Urinary iodine excretion is currently the most convenient laboratory marker of iodine deficiency. Accelerating international interest in correcting this condition demands rapid, simple methods for assessment and monitoring. We describe two adaptations of the Sandell-Kolthoff reaction, in which urine is first digested with chloric acid and iodine then determined from its catalytic reduction of ceric ammonium sulfate in the presence of arsenious acid. Both methods use gentle digestion by chloric acid in a heating block. Method A detects iodine in a colorimeter, method B by the indicator ferroin and a stopwatch. Results with 12 samples ranging from 1.8 to 19.0 micrograms/dL (0.14-1.48 mumol/L) differed from those in a reference laboratory by a mean of 9.1% for method A and 15.7% for method B. One technician can perform at least 150 tests per day at a total cost of less than $0.50 each. The speed, low cost, and simple instrumentation make these methods well suited to epidemiological assessment of iodine deficiency in developing countries.

The fetus is totally dependent in early pregnancy on maternal thyroxine for normal brain development. Adequate maternal dietary intake of iodine during pregnancy is essential for maternal thyroxine production and later for thyroid function in the fetus. If iodine insufficiency leads to inadequate production of thyroid hormones and hypothyroidism during pregnancy, then irreversible fetal brain damage can result. In the United States, the median urinary iodine (UI) was 168 microg/L in 2001-2002, well within the range of normal established by the World Health Organization (WHO), but whereas the UI of pregnant women (173 microg/L; 95% CI 75-229 microg/L) was within the range recommended by WHO (150-249 microg/L), the lower 95% CI was less than 150 microg/L. Therefore, until additional physiologic data are available to make a better judgment, the American Thyroid Association recommends that women receive 150 microg iodine supplements daily during pregnancy and lactation and that all prenatal vitamin/mineral preparations contain 150 microg of iodine.

Iodine deficiency is the leading cause of preventable mental retardation. Universal salt iodization (USI), calling for all salt used in agriculture, food processing, catering and household to be iodized, is the agreed strategy for achieving iodine sufficiency. This article reviews published information on programs for the sustainable elimination of the iodine deficiency disorders and reports new data on monitoring and impact of salt iodization programs at the population level. Currently, 68% of households from areas of the world with previous iodine deficiency have access to iodized salt, compared to less than 10% a decade ago. This great achievement, a public health success unprecedented in the field of noncommunicable diseases, must be better recognized by the health sector, including thyroidologists. On the other hand, the managers and sponsors of programs of iodized salt must appreciate the continuing need for greatly improved monitoring and quality control. For example, partnership evaluation of iodine nutrition using the ThyroMobil model in 35,223 schoolchildren at 378 sites of 28 countries has shown that many previously iodine deficient parts of the world now have median urinary iodine concentrations well above 300 microg/L, which is excessive and carries the risk of adverse health consequences. The elimination of iodine deficiency is within reach but major additional efforts are required to cover the whole population at risk and to ensure quality control and sustainability.

The thyroid concentrates iodide from the serum and oxidizes it at the apical membrane, attaching it to tyrosyl residues within thyroglobulin (Tg) to make diiodotyrosine and monoiodotyrosine. Major players in this process are Tg, thyroperoxidase (TPO), hydrogen peroxide, pendrin, and nicotinamide adenine dinucleotide phosphate (NADPH). Further action of TPO, hydrogen peroxide (H2O2), and iodinated Tg produce thyroxine (T4) and triiodothyronine (T3). Hormone-containing Tg is stored in the follicular lumen, then processed, most commonly by micropinocytosis. The lysosomal enzymes cathepsins B, L, and D are active in Tg proteolysis. Tg digestion leaves T4 and T3 intact, to be released from the cell, while the 3,5'-diiodotyrosine (DIT) and 3-iodotyrosine (MIT) are retained and deiodinated for recycling within the thyroid. Some areas of especially active recent research include: (1) the role of molecular chaperones in directing properly folded TPO and Tg to the apical membrane; (2) details of proteolytic pathways; (3) modulation of iodine metabolism, not only by thyrotropin (TSH) but by iodine supply and by feedback effects of Tg, glutathione, and inhibitory elements in the N-terminal region of Tg; and (4) details of Tg structure and iodotyrosyl coupling. Despite general agreement on the major steps in intrathyroidal iodine metabolism, new details of mechanisms are constantly being uncovered and are greatly improving understanding of the overall process.

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