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Context: Iodine, an essential constituent of thyroid hormones, is required for proper growth and development., Objective: To investigate whether growth parameters at birth are associated with maternal urinary iodine concentration (UIC) or normal ranges of thyroid hormones during pregnancy., Data Sources: Using the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines, electronic databases (namely, MEDLINE, Web of Science, the Cochrane Library, Scopus, and Google Scholar) were searched between January 1988 and November 2018 to identify relevant articles., Data Extraction: Data from the studies included were independently extracted by 2 investigators using standardized forms developed for this review., Data Analysis: The pooled mean birth weight, length, and head circumference values, and 95% confidence intervals were estimated in newborns born to women with UIC < 150 and UIC ≥150 μg/L during pregnancy. Possible linear or nonlinear associations between maternal UIC and the aforementioned anthropometric measures were evaluated. A narrative synthesis of the data was performed for thyroid hormones with levels within the normal range., Results: Of the 123 studies identified, 11 were eligible for inclusion in the meta-analysis. The pooled mean birth weight, length, and head circumference in newborns whose mothers had UIC < 150 μg/L vs UIC ≥150 μg/L were 2898 g vs 2900 g (P = 0.970), 49.6 cm vs 49.4 cm (P = 0.880), and 34.0 cm vs 34.1 cm (P = 0.933), respectively. Dose-response meta-analyses revealed no significant linear or nonlinear associations between maternal UIC during pregnancy and anthropometric measures at birth. Among the different thyroid function parameters evaluated, high-normal values of maternal free thyroxine and thyrotropin during pregnancy were inversely associated with neonatal birth weight., Conclusion: This systematic review showed that birth weight may be affected by even mild variations in the normal concentrations of maternal thyroid hormones. However, in the current meta-analysis, birth anthropometric measures were not associated with maternal UIC during pregnancy., (© The Author(s) 2020. Published by Oxford University Press on behalf of the International Life Sciences Institute. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: Findings from national surveys suggest that everyone in the United States is exposed to perchlorate. At high doses, perchlorate, thiocyanate, and nitrate inhibit iodide uptake into the thyroid and decrease thyroid hormone production. Small changes in thyroid hormones during pregnancy, including changes within normal reference ranges, have been linked to cognitive function declines in the offspring., Objectives: We evaluated the potential effects of low environmental exposures to perchlorate on thyroid function., Methods: Serum thyroid hormones and anti-thyroid antibodies and urinary perchlorate, thiocyanate, nitrate, and iodide concentrations were measured in 1,880 pregnant women from San Diego County, California, during 2000-2003, a period when much of the area's water supply was contaminated from an industrial plant with perchlorate at levels near the 2007 California regulatory standard of 6 μg/L. Linear regression was used to evaluate associations between urinary perchlorate and serum thyroid hormone concentrations in models adjusted for urinary creatinine and thiocyanate, maternal age and education, ethnicity, and gestational age at serum collection., Results: The median urinary perchlorate concentration was 6.5 μg/L, about two times higher than in the general U.S., Population: Adjusted associations were identified between increasing log10 perchlorate and decreasing total thyroxine (T4) [regression coefficient (β) = -0.70; 95% CI: -1.06, -0.34], decreasing free thyroxine (fT4) (β = -0.053; 95% CI: -0.092, -0.013), and increasing log10 thyroid-stimulating hormone (β = 0.071; 95% CI: 0.008, 0.133)., Conclusions: These results suggest that environmental perchlorate exposures may affect thyroid hormone production during pregnancy. This could have implications for public health given widespread perchlorate exposure and the importance of thyroid hormone in fetal neurodevelopment., Citation: Steinmaus C, Pearl M, Kharrazi M, Blount BC, Miller MD, Pearce EN, Valentin-Blasini L, DeLorenze G, Hoofnagle AN, Liaw J. 2016. Thyroid hormones and moderate exposure to perchlorate during pregnancy in women in Southern California. Environ Health Perspect 124:861-867; http://dx.doi.org/10.1289/ehp.1409614.

Background: Polybrominated diphenyl ethers (PBDEs) are flame-retardant chemicals that are added to many consumer products. Multiple animal studies have shown PBDEs to be thyroid hormone (TH) disruptors. Epidemiologic evidence of PBDE exposure associated with TH disruption has been inconclusive., Objectives: We used repeated measures to estimate associations between serum PBDE concentrations and THs in a North American adult cohort., Methods: From 2010 to 2011, we collected ≤ 3 serum samples at approximately 6-month intervals from 52 healthy adult office workers from Boston, Massachusetts, for analysis of PBDE congeners and THs., Results: The geometric mean sum concentrations of the most prevalent PBDE congeners (BDE-28, BDE-47, BDE-99, BDE-100, and BDE-153) were 22 ng/g lipid in winter 2010, 23 ng/g lipid in summer 2010, and 19 ng/g lipid in winter 2011. BDE-47 was the predominant congener. Based on a multivariable mixed regression model, we estimated that on average, a 1-ng/g serum increase in BDE-47 was associated with a 2.6-μg/dL decrease in total thyroxine (T4) (95% CI: -4.7, -0.35). Total T4 was inversely associated with each PBDE congener. Serum concentrations of PBDEs were not strongly associated with total triiodothyronine (T3), free T4, or thyroid-stimulating hormone (TSH)., Conclusion: These results are consistent with those from animal studies showing that exposure to PBDEs is associated with a decrease in serum T4. Because the other TH concentrations did not appear to be associated with BDE exposures, our findings do not indicate effects on the pituitary-thyroid axis. Taken together, our findings suggest that PBDE exposure might decrease the binding of T4 to serum T4 binding proteins., Citation: Makey CM, McClean MD, Braverman LE, Pearce EN, He XM, Sjödin A, Weinberg JM, Webster TF. 2016. Polybrominated diphenyl ether exposure and thyroid function tests in North American adults. Environ Health Perspect 124:420-425; http://dx.doi.org/10.1289/ehp.1509755.

Background: Thyroid hormone is essential for normal mental and physical development in infancy and childhood and is dependent on adequate iodine intake. During the first few months of life, infants are reliant on breastmilk and/or infant formula as their sole sources of dietary iodine. The iodine status of U.S. infants has not been well studied., Methods: This was a cross-sectional study of 95 breastfed and/or formula-fed infants less than 3 months of age in the Boston area. We measured iodine content from infants' single spot urine samples and assessed associations with infant feeding type as well as maternal demographic data, salt and multivitamin use, smoking status, and diet., Results: The median infant urine iodine concentration was 197.5 μg/L (range 40-897.5 μg/L). Median infant urine iodine concentrations were similar between infants who were exclusively breastfed (n=39, 203.5 μg/L; range 61.5-395.5 μg/L), formula-fed (n=44, 182.5 μg/L; range 40-897.5 μg/L), and mixed (n=10, 197.8 μg/L; range 123-592.5) (p=0.88). There were no significant correlations of infant urinary iodine with maternal salt or multivitamin use (regularly or in the past 24 hours), active or secondhand cigarette smoke exposures, infant weight, infant length, or recent maternal ingestion of common iodine-containing foods, although the correlations with iodine-containing foods are difficult to accurately determine due to the small sample sizes of these variables., Conclusions: Both breastfed and formula-fed infants less than 3 months of age in the Boston area were generally iodine sufficient. Larger studies are needed to confirm these observations among infants nationwide and elucidate other factors that may contribute to infant iodine nutrition.

Purpose of Review: To review several of the most recent and most important clinical studies regarding the effects of thyroid treatments on weight change, associations between thyroid status and weight, and the effects of obesity and weight change on thyroid function., Recent Findings: Weight decreases following treatment for hypothyroidism. However, following levothyroxine treatment for overt hypothyroidism, weight loss appears to be modest and mediated primarily by loss of water weight rather than fat. There is conflicting evidence about the effects of thyroidectomy on weight. In large population studies, even among euthyroid individuals, serum thyroid-stimulating hormone is typically positively associated with body weight and BMI. Both serum thyroid-stimulating hormone and T3 are typically increased in obese compared with lean individuals, an effect likely mediated, at least in part, by leptin. Finally, there is no consistent evidence that thyroid hormone treatment induces weight loss in obese euthyroid individuals, but thyroid hormone analogues may eventually be useful for weight loss., Summary: The interrelationships between body weight and thyroid status are complex.

Context: Gestational hypothyroidism leads to adverse obstetric outcomes and intellectual impairment in offspring. Pregnancy thyroid screening is controversial., Objective: Our objective was to determine thyroid function testing and thyroid dysfunction rates in pregnant women at Boston Medical Center (BMC)., Methods: We retrospectively enrolled 1000 pregnant women aged 18-46 yr seen in BMC's Obstetrics/Gynecology (OB/GYN) or Family Medicine (FM) Clinics for their initial prenatal visit during 2008. Age, race, insurance, gestational age (GA), medical history (thyroid or other autoimmune disorders), obstetric history, and thyroid function tests were ascertained., Results: A total of 983 women were included (17 excluded for coding error). Median maternal age was 28 yr and GA 9.4 wk. Thyroid testing rates were similar in the 918 (93%) followed by OB/GYN and 65 (7%) followed by FM (84 vs. 86%). Thirty-nine women had previous thyroid disease, of whom 19 took thyroid medications. Four had type 1 diabetes, and nine had other autoimmune diseases. Serum TSH was obtained in 832 women (84.6%) at median GA 9.7 wk (range, 0.1-39.7). The majority were tested during their first trimester (65.5%). Of the 832 tested, 56 (6.7%) had trimester-specific elevated TSH, of whom nine had a previous history of thyroid disease, two had type 1 diabetes, and one had dyschromia. Based on current case-finding guidelines, 45 of 56 women (80.4%) with an elevated TSH in pregnancy might not have been tested., Conclusion: BMC has a high rate of thyroid function testing in pregnancy. Targeted thyroid testing in only high-risk patients would have missed 80.4% of pregnant women with hypothyroidism.

Premature, very-low-birth-weight female twins were diagnosed with congenital hypothyroidism (CH). Thyroid hormone antibodies (THAb) directed against triiodothyronine (T3) and thyroxine (T4) of both the IgM and IgG class were detected in both twins. At age 10 months, a rise in thyroid stimulating hormone (TSH) occurred in both infants and measurement of THAb at the same time revealed the appearance of IgM-T4 and IgG-T4 and an increase in IgG-T3 levels in twin 1 (permanent CH), and with a slight increase of IgM-T4 and IgG-T4 levels and appearance of IgM-T3 in twin 2 (transient CH). THAb may contribute to the induction of hypothyroidism in neonates and infants, especially those with underlying autoimmune thyroid disease.

Iodine is an essential component of the hormones produced by the thyroid gland and is, therefore, essential for mammalian life. A landmark trial in the early 20th century definitively demonstrated that iodine supplementation could prevent what was then known as "endemic goiter." Subsequent studies over the next decades demonstrated that iodine deficiency causes a spectrum of disease, including not just goiter, but also cretinism, intellectual impairment, and adverse obstetric outcomes. Salt iodization, first used in Switzerland and the United States in the1920s, has become the mainstay of iodine deficiency prevention efforts. The dramatic reduction in the global prevalence of iodine deficiency disorders (IDD) over the past 30 years represents an outstanding and under-recognized public health achievement. This narrative review provides an overview of critical scientific discoveries and advances in public health nutrition related to the prevention of IDD in the United States and worldwide. This review was written to commemorate the centennial of the founding of the American Thyroid Association. [ABSTRACT FROM AUTHOR]

Purpose: There is some uncertainty about the optimal ranges for urinary iodine concentration (UIC) during pregnancy. This study aimed to explore associations between maternal UIC and thyroid function in iodine sufficient and mildly iodine deficient areas. Methods: It was a cross-sectional study in which 1461 healthy pregnant women were enrolled to collect their blood and urine samples during their routine antenatal care in Tianjin and Wuqiang, China. Wuqiang was a mildly iodine-deficient region, while Tianjin was iodine sufficient. UIC, free triiodothyronine (FT3), free thyroid hormone (FT4), thyroid stimulating hormone (TSH), thyroid peroxidase antibody (TPOAb), thyroglobulin antibody (TgAb), serum iodine concentration (SIC) including total serum iodine concentration (tSIC) and non-protein bound serum iodine concentration (nbSIC) were assessed during the routine antenatal care visits. Results: The median UIC in pregnant women was 174 (113, 249) μg/L in Tianjin and 111 (63, 167) μg/L in Wuqiang, respectively. Compared with Tianjin, UIC, FT3 and TSH were lower, and FT4, tSIC, nbSIC, rates of TPOAb and TgAb positivity and the thyroid dysfunction rate (TDR) were higher in Wuqiang (P < 0.001). FT3, FT4, tSIC and nbSIC increased during pregnancy in Tianjin with increasing UIC, while only FT3 and nbSIC increased in Wuqiang (P < 0.05). In Tianjin, the TDR increased with UIC and peaked at UIC ≥ 500 μg/L (P = 0.002), while in Wuqiang, the TDR showed a weak "U-shaped" relationship with UIC and the rate was lowest with UIC 100–149 μg/L. Conclusions: In iodine-deficient areas, there was a lower TDR in pregnant women with UIC 100–149 μg/L. We suspected that the optimal UIC criteria recommended by WHO may be a little high for pregnant women in mild-to-moderate iodine-deficient countries. [ABSTRACT FROM AUTHOR]

Objective: Examine the associations of maternal thyroid hormones, maternal dietary information, and newborn T4 levels with cognitive outcomes in mid-childhood. Methods: We studied 921 children born 1999–2003 at gestational age ≥ 34 weeks, who were participants in Project Viva, a prospective pre-birth cohort study in Massachusetts. We examined maternal dietary information, maternal thyroid hormone levels, and neonatal levels of T4. Research staff performed cognitive testing in mid-childhood (median age 7.7 years). Results: We included 514 women with measured first trimester thyroid hormone concentrations (mean 10.2 weeks); 15% of women had a thyroid stimulating hormone (TSH) level ≥ 2.5 mU/L, and 71% were college graduates. Newborn T4 was collected from 375 infants (mean 17.6 μg/dl; SD 4.0), on day 2 (mean 1.9 days; SD 0.7) as part of the newborn screening program. Mean (SD) verbal and nonverbal IQ, memory, and motor scores of children were 113.2 (14.3), 107.1 (16.7), 17.1 (4.4), and 92.5 (16.6) points, respectively. In multivariable analysis, first trimester maternal thyroid function (total T3, total T4, free T4, thyroid stimulating hormone (TSH) or total thyroid peroxidase (TPO) antibody levels) or newborn T4 were not associated with any of the cognitive outcomes in mid-childhood after adjustment for sociodemographic and perinatal variables. Conclusions for Practice: Maternal or neonatal thyroid hormone levels were not associated with cognitive outcomes in mid-childhood in this population with generally normal thyroid function. As we studied a highly educated cohort residing in an iodine-sufficient area, findings may not be generalizable. [ABSTRACT FROM AUTHOR]

Background: An alternative feasible and convenient method of assessing iodine intake is needed.Objective: The aim of this study was to examine the utility of serum iodine for assessing iodine intake in children.Methods: One blood sample and 2 repeated 24-h urine samples (1-mo interval) were collected from school-age children in Shandong, China. Serum free triiodothyronine (FT3), free thyroxine (FT4), thyroid-stimulating hormone (TSH), thyroglobulin (Tg), total iodine (StI), and non-protein-bound iodine (SnbI) concentrations and urine iodine (UIC) and creatinine (UCr) concentrations were measured. Iodine intake was estimated based on two 24-h urine iodine excretions (24-h UIE). Associations between serum iodine and other factors were analyzed using the Spearman rank correlation test. Receiver operating characteristic (ROC) curves were used to illustrate diagnostic ability of StI and SnbI.Results: In total, 1686 children aged 7-14 y were enrolled. The median 24-h UIC for the 2 collections was 385 and 399 μg/L, respectively. The median iodine intake was estimated to be 299 μg/d and was significantly higher in boys than in girls (316 μg/d compared with 283 μg/d; P < 0.001). StI and SnbI were both positively correlated with FT4 (ρ = 0.30, P < 0.001; and ρ = 0.21, P < 0.001), Tg (ρ = 0.21, P < 0.001; and ρ = 0.19, P < 0.001), 24-h UIC (ρ = 0.56, P < 0.001; and ρ = 0.47, P < 0.001), 24-h UIE (ρ = 0.46, P < 0.001; and ρ = 0.49, P < 0.001), urine iodine-to-creatinine ratio (ρ = 0.58, P < 0.001; and ρ = 0.62, P < 0.001), and iodine intake (ρ = 0.49, P < 0.001; and ρ = 0.53, P < 0.001). The areas under the ROC curves for StI and SnbI for the diagnosis of excessive iodine intake in children were 0.76 and 0.77, respectively. The optimal StI and SnbI threshold values for defining iodine excess in children were 101 and 56.2 μg/L, respectively.Conclusions: Serum iodine was positively correlated with iodine intake and the serum FT4 concentration in children. It is a potential biomarker for diagnosing excessive iodine intake in children. This trial was registered at clinicaltrials.gov as NCT02915536. [ABSTRACT FROM AUTHOR]

Background: The adverse effects of iodine excess on the thyroid in children are not well understood, and the Tolerable Upper Intake Level for iodine in children is unclear. Objectives: The aims of this study were to assess the effects of chronic long-term iodine excess on thyroid function in children and to explore the safe Tolerable Upper Intake Level of iodine in Chinese children. Design: A multistage cross-sectional study was conducted in 2224 children from areas with adequate to excessive iodine content in drinking water. Repeated samples of 24-h urine and spot urine samples were collected to estimate habitual daily iodine intakes of children. The thyroid volume in children was measured and blood samples were collected to determine thyroid function. Results: The habitual iodine intake of children was 298 µg/d (range: 186-437 µg/d). The total goiter rate was 9.7%, 232 (11.2%) children had hyperthyrotropinemia, and 232 (11.2%) children had thyroglobulin (Tg) concentrations >40 µg/L. The prevalence of hyperthyrotropinemia was >10% in children at iodine intakes of 200300 µg/d. Tg concentrations increased with increased iodine intake (β = 0.5; 95% CI: 0.4, 0.6), and the prevalence of Tg >40 µg/L was >3% in all iodine-intake groups. Multivariate logistic regression analysis indicated that the risk of total goiter significantly increased at iodine intakes ≥250-299 µg/d in 7- to 10-y-old children (OR: 8.8; 95% CI: 2.3, 34.0) and at iodine intakes ≥300-399 µg/d in 11- to 14-y-old children (OR: 5.2; 95% CI: 1.5, 18.3). However, there were no consistent differences in the risk of hyperthyrotropinemia and Tg >40 µg/L in children between different iodine-intake groups. Conclusions: Thyroid volume and goiter appear to be more sensitive indicators of thyroid stress than thyrotropin and Tg in children with long-term excess iodine intakes. We recommend 250 and 300 µg/d as safe Tolerable Upper Intake Levels of iodine for children aged 7-10 y and 11-14 y, respectively. [ABSTRACT FROM AUTHOR]

Objective Thyroid hormone, requiring adequate maternal iodine intake, is critical for neurodevelopment in utero. Perchlorate and, less so, thiocyanate decrease uptake of iodine into the thyroid gland by competitively inhibiting the sodium/iodide symporter (NIS). It remains unclear whether environmental perchlorate exposure adversely affects thyroid function in first-trimester pregnant women. Design Cross-sectional. Patients 134 pregnant women from Athens, Greece, at mean ± SD 10·9 ± 2·3 weeks' gestation. Measurements Urinary iodide, perchlorate, and thiocyanate and thyroid function tests were measured. Results The median urinary iodide was 120 μg/l. Urinary perchlorate levels were detectable in all women: median (range) 4·1 (0·2-118·5) μg/l. Serum thyroperoxidase antibodies (TPO Ab) were detectable in 16% of women. Using Spearman's rank correlation analyses, there was no correlation between urinary perchlorate concentrations and serum TSH, although inverse correlations were seen between urine perchlorate and free T3 and free T4 values. In univariate analyses, urine thiocyanate was positively correlated with serum TSH, but was not associated with serum free T3 or free T4. Urine perchlorate was positively correlated with gestational age. In multivariate analyses adjusting for urinary iodide concentrations, urine thiocyanate, gestational age, maternal age and TPO Ab titres, urine perchlorate was not a significant predictor of thyroid function. Conclusions Low-level perchlorate and thiocyanate exposure is ubiquitous, but, in adjusted analyses, is not associated with alterations in thyroid function tests among mildly iodine-deficient Greek women in the first trimester of pregnancy. [ABSTRACT FROM AUTHOR]

Background: Breastfed infants rely on maternal iodine for thyroid hormone production required for neurodevelopment. Dietary iodine among women of childbearing age in the United States may be insufficient. Perchlorate (competitive inhibitor of the sodium/iodide symporter [NIS]) exposure is ubiquitous. Thiocyanate, from cigarettes and diet, is a weaker NIS inhibitor. Environmental perchlorate and thiocyanate exposures could decrease breast milk iodine by competitively inhibiting NIS in lactating breasts (thus impairing infants' iodine availability), and/or infants' thyroidal NIS to directly decrease infant thyroid function. The current study assessed the relationships between environmental perchlorate and thiocyanate exposures and infant serum thyroid function. Methods: Iodine, perchlorate, and thiocyanate in breast milk, maternal and infant urine, and infant serum thyroid function tests were cross-sectionally measured in Boston-area women and their 1-3 month-old breastfed infants. Univariate and multivariable analyses assessed relationships between iodine, perchlorate, thiocyanate, thyroid-stimulating hormone (TSH), and free thyroxine (FT4) levels. Results: In 64 mothers and infants, median (range) iodine levels were 45.6 μg/L (4.3-1080) in breast milk, 101.9 μg/L (27-570) in maternal urine, and 197.5 μg/L (40-785) in infant urine. Median perchlorate concentrations were 4.4 μg/L (0.5-29.5) in breast milk, 3.1 μg/L (0.2-22.4) in maternal urine, and 4.7 μg/L (0.3-25.3) in infant urine. There were no correlations between infant TSH or FT4 and iodine, perchlorate, and thiocyanate levels in breast milk, maternal urine, and infant urine. In multivariable analyses, perchlorate and thiocyanate levels in breast milk, maternal urine, and infant urine were not significant predictors of infant TSH or FT4. Conclusions: Boston-area mothers and their breastfed infants are generally iodine sufficient. Although environmental perchlorate and thiocyanate are ubiquitous, these results do not support the concern that maternal and infant environmental perchlorate and thiocyanate exposures affect infant thyroid function. [ABSTRACT FROM AUTHOR]

Iodine is a necessary element for the production of thyroid hormone. We will review the impact of dietary iodine status on thyroid function in pregnancy. We will discuss iodine metabolism, homeostasis, and nutritional recommendations for pregnancy. We will also discuss the possible effects of environmental contaminants on iodine utilization in pregnant women. [ABSTRACT FROM AUTHOR]

Adequate levels of iodine, a trace element variably distributed on the earth, are required for the synthesis of the thyroid hormones thyroxine (T4) and triiodothyronine (T3). The iodide cycle consists of a series of transport, oxidation and coupling steps in thyroid follicular cells to produce thyroid hormone. The sodium/iodide symporter (NIS) transports iodide into the thyrocyte. Competitive inhibitors of NIS, such as perchlorate and thiocyanate, can decrease the entrance of iodide into the follicular cell. Pendrin is the primary protein that is responsible for iodide efflux out of the thyrocyte and into the follicular lumen. T4 is deiodinated in target tissues to produce the active form of thyroid hormone, T3, and other metabolites. Exposure to excessive iodine or chronic iodine deficiency may result in various clinical disorders. The Wolff-Chaikoff effect and Jöd-Basedow phenomenon describe mechanisms of thyroid autoregulation and dysregulation, respectively, during iodine excess. Population studies have determined that iodine deficiency exists in approximately 38% of the world's population, is the leading cause of preventable mental retardation, and is of particular concern to women and their infants. Finally, the unique role of iodine utilization in thyroid physiology has applications in many important clinical areas. INSETS: Box 1. Risk factors for iodine-induced hypothyroidism …;Key issues. [ABSTRACT FROM AUTHOR]

In pharmacologic doses, perchlorate inhibits thyroidal iodine uptake and subsequently decreases thyroid hormone production. Although pharmacologic doses may be used in the treatment of hyperthyroidism, recent literature has focussed on the detection of low levels of perchlorate in the environment, groundwater and foodstuffs and their potential adverse effects on human thyroid function. This is of particular concern to the developing foetus and infant, whose normal neurodevelopment depends on adequate iodine intake for the production of thyroid hormones. Further research is needed to clarify the potential health effects of low-level chronic environmental perchlorate exposure. The health impact of environmental perchlorate may be dependent upon adequate iodine intake and should be interpreted in combination with other environmental exposures that are also potential thyroidal endocrine disruptors. [Copyright &y& Elsevier]

In recent decades, the prevalence of thyroid nodules (TNs) has steadily increased in pregnant women. Therefore, this study aimed to investigate associations between TNs and iodine intake in pregnant women. From March 2016 to May 2017, serum and spot urine samples, as well as demographic data and medical history, were collected from 2353 pregnant women. Urine iodine concentration (UIC) and creatinine (Cr) level were determined in spot urine samples; serum thyroid hormones and thyroid autoantibodies were also determined. We examined the hypothesis that excess iodine intake influences incidence of TNs. Herein, TNs were diagnosed by ultrasonography, whereas demographic data and medical history were collected by questionnaire. Multivariate logistic regression models were used to calculate the odds ratios and their corresponding confidence intervals for TN risk factors. Generalized linear mixed model was used to assess the random effects of the regions. The UIC and UIC to creatinine ratio (I/Cr ratio) were significantly higher in pregnant women with TNs (168 and 190 μ g/L, respectively, for UIC [ P <.01]; 139 and 155 μ g/g, respectively, for I/Cr ratio [ P <.01]). Thyroglobulin, age, pre-pregnancy body mass index, and iodine-excessive region were associated with TNs (odds ratio = 1.01, 1.06, 1.04, and 2.38, respectively). Whereas I/Cr ratio was not a significant risk factor for TNs in pregnant women when adjusted for potential confounders, iodine excess (I/Cr ratio >500 μ g/g) was a risk factor in pregnant women in their second trimester. People living in areas with excessive iodine in drinking water should decrease their iodine intake, and a safe water source should be provided to ensure that the I/Cr ratio of pregnant women can be maintained at an optimal level. [ABSTRACT FROM AUTHOR]

Triphenyl phosphate (TPHP) is a commonly used organophosphate flame retardant and plasticizer with widespread human exposure. Data on health effects of TPHP are limited. Recent toxicological studies suggest TPHP may alter thyroid function. We used repeated measures to assess the temporal variability in urinary concentrations of the TPHP metabolite, diphenyl phosphate (DPHP), and to examine relationships between DPHP concentrations and thyroid hormones. We sampled 51 adults at months 1, 6, and 12 from 2010 to 2011. Urine samples were analyzed for DPHP. Serum samples were analyzed for free and total thyroxine (fT 4 , TT 4 ), total triiodothyronine (TT 3 ), and thyroid stimulating hormone (TSH). We assessed variability in DPHP using intraclass correlation coefficients (ICCs) and kappa statistics. We used linear mixed-effects models to examine associations between DPHP and thyroid hormones. DPHP was detected in 95% of urine samples. Mean DPHP concentrations were 43% higher in women than men. DPHP showed high within-subject variability (ICC range, 0.13–0.39; kappa range, 0.16–0.39). High versus low (≥ 2.65 vs. < 2.65 ng/mL) DPHP in all participants was associated with a 0.43 μg/dL (95% confidence interval: 0.15, 0.72) increase in mean TT 4 levels. In sex-stratified analyses, high versus low DPHP was associated with a 0.91 μg/dL (95% CI: 0.47, 1.36) increase in mean TT 4 in women. The association was attenuated in men (βeta = 0.19; 95% CI: − 0.15, 0.52). We found no significant associations between DPHP and fT 4 , TT 3 , or TSH. We found evidence that TPHP exposure may be associated with increased TT 4 levels, especially in women. [ABSTRACT FROM AUTHOR]