The only known mechanism of toxicity for perchlorate is interference with iodide uptake at the sodium-iodide symporter (NIS). The NIS translocates iodide across basolateral membranes to the thyroid gland so it can be used to form thyroid hormones (TH). NIS is also expressed in the mammary gland during lactation, so that iodide can be transferred from a mother to her child. Without adequate iodide, an infant cannot produce sufficient TH to meet its developmental needs. Effects expected from perchlorate are those that would be seen in conditions of hypothyroidism or hypothyroxinemia. The probability of a permanent adverse effect is greatest during early life, as successful neurodevelopment is TH-dependent. Study of perchlorate risk is complicated by a number of factors including thyroid status of the mother during gestation, thyroid status of the fetus, maternal and infant iodine intake, and exposure of each to other TH-disrupting chemicals. Perhaps the greatest standing issue, and the issue most relevant to the field of analytical chemistry, is the simple fact that human exposure has not been quantified. This review will summarize perchlorate's potential to adversely affect neurodevelopment. Whether current environmental exposures to perchlorate contribute to neuro-impairment is unknown. Risks posed by perchlorate must be considered in conjunction with iodine intake.