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Trace Elements in Abiotic and Biotic Environments
Observations of Mo deficiency have been limited to genetic defects, that interfere
with the ability of the Mo cofactor to activate molybdoenzymes, and to the one case
of feeding Mo-free total parenteral nutrition (TPN). Human dietary deficiency of Mo
has not been reported (EFSA 2010).
A congenital Mo cofactor deficiency disease, seen in infants, results in interference with the ability of the body to use Mo in enzymes. It causes high levels of sulfite and urate, and neurological damage. A Crohn’s disease patient, receiving TPN
without Mo added to the TPN solution, developed tachycardia, tachypnoea, severe
headache, night blindness, nausea, vomiting, central scotomas, generalized edema,
lethargy, disorientation, and coma (WHO 2011d).
In humans, tetrathiomolybdate therapy has been developed for Wilson’s disease,
a genetic disease in which the accumulation of Cu in tissues leads to liver and brain
damage. More recently, the use of tetrathiomolybdate has been explored for the treatment of cancer and inflammatory diseases.
The rate of gastrointestinal absorption of Mo is influenced by its chemical forms.
Tetravalent Mo is not readily absorbed. Sodium tungstate is a competitive inhibitor
of Mo. Dietary W reduces the concentration of Mo in tissues. High levels of Mo
can interfere with the body’s uptake of Cu, producing Cu deficiency. Molybdenum
prevents plasma proteins from binding to Cu, and it also increases the amount of Cu
that is excreted in urine.
An epidemiological study in India indicated that a form of lower-limb osteoporosis
may be associated with the high Mo content of the cereals consumed by the population. The results from a cross-sectional study in two settlements of a Mo-rich province
of the former Soviet Union suggested that the high incidence (18%–31%) of a goutlike disease was associated with high intake of Mo (10–15 mg/day). The disease was
characterized by joint pains of the legs and hands, enlargement of the liver, disorders
of the gastrointestinal tract, liver, and kidney, increased blood levels of Mo and uric
acid, increased XO activity, decreased blood levels of Cu, and increased urinary Cu.
The toxicity of Mo compounds appears to be relatively low in humans. But dusts
and fumes, which are generated by mining or metal working, can be toxic, especially
if ingested. Prolonged exposure to Mo can cause irritation to the eyes and skin, joint
pains, back pains, headache, or hair changes. The maximum permissible Mo exposure, in 8 hours a day, is 5 mg/m 3 . Chronic exposure to 60–600 mg/m 3 can cause
symptoms including fatigue, headache, and joint pains.
Molybdenum content in food exceeds 1 mg/kg FW rarely (Table 28.2), the highest
concentrations are in nuts, pulses, and offal. The estimated safe and adequate daily
dietary intake for Mo is 0.075–0.250 mg. The recommended dietary allowance for
Mo is different for various groups, by age and gender; for adult male and female, it
was set at 0.045 mg/day (FNB/IOM 2001).
Estimated daily intake varies widely regionally, depending on the soil type. Its
intakes in the United States range from 0.240 mg/day for adult men to 0.100 mg/day for
women (WHO 2011d). For adults, the representative range of mean estimates of Mo
intakes in different countries is 0.080–0.250  mg/day. Intakes of Mo in EU countries range from 0.096  mg/day, in the Netherlands, to 0.500  mg/day, in Germany.
Its intake by children (1–17 years old) varies between 0.0064 and 0.0144 mg/day.
However, in France, it is estimated at 0.106–0.119 mg/day (EFSA 2009a).