Thyroid disruption: mechanism and clinical implications in human health

Altern Med Rev. 2009 Dec;14(4):326-46.


Exposure to specific environmental toxins, including polychlorinated biphenyls, dioxins, phthalates, polybrominated diphenyl ethers (PBDEs), and other halogenated organochlorines, has been shown to interfere with the production, transportation, and metabolism of thyroid hormones by a variety of mechanisms. A broad range of chemicals, with structural similarity to thyroid hormone, have been shown to bind to thyroid receptors with both agonist and antagonist effects on thyroid hormone signaling. The incidence of thyroid disease in the United States, particularly for thyroid cancer and thyroid autoimmune disease, is increasing substantially. The evidence for the significant effects of background levels of thyroid-disrupting chemicals, the known pathways for thyroid disruptors, and the evidence and implications for neurodevelopmental damage due to thyroid-disrupting chemicals is reviewed.

Publication types

  • Review

MeSH terms

  • Dioxins / toxicity
  • Environmental Exposure / statistics & numerical data*
  • Environmental Pollutants / toxicity*
  • Flame Retardants / toxicity
  • Halogenated Diphenyl Ethers / toxicity
  • Health Knowledge, Attitudes, Practice
  • Humans
  • Pesticides / toxicity
  • Polychlorinated Biphenyls / toxicity
  • Thyroid Diseases / chemically induced*
  • Thyroid Diseases / epidemiology*
  • Thyroid Diseases / prevention & control
  • Thyroid Gland / drug effects*
  • Thyroid Neoplasms / chemically induced
  • Thyroid Neoplasms / epidemiology
  • United States / epidemiology


  • Dioxins
  • Environmental Pollutants
  • Flame Retardants
  • Halogenated Diphenyl Ethers
  • Pesticides
  • Polychlorinated Biphenyls