Thyroid hormones
Thyroid hormones are two hormones produced and released by the thyroid gland, namely triiodothyronine (T) and thyroxine (T). They are tyrosine-based hormones that are primarily responsible for regulation of metabolism. T and T are partially composed of iodine. A deficiency of iodine leads to decreased production of T and T, enlarges the thyroid tissue and will cause the disease known as simple goitre. The major form of thyroid hormone in the blood is thyroxine (T), which has a longer half-life than T. In humans, the ratio of T to T released into the blood is approximately 14:1. T is converted to the active T (three to four times more potent than T) within cells by deiodinases (5'-iodinase). These are further processed by decarboxylation and deiodination to produce iodothyronamine (Ta) and thyronamine (Ta). All three isoforms of the deiodinases are selenium-containing enzymes, thus dietary selenium is essential for T production. Edward Calvin Kendall was responsible for the isolation of thyroxine in 1915.
Flame retardant
Many halogenated flame retardants with aromatic rings, including most brominated flame retardants, are likely thyroid hormone disruptors. The thyroid hormones triiodothyronine (T3) and thyroxine (T4) carry iodine atoms, another halogen, and are structurally similar to many aromatic halogenated flame retardants, including PCBs, TBBPA, and PBDEs. Such flame retardants therefore appear to compete for binding sites in the thyroid system, interfering with normal function of thyroid transport proteins (such as transthyretin) in vitro and thyroid hormone receptors. A 2009 "in vivo" animal study conducted by the US Environmental Protection Agency (EPA) demonstrated that deiodination, active transport, sulfation, and glucuronidation may be involved in disruption of thyroid homeostasis after perinatal exposure to PBDEs during critical developmental time points in utero and shortly after birth. Disruption of deiodinase as reported in the Szabo et al., 2009 "in vivo" study was supported in a follow-up "in vitro" study. The adverse effects on hepatic mechanism of thyroid hormone disruption during development have been shown to persist into adulthood. The EPA noted that PBDEs are particularly toxic to the developing brains of animals. Peer-reviewed studies have shown that even a single dose administered to mice during development of the brain can cause permanent changes in behavior, including hyperactivity.