by Mark D Miller, et al.
August 10, 2009
[Note: to read the full text of this free access article, which notes chemicals known to affect thyroid function (such as bisphenol A, which can leach from polycarbonate drink containers, for example), click here.]
Background: There is increasing evidence in humans and in experimental animals for a relationship between exposure to specific environmental chemicals and perturbations in levels of critically important thyroid hormones (THs). Identification and proper interpretation of these relationships are required for accurate assessment of risk to public health.
Objectives: We review the role of TH in nervous system development and specific outcomes in adults, the impact of xenobiotics on thyroid signaling, the relationship between adverse outcomes of thyroid disruption and upstream causal biomarkers, and the societal implications of perturbations in thyroid signaling by xenobiotic chemicals.
Data sources: We drew on an extensive body of epidemiologic, toxicologic, and mechanistic studies.
Data synthesis: THs are critical for normal nervous system development, and decreased maternal TH levels are associated with adverse neuropsychological development in children.
In adult humans, increased thyroid-stimulating hormone is associated with increased blood pressure and poorer blood lipid profiles, both risk factors for cardiovascular disease and death.
These effects of thyroid suppression are observed even within the “normal” range for the population.
Environmental chemicals may affect thyroid homeostasis by a number of mechanisms, and multiple chemicals have been identified that interfere with thyroid function by each of the identified mechanisms.
Conclusions:
Individuals are potentially vulnerable to adverse effects as a consequence of exposure to thyroid-disrupting chemicals.
Any degree of thyroid disruption that affects TH levels on a population basis should be considered a biomarker of adverse outcomes, which may have important societal outcomes.
Source: Environmental Health Perspectives, Jul 2009; 117(7):1033-41. PMID: 19654909, by Miller, MD, Crofton KM, Rice DC, Zoeller RT. Office of Environmental Health Hazard Assessment, California Environmental Protection Agency, Oakland, California; Pediatric Environmental Health Specialty Unit, University of California at San Francisco, California; National Health and Environmental Effects Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina; Maine Center for Disease Control, Augusta, Maine; Biology Department, Morrill Science Center, University of Massachusetts at Amherst, Amherst, Massachusetts, USA. [E-mail: mmiller@oehha.ca.gov]
|
