ABSTRACT
INTRODUCTION In the adult human, thyroid hormone (TH) defi ciency or excess can lead to a wide array of neurological and psychiatric symptoms, which are largely reversible with adequate treatment ( 1-3 ). In contrast, TH defi ciency or excess during nervous system development leads to neurological and psychiatric symptoms that are not reversible, and are associated with permanent alterations in brain structure and function (4) . Recently, the potential for environmental contaminants that disrupt the thyroid axis to induce neurodevelopmental impairments has been a topic of considerable interest ( 5-10 ). A large number of environmental contaminants with diverse structures have been shown to decrease circulating levels of TH ( 6 , 11-13 ). Animal studies have indicated that this action of xenobiotics on the thyroid system may contribute to alterations in nervous system development and function ( 5 , 6 , 9 , 11-21 ). Some of these environmental contaminants have also been evaluated in humans and been found to lower serum TH levels ( 22-24 ). Moreover, human exposures to some of these same contaminants are associated with neurodevelopmental impairments ( 25-29 ). Thus, an important mechanism by which some environmental contaminants may produce neurotoxic effects on the developing or adult human is by interfering with thyroid function, or with TH action.
