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Boice
Radiation-induced thyroid cancer--what's new?Boice JD Jr. J Natl Cancer Inst. 2005 May 18;97(10):703-5. Review.
"Several years ago I wrote that there was little more to be learned about radiation-induced thyroid cancer. I was mistaken. After 50 years of research, it was known that the thyroid gland of children, but not adults, was especially sensitive to the carcinogenic action of ionizing radiation, that a straight line adequately represented the relationship between dose of radiation and effect, that effects for thyroid cancer were seen at lower dose levels (on the order of 0.10 Gy) than those observed for most other radiation-induced cancers, that very high dose levels resulted in a lowering of risk because of cell killing, that screening had a profound influence, and that mixtures of radioiodines could cause thyroid cancer. However, the carcinogenic effect of 131I exposure of children was uncertain. The article by Cardis et al. in this issue of the Journal has provided new and, if confirmed, provocative information on the risk of radiation-induced thyroid cancer and on the modifying role of diets deficient in stable iodine and of administering iodine supplements months after the exposure has occurred....
"The findings from Cardis et al., however, newly suggest that diets deficient in stable iodine potentiate the risk of radiation-induced thyroid cancer and that continued use of dietary supplements containing potassium iodide substantially reduces the risk of radiation-induced thyroid cancer, even if taken many months or years after the exposure has occurred. The first observation would caution against generalizing the Chernobyl findings to other exposed populations of children whose diets are not deficient in iodine. The second finding might have substantial public health and clinical implications if continued administration of potassium iodide reduces the risk of radiation-induced thyroid cancer and presumably other types of thyroid cancer, at least in areas of endemic goiter or iodine deficiency. "
Thyroid cancer risk after thyroid examination with 131I: a population-based cohort study in Sweden.Dickman PW, Holm LE, Lundell G, Boice JD Jr, Hall P. Int J Cancer. 2003 Sep 10;106(4):580-7. [abstract only]
"Ionizing radiation is the only established cause of thyroid cancer, though the effect of diagnostic administration of (131)I on thyroid cancer risk appears minimal. The annual number of thyroid examinations using radioiodine is currently 5 per 1,000 individuals worldwide, so this issue is of public health importance. Our objective was to evaluate the excess risk of thyroid cancer following a range of known doses of (131)I administered for diagnostic purposes. We conducted a nationwide, population-based cohort study in Sweden including all 36,792 individuals who received (131)I for diagnostic purposes during 1952-1969 and were alive and free of thyroid cancer 2 years after exposure. Accrual of person-time at risk commenced 2 years after the first (131)I administration. Follow-up for cancer was to the end of 1998. Standardized incidence ratios (SIRs) were calculated as the ratio between the observed and expected numbers of thyroid cancers. Estimates were stratified by previous exposure to external radiation therapy to the neck, reason for thyroid examination, (131)I dose, sex, age at exposure and time since exposure. Thyroid cancers (n = 129) were diagnosed during 886,618 person-years at risk. Excess thyroid cancers were observed only among the 1,767 patients who reported previous external radiation therapy to the neck [SIR = 9.8, 95% confidence interval (CI) 6.3-14.6] and among those originally referred due to suspicion of a thyroid tumor (SIR = 3.5, 95% CI 2.7-4.4 for 11,015 patients without previous external radiation therapy). The 24,010 patients without previous exposure to external radiation therapy to the neck who were referred for a reason other than suspicion of a thyroid tumor received an estimated dose to the thyroid of 0.94 Gy. Among these patients, 36 thyroid cancers were observed compared to 39.5 expected (SIR = 0.91, 95% CI 0.64-1.26). We found no evidence that administration of (131)I for diagnostic purposes increases risk of thyroid cancer. However, our study included few patients under age 20, so the results apply primarily to exposure among adults. Our data suggest that protraction of dose may result in a lower risk than brief X-ray exposure of the same total dose."
Thyroid cancer after exposure to external radiation: a pooled analysis of seven studies.Ron E, Lubin JH, Shore RE, Mabuchi K, Modan B, Pottern LM, Schneider AB, Tucker MA, Boice JD Jr. Radiat Res. 1995 Mar;141(3):259-77. [abstract only]
"The thyroid gland of children is especially
vulnerable to the carcinogenic action of ionizing radiation. To
provide insights into various modifying influences on risk, seven
major studies with organ doses to individual subjects were
evaluated. Five cohort studies (atomic bomb survivors, children
treated for tinea capitis, two studies of children irradiated for
enlarged tonsils, and infants irradiated for an enlarged thymus
gland) and two case-control studies (patients with cervical
cancer and childhood cancer) were studied. The combined studies
include almost 120,000 people (approximately 58,000 exposed to a
wide range of doses and 61,000 nonexposed subjects), nearly 700
thyroid cancers and 3,000,000 person years of follow-up. For
persons exposed to radiation before age 15 years, linearity best
described the dose response, even down to 0.10 Gy. At the highest
doses (> 10 Gy), associated with cancer therapy, there appeared
to be a decrease or leveling of risk. For childhood exposures,
the pooled excess relative risk per Gy (ERR/Gy) was 7.7 (95% CI =
2.1, 28.7) and the excess absolute risk per 10(4) PY Gy
(EAR/10(4) PY Gy) was 4.4 (95% CI = 1.9, 10.1). The attributable
risk percent (AR%) at 1 Gy was 88%. However, these summary
estimates were affected strongly by age at exposure even within
this limited age range. The ERR was greater (P = 0.07) for
females than males, but the findings from the individual studies
were not consistent. The EAR was higher among women, reflecting
their higher rate of naturally occurring thyroid cancer. The
distribution of ERR over time followed neither a simple
multiplicative nor an additive pattern in relation to background
occurrence. Only two cases were seen within 5 years of exposure.
The ERR began to decline about 30 years after exposure but was
still elevated at 40 years. Risk also decreased significantly
with increasing age at exposure, with little risk apparent after
age 20 years. Based on limited data, there was a suggestion that
spreading dose over time (from a few days to > 1 year) may lower
risk, possibly due to the opportunity for cellular repair
mechanisms to operate. The thyroid gland in children has one of
the highest risk coefficients of any organ and is the only tissue
with convincing evidence for risk about 1.10 Gy." |
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