Abstract
Common environmental exposures may affect thyroid function in humans. Foetuses and infants are most vulnerable to these effects because they need thyroid hormone for normal neurodevelopment. Perchlorate, thiocyanate and nitrate are all competitive inhibitors of the sodium/iodine symporter (NIS) in pharmacologic doses, but their effects on human thyroid function at environmental exposure levels remain unclear. Many compounds, including polychlorinated biphenyls (PCBs), polybrominated diphenylethers (PBDEs), bisphenol-A (BPA) and triclosan, may have direct actions on the thyroid hormone receptor, but these effects are complex and are not yet well understood. Isoflavones inhibit thyroperoxidase (TPO) activity, and, therefore, may cause goitre and hypothyroidism if ingested at high levels, particularly in iodine-deficient individuals. Organochlorine pesticides and dioxins may decrease serum T(4) half-life by activating hepatic enzymes. Additional studies are needed to further elucidate the risk posed by these and other potentially thyroid-disrupting compounds.
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