While most cancer rates have declined over the last two decades, the incidence rate for thyroid cancer has been increasing.1 National Cancer Institute statistics suggest that the number of cases of thyroid cancer has increased by about 6.5% in recent years.2 It is not known why thyroid cancer has become more prevalent, but some medical professionals believe it is not due solely to an increase in detection. There may be a biological basis for the change in disease prevalence.2
The relationship between human diseases of the endocrine system such as thyroid cancer and exposure to environmental contaminants is poorly understood and is the subject of much research and debate within the scientific community. The Food Quality Protection Act and Safe Drinking Water Act Amendments in 1996 gave the EPA the authority to screen chemicals for endocrine effects. The EPA’s Endocrine Disruptor Screening Program (EDSP), announced in 2009, mandates that certain pesticides, commercial chemicals, and environmental contaminants be screened in a series of assays to identify the potential of these chemicals to interact with estrogen, androgen, and the thyroid hormonal systems in humans and wildlife. The first phase of the EDSP , Tier I, consists of a screening battery of in vitro and in vivo assays.
Several important features of the thyroid system are conserved across species, including the structure of thyroid hormones, the mechanism by which they are synthesized, and the complex interplay between the hypothalamus, pituitary, and thyroid gland.3 Because of this, extrapolation of results across species may be simplified. Three in vivo assays have been validated to screen chemicals for their potential to interact with the thyroid system – the pubertal male, pubertal female, and amphibian metamorphosis assays.3 The assay species are the rat and frog, respectively.
The first group of 67 chemicals were identified for testing by the EPA in 2009 and included pesticide active ingredients and High Production Volume (HPV) chemicals used as pesticide inert ingredients.4 In 2010, the EPA identified an additional 134 chemicals for testing in the EDSP including pesticides, two perfluorocarbon compounds, three pharmaceuticals (erythromycin, nitroglycerin, and quinoline), and an array of other chemicals, ranging from those used for industrial manufacturing processes or in the production of pharmaceutical and personal care products.5 The deadlines for generation of data for Tier I screening range from the fall of 2011 through 2012.6
The EPA described their weight-of-evidence approach for interpretation of data collected from Tier I screening and their rationale for proceeding with additional, or Tier II, testing for potential endocrine disrupting chemicals in September 2011.7 The data from Tier I screening and its interpretation have yet to be made publicly available, so there are no specific examples which may be discussed and evaluated within the scientific community. Tier II testing will consist of in vivo assays that establish dose-response relationships for potential adverse effects for risk assessment. However, Tier II assays are still in development or the validation stages.8 Unraveling the complexities of the relationship between environmental contaminants and thyroid disease such as cancer will be a long term process.
1. The Washington Post, January 6, 2012. Most cancer rates declined over past two decades. Jennifer LaRue Huget.
2. USA Today, January 16, 2012. Doctors unsure why thyroid cancer cases on the rise. Shari Rudavsky.
3. OECD Environmental, Health, and Safety Publications, series on Testing and Assessment. Draft Detailed Review Paper on Thyroid Hormone Disruption Assays. O4 February 2005.
7. Office of Chemical Safety and Pollution Prevention, US EPA, September 14, 2011. Weight-of-Evidence: Evaluating Results of EDSP Tier 1 Screening to Identify the Need for Tier 2 Testing.
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