human tissue remains remarkably constant throughout adult life. The highest concentrations of manganese occur in the liver, pancreas, intestinal tract and kidney. Manganese absorption can be influenced by dietary level of manganese and iron, the type of manganese compound, iron deficiency and age ⁽⁶⁾ .

Food is the major natural source of manganese intake (approx. 3 mg/day) however only a very small proportion (ca.1%) is absorbed. Inhaled manganese is mostly swallowed (60-70%) after being cleared by the lung. Human volunteers who inhaled an aerosol containing MnCl₂ and MnO₂ were found to resorb manganese via the lungs ⁽⁷⁾ . The body is able to handle efficiently relatively large quantities of manganese, homeostasis being regulated by the liver, with excess excreted in the bile. The biological half-life of ⁵⁴Mn in normal individuals was found to be 37 days, though miners exposed to ore dust at 5 mg/m³ were shown to excrete manganese with a half-life of 15 days (Ref 5, p 1759. Manganese retention by the brain is much longer than by the whole body.

Although organo-manganese compounds can have significant absorption through the skin, it appears that absorption of inorganic manganese through the skin is negligible ⁽⁸⁾ .

In regard to biological monitoring, the significance of manganese in urine is still difficult to assess. On a group basis, manganese in blood seems to be more of an index of body burden than of current exposure ⁽²⁾ . Accordingly, results from biological monitoring for manganese need to be treated with particular caution.

5. HEALTH EFFECTS

In its acute form, manganese poisoning has an effect characteristic of other heavy metals, leading to "metal fume fever" if dust or fume is inhaled in sufficient quantity. An airborne concentration thought to be immediately dangerous to life or health is in the order of 10,000 mg/m^{3 (9)} .

In an occupational context, chronic exposure to manganese has been associated with two major effects; bronchitis/pneumonitis after inhalation of manganese dust, and 'manganism', a neuropsychiatric disorder that may also result from inhalation. The airborne manganese concentration which gives rise to these effects is different.

Manganism is the salient effect of chronic manganese poisoning. This disease, which arises from damage to the central nervous system (CNS), usually begins with psychological symptoms such as hallucinations, emotional instability and disturbances in behaviour. These may be followed by neurological symptoms such as muscular weakness, speech disturbances and headaches, as well as symptoms resembling those of Parkinson's disease (tremors, stiffness, motor dysfunction).

These toxic effects are considered to result from interference by manganese in the metabolism of biogenic amines such as dopamine. If exposure is terminated soon after the neurological symptoms appear, the individual generally recovers, but some speech and balance problems may remain ⁽⁷⁾ .

Individual susceptibility to the adverse effects of manganese varies considerably. The minimum dose that produces effects on the CNS is not known, but signs of adverse effects may occur at manganese concentrations ranging from 2 to 5 mg/m³ in air ⁽¹⁰⁾ . An explanation for this highly variable individual susceptibility may be related to the close relationship between manganese and iron metabolism and the intestinal absorption of manganese ⁽¹¹⁾ . Nutritional deficiency states may predispose workers to anaemia and thus increase susceptibility to manganese.

An increased incidence of pneumonia has been reported among individuals exposed to manganese. Some examples of these have been reported. From these data, it has not been possible to establish a dose-response relationship.

Table 1. Summary of reported respiratory effects associated with manganese exposure

It has been suggested that manganese may act as an aggravating factor, and that particle size distribution, type of manganese compound and oxidation state may be more important than the mass concentration of manganese in air ^(7,8) . This may also be true for the non-specific effects on the respiratory tract reported in manganese workers. Smoking appears to act synergistically with manganese in causing such effects, and it has been also suggested that inhalation exposure to manganese may also act synergistically with bacteria/viruses in the respiratory system thereby accounting for an increased prevalence of respiratory disease.

As background to the assignment of an exposure standard for manganese, two organisations, the American Conference for Governmental Industrial Hygiensts (ACGIH ⁽²⁾ ) and the Swedish National Board of Occupational and Safety and Health (SNBOSH ⁽⁷⁾ ), have reviewed the relationship between occupational exposure to manganese and the development of health effects in exposed individuals. An outline of the studies examined in these reviews are presented, along with summaries of more recent articles from the literature below.

Table 2. Summary of dose/effect relationships observed in some reported cases of exposure to manganese

6. DISCUSSION

From the data outlined above the following summary can be made.

Although little is known about the monitoring regime undertaken, Flinn et al (1940) and Rodier (1955), claimed that no cases of manganism were observed at concentrations considerably higher than 5 mg/m³. Tanaka and Lieben (1969) reported no cases of manganism at less than 5 mg/m³ for either fume or dust, wherease Kesic and Hausler (1954) reported that the incidence of manganese intoxication was low at exposures of 3-9 mg/m³. Reports cited for Whitlock (1966) and Chandra (1981) claim neurological symptoms consistent with manganism at exposures somewhat less than 5 mg/m³; however it has been suggested that the reported exposures are too low.

Schuler et al (1957) reported possible manganese poisoning when only one-third of exposures exceeded 5 mg/m³, and Emara et al (1971) noted that two workers displayed clinical neuropsychiatric effects of chronic manganese poisoning at 6.8 mg/m³ and six others at 32 mg/m³. Wang et al (1989) found six cases of Parkinsonism in eight workers exposed to >28 mg/m³ for at least 30 minutes per day, for seven days a week, over eight months (i.e. possibly > 2 mg/m³ TWA).

Recently, a number of authors have reported sub-clinical indicators of manganism following neurological assessment of exposed workers (e.g. abnormal psychomotor tests, tremors, exaggerated reflexes). Saric (1977) observed differences in 'rest tremor' following exposure at or above 5 mg/m³. Siegl et al (1982) noted increased reaction times in workers exposed to fume at 1.1 - 4.0 mg/m³ and a positive correlation with duration of exposure. Cizinsky et al (1989) reported differences in psychometric examinations at 0.2 - 0.45 mg/m³.

Roels et al (1987) reported significant alteration in psychomotor tests (reaction time, short-term memory capacity and hand tremor) in workers exposed at approximately 1 mg/m³. Roels et al concluded that a TWA exposure of about 1 mg/m³ (total Mn dust) for less than 20 years may present preclinical signs of intoxication.

An epidemiological study by Smyth (1973), supported by a fairly comprehensive monitoring program of TWA personal samples at various workstations, found evidence of clinical manganism in 5 out of 71 workers at a ferromanganese plant. Two workers were each exposed to manganese dust at 6.3 and 12.9 mg/m³, and two other workers were each exposed to fume at 0.3-3.6 and 13 mg/m³. One worker developed symptoms at 0.3 mg/m³ (fume). The author concluded that "the TLV for manganese-in-air concentrations provided little or no factor of safety, ... and that serious manganese intoxication might occur when weighted manganese-in-air concentrations were below the TLV as defined: 5 mg/m³, ceiling value".

The role of past high intermittent exposures in the development of these symptoms was not adequately addressed by Smyth. However, given that three years had elapsed since these significant exposures had been brought under control, it is unlikely that the symptoms displayed can be confidently divorced from the cited exposure data.

No reports indicating possible mutagenic or carcinogenic effects in humans have been found in the literature for inorganic manganese.

7. ASSIGNMENT OF STANDARDS BY OTHER AGENCIES

The ACGIH established a TLV of 6 mg/m³ for manganese in 1946. This value would appear to be based upon work by Flinn et al on dust exposures in a manganese ore mill. It would appear to have a very tentative basis.

The ACGIH adopted a ceiling value of 5 mg/m³ for manganese dust and compounds (as Mn) in 1963. This value, confirmed in the 1986 documentation ⁽²⁾ , was based upon a study of dust exposures at a ferromanganese steel plant where adverse effects were only shown at levels in the range of six to ten times the 5 mg/m³ limit, and through a personal communication to the TLV Committee in 1973, where it was claimed that no cases of manganism were ever reported for exposure to MnO₂ dust in the range of 1 to 5 mg/m³.

In 1988-89, the ACGIH deleted its ceiling limit for manganese in line with its policy that the ceiling notation only be applied where there is evidence of immediate health effects after brief exposures. On the basis that workers exposed to manganese fume developed symptoms of manganism at exposure levels below those of affected workers exposed to dust, the ACGIH recommends a TLV for manganese fume of 1 mg/m³ with a STEL of 3mg/m³. Acknowledging that this level is above that experienced by two (adversely affected) workers exposed to fume in the study by Smyth ⁽¹³⁾ , the ACGIH ⁽¹⁷⁾ states that "a lower limit may be recommended when more data become available".

The UK Health and Safety Executive (HSE ⁽¹⁸⁾ ) has assigned an eight-hour TWA of 5 mg/m³, with 5 mg/m³ ceiling (as Mn). The German DFG ⁽¹⁹⁾ has assigned an MAK (maximum allowable concentration) of 5 mg/m³ for manganese, allowing an excursion of 10 times the MAK value, as a 30 minute average, once per shift. These values, like the current NOHSC standard, have probably been adopted from the ACGIH.

In 1984, the EPA found that epidemiological studies in humans indicate effects on the respiratory system at levels below 1 mg/m³, whereas evidence of effects on the CNS below 0.5 mg/m³ was judged to be equivocal. The EPA concluded ⁽²⁰⁾ that a threshold for neurological effects from occupational exposure to manganese is 300 µg/m³ (0.3 mg/m³).

The World Health Organisation ⁽¹¹⁾ feels that signs and symptoms of effects on the central nervous system may already occur at air concentrations of manganese in the range of 2 to 5 mg/m³. The WHO believes that a minimum exposure effect level cannot be assessed, but considering human and animal data as well as the highly variable individual susceptibility to manganese, WHO also believes that it is probably less than 1 mg/m³.

The SNBOSH concluded that the critical effects of occupational exposure to manganese are respiratory and CNS effects. Manganism is acknowledged at manganese concentrations of 1 to 5 mg/m³, with early symptoms of manganism arising at lower concentrations. In 1983, the SNBOSH ⁽²¹⁾ assigned the following exposure limits to manganese and inorganic compounds (as Mn):

8. RECOMMENDATION FOR EXPOSURE STANDARD

There is a significant individual variation in the effects of exposure to airborne concentrations of manganese at about 5 mg/m³. It would appear, however, that the risk of manganism is not great below 5 mg/m³. Nonetheless, a number of studies have shown that susceptibility to the effects of manganese at or about 1 to 5 mg/m³ (TWA) can lead to both clinical manifestations of manganism or, more commonly, to the development of indicators of sub-clinical manganism (e.g. hand tremor, exaggerated reflexes, short-term memory deficits, headaches, poor psychomotor performance). Both clinical and sub-clinical indicators have been reported as low as 0.3 mg/m³, however the significance of these results is unclear.

Long-term exposure at, or below, 0.5 to 1 mg/m³ should afford protection for those individuals who may be susceptible to the neurological effects of prolonged exposure to manganese. Accordingly, the Exposure Standards Working Group recommends an eight-hour TWA exposure standard of 1 mg/m³ for manganese and inorganic compounds. A further review of this standard may be appropriate when more is known about the significance of the sub-clinical neurological effects of prolonged manganese exposure.

Fume arising from many industrial uses of manganese is often in the form of manganese tetroxide (Mn₃O₄). Although there is acknowledgement that the particle size distribution, type of manganese compound and oxidation state may play an important role in the development of both the neurological and respiratory effects of manganese, there is insufficient evidence to distinguish confidently between manganese fume, dust and other inorganic manganese compounds. For this reason it is recommended that a single exposure standard be applied for all inorganic manganese compounds, measured as inspirable dust (as Mn).

Provided that the eight-hour TWA exposure standard is not exceeded, short-term exposures should not exceed three times the TWA exposure standard for more than a total of 30 minutes per eight-hour working day; and under no circumstances should the short-term values exceed five times the exposure standard (the general excursion limit approach).

1. NOHSC, Exposure Standards for Atmospheric Contaminants in the Occupational Environment, National Occupational Health and Safety Commission, Australian Government Publishing Service, Canberra, 1990.

2. ACGIH, Documentation of the Threshold Limit Values and Biological Exposure Indices, 5th ed, American Conference of Governmental Industrial Hygienists, Cincinnati, Ohio, 1986.

3. Sax NX & Lewis RJ, Dangerous Properties of Materials, Vol III, 7th ed, Van Nostrand Reinhold, New York, 2159, 1989.

4. Cotton FA & Wilkinson GW, Advanced Inorganic Chemistry, 3rd ed, Interscience New York, 1972.

5. Clayton GD & Clayton FE (eds), Patty's Industrial Hygiene and Toxicology, 3rd ed, John Wiley and Sons, New York, 1981.

6. Roels H et al, "Epidemiological survey among workers exposed to manganese: effects on lung, central nervous system and some biological indices", Am J Industr Med, 11,307-327, 1987

7. SNBOSH, Scientific Basis for Swedish Occupational Standards IV - Consensus Report for Manganese, 36, Swedish National Board of Occupational Safety and Health, Solna, Sweden, 104-113, 1983.

8. ILO, Encyclopaedia of Occupational Health and Safety, 3rd ed, International Labor Office, Geneva, 1279-82, 1983.

9. OSHA, Industrial Exposure and Control Technologies for OSHA Regulated Substances - Manganese and Compounds, PB89-2,10199, US Occupational Safety and Health Administration, NTIS, Washington DC, 1193-1196, 1989.

10. IPCS, Environmental Health Criteria 17- Manganese, International Programme on Chemical Safety, World Health Organisation, Geneva, p 13, 1981.

11. Ibid, p 85.

12. Emara AM et al, "Chronic manganese poisoning in dry battery industry", Brit J Industr Med, 28, 78-82, 1971.

13. Smyth LT et al, "Clinical manganism and exposure to manganese in the production and processsing of ferromanganese alloy", J Med, 15, 2, 101-109, 1973.

14. Siegl P & Bergert KD, "Eine Fruhdiagnostische Uberwachungsmethode bei Manganexposition", Z Ges Hyg, 28, 524-526, 1982 [in German].

15. Cizinsky G et al, "Manganese exposure in Swedish steel smelteries & plants - a health hazard to the nervous system", NBOSH Newslett, Sweden, 4/89, 1989.

16. Wang JD et al, "Manganese induced Parkinsonism: an outbreak due to an unrepaired ventilation control system in a ferromanganese smelter", Brit J Industr Med, 46, 856-859, 1989.

17. ACGIH, Documentation of the Threshold Limit Values and Biological Exposure Indices, 6th ed, American Conference of Governmental Industrial Hygienists, Cincinnati, Ohio, 1990.

18. HSE, Occupational Exposure Limits 1987, Guidance Note EH40, UK Health and Safety Executive, London, 1989.

19. DFG, Maximum Concentrations at the Workplace and Biological Tolerance Values for Working Materials 1989, Report No. XXIII, Deutsche Forschungsgemein-schaft, Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, VCH Verlagsgesellschaft mbH, Weinheim, Germany, 1989.

20. EPA, Health Effects Assessment for Manganese (and compounds), US Environmental Protection Agency, 1984.

21. SNBOSH, Occupational Exposure Limit Values, Ordinance AFS 1984 5, National Board of Occupational Safety and Health, Solna, Sweden, 1984.

* Fume arising from molten ferromanganese or strong heating of manganese oxides inair is largely manganese tetraoxide (Mn₃O₄)⁽²⁾.