© The Author 2006. Published by Oxford University Press.
CORRESPONDENCE |
Re: Risk of Thyroid Cancer After Exposure to 131I in Childhood
Affiliations of authors: Department of Medicine, Legacy Good Samaritan Hospital, Portland, OR (CMG); Department of Physics and Environmental Sciences, Portland State University, Portland, OR (RHN)
Correspondence to: Rudi H. Nussbaum, PhD, 2393 SW Park Pl., #301, Portland, OR 97205 (e-mail: D4RN{at}odin.pdx.edu).
In his editorial, Boice (1) summarized "what is new" about radiogenic thyroid cancer in children as a result of the April 1986 Chernobyl nuclear accident, as presented by Cardis et al. (2). One of their puzzling findings is the fact that potassium iodide given to children months to years after exposure reduced the cancer risk by threefold. Cardis et al. hypothesize that the reduction in risk might be the result of shrinkage in the size of the thyroid due to prolonged administering of dietary iodine supplements.
Neither Cardis et al. nor Boice considered the fact that the release of 131I (half-life = 8 days) into the environment from the molten fuel rods was accompanied by large amounts of 129I (half-life = 16 million years), probably in higher proportion than that released by the Hanford, WA, plutonium production process (3).
In a report that suggests excess cancers, including thyroid cancers, among a population of residents downwind of the reactors in Hanford, WA, during periods of large releases of radioiodine into the atmosphere (downwinders), Grossman et al. (4) referred to several studies that show that the commonly assumed biological clearance half-time for iodine (80 days from the thyroid and 12 days for the rest of the body) (3) is inconsistent with several well-documented observations of much longer iodine retention times in tissue. Therefore, in contrast to statements that contributions to dose from uptake of 129I by the thyroids of residents downwind of Hanford, WA, were negligible (3), we suggested that a long retention time, combined with the considerably higher relative biological effectiveness of the very low-energy radiation from the radioactive decay of 129I compared with 131I emissions may contribute substantially to damage of thyroid tissue, including cancer induction (4).
The sizable reduction of risk by administering potassium iodide to children long after exposure to Chernobyl fallout supports our hypothesis of an important role of 129I in thyroid cancer induction, mitigated by long-term metabolic exchange between stable and radioactive iodine, and would explain the puzzle presented by the findings of Cardis et al.
REFERENCES
(1) Boice JD Jr. Radiation-induced thyroid cancer—what's new? J Natl Cancer Inst 2005;97:703–5.
(2) Cardis E, Kesminiene A, Ivanov V, Malakhova I, Shibata Y, Khrouch V, et al. Risk of thyroid cancer after exposure to 131I in childhood. J Natl Cancer Inst 2005;97:724–32.
(3) Robkin MA, Shleien B. Estimated maximum thyroid doses received from 129I releases from the Hanford site for the years 1944–1995. Health Phys 1995;69:917–22.[Web of Science][Medline]
(4) Grossman CM, Nussbaum RH, Nussbaum FD. Cancers among residents downwind of the Hanford, Washington, plutonium production site. Arch Environ Health 2003;58:261–74.[Medline]
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Del.icio.us What's this?
J Natl Cancer Inst 2006 98: 641-642.
J Natl Cancer Inst 2006 98: 642.
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