tary basis by manufacturers and extensive public education programs by health officials to encourage consumer use of this product resulted in the virtual elimination of goiter in high-risk regions. The question then arises as to whether strategies to reduce salt intake by the U.S. population will result in the unintended consequence of increasing the risk of iodine insufficiency and deficiency among high-risk groups.
To answer this question, it is important to determine the current iodine status of the U.S. population and to anticipate the potential effect of reduced salt intake on iodine status. However, assessing the iodine status of the U.S. population is challenging. Intake data are generally unreliable because they cannot accurately estimate the amount of table salt used by consumers, and information about whether iodized or non-iodized salt is used in food preparation at home or away from home is rarely captured in food composition databases or in dietary interviews. There are wide variations in the iodine content of some common foods. For example, the iodine content per slice of bread was > 300 μg for three varieties of bread and averaged 10 μg for 17 other brands in 2002 (Pearce, 2007), thus making it difficult to assign meaningful composition values to specific food items. The labeling of the iodine content of foods is not mandatory unless claims are made or iodine is added as a nutrient fortificant—practices that to date have been rare. On the other hand, dietary supplements, particularly multivitamin and multimineral supplements, often contain 150 μg of iodine per daily dose and the iodine content of these products is declared on the label.
Because of the difficulty of obtaining accurate estimates of dietary intake, iodine status is generally assessed by urinary excretion of iodine. Iodine is renally excreted, therefore urinary iodine concentrations are an indication of dietary iodine sufficiency (Pearce, 2007). The National Health and Nutrition Examination Surveys (NHANES) have periodically collected casual urine samples from which iodine values have been determined since NHANES I was conducted from 1971–1974. These data have been used to examine trends in urinary iodine excretion over time (Caldwell et al., 2005).
NHANES I levels were considered to be “adequate to excessive” for iodine (Pearce, 2007). Then, a downward trend was noted in urinary iodine concentration between NHANES I (320 ± 6 μg/L in 1971–1974) and NHANES III (145 ± 3 μg/L in 1988–1994). However, NHANES 2001–2002 data indicate that the urinary excretion of iodine stabi2lized (167.8 μg/L; 95 percent confidence interval: 159.3–177.6 μg/L). NHANES III and NHANES 2001–2002 urinary iodine excretion concentrations are within the range generally considered to be “optimal” for iodine nutriture (Caldwell et al., 2005; Pearce, 2007).
The reasons for the reductions in urinary iodine concentration between