An Iodine excess also can be harmful to the thyroid of infants by inhibiting the process of synthesis and release of thyroid hormones (Wolff-Chaikoff effect).

The threshold upper limit of Iodine Intake (the intake beyond which thyroid function is inhibited) is not easy to define because it is affected by the level of iodine intake before exposure to iodine excess. Indeed, long-standing moderate iodine deficiency is accompanied by an accelerated trapping of iodide and by a decrease in the iodine stores within the thyroid.

Under these conditions, the critical ratio between iodide and total iodine within the thyroid, which is the starting point of the Wolff-Chaikoff effect, is more easily reached during iodine depletion than under normal conditions. In addition, the neonatal thyroid is particularly sensitive to the Wolff-Chaikoff effect because the immature thyroid gland is unable to reduce the uptake of iodine from the plasma to compensate for increased iodine ingestion.

For these reasons transient neonatal hypothyroidism or transient hyperTSHemia after iodine overload of the mother, especially after the use of povidone iodine, has been reported more frequently in European countries such as in Belgium, France, and Germany, which have prevailing moderate iodine deficiency.

Iodine intake in areas of moderate iodine deficiency In a study in Belgium, iodine overload of mothers (cutaneous povidone iodine) increased the milk iodine concentration and increased iodine excretion in the term newborns (mean weight about 3 kg). Mean milk iodine concentrations of 18 and 128 μg/dl were associated with average infant urinary iodine excretion levels of 280 and 1840 μg/l (2.20-14.48 μmol/l), respectively (30). Estimated average iodine intakes would be 112 and 736 μg/day, or 37 and 245 μg/kg/day, respectively.

The lower dose significantly increased the peak TSH response to exogenous thyroid releasing hormone but did not increase the (secretory) area under the TSH response curve. The larger dose increased both the peak response and secretory area as well as the baseline TSH concentration. Serum T4 concentrations were not altered, however.

Thus, these infants had a mild and transient, compensated hypothyroid state. Non-contaminated mothers secreted milk containing 9.5 μg iodine/dl, and the mean urinary iodine concentration of their infants was 144 μg/l (1.13 μmol/l). These data indicate that modest iodine overloading of term infants in the neonatal period in an area of relative dietary iodine deficiency (Belgium) also can impair thyroid hormone formation. 

Similarly, studies in France indicated that premature infants exposed to cutaneous povidone iodine or fluorescinated alcohol-iodine solutions and excreting iodine in urine in excess of 100 μg/day manifested decreased T4 and increased TSH concentrations in serum. 

The extent of these changes was more marked in premature infants with less than 34 weeks gestation than in those with 35–37 weeks gestation. The full-term infants were not affected. These studies suggest that in Europe the upper limit of iodine intake, which predisposes to blockage of thyroid secretion in premature infants (about 200 μg/day) is 2 to 3 times the average intake from human milk and about equivalent to the upper range of intake.

Similar studies have not been conducted in the United States, where transient hypothyroidism is rarely seen perhaps because iodine intake is much higher. For example, urinary concentrations of 50 μg/dl and above in neonates, which can correspond to a Wolff-Chaikoff effect in Europe, are frequently seen in healthy neonates in North America.

The average iodine intake of infants in the United States in 1978, including infants fed whole cow milk, was estimated by the market-basket approach to be 576 μg/day (standard deviation [SD] 196); that of toddlers was 728 μg/day (SD 315) and of adults was 952 μg/day (SD 589). The upper range for infants (968 μg/day) would provide a daily intake of 138 μg/kg for a 7-kg infant, and the upper range for toddlers (1358 μg/day) would provide a daily intake of 90 μg/kg for a 15-kg toddler.

Table 38 summarises the recommended dietary intake of iodine for age and approximate level of intake which appear not to impair thyroid function in the European studies of Delange in infants, in the loading studies of adults in the United States, or during ingestion of the highest estimates of dietary intake (just reviewed) in the United States.

Except for the values for premature infants, these probably safe limits are 15–20 times more than the recommended intakes. These data refer to all sources of iodine intake. The average iodine content of infant formulas is approximately 5 μg/dl.

The upper limit probably should be one that provides a daily iodine intake of no more than 100 μg/kg. For this limit and with the assumption that the total intake is from infant formula, with a daily intake of 150 ml/kg (100 kcal/kg), the upper limit of the iodine content of infant formula would be about 65 μg/dl. The current suggested upper limit of iodine in infant formulas of 75 μg/100 kcal (89μg/500 kJ or 50 μg/dl), therefore, seems reasonable.

Excess iodine intake is more difficult to define. Many people regularly ingest huge amounts of iodine – in the range 10–200 mg/day – without apparent adverse effects. Common sources are medicines (e.g., amiodarone contains 75 mg iodine per 200-mg capsule), foods (particularly dairy products), kelp (eaten in large amounts in Japan), and iodine-containing dyes (for radiologic procedures). 

Excess consumption of salt has never been documented to be responsible for excess iodine intake. Occasionally each of these may have significant thyroid effects, but generally they are tolerated without difficulty. Braverman et al.  showed that people without evidence of underlying thyroid disease almost always remain euthyroid in the face of large amounts of excess iodine and escape the acute inhibitory effects of excess intra-thyroidal iodide on the organification (i.e., attachment of `oxidized iodine' species to throsyl residues in the thyroid gland for the synthesis of thyroid hormones) of iodide and on subsequent hormone synthesis (escape from or adaptation to the acute Wolff-Chaikoff effect).

This adaptation most likely involves a decrease in thyroid iodide trapping, perhaps corresponding to a decrease in the thyroid sodium-iodide transporter recently cloned. Some people, especially those with long-standing nodular goitre who live in iodine deficient regions and are generally ages 40 years or older, may develop iodine-induced hyperthyroidism after ingestion of excess iodine in a short period of time.