Exposure to arsenic (As) from drinking water has been linked to neurocognitive impairment, however, the physiological mechanisms of As-induced neurotoxicity are not known. Emerging evidence from animal studies suggest disruption of the endocrine system in early life as a plausible mechanism. We examined neu-robehavioral performance and serum thyroid hormone (TH) among adolescents living inAraihazar, Bangladesh who have been consistently exposed to water arsenic (WAs) above and below 10 μg L−1 since in utero. Mothers of these children are participants of the Health Effects of Arsenic Longitudinal Study (HEALS). We have observed inverse relationships between As exposure and TH biomarkers as well as between TH and multiple neurobehavioral outcomes in these adolescents. Findings from this study suggest that As-induced neurotoxicity may be mediated via disruption of thyroid hormone.