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The thyroid gland is highly sensitive to the tumorigenic effects of
external radiation. A causal relationship between X-ray exposure and thyroid
cancer was for the first time suggested in 1950 (30) and then confirmed
in several studies. The elevated risk of thyroid neoplasia was demonstrated
in patients treated with radiation for tinea capitis (31), enlarged thymus
gland (32), lymphnodes abnormalities (33), or for a variety of benign neck
and head conditions (34). The average dose of ionizing radiation varied
from 10 mGy to 6 Gy. Extensive studies indicated a linear dose response
relationship between radiation exposure and the induction of both malignant
and benign thyroid tumors with no clear threshold and extending through
0.7-10 Gy (35-37). In other words there is no threshold below which exposure
of the thyroid to external radiation does not carry a risk of cancer. The
risk per unit dose of radiogenic thyroid tumors was found to be significantly
higher among children as compared to adults. It was suggested (33) that
there are three age groups with different sensitivity to carcinogenic effects
of X-ray exposure. The highest sensitivity would be characteristic for
very young children aged up to 5 years, followed by the age group of 6
to 20 years while the lowest sensitivity was found in persons aged above
20 years. In general it can be stated that infants and young children might
be up to 8 times more sensitive than adults to the effects of external
radiation (35-37). It was also concluded that females are more sensitive
to the thyroidal tumorigenic effects of radiation than males, and the absolute
excess risk per Gy was found to be 2 to 3 times higher as compared to males
(32). Generally the risk compared to the spontaneous rate of occurrence
of thyroid malignancies is 2-3 fold for individuals exposed to 100-200
mGy and 50-100 fold for individuals exposed to 5 Gy (35-38). There is a
well-established latency period between external radiation and occurrence
of thyroid neoplasia (36,37). The latency period has a log-normal distribution
and varies from 5 to 40 years with a peak incidence of around 15 years
after exposure. External radiation of the thyroid gland leads not only
to significantly higher incidence of thyroid malignancies but also to damage
of thyroid tissue. With larger doses in the range of 30-50 Gy the damage
to thyroid cells is rapid, extensive and results in hypothyroidism. Doses
below 100 mGy can produce fibrosis, hyperplasia, some damage to vascular
tissues and possibly immune mediated changes in the thyroid (37).
In survivors of the atomic bombings of Hiroshima and Nagasaki (39) and residents of the Marshall Islands (40) accidentally exposed to both external and internal radiation from fallout of nuclear weapons testing, an increased risk for both malignant and benign thyroid neoplasia has been observed. In Nagasaki, in survivors directly exposed to a dose of radiation below 1 Gy, the prevalence of thyroid nodularity and malignancy was about 7 fold increased, while in those exposed to a dose above 1 Gy the frequency of malignant tumors was up to 10 times higher than in non-exposed age and sex matched controls (41). In addition to radiation induced thyroid nodularity, a significant increase in the prevalence of hypothyroidism was observed in a group of survivors exposed to low radiation in a range of 1 mGy to 49 mGy (40). The Marshall Islands experience was the first to show the risk from radioactive iodine fallout to the thyroid gland in man (40,42). In the Rongelap Island accident the external radiation in adults, 9 year old and 1 year old children contributed to about 16%, 9% and 4%, respectively, of total thyroid absorbed dose estimates. In the same age groups, who were exposed to a maximal dose of radiation, the external radiation contributed to 4.5%, 2.3% and 0,95% of total thyroid adsorbed dose respectively, thus showing first time, that internal radiation can be carcinogenic in men (42). In Rongelap Island the mean total thyroid uptake of radioactivity from short-lived radioiodines (132I, 133I, 134I and 135I) and tellurium (131Te and 132Te) was about 8000 uCi while that from 131I was 100uCi (42). Resulting thyroid cancer risk for all Marshallese was calculated to be about 2/106 persons/10 mGy/year, a value similar to that for survivors of Hiroshima and Nagasaki and a person exposed in childhood to X-ray therapy (38,39,42). The medical findings in the Marshallese population gave a proof that radiation by short-lived isotopes of iodine is tumorigenic for the thyroid. Contrary to X-ray, or radiation by short-lived radioiodines data on effects of 131I in humans are insufficient to draw firm conclusions. In four independent studies, which when combined consisted of more than 60000 thyrotoxic adult patients no relation was found between 131I treatment and subsequent development of thyroid carcinoma (43-46). Also Safa et al (47), studying hyperthyroid children were unable to show, that administration of therapeutic doses of 131I can lead to carcinogenesis in the thyroid. Finally, thyroid cancer cases which were suggested to result from 131I treatment did not share characteristics of radiation induced malignant tumors (48). The theoretical but not proven risk for thyroid cancer after exposure to therapeutic doses of 131I in a person younger than 20 years of age was calculated to be 0.064/106 persons/ 10 mGy/year. The largest study up to date on the effects of diagnostic doses of 131I also failed to show carcinogenicity (49). Until the Chernobyl catastrophe it was therefore suggested, that 131I in humans does not increase the risk of thyroid cancer, or if it does, its carcinogenic effectiveness is several times lower, than that of external radiation (48,50). It should be pointed out that contrary to humans, 131I in rats is carcinogenic to the thyroid and this effect is comparable to that of external X-ray radiation in the same species (51). |
