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Trace Elements in Abiotic and Biotic Environments
flooded river valleys, such as the Ganges, are among the most severely I-deficient
areas in the world.
Globally, it is estimated that two billion individuals have insufficient I intake.
Although goiter is the most visible sequelae of I deficiency, the major impact of hypothyroidism, due to I deficiency, is impaired neurodevelopment, particularly early in
life. In the fetal brain, inadequate thyroid hormone impairs myelination, cell migration, differentiation, and maturation. Moderate-to-severe I deficiency during pregnancy increases rates of spontaneous abortion, reduces birth weight, and increases
infant mortality. Offsprings of deficient mothers are at high risk for cognitive disability, with cretinism, being the most severe manifestation. Moderate-to-severe I deficiency during childhood reduces somatic growth. Correction of mild-to-moderate
I deficiency in primary school-aged children improves cognitive and motor function.
Iodine prophylaxis of deficient populations with periodic monitoring is an extremely
cost-effective approach to reduce the substantial adverse effects of I deficiency,
throughout the life cycle (Zimmermann 2011).
Iodine deficiency can lead to a wide spectrum of health problems, ranging
from mild intellectual impairment to severe mental retardation, growth stunting,
apathy, and impaired movement, speech, or hearing. Cretinism, in which most of
these abnormalities occur, represents the extreme form of early I deficiency and is
rare. Much more widespread is intellectual blunting, which may afflict as many as
50 million of the estimated 1.6 billion at-risk people, living in I-deficient regions.
Because of decreased production of thyroid hormones, I deficiency causes compensatory hypertrophy of the thyroid gland, as it attempts to make more thyroid
hormone, resulting in a goiter—a disfiguring condition that is common in high-risk
areas. Health problems arising from the lack of I are known as IDD (Zimmermann
2011). Universal salt iodization provides the most effective and affordable means to
prevent IDD throughout the world.
Selenium deficiency can exacerbate the effects of I deficiency. Iodine is essential
for the synthesis of thyroid hormone, but selenium-dependent enzymes (iodothyronine deiodinases) are also required for the conversion of thyroxine (T 4 ) to the biologically active thyroid hormone, triiodothyronine (T 3 ). Additionally, deficiencies of
vitamin A or Fe may exacerbate the effects of I deficiency (FNB/IOM 2001).
Numerous measures have been undertaken to improve I supply to human diets,
for example, using iodized salts, other vehicles for I, supplementation of foods of
plant or animal origin or supplementing I to animal feed, in order to increase its
content of food of animal origin (Flachowsky 2007).
Estimated dietary requirements for adult humans range from 0.08 to 0.150 mg/
day. In 1988, Joint FAO/WHO Expert Committee on Food Additives set a provisional maximum tolerable daily intake (PMTDI) for I at 1 mg/day (0.017 mg/kg bw/
day) from all sources, based primarily on data on the effects of iodide. However,
recent data from studies in rats indicate that the effects of I in drinking water on
thyroid hormone concentrations in the blood differ from those of iodide (WHO
2011a).
Iodine content in food and water primarily depends on its contents in soils. Thus,
the average I content in foods shown in Table 21.2 cannot be used universally for
estimating its intake by people of various regions.