Ionizing radiation may, depending on the dose, cause damage to organic tissue. The mechanisms by which radiation damages the human body are two-fold:
- radiation directly damages the DNA of the cells by ionizing atoms in its molecular structure and
- radiation creates free radicals, which are atoms, molecules, or ions with unpaired electrons.
Unpaired electrons are usually highly reactive, so radicals are likely to take part in chemical reactions that eventually change or harm the cellular DNA. The human body is able to repair damaged cells to a certain extent, but if exposed to a high amount of radiation beyond a given threshold in a short period of time, “deterministic” damage will occur. This term implies that radiation poisoning has definitely occurred; in addition, the damage is dependent on the amount of radiation received. Deterministic radiation damage includes changes of the blood count, hair loss or tissue necrosis. Exposure levels of typical medical diagnostic imaging procedures are far below the threshold for deterministic radiation damage. However, deterministic effects are an important consideration in external radiation therapy and radionuclide therapy.
All levels of radiation may cause long-term or “stochastic” damage. In this context, “stochastic” means that the probability of suffering a disease caused by radiation is proportional to the amount of radiation received in years prior. Cellular self-repair mechanisms may fail, and some cells may experience non-lethal DNA modifications that are passed on through subsequent cell divisions. Years after exposure, diseases such as solid cancer or leukemia may occur.
In fact, the effect of the very low amounts of radiation encountered under normal circumstances (from both natural and artificial sources, such as cosmic rays or medical X-rays) is subject to constant debate. There are three main models used to predict the effects of low amounts of radiation: the linear, no-threshold model, the threshold model and the hormetic model, which is a non-linear model that even assumes a lower risk at low levels of radiation due to a “training effect” of the immune system.
The linear, no-threshold model assumes that the response is linear (i.e., directly proportional to the amount) at all levels of radiation exposure. The more radiation received, the more likely a disease caused by radiation will occur.
The threshold model proposes that anything below a certain level of radiation is safe, and only if this level is exceeded the probability of radiation damage increases proportionally to the received radiation (Figure 1).
The linear no-threshold model is currently the most accepted risk model for low levels of radiation as well. The Committee to Assess Health Risks from Exposure to Low Levels of Ionizing Radiation of the National Academy of Sciences concluded:1
“The committee concludes that current scientific evidence is consistent with the hypothesis that there is a linear, no-threshold dose-response relationship between exposure to ionizing radiation and the development of cancer in humans.”
But it also noted:
“New data and analyses have reduced sampling uncertainty, but uncertainties related to estimating risk for exposure at low doses and dose rates and to transporting risks from Japanese A-bomb survivors to the U.S. population remain large. Uncertainties in estimating risks of site-specific cancers are especially large.”
Radiation dose reflects the potential damage to organic tissue that cannot be defined simply as a certain amount of radiation energy per kg or cm2 of body surface. This is why three different definitions are used: absorbed, equivalent and effective dose.
1Health Risks from Exposure to Low Levels of Ionizing Radiation: BEIR VII – Phase
2Committee to Assess Health Risks from Exposure to Low Levels of Ionizing Radiation, National Research Council, National Academies Press, Washington D.C., 2006, p. 15.
The absorbed dose D, measured in Gray (Gy) units, characterizes the amount of energy deposited in tissue. It is defined as the amount of radiation required to deposit 1 Joule (J) of energy in 1 kilogram of any kind of matter (1 Gy = 1 J/kg).
Unfortunately, this rather simple definition is a physical quantity and does not reflect the biological effects of radiation since it does not take into account the type of radiation or the damage it might cause in different tissues.
The biological damages caused by different types of radiation differ; i.e. a similar absorbed dose of X-rays or α-rays can lead to dramatically different damage.
The equivalent dose H takes in account the damage caused by different types of radiation. It is defined as the absorbed dose D multiplied by a factor (wf) that weighs the damage caused to biological tissue by a particular type of radiation (H = D · wf). The unit used to measure the equivalent dose H is the Sievert (Sv).
In the case of X-rays, γ-rays, β-rays and positrons, the weighting factor is 1; therefore the equivalent dose is the same as the absorbed dose. In the case of α-rays, which occur naturally and are emitted, for example, by some types of uranium isotopes, the absorbed dose must be multiplied by a factor of 20. This indicates that α-rays and other heavy particles such as neutrons and protons cause much more damage to biological tissue than X-rays. Please note that as long as alpha emitting substances don’t get inside the body they don’t cause any harm because alpha rays are completely shielded by the skin.
The sensitivity of different types of organic tissue to radiation is not identical; for example, red bone marrow is very sensitive to radiation, whereas the liver is much less sensitive.
The effective dose E, also measured in Sievert (Sv) units, is an approximate measure that was introduced to compare the stochastic risk taking into account these differences in sensitivity.
When estimating the stochastic damage caused by irradiation of the human body, these differences must be considered. The coefficient wi quantifies the sensitivity of the particular organic tissue to the radiation received. The effective dose reflects this, because it is a weighted average of the equivalent dose received by the organs: E = Σ wi x Horg,i
The weighting factors wi are estimated and published by the International Commission on Radiological Protection. The Recommendations of the International Commission on Radiological Protection of 2007 (ICRP 103) has different coefficients than that of 1990 (ICRP 60).1 In particular, gonads are less radiosensitive and the breast is more radiosensitive than previously assumed (Table 1).
Effective dose E depends on model assumptions that may not be valid for an individual. Hence, E is not useful for determining the specific risk of an individual after receiving a certain amount of radiation. As research and quantification technologies advance, these factors may change.
1The 2007 Recommendations of the International Commission on Radiological Protection. ICRP publication 103. Ann ICRP. 2007;37(2-4):1-332. 1990 Recommendations of the International Commission on Radiological Protection. ICRP Publication 60. Ann ICRP. 1991;21(1-3):1-201.