Abstract:Potassium iodide (KI) is recommended as an emergency treatment for exposure to radioiodines, most commonly associated with nuclear detonation or mishaps at nuclear power plants. Protecting the thyroid gland of infants and children remains a priority because of increased incidence of thyroid cancer in the young exposed to radioiodines (such as 131I and 133I). There is a lack of clinical studies for KI and radioiodines in children or infants to draw definitive conclusions about the effectiveness and safety of KI… Show more
“…A review of the functional aspects of the thyroid axis across life-stages provides supporting evidence that thyroid functions in infants and children are accelerated compared to adults [31]. The current recommendations for KI dose and duration were adjusted downward by age group in consideration of body size, assuming thyroid function scales linearly with development and age.…”
Section: Evidence From Accidental Exposuresmentioning
Children are at a greater risk than adults of developing cancer after being exposed to ionizing radiation. Because of their developing bodies and long life expectancy post-exposure, children require specific attention in the aftermath of nuclear accidents and when radiation is used for diagnosis or treatment purposes. In this review, we discuss the carcinogenic potential of pediatric exposures to ionizing radiation from accidental, diagnostic, and therapeutic modalities. Particular emphasis is given to leukemia and thyroid cancers as consequences of accidental exposures. We further discuss the evidence of cancers that arise as a result of radiotherapy and conclude the review with a summary on the available literature on the links between computer tomography (CT) and carcinogenesis. Appropriate actions taken to mitigate or minimize the negative health effects of pediatric exposures to ionizing radiation and future considerations are discussed.
“…A review of the functional aspects of the thyroid axis across life-stages provides supporting evidence that thyroid functions in infants and children are accelerated compared to adults [31]. The current recommendations for KI dose and duration were adjusted downward by age group in consideration of body size, assuming thyroid function scales linearly with development and age.…”
Section: Evidence From Accidental Exposuresmentioning
Children are at a greater risk than adults of developing cancer after being exposed to ionizing radiation. Because of their developing bodies and long life expectancy post-exposure, children require specific attention in the aftermath of nuclear accidents and when radiation is used for diagnosis or treatment purposes. In this review, we discuss the carcinogenic potential of pediatric exposures to ionizing radiation from accidental, diagnostic, and therapeutic modalities. Particular emphasis is given to leukemia and thyroid cancers as consequences of accidental exposures. We further discuss the evidence of cancers that arise as a result of radiotherapy and conclude the review with a summary on the available literature on the links between computer tomography (CT) and carcinogenesis. Appropriate actions taken to mitigate or minimize the negative health effects of pediatric exposures to ionizing radiation and future considerations are discussed.
Iodine is essential for production of thyroid hormones (TH). Perchlorate is an environmental contaminant that interferes with iodine uptake into the thyroid gland to reduce TH synthesis. As TH are critical for brain development, exposure to perchlorate during pregnancy is of concern for the developing fetal brain. In this study we 1) define profiles of TH in the maternal and fetal compartments of pregnant rats in response to inhibition of the sodium-iodine symporter (NIS) by perchlorate, 2) expand inquiry previously limited to serum to include fetal thyroid gland and brain. Perchlorate was added to the drinking water (0, 1, 30, 300, 1000 ppm) of pregnant rat dams from gestational days (GD) 6-20. On GD20, blood, thyroid gland and brain were collected from the fetus and dam for TH and molecular analyses. Thyroid gland and serum TH were dose-dependently reduced, with steeper declines evident in fetus than the dam. The thyroid gland revealed perturbations of TH-action with greater sensitivity in fetus than dam. TH and TH-responsive gene expression were reduced in the fetal cortex portending effects on brain development. These findings are the first quantitative assessments of perchlorate-induced deficits in the fetal thyroid gland and fetal brain. We provide a conceptual framework to develop a quantitative NIS AOP for serum TH deficits and the potential to impact the fetal brain. Such a framework may also facilitate the translation of in vitro bioactivity to the downstream in vivo consequences of NIS inhibition in the developing fetus.
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