Update on radiation protection of the thyroid gland

Abstract

In recent years, concern about the effects of ionizing radiation on exposed individuals has led to the need to regulate and quantify the use of diagnostic and therapeutic techniques. Geopolitical events in recent times have also increased the population's perception of insecurity regarding ionizing radiation, and we increasingly face patients reluctant to undergo certain types of scans in our nuclear medicine services and, albeit less frequently, in radiology services. This article aims to summarise the extent to which ionizing radiation is present in our daily lives and how diagnostic and therapeutic procedures can affect our health, particularly from the perspective of their effects on the thyroid gland, one of the body's most radiation-sensitive organs.

Resumen

En los últimos años, la preocupación sobre los efectos que la radiación ionizante ejerce sobre las personas expuestas ha obligado a regular y cuantificar el uso de las técnicas diagnósticas y terapéuticas. Los acontecimientos geopolíticos de los últimos tiempos han incrementado también la percepción de inseguridad de la población en relación con la radiación ionizante y cada vez más nos encontramos con pacientes reacios a realizar según qué tipo de exploraciones en nuestros servicios de medicina nuclear y, aunque de forma menos frecuente, en los servicios de radiología. Este artículo pretende resumir hasta qué punto la radiación ionizante está presente en nuestra vida cotidiana y en como los procedimientos diagnósticos y terapéuticos pueden influir en nuestra salud, sobre todo desde el punto de vista de los efectos sobre la glándula tiroides, uno de los órganos más radiosensibles del organismo.

The effects of radiation on health

A well-known example of the harmful effects of radiation was presented by the famous discoverer of radioactivity, Madame Curie. Her scientific activity led her to be immersed in a highly radioactive environment during practically her whole adult life. She suffered partial chronic blindness due to cataracts and finally died of aplastic anemia in 1934. It is highly likely that these effects were caused by her elevated exposure to radiation.¹

Following the discovery of radiation in the 20th century, few studies were carried out on the effects of radioactivity on health. If we add the lobbying of the radioactive industry with the regulating authorities, examples such as that of Madame Curie demonstrate the little importance initially given to the harmful risks of exposure to radiation. It was not until after World War II and the appearance of a powerful nuclear industry and the detonation of the atomic bomb that a glimpse of this potential began to emerge. After demonstrating the devastating effects on the population bombed, the current regulation and a tree of knowledge of the effects of radiation on health began to be developed, in addition, in part, to a justifiable radiophobic perception of society.²

There was an urgent need to obtain in depth knowledge of the molecular and cellular mechanisms that radiation activated at these levels and was capable of even producing death over a very short time. Studies aimed at radioprotection proliferated.² The cohorts of Hibakusha (survivors of the atomic bombs in Japan) were mainly studied and the knowledge obtained following the disasters of Chernobyl and Fukushima was more recently incorporated. In addition, a few studies in patients undergoing radiotherapy have been performed and the results adapted. Thus, until very recent times (the 90s), knowledge of the effects of radiation on health was mainly obtained from the observation of the effects derived from elevated rates of radiation and high cumulative exposures.^3,4

Experts of the United Nations · Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) and the International Commission on Radiological Protection (ICRP) collected the results of these studies in a series of publications.^4,6–9 They determined that high doses of ionizing radiation (greater than one gray — Gy) seriously harm the tissues exposed, and can even be lethal based on the dose, the duration of exposure and the quantity of volume irradiated. On the other hand, they concluded that irradiations with lower doses, of between hundredths and low Gy, present a palpable probability of causing cancer.⁹ In relation to doses less than hundredths of Gy, the studies present many uncertainties. Nonetheless, although not evidence-based,² they conservatively recommended the adoption of the linear non-threshold (LNT) model with which the harmful risks to health are probabilistically assumed and are proportional to the dose received.¹⁰

With these data, the theory considers that after exposure, once the corresponding physiochemical and biological processes originated by the incidence of the radiation in the center of the cell take place, the clinical effects manifest as a direct consequence of the probability of rupture of the DNA chains in the cellular nucleus and their capacity to repair. The irreparable rupture of cellular DNA induces cell death, and massive cell deaths lead to acute effects. While defective repairs lead to mutations which, in the case of the survival of somatic cells, a tumor develop and, in the case of germinal cells, this leads to genetic diseases.⁵ According to this scheme, the clinical effects derived from high doses (greater than Gy) described above are classified as determinist effects and, those derived from lower doses as random effects.^4,6–9 Determinist effects correspond to the accumulation of tissue lesions produced by the massive death of cells by radiation. Therefore, they depend on which part of the body has been irradiated and the duration of exposure, and only appear when the tissue or organ has been exposed to a minimum threshold of radiation. Once this threshold has been passed, the severity of the lesions is proportional to the dose of incident radiation, and this is conditioned by the characteristics of the individual affected. Age, the phase of the cell cycle in which the cells are exposed, their state of oxygenation, the volume and radiosensitivity of the tissues and organs affected and the general health status are considered. According to the effect, determinist lesions are produced after threshold doses of 1–3 Gy. They usually manifest after a prodromic phase during the first 48 h after the irradiation and a latent asymptomatic stage of 2 or 3 weeks. In general, the sooner the manifestations appear, the greater the dose received. The prodromic phase consists of nausea and vomiting (threshold dose of 1 Gy), headache (4 Gy), diarrhea and fever (6 Gy) and episodes of loss of consciousness (8 Gy). The lesions consist in different grades of burns on the skin based on the dose, alopecia, cataracts, glaucoma, sterility, abnormal fetal development or acute radiation syndromes: hematopoietic syndrome, and syndromes of the gastrointestinal tract (greater than 8 Gy) and the central nervous system (10 Gy).

Random effects refer to cancer or hereditary abnormalities in the individual. The risk of presenting these effects originates in the probability of defective repair (or non-repair) of the damaged cells.^4,7 In contrast, determinist effects do not require a minimum dose threshold to occur and can also be produced at “low doses”, although there is only evidence for doses greater than 100 mGy accumulated within a relatively short period of time.¹⁰ Up to now, the LNT model has been adopted for low doses and considers that the risk of presenting random effects is proportional to the dose accumulated, however low it is. Thus, the theory considers a mean extra increase in the probability of presenting cancer of 5% over the inherent risk for each Gy absorbed. It should be taken into account that this is a mean populational value, and that individually this value largely depends on the age of the individual and the phase in which the cells exposed are in. Therefore, the risk is significantly greater the lower the age of the individual, and to the contrary, reduces with age.

The technological developments and the resources that have become available in the 21st century, during the last 20 years, now allow low doses to be systematically estimated (less than 100 mGy), registries to be created and are capable of approaching an ever greater population, facilitating the inclusion of large cohorts. Entities such as the European Society of Nuclear Medicine have clearly noted in their agenda the need to study the reactions of normal tissue, the morbidities induced and the long-term health problems that exposures of medical radiological studies may produce.¹¹ Thus, initiatives such as the Multidisciplinary European Low Dose Initiative (MELODI)¹² and The Million Person Study¹³ are being promoted worldwide. These studies include large cohorts exposed to low doses of not only medical but also environmental or occupational origin. Assuming that the lower the dose the longer the latency period, long-term effects are expected. Therefore, due to the lack of more or greater solid evidence, the mechanisms of these low exposures have not yet been accurately defined. Nonetheless, the principal effects have been clarified. In principle, only three types of response to low doses have been observed: the bystander effect, adaptative protector response and genomic instability. The responses to radiation at a tissular, cellular and molecular level are different from those of the traditional theory based on cell death or repair after high doses.² They are, unquestionably, effects of the low doses and question the validity of the LNT model for the probability of cancer in these circumstances. For example, the findings to date suggest that the risk of leukemia and lung cancer is much lower than that predicted by the LNT model and, to the contrary, there is an increase in esophageal cancer. In addition, there is evidence of a relationship with non-cancerogenic effects such as cataracts, vascular and cardiac effects or neurological and cognitive effects and diseases such as Parkinson,^12,13 among others. It should be noted that the conclusions of all the studies state that more research is needed to improve our knowledge and provide more solid evidence of this range of low doses.

Knowledge of the effects of radiation on the thyroid gland follows the same scheme described to date. During the last decade the results of several combined analyses of multiple epidemiological studies performed over time have been published, including the first data of the accident of Fukusima.

With respect to the risk of presenting thyroid cancer, the high sensitivity of this gland to radiation has been well documented, with the main factors contributing to this risk being the quantity of dose received by the gland and the age of the individual at the time of the irradiation. It has been confirmed that for external radiation doses greater than 50−100 mGy the risk increases linearly up to approximately 30 Gy by about a 6.5–11.1 entrance exposure rate (EER)/Gy based on age at the time of exposure. In patients less than 4–5 years of age undergoing radiation, the excess risk is 5-fold compared to children between 10 and 14 years of age. Above 30 Gy the excess of risk by radiation seems to begin to fall due to massive cell death. Following radiation, there is a latency period of between 5–10 years, after which the risk of the appearance of cancer increases up to 25–30 years, and later diminishes over time. Nevertheless, the risk remains substantial even at 60 years after the exposure.

The analysis and evaluation of the risks to the thyroid gland due to doses of internal radiation are more complex. The results of the Chernobyl cohorts showed variable results with values between 1.9 and 48.7 EER/Gy depending on the persistence to exposure over time. On the other hand, the results of Fukushima (with 5 years of follow-up and a high sensitivity in the screening procedure) show that, at low doses less than 33 mSv, there was no evidence of excess of relative risk for thyroid cancer.

In medical practice, exposure of the thyroid to radiation may be produced both externally and internally. In addition to this difficulty, the usual lack of estimation of dose for each procedure can be added and that with the means currently available these estimations are still accompanied by a wide uncertainty that does not allow conclusions to be made. Furthermore, the studies on irradiated patients implicitly include a bias due to an underlying disease, thereby impeding comparison with other studies including previously “healthy” irradiated cohorts. The results should serve as an argument for justifying each medical irradiation individually, taking into account that the risk cannot be underestimated regardless of how low the dose is.

Sources of radiation

Although we are not aware of it, our lives go by with a constant invisible interaction with radiation. About 340 nuclides have been identified in nature, 70 of which are radioactive.¹⁴ Thus, it is understood that radiations are present in different scenarios of everyday life and the interaction of humans with these radiations is largely unavoidable (Fig. 1). Knowledge of these radiations has allowed the development of artificial sources and controlled use in clinical, industrial and investigational applications.

Fig. 1.

Relationship among the sources of radiation.

The different most prevalent sources of radiation are shown: (1) Galactic cosmogenic and solar radiation (¹⁴C, ³H, ⁷Be). (2) Terrigenous radiation of both primordial radiation from the rocks of the earth’s crust (²³⁸U, ²³⁵U, ²³²Th, ⁴⁰K) and secondary generated by the disintegration of the primordial radionuclide (²²⁷Ac, ²²⁸Ra, ²²⁶Ra, ²²²Rn, ²²⁰Rn, ²¹⁹Rn, ²¹⁶Po, ²¹⁰Pb). (3) Artificial radiation from nuclear centers, the industry and the field of medicine.

The figure represents the relationship with exposure in humans: external radiation originating from cosmogenic radiation (airplanes) which is later incorporated into the food chain by ¹⁴C and ³H (internal radiation in the form of ingestion); external radiation from the radiation of the earth’s crust and external and internal radiation in the form of inhalation of secondary radionuclides mainly due to the elements used for building construction (uranium and radon); external and internal radiation for medical purposes.

Sources of radiation

According to the origin of the radiation, it is classified as natural or artificial.

Sources of natural radiation

Three fourths of the radioactivity in the environment comes from natural elements.¹⁵ Natural radiation is that which depends on the physical characteristics of our planet (terrigenous radioactivity) and the surrounding cosmos (cosmogenic radioactivity) present since the formation of the solar system.

Terrigenous radioactivity: This radioactivity originates from our planet, the Earth. The radionuclides produced are classified as primordial and secondary.

• •

  Primordial radionuclides: these radionuclides were present before the solar era and have a half-life comparable to the age of the universe (>10⁸ years), and are thereby still detectable in significant quantity. They make up part of the rocks of the Earth’s crust. The most important radionuclides of this series are uranium (²³⁸U, ²³⁵U) and thorium (²³²Th), as well as potassium (⁴⁰K).¹⁴

• •

  Secondary radionuclides: these are generated by the disintegration of a primordial radionuclide and are also present in the rocks of the Earth’s crust. They include the group of actinium (²²⁷Ac), radium (²²⁸Ra, ²²⁶Ra), radon (²²²Rn, ²²⁰Rn, ²¹⁹Rn), polonium (²¹⁶Po) and lead (²¹⁰Pb), among others. Of note is the peculiar behavior of radon, a descendent of uranium and thorium. In gaseous form, this radionuclide is released during disintegration through the porous space of the mineral to the atmosphere.¹⁴

Terrigenous radioactivity is not the same in the different regions of the planet and depends on the composition of the underlying crust. For example, in certain zones of India terrigenous radioactivity is 10-fold greater than the mean in Europe, due to the presence of sand with an elevated quantity of ²³²Th.¹⁶

Cosmogenic radioactivity: This radioactivity comes from the cosmos. The most important interactions with humans are the following:

• •

  Galactic cosmic radiation: this high energy radiation comes from outside the solar system (composed mainly of helium [³H] protons and neutrons). Solar winds and the magnetic field of the Earth hinder its entry into the atmosphere.¹⁴

• •

  Solar cosmic radiation: this radiation is produced by solar eruptions, and is mainly composed of protons.¹⁴

In the atmosphere, the clinical rays interact with stable elements generating isotopes. The most relevant for human exposure are ¹⁴C, ³H and, to a lesser extent, ⁷Be.¹⁴¹⁴C makes up part of CO₂ and ³H of the particles of H₂O.

Sources of artificial radiation

Artificial radioactivity was discovered in 1932 by Frederic and Irene Joliot-Curie after the irradiation of aluminum with alpha particles from a source of polonium. They observed that high penetrance radiation was produced, which lasted following withdrawal of the initial source and exponentially decayed over time. They were awarded the Nobel Prize of Chemistry in 1935. The principle sources of artificial radiation emanating to the environment were those generated by the atmospheric testing of nuclear arms performed between 1945–1980 (which led to the generation of isotopes of fission) and later by the greatest nuclear accident registered to date, that of Chernobyl in 1986 (emission of more than 100 radioactive isotopes, including ¹³⁷Cs, among others).^14,17–19 Other sources of the generation of artificial isotopes have been and are the nuclear power plants, which generate controlled artificial radioactivity following established safety regulations related to the production of radionuclides and waste management. On the other hand, there is an application of these radiations in the field of medicine (for diagnostic or therapeutic purposes), industry (thickness measurement, density measurement, smoke detectors, cyclotrons) in research (in the field of physics, chemistry and technology) and agriculture (bactericidal, pesticidal agents) with legislation related to its use and waste management.^17–19

Routes of radiation exposure in humans: external and internal radiation

The interaction of humans with the natural radiations present in the environment involves two forms: that of external radiation (by proximity to sources of natural or artificial radiation) and that of internal radiation (inhalation or ingestion of radioactive isotopes). The main route of natural radiation is produced by the inhalation of radon, which emanates from the disintegration of uranium and thorium (52%, 1.2 mSv/year). This is followed by external radiation (16% cosmic 20% terrestrial) and internal radiation related to ingestion (12%).^14,17 See Fig. 2.

Fig. 2.

Exposure to natural radiation by humans.

Percentage of sources of exposure. Internal radiation 64% (inhalation 52%, ingestion 12%); External radiation 36% (20% terrigenous, 16% cosmogenic).

External radiation

• •

  Cosmic radiation: This radiation mainly affects the crew of aircraft and spacecraft since the terrestrial atmosphere has a protective or attenuating effect on this type of radiation. This protector effect is lower according to the altitude (airplane flight, mountain cities and towns). The dose received doubles for each 2000 m of height.¹⁴

• •

  Terrestrial radiation: This radiation is related to the radiation of the subsoil and the elements used for construction, both of which are principally rich in uranium. The median effective dose worldwide is 0.5 mSv/year, varying according to the geographical area studied.¹⁵ In Spain the mean terrestrial dose is 0.48 mSv/year, with the province of Murcia having the lowest value (0.39 mSv/year) and Pontevedra being the most exposed (1.45 mSv/year).²⁰

Internal radiation

The incorporation of radioactive elements in humans is produced by different routes of migration and transference, which are interlinked (Fig. 1).

• •

  Radioactive elements can be incorporated from the air by isotopes in suspension proceeding from cosmic radiation (¹⁴C, ³H mainly in the form of CO₂ and H₂O), which may be directly inhaled or indirectly introduced after precipitation, such as rain or snow, and deposit in continental waters or the soil. Likewise, these may reenter the atmosphere by phenomena of evaporation or wind and beginning a new cycle.^14,21 The presence of isotope ¹⁴C in the carbon cycle allows understanding the physical foundation of carbon dating. During their lifetime, living beings incorporate ¹⁴C from CO₂, a phenomenon which discontinues after death, after which the ¹⁴C incorporated progressively diminishes according to the law of radioactive decay. Calculation of residual activity is what allows dating.²² Radioactive elements can also be incorporated through the radon proceeding from terrestrial radiation in the form of aerosol and may present elevated concentrations in houses constructed on very permeable soils or those with a high content of ²²⁶Ra. Certain work activities present a greater risk of exposure to this gas (subterranean mining or exploration of thermal waters).^19,20

• •

  Internal radiation may be incorporated through water by the isotopes present in precipitation from the atmosphere or by erosion of the Earth’s crust. The most abundant isotopes are those of ²²⁶Ra due to its greater solubility (low concentration in shallow waters 0.4–40 m Bq/l, and reaching several Bq/l in deep waters, such as in wells).¹⁴

• •

  There is exposure to internal radiation through the food chain in which isotopes present in water, earth or air are absorbed by the plants. The isotopes present in water and in plants are ingested by the animals leading to the contamination of meat and other animal products (milk, eggs). Finally, the isotopes present in water, the plants and products of animal origin are ingested by humans. The predominant isotope is ⁴⁰K (0.3 mSv/year).^15,17 It is of interest to note that 0.0117% of the potassium in our body corresponds to the isotopic form ⁴⁰K, which remains in equilibrium with the non-radioactive forms.¹⁴ Remains of ¹³⁷Cs can still be found in pastures and cattle in Europe in relation to the Chernobyl accident.¹⁸

Relationship between ionizing radiation and thyroid cancer

The incidence of thyroid cancer has increased worldwide. In addition to having more accurate diagnostic systems, it has been proposed that environmental effects may influence this increase, with one of these effects being the exposure of the population to ionizing radiation.²³ Knowledge accumulated over more than 60 years has demonstrated a relationship between exposure to ionizing radiation and its harmful effects on the thyroid gland. Many publications have studied the effects of different types of radiation on the thyroid gland, such as nuclear radiation and medical diagnostic or therapeutic radiation.^24,25 To quantify the risk associated with the dose of radiation, most articles use epidemiological data of risk for measuring the frequency of the effects, such as relative risk (RR) or the risk of having the effect in those exposed that is due to exposure (excess relative risk — ERR).²⁶ Despite the great heterogeneity among the different studies and the populations studied largely due to the long time that has gone by between these studies and the geographical differences and the wide range of type of radiation exposure, they share several conclusions.

One of the most important conclusions is the effect of age on the sensitivity of the thyroid gland to radiation. Exposure of the thyroid gland to radiation during infancy is the most important factor associated with the development of benign or malignant thyroid tumors. Children are the most sensitive even to very low doses and the effects persist throughout life. During childhood tissue growth and consequently rapid cell division make children more susceptible to the mutational effects of ionizing radiation. Taking into account that the carcinogenic potential persists throughout life and that children have a longer life expectancy, the effects of radiation are greater in children compared to adults. A strong inverse relationship has been demonstrated between the age of exposure and the associated risk. While the RR of radiation in solid tumors decreases 17% for every 10 years of age in persons exposed, it decreases 56% in the thyroid.²⁶ The general consensus is that linearity is the best way to describe the dose-response relationship in children under 15 years of age exposed to radiation, with the age of greatest risk being between 0 and 9 years and significantly decreasing to a minimum from 10 to 20 years of age.^23–27 On analyzing all the types and doses of radiation, it has been demonstrated that the RR increases supra-linearly at a dose of 2−4 Gy, showing a linear increase at a dose of 10−30 Gy and diminishing at higher doses at which cytotoxic action plays a role.²⁴ Indeed, Ron and cols.²⁶ reported an ERR/Gy of 7.7 (95% confidence Interval [CI] = 2.1–28.7). It has also been demonstrated that the risk is not zero at a dose less than 0.10 Gy, and thus, there is no safe dose threshold, thereby supporting the “as low as reasonably achievable” (ALARA) concept.²⁸ No study has reported a statistically significant difference between sexes at an infant age. The period of latency calculated since the exposure may be 5–10 years and remains elevated during decades (40–50 years). Although almost all the studies published have not demonstrated a significant risk in the adult population, the study by Richardson²⁹ analyzed the risk of thyroid cancer in individuals over 20 years of age who had survived the atomic bombs of Hiroshima and Nagasaki, and found a positive relationship in female survivors (ERR/Gy = 0.70; 90% CI = 0.20–1.46), being much lower than in children exposed.

As explained above, there are two types of exposure to radiation in the thyroid, external and internal radiation. The main sources of external radiation are those that are secondary to medical exposure for diagnostic purposes, such as radiographies or computerized tomographies (CT) and those for therapeutic purposes such as radiotherapy. The sources of internal radiation are treatment of hyperthyroidism with radioiodine (¹³¹I) and exposure to contaminated foods or liquids or radioactive gases after the detonation of atomic bombs or nuclear accidents.

In the past, head and neck radiotherapy in benign or malignant disease was the principle source of external radiation to the thyroid gland, while at present, the main source is medical radiation for diagnostic purposes.²⁶ According to the different diagnostic techniques, there are clear differences in relation to the radiation doses, which have significantly decreased over the last three decades due to technological advances. The effective dose of a thoracic CT study may be of 8 mSv, being 10 mSv for a CT of the abdomen and 2 mSv for head and neck CT. The dose of a simple chest X-ray (posterior- anterior) is of around 0.02 mSv. In a metaanalysis published in Thyroid in 2017,³⁰ Han and Kim stated that radiological studies including the thyroid in the field of exposure are associated with an increase in the risk of thyroid cancer (odds ratio [OR] 1.52; 95% CI = 1.13–20.4). When analyzed by subtypes of exposure, dental X-rays (OR = 1.69; 95% CI = 1.17–2.44), CT studies of the thorax (OR = 1.71; 95% CI = 1.09–2.69) and head and neck (OR = 1.31; 95% CI = 1.02–1.69) are associated with the greatest increase in risk. No association was found with exposure to radiological techniques in the rest of the body and neither was any relationship found with performing chest X-rays or mammographies. However, in small children, and especially neonates, there is a risk due to the small body size and the possibility of irradiating parts of the body that are not the objective of study.²⁶

The principal source of internal radiation to the thyroid is currently nuclear medicine techniques, such as thyroid scintigraphy (^99mTc or ¹²³I), parathyroid scintigraphy (^99mTc-sestamibi), studies with ¹⁸F-FDG and the treatment of hyperthyroidism with radioiodine (¹³¹I). The effective dose of these different radiopharmaceuticals with affinity for the thyroid would, in all cases, be less than 1.5 mSv, except for therapy for hyperthyroidism with radioiodine, in which case the dose would be 11 mSv/MBq. Despite this dose being much higher, no significant increase in the risk of thyroid cancer has been demonstrated.^25,26,31,32 The studies describing a slight increase in the risk compared treated populations with normal individuals without thyroid disease. The study by Gronich et al.³³ compared patients with hyperthyroidism treated with radioiodine with patients treated with antithyroid agents and found no differences between the two, suggesting that the underlying disease may have influenced the previous results.

At a histological level, papillary thyroid cancer is the most frequent subtype diagnosed in patients exposed to ionizing radiation (85%), and normally presents bilateral involvement and extra-glandular extension.^24,25 At a molecular level, multiple specific molecular targets through which radiation affects the thyroid gland have been identified. Many genes, proteins and lipids are involved in the mechanism of action of the effects and the consequences of radiation. To date, the best studied mechanisms are the harmful effects on the DNA, which condition the rupture of one or the two DNA chains, leading to chromosome deletions or rearrangements, the most frequent being RET/PTC, as well as BRAF and < TRK.^24,25,31,34

In view of these results and taking into account that the current predominating source of radiation to the thyroid gland is medical, exposure to this radiation should be minimized, especially at pediatric ages. Possible strategies would be to avoid the use of techniques with ionizing radiation in the infant population, provided that there is an alternative and, if not, the ALARA criteria must be applied. If this were the case, techniques of current modulation should be used to optimize the dose in CT studies or use measures of external protection in the radiographic studies. However, the use of measures of external protection in studies with ionizing radiation is sometimes counterproductive, since it may deteriorate the quality of the image by the presence of artifacts, requiring repetition of the study and a consequent increase in the dose received. In all the studies analyzed possible confounding factors must be taken into account, such as genetic factors and the supply of iodine in the population studied, since iodine deficiency is inversely related to the incorporation of radioactive iodine and involves higher dosimetry to the gland or variability among the screening modalities used.

Measures of radiological protection

When there is exposure to ionizing radiation, the first action should be aimed at reducing or avoiding the emission of radiation.³⁵ If this is not possible, as in the case of radioactive leaks or other nuclear accidents, emergency or early measures are aimed at reducing exposure to not only external but also internal radiation. The measures of control of external radiation are based on the reduction of exposure time and shielding though confinement or in a shelter and even the need for evacuation in the zones closest to the emission of radiation. In the case of a leak, the first measure recommends confinement of the population in their home to avoid exposure. If this measure does not guarantee protection, the whole population can be evacuated up to 5 Km from the origin of contamination.

To reduce internal radiation, the relocation of animals is considered to seek non-contaminated pasture areas, and the restriction of food products from some zones may be necessary, especially milk, drinking water, cereals and other vegetables, as well as meat and fish, based on the localization of the accident (Fig. 3).³⁶

Fig. 3.

Measures of radiological protection.

On exposure to radiation secondary to a nuclear accident, the first measures should be distance and shielding, which, for the civilian population, is usually confinement (A) or a bomb shelter. In the case of a leak and to avoid internal contamination, the restriction of food products may be necessary including the products from animals grazing in non-exposed zones (B), and, as a more extraordinary measure, potassium iodide should be ingested (C) when it is impossible to obtain non-contaminated food products.

Prophylaxis with iodine

Another measure to avoid internal radiation to the thyroid gland is prophylaxis with potassium iodide. Potassium iodine acts at different levels. On one hand, it blocks active transport at the level of the sodium/potassium pump, and on the other hand, the massive entry by passive diffusion and its retention at a colloidal level produces cellular saturation. With both mechanisms, the entry of ¹³¹I is blocked both in the active form and by diffusion.

This measure is especially aimed at prophylaxis in children and fetuses or embryos. Although this measure is known by the population, generalized application should not be launched. The intake of potassium iodide is only recommended when the supply of non-contaminated food products is impossible, which is considered as 20 Km from the origin of the contamination (356). If necessary, ingestion within the first two hours after exposure to ¹³¹I is recommended secondary to internal contamination (inhalation or consumption of contaminated food products). The protector effect of potassium iodide has been estimated to be of around 75–80% at 2 h after exposure, but decreases exponentially and is completely lost at 24 h. After the first 12 h, the curve of radioactive iodine uptake remains stable, despite the ingestion of potassium iodide.³⁷

Different doses of potassium iodide have been studied according to age. However, the dose approved by the Food and Drug Administration is 16 mg for newborns, 32 mg for children under three years of age, 65 mg for the rest of infancy and adolescence and 130 mg for adults. It is recommended that adolescents with a weight similar to that of an adult (around 70 kg) take the dose of an adult.³⁷

Screening

There are different types of screening: massive screening is applied to all the population; selective screening is done in a population selected according to criteria of risk (i.e., according to exposure to radiation); community screening is that in which individuals are selected for screening at the time of consultation in the health care system, independently of the reason for the visit; and finally, multiple screening, which is applied in different diseases or clinical situations.³⁸

Following nuclear accidents, such as that of Fukushima or Chernobyl, some screening programs have been launched for early detection of thyroid cancer and include physical examination and ultrasonography of the cervical region. The screening programs were initiated one decade after the Chernobyl accident to correctly register the increase in thyroid cancer in the young and adolescent population. In relation to the Fukushima accident, screening programs were initiated in the pediatric population of 3–18 years of age one year after the accident. The latter program revealed that the detection of nodules greater than 5 mm or cysts greater than 20 mm was of 0.5−0.8%, while in other cities far from the focus of radiation the presence of nodules was 1%, and thus, with no differences in the detection of thyroid nodules.³⁹ No impact on mortality was observed, however, there was a negative impact on the emotional state of the population submitted to screening, with a marked reduction in adherence to the program over time.^39,40 The implementation of a massive screening program is therefore not recommended, but access to screening should be performed if requested by patients, including periodic cervical ultrasound study.

Other recommendations

Lastly, in some circumstances, some remedial (and protector) measures should be taken into account provided that these measures provide greater benefits than disadvantages and respect the criteria of equity among the population. Some remedial measures include corrective measures of the buildings close to the source of exposure and new construction buildings with the objective of reducing the levels of radon (²²²Rn). Other measures focus on the rehabilitation of zones with residual radioactive material and restrict the use of determined construction materials.

In regard to the time of beginning and finalizing the measures, it is evident that the initiation of any of radioprotection measures should follow the ASAP criteria, that is, the sooner the better. Simple measures, such as maintaining the distance or avoiding the inhalation of contaminated gases, have been developed and should be implemented immediately. In addition, the intake of contaminated food products should be avoided from the beginning, or if this is impossible, iodine should be ingested within the first two hours after exposure to these food products. However, it is difficult to determine when the use of these measures should finalize. The safety guidelines of the International Atomic Energy Agency or General Safety Regulations indicate a reference level of radiation or residual dose, which include the dose received by all the external and internal exposures. This residual dose is that which is estimated to be received after which the use of the protector measures are finalized, and ranges getween 20 and 100 mSv. Thus, when this threshold is reached, the measures of protection can be finalized.

Conclusions

Radiation is present in our everyday life due to the structure of the cosmos itself, the Earth’s crust as well as the evolution of our species. Exposure differs according to altitude, the geology of the land and the infrastructures that surround us, the chemical characteristics of the water and the contamination generated by secondary radioactive events.

The recommendations to follow after a nuclear accident are to prioritize the avoidance of exposure, mainly by distance and shielding before evacuation or potassium iodide ingestion for thyroid saturation, with the latter two being considered exceptional. Screening has not shown an impact on the survival of individuals and has been accompanied by program abandonment due to an increase in anxiety associated with the controls.

Nonetheless, the current predominant source of radiation to the thyroid is medial and exposure should be minimized, especially at the pediatric age. Possible strategies are the modulation and reduction in the dosimetry of CT studies, measures of external protection in radiographic studies, avoidance of iodine contrast as far as possible and avoidance of the use of techniques with ionizing radiation in the infant population, provided that another alternative is available and if this is not the case, the ALARA criteria are followed.

Radiation is part of our lives, and thus, without fear but with care, we are learning to live with it.

Funding

None.

Conflicts of interest

None.

Declaration of the use of Generative AI and AI assisted technologies in the writing process

During the preparation of this study the authors used Copilot/Microsoft Edge and DALL-E/ChatGPT to aid in the creation of images. After the use of these tools, the authors reviewed and edited the content ad necessary, and assume full responsibility for the content of the publication.

Acknowledgments

We would like to thank the Societat Catalana de Tiroides (SCT) for the initiative to carry out this collaborative study, building bridges between scientific societies.