Thyroid hyperplasia

PCB 77 given 20 mg/kg BW 3 times over a 28-day period Thyroid hyperplasia caused by low iodine diet was not enhanced by PCB 77 14... 

PCB 77 single dose of 60 mg/kg BW Thyroid hyperplasia reversed within 7 days 14... 

Endocrine Effects. Thyroid hyperplasia and pituitary cysts were observed in rats, but not mice, in a chronic bioassay study with endrin administered in the feed (NCI 1978). Treon et al. (1955) found diffuse degeneration of the adrenal glands in rats dosed with >1.25 mg/kg/day in their feed for 2 years however, the adrenal effects were absent at the 0.25 mg/kg/day dose. There has been no evidence of endocrine effects in occupationally exposed human populations. 

Endocrine Effects. Thyroid hyperplasia and pituitary cysts were observed in rats, but not in mice, in a chronic bioassay study with endrin administered in the feed (NCI 1978). There has been no evidence of endocrine effects in occupationally exposed populations. 

Mutations with similar outcomes have been identified in nonautoimmune autosomal dominant hyperthyroidism (toxic thyroid hyperplasia) (25,26,28,32,33). These variants are located in the third TM (Val509Ala), the seventh TM (Cys672Tyr), and the carboxyl tail (Asp727Glu) regions (34). These variants result in a form of congenital hyperthyroidism that is the germline counterpart of a hyperfunctioning thyroid adenoma, with similar functional characteristics (25,33). 

Thyroid effects that have mainly included reduced serum T4 hormone levels and follicular cell hyperplasia were consistently observed in rats and mice orally exposed to PBDEs. Accompanying changes in serum TSH levels were not found and the depression of serum T4 is likely related to hepatic enzyme induction. Acute duration studies showed decreases in serum T4 in rats exposed to >10 mg/kg/day octaBDE or >30 mg/kg/day pentaBDE for 4 days and in rats and mice exposed to >18 mg/kg/day pentaBDE for 14 days. Effects observed in intermediate-duration studies include thyroid hyperplasia in rats exposed to >8 mg/kg/day octaBDE for 30 days and reduced serum T4 in rats exposed to >10 mg/kg/day pentaBDE for 90 days. Exposure to pentaBDE on gestation day 6 through postnatal day 21 caused serum T4... 

Research Laboratories 1984). Effects observed in both sexes included significantly reduced plasma T4 levels at 10 mg/kg/day and increased follicular cell hyperplasia at 100 mg/kg/day. Incidences of follicular cell hyperplasia in the 0, 2, 10, and 100 mg/kg/day dose groups of this study were 0/10, 2/10, 2/10, and 5/10 in males and 0/10, 0/10, 1/10, and 4/10 in females. The thyroid hyperplasia was mild and transient as it was characterized as very slight in severity at all doses and was no longer observed at 24 weeks postexposure in any animals. Thyroid hyperplasia was equivocally increased in male CD rats that were exposed to 90 mg/kg/day of pentaBDE (unspecified mixture) in the diet for 28 days (IRDC... 

Mancozeb has effects on various organ systems. Its primary mechanism of toxicity is via skin contact, leading to contact dermatitis and dermal sensitization. Mancozeb has also been shown to have teratogenic and reproductive effects. Mancozeb exposure also alters the reproductive and endocrine structures, leading to decreased fertility. Animals orally exposed to mancozeb showed thyroid hyperplasia, probably via its ability to inhibit the synthesis of thyroxin. Additionally, mancozeb exposure produces neurotoxicity via yet an unknown mechanism. 

Ethylene thiourea is toxic and known to produce thyroid neoplasms (thyroid hyperplasia) in rats and liver neoplasms in mice following long-term administration NIOSH potential occupational carcinogen NTP Suspect carcinogen OSHA Possible suspect carcinogen. Acute oral toxicity (LD50) 1832 mg/kg [Rat],... 

Casey MB, Lohse CM, Lloyd RV. Distinction between papillary thyroid hyperplasia and papillary thyroid carcinoma by immunohistochemical staining for cytokeratin 19, galectin-3 and HBME-1. Endocr Pathol. 2003 14 55-60. 

Maneb or mancozeb. The reader is referred to Section 2.2.1.2 regarding endocrine effects in humans following potential dermal exposure to maneb or mancozeb. Thyroid hyperplasia was observed in 3 female newts dermally exposed to 20 ppm maneb for 5 months (Pacces Zaffaroni et al. 1978). 

Human Toxicity Large amounts of CoCl2 depress erythrocyte production. May lead to death in children. Other effects include cutaneous flushing, chest pains, dermatitides, tinnitus, nausea and vomiting, nerve deafness, thyroid hyperplasia, myxedema, congestive heart failnre. See E. Beut-ler et al.. Clinical Disorders of Iron Metabolism (Grime Stratton, New York, 1963) pp 175-178. 

A deficiency in iodine causes goiter even in fish (thyroid hyperplasia, increased mortality) (Anonymous 1983). Polychlorinated biphenyls caused severe endemic goiter in predator fish in the Great Lake (USA) waters (Matovinovic and Trowbridge 1980). 

Mutations of the TSH receptor result in clinical thyroid dysfunction. Germline mutations can present as autosomal dominant toxic thyroid hyperplasia (gain-of-frmction mutations) or as gestational hyperthyroidism due to receptor hypersensitivity to hCG. Somatic mutations that result in constitutive activation of the receptor are associated with hyperfrmctioning thyroid adenomas. 

It is often assumed that eradication of severe ID is enough to avoid the most important IDD, including those affecting mental processes. Present experimental results stress that this is not so, and countries with areas of mild-to-moderate ID, should actively correct it an important proportion of their inhabitants, and their future progeny, may still suffer from easily preventable impairment of mental functions and the consequent socioeconomic implications (Morreale de Escobar et ai, 2004), as well as the increased incidence of thyroid disorders accompanying thyroid hyperplasia. 

Any degree of ID, even if mild, ought to be avoided because it rapidly activates TSH-independent autoregu-latory mechanisms that result in goiter, and an increased incidence of thyroid disorders accompanying thyroid hyperplasia. 

Urinary iodine concentration and palpation of goiter among schoolchildren is the most frequent method used by cross-sectional surveys to measure iodine deficiency. Because iodine is excreted by the kidneys, the urinary concentration of iodine is an indicator of iodine intake. Lower production of thyroxine leads to increased production of the thyroid-stimulating hormone, which results in thyroid hyperplasia known as goiter. The World Health Organization (2001) classifies iodine deficiency into mild, moderate and severe when urinary excretion is, respectively, 50—99, 20 9 and <20 p,g/l of urine. 

Dose-related increases in liver and thyroid weight were reported in pigs administered 60,296, or 1551 mg/kg of turmeric oleoresin daily for 102 days. Inflammation of the bile duct, thyroid hyperplasia, and epithelial changes in the kidney and urinary bladder were observed in the two higher dose groups (Bille et al. 1985). 

We need more information on the structure and ultrastructure of the thyroid in the two types of cretinism. We need to know whether there are specific aspects of thyroid morphology in hypothyroid newborns and stillbirths in endemic areas. We also need to know whether there are age-related changes in the thyroid of hypothyroid infants and children. In other words, how valid is the hypothesis that only progressive atrophy of the thyroid will result in permanent hypothyroidism and myxedematous cretinism in some individuals while the development of compensatory thyroid hyperplasia explains the transient character of hypothyroidism in others (5). Finally, is there any morphological evidence of an autoimmune process within the thyroid ... 

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