Monitoring manganese exposure
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Manganese (Mn) is a trace essential element with many industrial uses. The twelfth most abundant element in the earth's crust, nearly all mined manganese is consumed in the production of ferromanganese, which is then used to remove oxygen and sulfur impurities from steel. These industrial processes cause elevated environmental exposures to airborne manganese dust and fumes, which in turn have led to well-documented cases of neurotoxicity among exposed workers. Mining and iron and steel production have been implicated as sources of exposure.
Inhalation is the primary source of entry for manganese toxicity. Signs of toxicity may appear quickly, and neurological symptoms are rarely reversible. Manganese toxicity is generally recognized to progress through 3 stages. Levy describes these stages. "The first stage is a prodrome of malaise, somnolence, apathy, emotional lability, sexual dysfunction, weakness, lethargy, anorexia, and headaches. If there is continued exposure, progression to a second stage may occur, with psychological disturbances, including impaired memory and judgement, anxiety, and sometimes psychotic manifestations such as hallucinations. The third stage consists of progressive bradykinesia, dysarthrian axial and extremity dystonia, paresis, gait disturbances, cogwheel rigidity, intention tremor, impaired coordination, and a mask-like face. Many of those affected may be permanently and completely disabled."(1) Few cases of manganese deficiency or toxicity due to ingestion have been documented. Only 1% to 3% manganese is absorbed via ingestion, while most of the remaining manganese is excreted in the feces.
As listed in the United States National Agriculture Library, manganese adequate intake is 1.6 mg/day to 2.3 mg/day for adults. This level of intake is easily achieved without supplementation by a diverse diet including fruits and vegetables, which have higher amounts of manganese than other food types. Patients on a long-term parenteral nutrition should receive manganese supplementation and should be monitored to ensure that circulatory levels of manganese are appropriate.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
Reference values have not been established for patients that are <18 years of age.
Serum manganese results above the reference values suggest recent exposure.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
Specimens collected from healthy, unexposed adults have extremely low levels of manganese. Because of the high environmental concentration of manganese, contamination is always a possibility when considering elevated results. Precautions must be taken to ensure the specimen is not contaminated. Metal-free serum collection procedures must be followed and centrifuged serum must be aliquoted into an acid-washed Mayo metal-free vial.
High concentrations of gadolinium and iodine are known to interfere with most metals tests. If either gadolinium- or iodine-containing contrast media has been administered, a specimen should not be collected for 96 hours.
Clinical Reference Provides recommendations for further in-depth reading of a clinical nature
1. Levy BS, Nassetta WJ: Neurologic effects of Manganese in humans: A review. Int J Occup Environ Health Apr/Jun 2003;9(2):153-163
2. Chiswell B, Johnson D: Manganese: In Handbook on Metals in Clinical and Analytical Chemistry. Edited by HG Sigel, H Sigel. Marcel Dekker, Inc, New York, 1994, pp 479-494
3. Finley J, Davis C: Manganese deficiency and toxicity: Are high or low dietary amounts of manganese cause for concern? Biofactors 1999;10:15-24