Thyroid hormone is essential for normal brain development and recognition of this has led to universal screening of newborns for thyroid function to ensure that circulating levels of thyroid hormone are within a range known to be supportive of normal growth and mental development. Environmental chemicals that interfere with thyroid function are known to inhibit normal growth and mental development. Work from our lab and from labs internationally demonstrates in animal systems that some industrial chemicals such as PCBs, PBDEs, and others may interact with the thyroid hormone receptor(s) in ways that are not predicted by changes in serum thyroid hormone levels. Our work demonstrates that the enzyme CYP1A1 must metabolize some individual PCB congeners before they can interact with the thyroid receptor. In animals, this requirement appears to be manifested in part by a strong correlation between CYP1A1 and TH target gene expression. Here we present that this pattern extends to humans by demonstrating a correlation between increased CYP1A1 mRNA and an abundance of thyroid hormone responsive gene mRNA.