Home | | Introduction to Human Nutrition | Iodine: Toxicity, Genetic diseases, Requirements, dietary sources, Micronutrient interactions

Chapter: Introduction to Human Nutrition: Minerals and Trace Elements

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Iodine: Toxicity, Genetic diseases, Requirements, dietary sources, Micronutrient interactions

Iodine is a nonmetallic element of the halogen group with common oxidation states of −1 (iodides), +5 (iodates), and +7 (periodates), and less common states of +1 (iodine monochloride) and +3 (iodine trichloride).

Iodine

 

Iodine is a nonmetallic element of the halogen group with common oxidation states of 1 (iodides), +5 (iodates), and +7 (periodates), and less common states of +1 (iodine monochloride) and +3 (iodine trichloride). Elemental iodine (0) is a soft blue–black solid, which sublimes readily to form a violet gas.

 

The principal industrial uses of iodine are in the pharmaceutical industry, medical and sanitary uses (e.g., iodized salt, water treatment, protection from radioactive iodine, and disinfectants), as catalysts (synthetic rubber, acetic acid synthesis), and in animal feeds, herbicides, dyes, inks, colorants, photographic equipment, lasers, metallurgy, conductive polymers, and stabilizers (nylon). Naturally occurring iodine minerals are rare and occur usually in the form of calcium iodates. Commercial production of iodine is largely restricted to extraction from Chilean deposits of nitrates (saltpeter) and iodine in caliche (soluble salts precipitated by evaporation), and from concen-trated salt brine in Japan. Iodine is the least abundant halogen in the Earth’s crust, at concentrations of 0.005%. The content of iodine in soils varies and much of the original content has been leached out in areas of high rainfall, previous glaciation, and soil erosion.


Toxicity

 

A wide range of iodine intakes is tolerated by most individuals, owing to the ability of the thyroid to regulate total body iodine. Over 2 mg iodine/day for long periods should be regarded as excessive or poten-tially harmful to most people. Such high intakes are unlikely to arise from natural foods, except for diets that are very high in seafood and/or seaweed or com-prising foods contaminated with iodine. In contrast to iodine-replete individuals, those with IDDs or pre-viously exposed to iodine-deficient diets may react to sudden moderate increases in iodine intake, such as from iodized salt. Iodine-induced thyrotoxicosis (hyperthyroidism) and toxic nodular goiter may result from excess iodine exposure in these indivi-duals. Hyperthyroidism is largely confined to those over 40 years of age and symptoms are rapid heart rate, trembling, excessive sweating, lack of sleep, and loss of weight and strength.


Individuals who are sensitive to iodine, usually have mild skin symptoms, but very rarely fever, sali-vary gland enlargement, visual problems, and skin problems, and, in severe cases, cardiovascular col-lapse, convulsions, and death may occur. The occur-rence of allergic symptoms, for example to iodine medications or antiseptics, however, is rare.


Genetic diseases

Pendred’s syndrome is an autosomal recessive inher-ited disorder with a frequency of 100 or less per 100 000. It is characterized by goiter and profound deafness in childhood and is caused by mutations in the Pendrin gene located on chromosome 7. The gene codes for pendrin, a transporter protein for chloride/ iodine transport across the thyroid apical membrane. This results in defective iodination of thyroglobulin. Mutations in another gene, the sodium/iodide sym-porter (NIS) gene, occasionally cause defective iodide transport and goiter, whereas single nucleotide poly-morphisms in the TSH receptor gene may predispose individuals to the hyperthyroidism of toxic multi-nodular goiter and Graves’ disease.


Assessing status

The critical importance of iodine for the thyroid indicates that iodine status is assessed by thyroid function. A standard set of indicators (goiter by palpation, thyroid volume by ultrasound, median urinary iodine, and whole blood TSH) is used to determine prevalence in countries with endemic deficiency. Measurement of plasma thyroid hormones (TSH, T4, and T3) provides useful indicators of func-tional iodine status in the individual. Of these, TSH is the most sensitive functional indicator of subopti-mal iodine status. Concentrations of T4 decline in more severe iodine deficiency whereas T3 concentra-tions decline only in the most severe of iodine deficiencies.


Dietary intakes and requirements

Requirements in infancy and childhood range from 40 to 150 μg iodine/day. Adult requirements are esti-mated at 150 μg iodine/day, increasing to 175 and 200 μg/day for pregnancy and lactation. The UL for adults is set at 600 μg/day (EU) and at 1.1 mg/day (USA).

Under normal circumstances, about 90% of iodine intake is from food, with about 10% from water. The concentration of iodine in most foods is low and, in general, reflects the iodine content of the soil, water, and fertilizers used in plant and animal production. In most countries other sources, such as iodized salts or foods, are required. Seafoods and seaweed concen-trate iodine from seawater and are particularly rich sources. In some populations, milk has become a major source of iodine, owing to the use of iodized salt licks and iodine-enriched cattle feed for dairy herds. Minor amounts may come from adventitious contamination from iodophor disinfectants (teat-dip). Iodine-enriched cattle feed will also increase the iodine content of meat for beef herds raised on con-centrated feedstuffs. Processed foods contribute some additional iodine from food additives, such as calcium iodate used in the baking industry.


Micronutrient interactions

From a public health viewpoint, the most important metabolic interaction of iodine with other micronu-trients is with selenium. Adequate selenium status is essential for thyroid hormone metabolism and, there-fore, normal growth development, by ensuring suffi-cient T3 supply to extrathyroidal tissues. Most T3 is formed from T4 by the selenium-dependent de-iodinases. Iodine and selenium deficiencies overlap in various parts of the world and concurrent deficiencies of both may contribute to the etiologies of Kashin– Beck disease in Russia, China, and Tibet, and myxede-matous congenital hypothyroidism in Zaire. In addi-tion, both nutrients are required for normal repro-duction, normal gene expression, synthesis of zeno-biotic and metabolizing enzymes in the liver, and normal tolerance against cold stress. It is possible that hypothyroidism associated with suboptimal selenium status may explain some of the etiology of cardiovas-cular disease and certain cancers.

 

Hypothyroidism is associated with deficiencies of other trace elements, including zinc, iron, and copper, while there are close metabolic relationships at the molecular and transport levels between iodine and vitamin A. Conversely, the widespread disruption of metabolism in IDDs can affect the proper utilization of a host of other nutrients.

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