following doses above J000 rads for external irradiation and 20 rads following 1311 exposure. From the review of Maxon et al., the BEIR Canmittee concluded that the threshold for the induction of hypothyroidism was 2000 rads in externa! exposure and 5000 rads for '311 (NAS, 1980). Means of Protection The thyroid gland's affinity for todine not only makes it the target organ for radioiodine but also provides a means by which the thyroid may be protected fran radfofodine. The administration of stable fodine suppresses the uptake of radiotodine by the thyroid by dfluting the radioactive fsotope and by invoking homeostatic mechanisms within the gland that reduce the anount of fodide taken up by the gland. This so-called “blocking” ability of the thyroid gland was demonstrated svor after 1311 became available (Perlman et al., 1941), when rats were given 131] with either 0.5 mg iodine as potassium fodide, 0.03 mg iodine, or no fodine, that fs, carrfer-free. Subsequent peak uptakes by thyroid glands were 2 percent and 7 percent for rats that received 0.5 or 0.03 mg fodine, respect ive- ly. Rats receiving only the tracer had peak uptakes of 65 percent. The blocking ability of the thyroid has been the subject of many papers, including those by Adams and Bonnell] (1962) and Blum and Efsenbud (1967). The National Counci] on Radfation Protection and Measurements (NCRP, 1977b) recommended the adequate blocking dose in cases of radioiodine exposures to be a daily dose of 130 milligrams of potassium iodide (and half that amount to infants under one year of age). Administration of the blocking agent was recaumended to occur at thyroid doses of 10-30 rads or more. Data from a later study (Sternthal et al., 1980) suggested that thyroidal uptake can he suppressed bn Me eteees Be