Radioactive iodine can cause thyroid cancer primarily through its emission of ionizing radiation, which damages the DNA within thyroid cells. The thyroid gland naturally absorbs iodine from the bloodstream to produce thyroid hormones, so when radioactive iodine, such as iodine-131, enters the body, it is selectively taken up by thyroid cells. This targeted uptake means that the radiation emitted by radioactive iodine directly affects the thyroid tissue.
The radiation from radioactive iodine consists mainly of beta particles and gamma rays. Beta particles have enough energy to penetrate cells and cause breaks in the DNA strands. When DNA is damaged, the cell attempts to repair it, but sometimes the repair is imperfect or incomplete. These DNA errors can lead to mutations, which may disrupt normal cell function and regulation. If mutations occur in genes that control cell growth and division, such as oncogenes or tumor suppressor genes, the affected thyroid cells can begin to grow uncontrollably, leading to the development of thyroid cancer.
The risk of thyroid cancer from radioactive iodine exposure depends on several factors, including the dose of radiation, the age at exposure, and the duration of exposure. Children and young adults are more sensitive to radiation-induced thyroid damage because their thyroid cells are dividing more rapidly, making DNA damage more likely to result in cancerous changes. Moderate doses of radioactive iodine have been linked to an increased risk of thyroid cancer, while very high doses may destroy thyroid tissue outright, reducing the risk of cancer but causing other health issues.
One well-documented example of radioactive iodine causing thyroid cancer is the increased incidence of thyroid cancer observed after nuclear accidents, such as the Chernobyl disaster. In these cases, radioactive iodine released into the environment was absorbed by the thyroid glands of exposed populations, especially children, leading to a significant rise in thyroid cancer cases years later. Molecular studies of these cancers have shown specific genetic alterations, such as RET/PTC gene fusions, which are characteristic of radiation-induced thyroid tumors. These genetic changes result from the DNA damage caused by ionizing radiation and contribute to the cancerous transformation of thyroid cells.
In medical settings, radioactive iodine is used therapeutically to treat thyroid cancer and hyperthyroidism by delivering high doses of radiation to destroy abnormal thyroid tissue. While this treatment is effective, it also carries a risk of inducing secondary cancers if not carefully managed. The balance between therapeutic benefit and risk is carefully considered by physicians, especially in children and young adults.
In summary, radioactive iodine causes thyroid cancer by delivering ionizing radiation directly to thyroid cells, leading to DNA damage and mutations that can trigger uncontrolled cell growth. The thyroid’s natural iodine uptake mechanism makes it particularly vulnerable to radioactive iodine exposure, and the risk is influenced by dose, age, and genetic susceptibility. This mechanism explains both the increased thyroid cancer rates after environmental radioactive iodine exposure and the careful use of radioactive iodine in medical treatments.