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      The ETA–ESE statement on the European Chemicals Agency opinion on iodine as an endocrine disruptor

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          Abstract

          In 2022, the European Chemicals Agency (ECHA) made a statement concluding that iodine is an endocrine disruptor (ED). We stress the fact that the ECHA opinion ECHA/BPC/357/2022 is based on their misguidedly zooming in on exclusively the biocidal products (e.g. hand disinfectants, disinfection of animals’ teats/udder, embalming fluids before cremation) that contain molecular iodine (I 2), entirely neglecting the 2013 ECHA Regulation (EU) no. 528/2012 describing iodine as being of ‘great importance for human health’. Clearly, the current sweeping and erroneous classification of ‘iodine’ as an endocrine disruptor is ill-advised. We moreover call upon the scientific and medical community at large to use the accurate scientific nomenclature, i.e. iodide or iodate instead of ‘iodine’ when referring to iodized salts and food prepared there with. Drugs, diagnostic agents, and synthetic chemicals containing the element iodine in the form of covalent bonds must be correctly labeled ‘iodinated’, if possible, using each time their distinctive and accurate chemical or pharmacological name.

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          Iodine deficiency.

          Iodine deficiency has multiple adverse effects in humans, termed iodine deficiency disorders, due to inadequate thyroid hormone production. Globally, it is estimated that 2 billion individuals have an insufficient iodine intake, and South Asia and sub-Saharan Africa are particularly affected. However, about 50% of Europe remains mildly iodine deficient, and iodine intakes in other industrialized countries, including the United States and Australia, have fallen in recent years. Iodine deficiency during pregnancy and infancy may impair growth and neurodevelopment of the offspring and increase infant mortality. Deficiency during childhood reduces somatic growth and cognitive and motor function. Assessment methods include urinary iodine concentration, goiter, newborn TSH, and blood thyroglobulin. But assessment of iodine status in pregnancy is difficult, and it remains unclear whether iodine intakes are sufficient in this group, leading to calls for iodine supplementation during pregnancy in several industrialized countries. In most countries, the best strategy to control iodine deficiency in populations is carefully monitored universal salt iodization, one of the most cost-effective ways to contribute to economic and social development. Achieving optimal iodine intakes from iodized salt (in the range of 150-250 microg/d for adults) may minimize the amount of thyroid dysfunction in populations. Ensuring adequate iodine status during parenteral nutrition has become important, particularly in preterm infants, as the use of povidone-iodine disinfectants has declined. Introduction of iodized salt to regions of chronic iodine deficiency may transiently increase the incidence of thyroid disorders, but overall, the relatively small risks of iodine excess are far outweighed by the substantial risks of iodine deficiency.
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            Iodine deficiency and thyroid disorders.

            Iodine deficiency early in life impairs cognition and growth, but iodine status is also a key determinant of thyroid disorders in adults. Severe iodine deficiency causes goitre and hypothyroidism because, despite an increase in thyroid activity to maximise iodine uptake and recycling in this setting, iodine concentrations are still too low to enable production of thyroid hormone. In mild-to-moderate iodine deficiency, increased thyroid activity can compensate for low iodine intake and maintain euthyroidism in most individuals, but at a price: chronic thyroid stimulation results in an increase in the prevalence of toxic nodular goitre and hyperthyroidism in populations. This high prevalence of nodular autonomy usually results in a further increase in the prevalence of hyperthyroidism if iodine intake is subsequently increased by salt iodisation. However, this increase is transient because iodine sufficiency normalises thyroid activity which, in the long term, reduces nodular autonomy. Increased iodine intake in an iodine-deficient population is associated with a small increase in the prevalence of subclinical hypothyroidism and thyroid autoimmunity; whether these increases are also transient is unclear. Variations in population iodine intake do not affect risk for Graves' disease or thyroid cancer, but correction of iodine deficiency might shift thyroid cancer subtypes toward less malignant forms. Thus, optimisation of population iodine intake is an important component of preventive health care to reduce the prevalence of thyroid disorders.
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              Iodine and Iodine Deficiency: A Comprehensive Review of a Re-Emerging Issue

              Iodine is a mineral nutrient essential for the regulation of a variety of key physiological functions including metabolism and brain development and function in children and adults. As such, iodine intake and status within populations is an area of concern and research focus. This paper will review recently published studies that focus on the re-emerging issue of iodine deficiency as a global concern and declining intake among populations in developed countries. Historically, the implementation of salt-iodization programs worldwide has reduced the incidence of iodine deficiency, but 30% of the world’s population is still at risk. Iodine nutrition is a growing issue within industrialized countries including the U.S. as a result of declining iodine intake, in part due to changing dietary patterns and food manufacturing practices. Few countries mandate universal salt iodization policies, and differing agriculture and industry practices and regulations among countries have resulted in inconsistencies in supplementation practices. In the U.S., in spite of salt-iodization policies, mild-to-moderate iodine deficiency is common and appears to be increasing. European countries with the highest incidence of deficiency lack iodization programs. Monitoring the iodine status of at-risk populations and, when appropriate, public health initiatives, appear to be warranted.

                Author and article information

                Journal
                Eur Thyroid J
                Eur Thyroid J
                ETJ
                European Thyroid Journal
                Bioscientifica Ltd (Bristol )
                2235-0640
                2235-0802
                23 February 2024
                06 February 2023
                01 February 2024
                : 13
                : 1
                : e230244
                Affiliations
                [1 ]Department of Nuclear Medicine , Hospital Erasme, Université Libre de Bruxelles, Brussels, Belgium
                [2 ]Department of Endocrinology and Metabolism , University Hospital Rigshospitalet, and Faculty of Ηealth and Clinical Sciences, University of Copenhagen, Copenhagen, Denmark
                [3 ]Centre of Postgraduate Medical Education , Centre of Translational Research, Department of Biochemistry and Molecular Biology, Warsaw, Poland: Basic Lead of the European Society of Endocrinology Focus Area on Thyroid
                [4 ]Public Health Unit , ULS Baixo Mondego, Figueira da Foz, Portugal Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal Health Investigation and Innovation Institute (i3S), University of Porto, Porto, Portugal
                [5 ]National Institute of Endocrinology "C. Davila" University of Medicine and Pharmacy , Bucharest, Romania
                [6 ]Charité-Universitätsmedizin Berlin , Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institut für Experimentelle Endokrinologie, Berlin, Germany: Co-Lead of the European Society of Endocrinology Focus Area on Environmental Endocrinology
                [7 ]Evgenideion Hospital , Unit of Endocrinology, Metabolism and Diabetes, National Kapodistrian University of Athens, Athens, Greece
                Author notes
                Correspondence should be addressed to L H Duntas: lduntas@ 123456eugenideio.uoa.gr or leonidas@ 123456duntas.gr
                Author information
                http://orcid.org/0000-0001-6392-9130
                http://orcid.org/0000-0001-9133-4089
                Article
                ETJ-23-0244
                10.1530/ETJ-23-0244
                10959048
                38320401
                b56d4b79-4ba2-42a6-bde4-a8502c4b584f
                © the author(s)

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

                History
                : 01 December 2023
                : 05 February 2023
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                eta-ese,iodine statement,iodine,echa
                eta-ese, iodine statement, iodine, echa

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