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MNB
89120
Clinical Information: Manganese (Mn) is an essential trace element with many industrial uses.
Manganese is the 12th most abundant element in the earth's crust and is used predominantly in the
production of steel. These industrial processes cause elevated environmental exposures to airborne
manganese dust and fumes, which in turn have lead 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
or not at all; 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 judgment, 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.
Useful For: Monitoring manganese exposure Nutritional monitoring Clinical trials
Interpretation: Manganese in urine represents the excretion of excess manganese from the body.
Elevated levels may indicate occupational exposure or excessive nutritional intake. Specimens from
normal individuals have very low levels of manganese.
Reference Values:
0-15 years: not established
> or =16 years: 0.1-1.2 mcg/specimen
Clinical References: 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. Paschal DC, Ting BG, Morrow JC,
et. at. Trace metals in urine of United States residents: Reference range concentrations. Environmental
Research 1998;7:53-59
Manganese, Blood
Clinical Information: Manganese is a trace element that is an essential cofactor for several
enzymes, including one form of superoxide dismutase and the gluconeogenic enzymes pyruvate
carboxylase and isocitrate dehydrogenase. It circulates in the serum as a metalloprotein complex with
any of several proteins. The +2 and +3 states are of biological significance, but speciation in the
analysis has not been studied sufficiently to determine its value. The required daily intake of 1 mg to 6
mg is readily supplied by a normal diet with a diverse mixture of fruits and vegetables. Manganese ores
and alloys are refined and used in the making of batteries, welding rods, and high-temperature
refractory materials. Environmental exposure occurs from inhalation and ingestion of
manganese-containing dust and fumes occurring from the refinement processes. It is likely that inhaled
Mn is mobilized up the trachea and swallowed; uptake through the gut is inefficient, about 10%. The
major compartment for circulating Mn is the erythrocytes, bound to hemoglobin, with whole blood
concentrations of Mn (in normals) being 10 times that of the serum. Mn passes from the blood to the
tissues quickly. Concentrations in the liver are highest, with 1 mg Mn/kg to 1.5 mg Mn/kg (wet weight)
in normal individuals. The half-life of Mn in the body is about 40 days, with elimination primarily
through the feces. Only small amounts are excreted in the urine. Environmental sources of Mn can lead
to toxicity. The primary sites of toxicity are the central nervous system (CNS) and the liver. Acute
exposure to Mn fumes gives rise to symptoms common to many metal exposures including fever, dry
mouth, and muscle pain. Chronic exposure of several months or more gives rise to CNS symptoms and
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