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Trace Elements in Abiotic and Biotic Environments
(EFSA  2013). It is also a cofactor for a number of important enzymes, including
cholinesterase, oxidoreductases, transferases, hydrolases, lyases, isomerases, ligases
phosphoglucomutase, pyruvate carboxylase, mitochondrial superoxide dismutase
and several phosphates, peptidases, and glycosyltransferases. In certain instances,
Mn 2+ may be replaced by Co 2+ or Mg 2+ .
Mn and Fe have many physicochemical similarities, and there is a possibility
of competition between these elements. Excess Mn interferes with the absorption
of dietary Fe. Increased Mn concentrations inhibit the metabolic function of the
Fe-dependent enzyme, aconitase. Because Fe is the most prevalent nutritional deficiency in the world, there is the potential health risk associated with Fe deficiencies
exacerbating the brain Mn burden. Long-term exposure to excess Mn levels may
result in the Fe-deficiency anemia. Increased Mn intake impairs also the activity of
Cu metalloenzymes.
Adverse effects resulting from the Mn exposure in humans are associated primarily with inhalation in occupational settings. In the workplace, exposure to Mn
is most likely to occur by inhalation of Mn fumes or Mn-containing dusts. This is a
concern mainly in the ferromanganese, iron and steel, dry-cell battery, and welding
industries. Exposure may also occur during Mn mining and ore processing. Workers
in the Mn-processing industry are at the most risk.
Oral exposure to Mn, especially from contaminated water, can also cause adverse
health effects, which are similar to those observed from inhalation exposure. An
actual threshold level, at which exposure to Mn produces neurological effects in
humans, has not been established (EFSA 2013). Well water rich in Mn can be the
cause of its excessive intake.
Chronic low-dose Mn intoxication is strongly implicated in a number of neurodegenerative disorders, including Alzheimer’s disease, Parkinson’s disease, and
amyotrophic lateral sclerosis.
It may also play a role in the development of multiple sclerosis, restless leg syndrome, and Huntington’s disease. Excess accumulation of Mn in the brain results
in a neurological syndrome with cognitive, psychiatric, and movement abnormalities. Highest concentrations of Mn in the brain are at the basal ganglia, which may
precipitate a form of parkinsonism, with some clinical features that are similar, and
some that are different to those in Parkinson’s disease (Guilarte 2010).
Manganese overexposure, by both ingestion and inhalation, is most frequently
associated with manganism, a rare neurological biphasic disorder.
Manganese is a natural component of most foods (Table 26.2). Oral exposure is
the primary source of absorbed Mn, although its absorption through gastrointestinal
is relatively low. Dietary Mn intakes were significantly lower in nontea drinkers
(3.2 mg/day) than in tea drinkers (5.5 mg/day), depending upon the value used for
Mn levels of black tea. Tea drinking is a major source of dietary Mn, and Mn intakes
commonly exceed proposed adequate values of 1.8–2.3 mg Mn/day, and may exceed
upper limits of 10–11 mg/day (Hope et al. 2006). Nuts, chocolate, cereal-based products, pulses, fruits, and fruit products are rich sources of Mn (Table 26.2).
Formal recommended dietary allowance for Mn has not been established, but
WHO has proposed the estimated safe and adequate dietary intake at 2–5 mg/day,
for adults (WHO 2004).