Environmental Agents Trigger Autoimmune Thyroid Disease

Paul W. Mamula, PhD

May 20, 2010

May 20 2010 (Minneapolis, Minnesota) — Multiple genetic and environmental risk factors can trigger autoimmune thyroid disease in humans, according to experts here at the American Thyroid Association (ATA) Spring 2010 Meeting.

Gregory A. Brent, MD, professor of medicine and physiology at the David Geffen School of Medicine at the University of California at Los Angeles, presented the findings.

He reported that "genetic background accounts for about 70% of the risk for autoimmune thyroid disease. The remainder is likely related to a range of environmental triggers."

A number of toxicants affect iodine uptake and thyroid hormone synthesis, metabolism, binding, and action, he explained.

He noted that among the more common agents that affect thyroid metabolism are perchlorates (a rocket fuel additive), thiocyanates (a compound in cigarettes), and dioxins (a class of pesticides). Few studies assess how these agents affect humans, he added.

"The problem is that most of these thyroid toxicants have been identified in vitro and in animal models. The significance for humans is much more difficult to assess," said Dr. Brent.

Dr. Brent reported that some of the risk factors for humans are medical radiation, environmental releases of radiation (such as from the Chernobyl nuclear reactor accident and the Hiroshima atomic bomb), environmental pollutants, and excess iodine intake.

Medical radiation can trigger antithyroid antibodies and autoimmune thyroid disease. Dr. Brent pointed out that some patients treated with radioactive iodine for non-Graves' disease hyperthyroidism eventually develop Graves' disease.

Environmental releases have served as the basis for many studies of exposure and thyroid disease, according to Dr. Brent. "Toxicologists want to know the dose given. For these radiation accidents, we have the best evidence of the [disease] relationship because the dose is known," he added.

He presented examples from selected studies in humans that demonstrated the effects of I131 releases in nuclear accidents and after the atomic bomb. One study that followed a cohort of atomic bomb survivors found that many people developed antithyroid antibodies and hypothyroidism. The disorders manifested a U-shaped relationship, as did findings in studies of the Chernobyl survivors.

Iodine added to the diet can trigger disease in select individuals and populations, according to Dr. Brent. He noted that among people in iodine-deficient areas, giving them iodine can stimulate immune response and antibodies.

Researchers have the least evidence for environmental toxicant effects in humans, Dr. Brent stated.

"A whole range of compounds are being increasingly recognized that are associated with the impairment of thyroid hormone action," he told meeting attendees.

The thyroid is influenced by toxicants. Researchers know very little about their effects in humans. These compounds include polychlorinated biphenyls (PCBs), pesticides, polybrominated diphenyl ethers (PBDEs), and bisphenol A (BPA).

In experimental animals, BPA has been shown to affect thyroid receptors and thyroid function, said Dr. Brent. Although BPA is of concern now, evidence of its effects in humans is sparse. Some evidence exists for industrial exposure to other compounds, but these lack dose-response data.

The way to avoid thyroid problems is to recognize risk factors and try to avoid them, Dr. Brent said. He noted that environmental factors account for about 30% of the risk for autoimmune thyroid disease. Risk factors that are easily avoided include certain drugs, cigarette smoke, stress (although difficult to prove), selenium deficiency, and contaminated well water (perchlorates).

Yaron Tomer, MD, vice chair of research at Mount Sinai School of Medicine in New York City, and a presenter at the ATA, told Medscape Diabetes & Endocrinology that "physicians don't have good human data for environmental insults, but Dr. Brent's presentation summarized the existing data well and without bias."

All of the reviews presented at this meeting will appear in the July 2010 issue of Thyroid.

Dr. Brent has disclosed no relevant financial relationships. Dr. Tomer reports receiving research grants from the National Institutes of Health, but reports no other relevant financial relationships.

American Thyroid Association (ATA) Spring 2010 Meeting. Presented May 15, 2010.

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