in investigation and treatment of thyroid disease and on studies of populations exposed to fallout from various nuclear incidents. Radiation effects can result from external radiation (from a source of radiation outside the body, such as x rays) and from internal radiation (from a source of radiation in the body, such as radioisotopes absorbed from food or drink or absorbed from the air). The effects of internal radiation from iodine radioisotopes on the thyroid depend on the gland’s ability to concentrate and store the isotopes, which lead to a much higher radiation dose to the thyroid than to other tissues. Some other tissues (such as salivary glands, breast, and stomach) concentrate radioiodine but do not store it, so their dose, although more than that to most tissues, is much less than that to the thyroid.

Radiation from any source—including ingested or inhaled isotopes, medical or dental investigations with x rays, and direct radiation from an atomic bomb—can damage DNA and thus pose a risk of tumors and, in high doses, cell death. The main expected consequences of exposure of the thyroid to radiation are an increase in the incidence of thyroid tumors and an increase in the occurrence of loss of thyroid function (hypothyroidism, myxedema). Tumors occur because DNA damage can lead, in a small minority of cells, to activation of genes that stimulate cell growth, to loss of function of genes that suppress cell growth, or to various other changes that give cells and their progeny the ability to multiply more rapidly than normal. Radiation can damage DNA directly or through the formation of free radicals. The damage can be double strand breaks, with resultant loss of a portion of a chromosome (deletions), or rearrangement, in which a piece of a chromosome is reinserted inappropriately. Misrepair of radiation-induced damage, including single strand breaks, can also lead to point mutation, in which a base is replaced by an inappropriate one. Many mutagenic chemicals lead to point mutations, but radiation causes mostly deletions and rearrangements (Sankaranarayanan, 1991). Much attention has recent been focused on genetic instability, a phenomenon observed in vitro in which radiation, of both high- and low-energy-transfer types, leads not only to mutations in irradiated cells but also to a persistent increase in mutation rate in the non-irradiated daughter cells (Little et al., 1997). Surprisingly, it has been shown that such instability is



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