Abstract
An increased incidence of thyroid cancer has been reported in many parts of the world including the United States during the past several decades. Recently emerging evidence has demonstrated that polyhalogenated aromatic hydrocarbons (PHAH), particularly polybrominated diphenyl ethers (PBDE), alter thyroid hormone homeostasis and cause thyroid dysfunction. However, few studies have been conducted to test whether exposure to PBDE and other PHAH increases the risk of thyroid cancer. Here, we hypothesize that elevated exposure to PHAH, particularly PBDE, increases the risk of thyroid cancer and may explain part of the increase in incidence of thyroid cancer during the past several decades. In addition, genetic and epigenetic variations in metabolic pathway genes may alter the expression and function of metabolic enzymes which are involved in the metabolism of endogenous thyroid hormones and the detoxification of PBDE and other PHAH. Such variation may result in different individual susceptibilities to PBDE and other PHAH and the subsequent development of thyroid cancer. The investigation of this hypothesis will lead to an improved understanding of the role of PBDE and other PHAH in thyroid tumorigenesis and may provide a real means to prevent this deadly disease.
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