Iodine concentration in commercial cat foods from three regions of the USA, 2008-2009.

Fluctuations in iodine concentration in food have been suggested as one risk factor for the development of feline hyperthyroidism, an epidemic disease first described in 1979. Three international studies have examined iodine concentrations of commercial cat foods. The iodine concentration of 112 commercial cat foods from across the USA was measured, and the daily iodine intake by hypothetical 4.5 kg adult cats or 1.4 kg kittens calculated in this descriptive epidemiologic study to examine differences in feline iodine intake due to (i) geographical source of foods, (ii) packaging type, (iii) brand-to-brand variation, (iv) form of iodine supplementation, (v) types and numbers of seafood ingredients and (vi) kitten and 'therapeutic' diets. Dramatic variation among canned foods (resulting in ingestion of approximately 49-9639 µg iodine/day) suggests that the disparity in iodine concentrations may lead to development of nodular hyperplasia and, later, clinical hyperthyroidism, if cats consume diets that are at first iodine-deficient and later contain excessive iodine. Manufacturers are encouraged to ensure adequate iodine supplementation across all products and areas of the USA.

Congenital hypothyroidism caused by excess prenatal maternal iodine ingestion.

We report the cases of 3 infants with congenital hypothyroidism detected with the use of our newborn screening program, with evidence supporting excess maternal iodine ingestion (12.5 mg/d) as the etiology. Levels of whole blood iodine extracted from their newborn screening specimens were 10 times above mean control levels. Excess iodine ingestion from nutritional supplements is often unrecognized.

Colostrum iodine and perchlorate concentrations in Boston-area women: a cross-sectional study.

OBJECTIVE: To measure levels of colostrum iodine, which has not been previously measured, and perchlorate and cotinine (a surrogate for thiocyanate derived from cigarette smoke) in women up to 60 h postpartum. Perchlorate and thiocyanate are environmental inhibitors of iodide transport into the thyroid and lactating breast. DESIGN: Cross-sectional. PATIENTS: Ninety seven postpartum women in Boston, Massachusetts, USA. MEASUREMENTS: Colostrum iodine and perchlorate, and spot urine iodine, perchlorate, cotinine and creatinine concentrations were measured. RESULTS: Sufficient colostrum was obtained to measure iodine in 61 samples and perchlorate in 46 samples. Median colostrum iodine content was 51.4 micromol/l (range 21.3-304.2 microg/l). Perchlorate was detectable in 43 of 46 colostrum samples (median 2.5 micromol/l; range, < 0.05-188.9 micromol/l). Median urine iodine in 97 samples was 82.2 micromol/l (range, 10.3-417.1 micromol/l). Perchlorate was detectable in all 97 urine samples (median 2.6 micromol/l; range, 0.2-160.6 micromol/l). Colostrum iodine content was not significantly correlated with levels of colostrum perchlorate or concentrations per litre of urinary iodine, perchlorate, or cotinine. Colostrum perchlorate concentrations were not significantly associated with urinary iodine, perchlorate, or cotinine levels. Urinary cotinine levels were not significantly associated with urinary iodine or perchlorate levels. There was no association between maternal urinary iodine and urinary perchlorate levels. CONCLUSIONS: Iodine is present in human colostrum and thus available for breastfeeding infants immediately after birth. Perchlorate was also present in 93% of samples measured, but the concentrations did not correlate with colostrum iodine concentrations.

Iodide concentrations in matched maternal serum, cord serum, and amniotic fluid from preterm and term human pregnancies.

OBJECTIVES: To characterize the matched maternal and cord plasma and the amniotic fluid concentrations of iodide in preterm and term human pregnancies. METHODS: Specimens were collected at the delivery of 121 singleton pregnancies (92 at term, 29 preterm) with no pre-existing medical complications. Plasma unbound iodide concentrations were measured by the difference between the protein bound iodine and the total iodine measured spectrophotometrically. Total iodide was measured in amniotic fluid. RESULTS: Maternal plasma iodide concentrations were 1.6 +/- 0.4 mcg/dL (mean +/- S.D.) for preterm deliveries and 1.5+/ -0.5 mcg/dL for term deliveries. Cord plasma iodide concentrations were 1.4 +/- 0.5 mcg/dL for preterm deliveries and 1.7 +/- 0.7 mcg/dL for term deliveries. Cord plasma iodide concentrations at birth correlated highly with maternal levels (p < 0.001). The cord:maternal plasma iodide ratio for all pairs was 1.2+/- 0.7. The average cord:maternal plasma iodide ratio was not significantly different between the preterm (0.9+/- 0.4) and term (1.3+/- 0.8) deliveries. Amniotic fluid iodide concentrations did not correlate significantly with cord plasma concentrations. CONCLUSION: Cord plasma concentrations of iodide correlate with paired maternal levels, indicating that, unlike the rabbit and other species, the human conceptus does not highly concentrate iodide.

Seaweed and soy: companion foods in Asian cuisine and their effects on thyroid function in American women.

Seaweeds and soy are two commonly eaten foods in Asia. Both have been reported to affect thyroid function, seaweed because of its iodine content and soy because of its goitrogenic effect. Twenty-five healthy postmenopausal women (mean age 58 years) completed a double-blinded randomized crossover study. Ten capsules (5 g/day) of placebo or seaweed (Alaria esculenta), providing 475 microg of iodine/day, were consumed daily for 7 weeks. A powdered soy protein isolate (Solae Co., St. Louis, MO), providing 2 mg of isoflavones/kg of body weight, was given daily during the last week of each treatment arm. On average, this provided 141.3 mg of isoflavones/day and 67.5 g of protein/day. Blood samples and 48-hour urine samples were collected before and after each intervention period, and urinary I/C (microg of iodine/g of creatinine) and serum thyroxine, free thyroxine index, total triiodothyronine, and thyroid stimulating hormone (TSH) were measured. Seaweed ingestion increased I/C concentrations (P < .0001) and serum TSH (P < .0001) (1.69 +/- 0.22 vs. 2.19 +/- 0.22 microU/mL, mean +/- SE). Soy supplementation did not affect thyroid end points. Seven weeks of 5 g/day seaweed supplementation was associated with a small but statistically significant increase in TSH. Soy protein isolate supplementation was not associated with changes in serum thyroid hormone concentrations.

Breast milk iodine and perchlorate concentrations in lactating Boston-area women.

CONTEXT: Breastfed infants rely on adequate maternal dietary iodine intake. OBJECTIVE: Our objective was to measure breast milk iodine and perchlorate, an inhibitor of iodide transport into the thyroid and potentially into breast milk, in Boston-area women. PARTICIPANTS: The study included 57 lactating healthy volunteers in the Boston area. MEASUREMENTS: Breast milk iodine and perchlorate concentrations and urine iodine, perchlorate, and cotinine concentrations were measured. For comparison, iodine and perchlorate levels in infant formulae were also measured. RESULTS: Median breast milk iodine content in 57 samples was 155 microg/liter (range, 2.7-1968 microg/liter). Median urine iodine was 114 microg/liter (range, 25-920 microg/liter). Perchlorate was detectable in all 49 breast milk samples (range, 1.3-411 microg/liter), all 56 urine samples (range, 0.37-127 microg/liter), and all 17 infant formula samples (range, 0.22-4.1 microg/liter) measured. Breast milk iodine content was significantly correlated with urinary iodine per gram creatinine and urinary cotinine but was not significantly correlated with breast milk or urinary perchlorate. CONCLUSIONS: Perchlorate exposure was not significantly correlated with breast milk iodine concentrations. Perchlorate was detectable in infant formula but at lower levels than in breast milk. Forty-seven percent of women sampled may have been providing breast milk with insufficient iodine to meet infants' requirements.

Effects of six months of daily low-dose perchlorate exposure on thyroid function in healthy volunteers.

CONTEXT: Perchlorate has been detected in U.S. drinking water supplies at levels ranging from 4 to 200 microg/liter as well as in agricultural products. Perchlorate is known to be a competitive inhibitor of iodine uptake by the thyroid through the sodium-iodide symporter. OBJECTIVE: The objective of the study was to determine whether prolonged exposure (6 months) to low levels of perchlorate would perturb thyroid function. DESIGN: This was a prospective, double-blinded, randomized trial. PARTICIPANTS: The study population consisted of 13 healthy volunteers. INTERVENTION: INTERVENTIONs included placebo vs. 0.5 mg or 3.0 mg potassium perchlorate daily. MAIN OUTCOME MEASURES: Serum thyroid function tests, 24-h radioactive iodine uptake, serum thyroglobulin (Tg), urinary iodine and perchlorate, and serum perchlorate were measured. RESULTS: Mean urinary perchlorate value during ingestion of 0.5 mg perchlorate daily was 332.7 +/- 66.1 microg per 24 h or 248.5 +/- 64.5 microg/g creatinine and mean values for the four subjects who received 3 mg perchlorate daily were 2079.5 +/- 430.0 microg per 24 h or 1941.7 +/- 138.5 microg/g creatinine. There was no significant change in the thyroid (123)I uptakes during perchlorate administration. There were no significant changes in serum T(3), free T(4) index, TSH, or Tg concentrations during the exposure period, compared to baseline or postexposure values. Urine iodine values for the 3-mg perchlorate group were higher, but not significantly so, at baseline than during perchlorate exposure. CONCLUSIONS: We observed that a 6-month exposure to perchlorate at doses up to 3 mg/d had no effect on thyroid function, including inhibition of thyroid iodide uptake as well as serum levels of thyroid hormones, TSH, and Tg.

The effect of perchlorate, thiocyanate, and nitrate on thyroid function in workers exposed to perchlorate long-term.

Perchlorate (ClO(4)(-)) and thiocyanate (SCN(-)) are potent and nitrate (NO(3)(-)) a weak competitive inhibitor of the thyroid sodium-iodide symporter. To determine the effects of long-term, high ClO(4)(-) exposure on thyroid function, we conducted a study of 29 workers employed for at least 1.7 yr (50% over 5.9 yr) in an ammonium ClO(4)(-) production plant in Utah. Serum ClO(4)(-), SCN(-), and NO(3)(-); serum T(4), free T(4) index, total T(3), thyroglobulin (Tg), and TSH; 14-h thyroid radioactive iodine uptake (RAIU); and urine iodine (I) and ClO(4)(-) were assessed after 3 d off (Pre) and during the last of three 12-h night shifts in the plant (During) and in 12 volunteers (C) not working in the plant. Serum and urine ClO(4)(-) were not detected in C; urine ClO(4)(-) was not detected in 12 of 29 and was 272 microg/liter in 17 Pre workers; serum ClO(4)(-) was not detected in 27 of 29 Pre; and serum and urine ClO(4)(-) were markedly elevated during ClO(4)(-) exposure to 868 microg/liter and 43 mg/g creatinine, respectively. Serum SCN(-) and NO(3)(-) concentrations were similar in all groups. Thyroid RAIUs were markedly decreased in During compared with Pre (13.5 vs. 21.5%; P < 0.01, paired t) and were associated with an increase in urine I excretion (230 vs. 148 microg I/g Cr; P = 0.02, paired t) but were similar to those in the C group (14.4%). Serum TSH and Tg concentrations were normal and similar in the three groups. Serum T(4) (8.3 vs. 7.7 microg/dl), free T(4) index (2.4 vs. 2.2), and total T(3) (147 vs. 134 ng/dl) were slightly but significantly increased in the During vs. Pre workers (P < 0.01, paired t). Thyroid volumes and patterns by ultrasound were similar in the 29 workers and 12 community volunteers. In conclusion, high ClO(4)(-) absorption during three nights work exposure decreased the 14-h thyroid RAIU by 38% in ClO(4)(-) production workers compared with the RAIU after 3 d off. However, serum TSH and Tg concentrations and thyroid volume by ultrasound were not affected by ClO(4)(-), suggesting that long-term, intermittent, high exposure to ClO(4)(-) does not induce hypothyroidism or goiter in adults.

Variability of iodine content in common commercially available edible seaweeds.

Dietary seaweeds, common in Asia and in Asian restaurants, have become established as part of popular international cuisine. To understand the possibility for iodine-induced thyroid dysfunction better, we collected samples of the most common dietary seaweeds available from commercial sources in the United States, as well as harvester-provided samples from Canada, Tasmania, and Namibia. Altogether, 12 different species of seaweeds were analyzed for iodine content, and found to range from 16 microg/g (+/-2) in nori (Porphyra tenera) to over 8165 +/- 373 microg/g in one sample of processed kelp granules (a salt substitute) made from Laminaria digitata. We explored variation in preharvest conditions in a small study of two Namibian kelps (Laminaria pallida and Ecklonia maxima), and found that iodine content was lowest in sun-bleached blades (514 +/- 42 microg/g), and highest amount in freshly cut juvenile blades (6571 +/- 715 microg/g). Iodine is water-soluble in cooking and may vaporize in humid storage conditions, making average iodine content of prepared foods difficult to estimate. It is possible some Asian seaweed dishes may exceed the tolerable upper iodine intake level of 1100 microg/d.

Sources of dietary iodine: bread, cows' milk, and infant formula in the Boston area.

Dietary iodine is essential for thyroid hormone production. Although U.S. dietary iodine is generally adequate, some groups, especially women of childbearing age, are at risk for mild iodine deficiency. Children's average urinary iodine is higher than that of adults. U.S. dietary iodine sources have not been assessed recently. A survey of iodine content in 20 brands of bread, 18 brands of cows' milk, and eight infant formulae was performed between 2001 and 2002. Three bread varieties contained more than 300 microg iodine per slice. Iodine content in other brands was far lower (mean +/- sd, 10.1 +/- 13.2 microg iodine/slice). All cows' milk samples had at least 88 microg iodine/250 ml, ranging from 88-168 microg (116.0 +/- 22.1 microg/250 ml). Infant formulae values ranged from 16.2 to 56.8 microg iodine/5 oz (23.5 +/- 13.78 microg/5 oz). The public should be aware of the need for adequate dietary iodine intake and should be aware that ingredient lists do not reflect the iodine content of foods.

Effects of chronic iodine excess in a cohort of long-term American workers in West Africa.

A cross-sectional survey of 102 Peace Corps volunteers in Niger, West Africa, in 1998 had previously demonstrated a high rate of thyroid dysfunction and goiter attributable to excess iodine from their water filters. The Peace Corps volunteers were followed-up a mean of 30 wk after they ceased using iodine-based water filtration systems. Goiter was present in 44% of subjects during excess iodine ingestion and in 30% after removal of excess iodine. Mean serum iodine decreased from 293 micro g/liter during excess iodine ingestion to 84 micro g/liter after cessation of excess iodine. Mean total serum T(4) values increased from 100.4 to 113.3 nmol/liter (7.8 to 8.8 micro g/dl). Mean serum free T(4) increased from 32.2 to 34.7 pmol/liter (2.5 to 2.7 ng/dl). Mean serum TSH decreased from 4.9 to 1.8 mU/liter. Mean serum thyroid peroxidase antibody levels decreased from 33,000 to 22,000 IU/liter (33 to 22 IU/ml). We found that during prolonged excess iodine exposure there were marked increases in serum total iodine concentrations, and the prevalence of goiter, elevated serum TSH values, and elevated serum thyroid peroxidase antibody values increased. The prevalence of all abnormalities decreased after removal of excess iodine from the drinking water system.