Iodine Exposure Research Articles

Trends in treatments of thyroid disease following iodine fortification in Denmark: a nationwide register-based study.

BackgroundLong-term iodine exposure may influence the frequency of thyroid disease treatments through fluctuations in thyroid diseases. Yet, the long-term fluctuations in thyroid disease treatments upon iodine fortification (IF) are not fully known. We aimed to examine the development in thyroid disease treatments in Denmark before and following the implementation of IF in 2000.MethodsNationwide data on antithyroid medication, thyroid hormone therapy, thyroid surgery, and radioiodine treatment were obtained from Danish registries. Negative binominal regression was applied to analyze annual changes in treatment rates adjusted for region of residence, sex, and age.ResultsIncidence of antithyroid medication transiently increased but fell and reached steady state from 2010 at an incidence rate ratio (RR) of 0.72 (95% confidence interval [CI] 0.67–0.77) compared to year 2000. Thyroid hormone therapy increased and reached steady state in 2010 at an incidence RR of 1.75 (95% CI 1.62–1.89) compared to year 2000. Thyroid surgery was constant except for higher rates in 2014–2015, and radioiodine treatment fluctuated with no apparent pattern.ConclusionTen years after IF, a steady state was observed for incident antithyroid medication below the level at IF, and thyroid hormone therapy above the level at IF. Only small changes were observed in thyroid surgery and radioiodine treatment. In the same period, changes in diagnostic and treatment practices and lifestyle factors are likely to have occurred and should be considered when evaluating the effects of IF on treatment of thyroid diseases.

The main determinants of iodine in cows' milk in Switzerland are farm type, season and teat dipping.

Milk and dairy products are important iodine sources and contribute about 30-40 % of total iodine in the Swiss diet. Information about variation in milk iodine concentration (MIC) in Switzerland is limited. We examined MIC and its potential determinants in milk from organic and conventional farms. We collected bulk milk samples at 3-month intervals over 1 year from thirty-two farms throughout Switzerland and Aosta valley, North-West Italy. We sampled all feed components including tap water, collected information on farm characteristics, feeding and teat disinfection practices by questionnaire and estimated the cows' winter and summer iodine intake. Iodine in milk and feed components was measured using inductively coupled plasma MS. The overall median MIC was 87 (range 5-371) µg/l. In multivariate analysis, predictors of MIC were as follows: (1) farm type: median MIC from organic and conventional farms was 55 and 93 µg/l (P=0·022); (2) season: 53, 97 and 101 µg/l in September, December and March (P<0·002); and (3) teat dipping: 97 µg/l with v. 56 µg/l without (P=0·028). In conclusion, MIC varied widely between farms because of diverse farming practices that result in large differences in dairy cow exposure to iodine via ingestion or skin application. Standardisation of MIC is potentially achievable by controlling these iodine exposures. In order for milk to be a stable iodine source all year round, dietary iodine could be added at a set level to one feed component whose intake is regular and controllable, such as the mineral supplement, and by limiting the use of iodine-containing teat disinfectants.

Gold and Nickel Extended Thiophenic-TTF Bisdithiolene Complexes.

Gold and nickel bisdithiolene complexes with methyl and tert-butyl substituted thiophenetetrathiafulavalenedithiolate ligands (α-mtdt and α-tbtdt) were prepared and characterized. These complexes were obtained, under anaerobic conditions, as tetrabutylammonium salts. The diamagnetic gold monoanion (n-Bu4N)[Au(α-mtdt)2] (3) and nickel dianionic species (n-Bu4N)x[Ni(α-mtdt)2] (x = 1,2) (4) were similar to the related non-substituted extended thiophenic-TTF (TTF = tetrathiafulvalene) bisdithiolenes. However the introduction of the large, bulky substituent tert-butyl, led to the formation of a Au (I) dinuclear complex, (n-Bu4N)2[Au2(α-tbtdt)2] (5). The neutral methyl substituted gold and nickel complexes were easily obtained through air or iodine exposure as polycrystalline or amorphous fine powder. [Au(α-mtdt)2] (6) and [Ni(α-mtdt)2] (7) polycrystalline samples display properties of a metallic system with a room temperature electrical conductivity of 0.32 S/cm and ≈4 S/cm and a thermoelectric power of ≈5 µV/K and ≈32 µV/K, respectively. While [Au(α-mtdt)2] (6) presented a Pauli-like magnetic susceptibility typical of conducting systems, in [Ni(α-mtdt)2] (7) large magnetic susceptibilities indicative of high spin states were observed. Both electric transport properties and magnetic properties for gold and nickel [M(α-mtdt)2] are indicative that these compounds are single component molecular conductors.

Biomonitoring Equivalents for interpretation of urinary iodine

Iodine is an essential nutrient whose deficiency or excess exposure can cause adverse health effects. The primary sources of iodine exposure in the general population are iodized salt, dairy products, bread and sea food. Urinary iodine concentrations (UIC) have been measured by Canadian Health Measures Survey (CHMS) and US National Health and Nutrition Examination Survey (NHANES). The Institute of Medicine (IOM), the US Agency for Toxic Substances and Disease Registry (ATSDR) and World Health Organization (WHO) have established exposure guidance values for nutrition (IOM Estimated Average Requirement (EAR), Recommended Dietary Allowance (RDA), WHO Recommended Nutrient Intake (RNI)) and toxicity (IOM Tolerable Upper Intake Level (UL); ATSDR Minimal Risk Level (MRL), WHO International Programme on Chemical Safety (IPCS) Tolerable Daily Intake (TDI)). Using a urinary excretion fraction of 0.9, Biomonitoring Equivalents (BE) for the EAR, RDA, UL and MRL were derived for adults (60, 100, 730 and 450 μg/L, respectively) and children (50, 80, 580 and 360 μg/L, respectively). The population median UIC values from NHANES and CHMS for adults (140–181, 122–126 μg/L, respectively) and children (232, 189 μg/L, respectively) were above the criteria for assessing iodine nutrition, indicating that US and Canadian populations are likely to have adequate population iodine nutrition. The median UIC from NHANES and CHMS do not exceed BE values derived from exposure guidance values for toxicity.

Exposure to DBP and High Iodine Aggravates Autoimmune Thyroid Disease Through Increasing the Levels of IL-17 and Thyroid-Binding Globulin in Wistar Rats

Autoimmune thyroid disease (AITD) is the most common autoimmune disease that causes hypothyroidism. High iodine is a well-known factor that can induce thyroid disorders, including Hashimoto's thyroiditis, one of the main types of AITD. Recent epidemiological studies have indicated that phthalates, especially di-n-butyl phthalate (DBP) may induce thyroid disease. In this study, we aim to determine the effects and underlying mechanisms of high iodine and/or DBP exposure on AITD. Female Wistar rats were modeled with thyroglobulin and exposed to high iodine and/or DBP. We investigated histopathological changes in the thyroid and measured thyroid hormone levels in serum to assess thyroid function. In the thyroid and liver, we detected oxidative stress, proinflammatory factors (IL-1β, IL-6, and IL-17) and the activation of activator protein 1 (AP-1), a transcription factor that is related to the synthesis of the thyroxine-binding globulin (TBG) and the activation of Th17. After blocking AP-1 with SP600125, we detected TBG and the Th17 related cytokines (IL-6 and IL-17). The data showed that thyroid damage and the alteration of thyroid hormones were greater when the rats were exposed to both high iodine and DBP. Coexposure to DBP and high iodine enhanced the activation of AP-1 in the liver and thyroid, and induced an increase in the levels of TBG in serum and IL-17 in the thyroid. Blocking AP-1 activation prevented the increase of TBG and IL-17. The results indicate that high iodine and/or DBP exposure exacerbated AITD through altering TBG levels in serum and aggravating IL-17 in the thyroid.

Transient hypothyroidism in the newborn: to treat or not to treat.

Transient congenital hypothyroidism (CH) refers to a temporary deficiency of thyroid hormone identified after birth, with low thyroxine (T4) and elevated thyrotropin (TSH), which later recovers to improved thyroxine production, typically in first few months of infancy. Approximately 17% to 40% of children diagnosed with CH by newborn screening (NBS) programs were later determined to have transient hypothyroidism. Causes of transient CH are prematurity, iodine deficiency, maternal thyrotropin receptor blocking antibodies, maternal intake of anti-thyroid drugs, maternal or neonatal iodine exposure, loss of function mutations and hepatic hemangiomas. The classic clinical symptoms and signs of CH are usually absent immediately after birth in vast majority of infants due to temporary protection from maternal thyroxine. NBS has been largely successful in preventing intellectual disability by early detection of CH by performing thyroid function tests in infants with abnormal screening results. In this review we present the evidence for decision making regarding treatment vs. withholding treatment in infants with transient CH and present a rational approach to identifying transient CH based on American Academy of Pediatrics (AAP) recommendation.

Dietary Iodine Exposure and Brain Structures and Cognition in Older People. Exploratory Analysis in the Lothian Birth Cohort 1936.

Iodine deficiency is one of the three key micronutrient deficiencies highlighted as major public health issues by the World Health Organisation. Iodine deficiency is known to cause brain structural alterations likely to affect cognition. However, it is not known whether or how different (lifelong) levels of exposure to dietary iodine influences brain health and cognitive functions. From 1091 participants initially enrolled in The Lothian Birth Cohort Study 1936, we obtained whole diet data from 882. Three years later, from 866 participants (mean age 72 yrs, SD±0.8), we obtained cognitive information and ventricular, hippocampal and normal and abnormal tissue volumes from brain structural magnetic resonance imaging scans (n=700). We studied the brain structure and cognitive abilities of iodine-rich food avoiders/low consumers versus those with a high intake in iodine-rich foods (namely dairy and fish). We identified individuals (n=189) with contrasting diets, i) belonging to the lowest quintiles for dairy and fish consumption, ii) milk avoiders, iii) belonging to the middle quintiles for dairy and fish consumption, and iv) belonging to the middle quintiles for dairy and fish consumption. Iodine intake was secured mostly though the diet (n=10 supplement users) and was sufficient for most (75.1%, median 193 µg/day). In individuals from these groups, brain lateral ventricular volume was positively associated with fat, energy and protein intake. The associations between iodine intake and brain ventricular volume and between consumption of fish products (including fish cakes and fish-containing pasties) and white matter hyperintensities (p=0.03) the latest being compounded by sodium, proteins and saturated fats, disappeared after type 1 error correction. In this large Scottish older cohort, the proportion of individuals reporting extreme (low vs. high)/medium iodine consumption is small. In these individuals, low iodine-rich food intake was associated with increased brain volume shrinkage, raising an important hypothesis worth being explored for designing appropriate guidelines.

Hypothyroidism in Infants With Congenital Heart Disease Exposed to Excess Iodine.

Thyroid hormone is critical for neonatal brain development, and even transient hypothyroidism can cause adverse neurocognitive outcomes. Infants exposed to excess iodine are at risk of developing hypothyroidism, especially those with congenital heart disease (CHD), because they are routinely exposed to excess iodine from intravenous iodinated contrast media and topical antiseptics. The aim of the present study was to identify the proportion of neonates with CHD exposed to iodine who developed hypothyroidism and to identify the associated risk factors. This was a retrospective study of neonates undergoing cardiac catheterization at Boston Children’s Hospital during a 3-year period, some of whom also underwent cardiac surgery. Hypothyroidism was defined as an elevated thyroid-stimulating hormone level (>20 mIU/L at 24 to 96 hours of age and >15 mIU/L at >96 hours of age by heel-stick sampling and >9.1 mIU/L at 1 to 20 weeks of age by serum testing). Multivariate logistic regression was performed to predict the odds of developing hypothyroidism. Hypothyroidism was diagnosed incidentally in 46 of 183 infants (25%) with CHD after iodine exposure. Controlling for baseline cardiac risk, postnatal age, and gestational age, we found a fourfold increase in odds of developing hypothyroidism in neonates with serum creatinine >0.9 mg/dL and a fourfold increase in those who underwent more than three procedures. Hypothyroidism in neonates with CHD exposed to excess iodine is associated with multiple procedures and impaired renal function. Routine serial monitoring of thyroid function in these neonates is warranted. Future studies should examine the association between hypothyroidism and neurocognitive function in this population.

Relationship between iodine levels and papillary thyroid carcinoma: A systematic review and meta‐analysis

Iodine excess has been suggested as an exogenous risk factor of papillary thyroid cancer (PTC). We performed a systematic review and meta-analysis to assess the relationship between iodine exposure measured in various forms and PTC prevalence. We searched MEDLINE, Embase, and the Cochrane Library for case-control studies on iodine and PTC published up to December 2015. Exposure to iodine was compared between PTC and control groups. From the 16 selected studies, the odds ratio (OR) for the overall effect size between high iodine exposure and PTC risk was 1.418 (95% confidence interval [CI] 1.054-1.909). Based on 7 studies conducted in high iodinated regions, a positive association between iodine exposure and PTC was observed (OR 2.200; 95% CI 1.389-3.483). This study demonstrated a higher exposure to iodine in patients with PTC compared with controls, especially for patients from high iodinated regions.

Influence of iodine in excess on seminiferous tubular structure and epididymal sperm character in male rats.

Excess iodine induced public health problems are now emerging in many iodine sufficient regions for indiscriminate intake of iodine through various iodized products. It has been reported that excess iodine can disrupt overall male reproductive physiology by generating oxidative stress in the testis. However, information on the possible effect of iodine in excess on spermatozoa found less. In the present investigation flow cytometric techniques and scanning electron microscopy (SEM) have been used to study the spermatozoal functional as well as structural status under the influence of excess iodine; generation of ROS in the spermatozoa as evident by DCFDA, altered acrosomal integrity as observed by fluorescence lectin staining method and depolarized mitochondrial membrane potential (ΔΨm ) noticed by JC-1 staining. Ultrastructure of seminiferous tubule after excess iodine exposure indicated severe deterioration of seminiferous tubular surface architecture. Significant increase in spermatozoal DNA fragmentation and apoptotic sperms were found by acridine orange and Annexin V, respectively, however the plasma membrane integrity/viability was decreased as evident by propidium iodide staining in various incremental doses and durations under iodine excess. The study reveals that excess iodine could cause apoptosis of spermatozoal cells by inducing ROS that ultimately affects male fertility potential.

Effect of excess iodine intake on thyroid on human health.

The recommended daily intake of iodide, is 150 μg for adolescents and adults, 250 μg for pregnancy and lactation. Thyroid gland is an effective collector of iodine. The active iodine uptake along the basolateral membrane of thyroid cell is followed by its transport to the apical edge of the cell and then to the follicle lumen. TSH acts through cAMP and stimulates NIS gene expression and protein synthesis. The major proportion of iodine in the thyroid gland is bound to Thyroglobulin. The non-organic intrathyroidal iodine is usually low, but significantly greater compared to plasma. Large doses of iodine reduce both the uptake and the organification (Wolff-Chaikoff effect) and cause partial inhibition of Tg proteolysis. The thyroid gland has several protective mechanisms resulting on the maintenance of normal thyroid function despite wide fluctuations of the daily iodine intake. Ingestion of several commonly used drugs and food conservatives results in acute or chronic excessive iodine intake. Failure to escape from the iodine induced organification inhibition can cause hypothyroidism, which is temporary and subsides after iodine exposure ceases. Iodine excess may also establish a status of excessive thyroid hormone synthesis and release, thus inducing autonomic thyroid function in iodopenic areas or can contribute to the development of iodine-induced hyperthyroidism in iodine abundant areas. The anti-arrhythmic Amiodarone, is a benzofuranic product with a very high iodine content, is associated with either hypo- or hyperthyroidism development. In the presence of defective auto-protective mechanisms, excessive iodine ingestion can divert the normal thyroid function.

Reversible intercalation of iodine monolayers between on-surface synthesised covalent polyphenylene networks and Au(111).

We report on post-synthetic decoupling of covalent polyphenylene networks from Au(111) by intercalation of a chemisorbed iodine monolayer. The covalent networks were synthesised by on-surface Ullmann polymerization of 1,3-bis(p-bromophenyl)-5-(p-iodophenyl)benzene precursors on Au(111) under ultra-high vacuum conditions. The present study relates to previous work, where successful detachment was demonstrated on Ag(111) by a combination of microscopic and spectroscopic techniques. On the more reactive Ag(111) surfaces, intercalation was readily accomplished by exposing the samples to iodine vapour at room temperature. On more noble Au(111), however, STM, XPS and NEXAFS consistently indicate that the same protocol merely results in co-adsorption of iodine on uncovered surface areas, whereas the covalent networks remain adsorbed on the metal. Yet, performing the iodine exposure at elevated surface temperatures similarly results in detachment of the organic networks via intercalation of an iodine monolayer also on Au(111) as evidenced by characteristic changes in STM. In addition, owing to the high thermal stability of the covalent networks and the comparatively low iodine desorption temperature, the reversibility of the process is demonstrated: sample annealing at 400 °C results in complete desorption of the iodine monolayer, whereby the covalent networks re-adsorb directly on Au(111).

Update on dietary intake of perchlorate and iodine from U.S. food and drug administration’s total diet study: 2008–2012

The U.S. Food and Drug Administration's (FDA) Total Diet Study (TDS) monitors the US food supply for pesticide residues, industrial chemicals, radionuclides, nutrients, and toxic elements. Perchlorate and iodine intakes based on concentrations in TDS samples collected between 2008 and 2012 were estimated in order to update an earlier TDS dietary assessment. Perchlorate is used as an oxidizing agent in rocket and missile fuel, is formed naturally in the atmosphere, and occurs naturally in some soils. Because of perchlorate's presence in soil, and in irrigation, processing, and source water, it is widely found in food. Iodine was included in the study because perchlorate at high doses interferes with iodide uptake in the thyroid. Iodine (the elemental form of iodide) is essential for growth and development, and metabolism. This study uses a novel statistical method based on a clustered zero-inflated lognormal distribution model to estimate mean and 95th percentile confidence interval concentrations for perchlorate and iodine in US foods. These estimates were used to estimate mean perchlorate and iodine exposures for the total US population and for 14 age/sex groups in the US population. Estimated mean perchlorate intake for the total US population was 0.13 μg/kg bw/day, with mean intakes for the 14 age/sex groups between 0.09 and 0.43 μg/kg bw/day. The estimated mean intakes of perchlorate for all age/sex groups were below EPA's reference dose (RfD) of 0.7 μg/kg bw/day. The estimated mean iodine intake for the total US population was 216.4 μg/person/day, with mean intakes ranging from 140.9 to 296.3 μg/person/day for the 14 age/sex groups, with all age/sex groups exceeding their respective estimated average requirements (EARs).

Thyroidal response following iodine excess for cardiac catheterisation and intervention in early infancy

BackgroundCardiac catheterisation requiring the use of contrast medium is increasingly utilised in infants with congenital heart disease. Thyroid function in infants is potentially vulnerable to relatively high doses of iodine. MethodsSingle-centre prospective study of 21 patients (10 neonates, 11 infants) exposed to iodine during cardiac catheterisation. Median age was 30days (1–180), median body weight 3.3kg (1.6–7.0). Serum-levels of thyroid-stimulating hormone (TSH), free triiodothyronine (fT3) and free thyroxine (fT4) were measured at baseline before, and at three different times points after intervention. ResultsBaseline thyroidal levels were within normal range in all patients. After applying contrast media of median 6.8ml/kg (range 4.5–14.9), we observed a wide range of TSH values: median 5.01μg/l (range 0.59–37.73; reference 0.72–11.0) three to five days after catheterisation. Five of the 10 neonates demonstrated transient TSH elevation consistent with latent hypothyroidism, and a sixth a transient drop in all hormone levels typical of non-thyroidal illness syndrome. However, circulating thyroid hormones remained within normal range, except for two borderline-low fT4 values within the first week after catheterisation that normalised without any medical intervention. ConclusionSystemic iodine exposure during cardiac catherterisation seems to be clinically well tolerated in early infancy. However, exposure to iodine has demonstrable but apparently reversible effects on thyroid hormones during a potentially important developmental period. The implications of this are unclear, but warrant further investigation in larger cohorts.

Iodine deficiency and thyroid cancer trends in three regions of Thailand, 1990–2009

BackgroundIodine deficiency may play a role in thyroid cancer carcinogenesis. Because Thailand has region-specific historical iodine deficiency, it is ideal to evaluate the potential impact of recent national iodine supplementation policies on thyroid cancer incidence trends. MethodsWe examined thyroid cancer trends in Thailand from 1990 to 2009 in three geographically separated populations (Songkhla Province [south], Chiang Mai Province [north], and Khon Kaen Province [northeast]), each with a different historical prevalence of iodine deficiency. We used Joinpoint analysis and age-period-cohort (APC) models to investigate trends in thyroid cancer incidence. ResultsPooled incidence of papillary cancers significantly increased (Males APC: 2.0, p<0.05; Females APC: 7.3 [1990–2001, p<0.05], −2.1 [2001–2009]) and incidence of follicular cancers significantly decreased (Males APC: −5.2, p<0.05; Females APC: −4.3 [1990–1998, p<0.05], 12.3 [1998–2001], −17.0 [2001–2005, p<0.05], 8.2 [2005–2009]) in both males and females between 1990 and 2009. The largest increases in papillary cancer incidence, and the largest decreases in follicular cancer incidence, occurred in historically iodine-deficient regions. Interestingly, the significant histological changes coincided with Thailand’s most recent national iodination policy. The thyroid cancer trends in females were better explained by period effects than cohort effects. ConclusionsThis study adds to the research indicating that papillary carcinoma incidence increases, and follicular carcinoma incidence decreases, as population-level iodine deficiency declines, and suggests that iodine exposure may affect late stages of thyroid carcinogenesis. However, our findings are limited by the ecological study design and lack of data prior to iodine supplementation.

Thyroid Function among Breastfed Children with Chronically Excessive Iodine Intakes.

Iodine excess may impair thyroid function and trigger adverse health consequences for children. This study aims to describe iodine status among breastfed infants with high iodine exposure in the Saharawi refugee camps Algeria, and further assess thyroid function and iodine status among the children three years later. In 2010, a cross-sectional study among 111 breastfed children aged 0–6 months was performed (baseline study). In 2013, a second cross-sectional study (follow-up study) was conducted among 289 children; 213 newly selected and 76 children retrieved from baseline. Urinary iodine concentration (UIC) and breast milk iodine concentration (BMIC) were measured at baseline. UIC, thyroid hormones and serum thyroglobulin (Tg) were measured at follow-up. At baseline and follow-up, 88% and 72% had excessive iodine intakes (UIC ≥ 300 µg/L), respectively. At follow-up, 24% had a thyroid hormone disturbance and/or elevated serum Tg, including 9% with subclinical hypothyroidism (SCH), 4% with elevated fT3 and 14% with elevated Tg. Children with SCH had poorer linear growth and were more likely to be underweight than the children without SCH. Excessive iodine intakes and thyroid disturbances were common among children below four years of age in our study. Further, SCH seemed to be associated with poor growth and weight.

Iodide Residues in Milk Vary between Iodine-Based Teat Disinfectants.

Majority of iodine found in dairy milk comes from the diet and teat disinfection products used during milking process. The objective of this study was to evaluate the effects of 4 iodine-based teat dips on milk iodide concentrations varying in iodine level (0.25% vs. 0.5%, w/w), normal low viscosity dip versus barrier dip, and application method (dip vs. spray) to ensure safe iodine levels in dairy milk when these products are used. The iodine exposure study was performed during a 2-wk period. The trial farm was purged of all iodine-based disinfection products for 21 d during a prestudy "washout period," which resulted in baseline milk iodide range of 145 to 182 ppb. During the experiment, iodine-based teat dips were used as post-milking teat disinfectants and compared to a non-iodine control disinfectant. Milk iodide residue levels for each treatment was evaluated from composited group samples. Introduction of different iodine-based teat disinfectants increased iodide residue content in milk relative to the control by between 8 and 29 μg/L when averaged across the full trial period. However, residues levels for any treatment remained well below the consumable limit of 500 μg/L. The 0.5% iodine disinfectant increased milk iodide levels by 20 μg/L more compared to the 0.25% iodine. Compared to dip-cup application, spray application significantly increased milk iodide residue by 21 μg/L and utilized approximately 23% more teat dip. This carefully controlled study demonstrated an increase in milk iodide concentrations from iodine disinfectants, but increases were small and within acceptable limits.

Iodine in commercial edible iodized salts and assessment of iodine exposure in Sri Lanka.

BackgroundIodine is an essential micronutrient used by the thyroid gland in the production of thyroid hormones. Both excessive and insufficient iodine intakes can cause thyroid diseases thus harmful to the human body. Inadequate iodine intake by human body causes Iodine Deficiency Disorders (IDD) and hypothyroidism. Excessive iodine intake causes Iodine Induced Hyperthyroidism (IIH). Universal Salt Iodization (USI) is the most effective way of preventing IDD. This study determined the concentrations of iodine species in commercial edible salt products, the stability of iodine at different conditions and iodine exposure at the consumer level.MethodsThe iodine contents of six commercial edible iodized salts were determined qualitatively and quantitatively for both iodide and iodate. Thereafter, the first three products of highest iodine contents, the stability of iodide at exposed to air and heat was measured after 24 hours. Risk assessment of exposure was done at four levels considering the WHO estimation.ResultsResults revealed that all of the salt products have excess iodine that is above the fortification level of 15–30 mg kg−1 level in Sri Lanka. Iodide stability was reduced at the average percentages of 13.1, 10.7 and 11.3. The iodate loss percentages were 0, 5.7 and 0 at open air. The iodide loss percentages at the temperature of 50 °C were 4.6, 7.8 and 8.6 while at 100 °C, loss percentages were 11.1, 11.4 and 15.9 for the same salt products. The iodine exposure at lower consumption during cooking ranged 244.4–432.2 μg/day while 325.9–576.3 μg/day for medium consumption, 407.4–720.4 μg/day for moderate high salt consumptions and 488.8–864.4 μg/day for high salt consumptions. As a total 95.8 % cases can cause IIH and only 4.1 % of them can provide optimal iodine nutrition in a population. Iodine exposure without cooking ranged 305.5–540.3 μg/day for low salt consumption, 407.4–720.4 μg/day for medium consumption and 509.2–900.5 μg/day for moderate high consumption and 611.1–1080.6 μg/day for high salt consumptions.ConclusionsAll of the incidents (100 %) of consumption without cooking at the household level can cause excessive iodine intake and IIH in a population.

Chemical RedOx Properties of a Donor-Acceptor Conjugated Microporous Dithienothiophene-Benzene co-Polymer FormedviaSuzuki-Miyaura Cross-coupling

An electron rich conjugated microporous polymer (CMP) was prepared after reacting a dithienothiophene (DTT) derivative and benzene as co-monomers by Suzuki-Miyaura polycondensation. Gas sorption measurements revealed a Brunauer–Emmett–Teller (BET) surface area of 421 m2g−1 for the network. Its chemical oxidation was performed via iodine exposure, which is fully reversible with ammonia treatment resulting in a complete removal of the oxidants. This was observed in a decrease and recovery of the initial porosity due to reversible introduction and removal of iodide within the micropores, which could also be monitored by IR and UV/Vis absorption spectroscopy during the RedOx process.

Maternal Iodine Exposure: A Case of Fetal Goiter and Neonatal Hearing Loss

A 27-year-old gravid 1 at 27 weeks 6 days with a history of hypothyroidism had an ultrasound that demonstrated a 3.9 × 3.2 × 3.3-cm well-circumscribed anterior neck mass, an extended fetal head, and polyhydramnios. Further characterization by magnetic resonance imaging (MRI) showed a fetal goiter. During her evaluation for the underlying cause of the fetal goiter, the patient revealed she was taking nutritional iodine supplements for treatment of her hypothyroidism. She was ingesting 62.5 times the recommended amount of daily iodine in pregnancy. The excessive iodine consumption caused suppression of the fetal thyroid hormone production, resulting in hypothyroidism and goiter formation. After the iodine supplement was discontinued, the fetal goiter decreased in size. At delivery, the airway was not compromised. The infant was found to have reversible hypothyroidism and bilateral hearing loss postnatally. This case illustrates the importance of examining for iatrogenic causes for fetal anomalies, especially in unregulated nutritional supplements.