© The Author 2006. Published by Oxford University Press.
CORRESPONDENCE |
RESPONSE: Re: Risk of Thyroid Cancer After Exposure to 131I in Childhood
Affiliation of author: International Epidemiology Institute, Rockville, MD, and Vanderbilt University School of Medicine, Nashville, TN
Correspondence to: John D. Boice, Jr., ScD, International Epidemiology Institute, 1455 Research Blvd., Ste. 550, Rockville, MD 20850 (e-mail: john.boice{at}vanderbilt.edu).
The contribution of 129I to thyroid dose compared with that of 131I released during the Chernobyl accident in 1986 and with the background radiation from natural sources is minor because of the long physical half-life (15.7 million years) of 129I and its short retention time in the body (1). There is no experimental evidence for a carcinogenic effect of 129I—the rate of decay is one billion times lower than that of 131I and is much too low to expect one. Exposure of 129I to rats at 1 cGy/day for life produced no excess of thyroid tumors or other thyroidal effects (2). 129I occurs naturally when high-energy particles interact with xenon in the upper atmosphere, and 129I is produced after nuclear detonations and in nuclear reactors. 129I is not considered a principal radioactive release product after Chernobyl (3). Any continued small exposure to 129I to those alive in 1986 would be at older ages than occurred for the short-lived radioiodines, and any carcinogenic risk would accordingly be reduced because risk decreases dramatically with age at exposure. The possible contribution of 129I to thyroid dose from the Hanford nuclear site releases in Washington State was estimated to be very small (4), and comprehensive epidemiologic studies of populations residing near Hanford have failed to identify an increased risk of thyroid cancer (or any of 14 measures of thyroid disease) associated with 131I exposure (5).
The areas near Chernobyl of highest fallout to radioactive iodines were also the areas most deficient in dietary stable iodine. The continued administration of potassium iodine (KI) reduced thyroid cancer risk, even after the time when blockage of 131I uptake was no longer possible. How this risk reduction could occur is not entirely clear. It has been postulated that diets deficient in iodine may interact with radioactive iodines to enhance the risk of thyroid cancer (6). Animal studies have shown that the tumorigenic effect of thyroid irradiation depends on the duration and extent of subsequent thyroid stimulation; i.e., thyroid stimulation resulting from iodine-deficient diets increased the number of radioiodine-induced thyroid tumors, and radiation-induced tumors were conversely reduced when excessive thyroid stimulation was removed (7). It is conceivable that restoring normal levels of stable iodine to the diet in areas of endemic goiter might quell the overactive thyroid gland so that any underlying damage from prior radioiodine exposures did not progress to cancer. If KI administration has influenced the patterns of thyroid cancer risk among children living near Chernobyl, this influence is unlikely because of any protective action against a hypothetical and implausible carcinogenic effect of 129I. It is more plausible that the higher levels of thyroxine associated with iodine supplements decreased the level of thyroid stimulation (and subsequent cancer risk) by indirect inhibition of thyrotropin secretion.
REFERENCES
(1) NCRP (National Council on Radiation Protection and Measurements). Induction of Thyroid Cancer by Ionizing Radiation. NCRP Report No. 80. Bethesda (MD): National Council on Radiation Protection and Measurements; 1985.
(2) Book SA. Iodine-129 uptake and effects of lifetime feeding in rats. Health Phys 1983;45:61–6.[ISI][Medline]
(3) World Health Organization. Health effects of the Chernobyl accident and special health care programmes. Report of the UN Chernobyl Forum. Expert Group "Health" (EGH). Working Draft, August 31, 2005. Available at http://www.iaea.org.
(4) Robkin MA, Shleien B. Estimated maximum thyroid doses from 129I releases from the Hanford site for the years 1944–1995. Health Phys 1995;69:917–22.[ISI][Medline]
(5) Davis S, Kopecky KJ, Hamilton TE, Onstad L; Hanford Thyroid Disease Study Team. Thyroid neoplasia, autoimmune thyroiditis, and hypothyroidism in persons exposed to iodine 131 from the Hanford nuclear site. JAMA 2004;292:2600–13.
(6) Shakhtarin VV, Tsyb AF, Stepanenko VF, Orlov MY, Kopecky KJ, Davis S. Iodine deficiency, radiation dose, and the risk of thyroid cancer among children and adolescents in the Bryansk region of Russia following the Chernobyl power station accident. Int J Epidemiol 2003;32:584–91.
(7) Williams D, Pinchera A, Karaoglou A, Chadwick KH, eds. Thyroid cancer in children living near Chernobyl. Report EUR 15248. (Luxembourg): Commission of the European Communities; 1993. p. 81.
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J Natl Cancer Inst 2006 98: 641.
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