of radiations
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 Case of exposure leading to the appearance of acute effects |
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Case of exposure leading to the appearance of deferred effects |
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Exposure to weak doses |
The
damage caused by ionising
radiation depends on the quantity of energy released by radiation
into the cells of each organ or tissue of the human body (exposure
dose). For a given quantity of absorbed energy (dose expressed in
Gray, Gy), the damage will vary according to the nature of the radiation
and the affected organ. These effects are of two types: acute effects
and deferred effects.
In the event of high doses received over a short period, ionising radiation can lead to the massive destruction of cells in exposed organs, and can produce health effects observable in the more or less short-term (from several hours to several months, depending on the dose and affected organ). We refer to "acute" effects (or "deterministic" effects). This can include skin burns (radiation dermatitis), vomiting or the destruction of the bone marrow or the intestinal mucous membrane, which can lead to the death of the exposed person. These effects appear starting from a dose threshold, which varies according to the tissue or organ (from 1 to several grays), and are more severe as the dose increases. As a general rule, the doses received, either by workers or by the public while carrying out activity resulting in ionising radiation, are not likely to result in acute effects. Such effects are only observed after accidental exposures (accidents within an installation, improper handling of highly active radioactive sources) or the deliberate exposure of patients for therapeutic purposes (radiation therapy).
Ionising radiation can also produce transformations in cells which, several years after exposure, may produce illnesses amongst the exposed population; these include leukemia and various cancers (thyroid, digestive tract, lungs, etc.). We then speak of "stochastic" effects; these effects are deferred in time. These pathologies can have many causes, and there is no biological means with which to differentiate, for example, between lung cancer due to tobacco and lung cancer due to ionising radiation. Given this particularity, and the fact that the risk of the occurrence of such effects is low relative to the natural frequency of cancer in the population, it is only possible to bring them to light by carrying out epidemiological studies on sufficiently large population groups which have been significantly exposed to ionising radiation (example: epidemiological study on the survivors exposed to the nuclear bombardments of Hiroshima and Nagasaki, Japan, 1946). Such studies show that the degree of exposure has an influence on the frequency of the occurrence of such pathologies, but not on their severity.
With regard to weak doses, spread out over time and falling within the range of a few millionths of sievert (known as microsieverts and written µSv), or even a few millisieverts, the effects, if any, are so weak that it would be very difficult if not impossible to identify them during epidemiological studies. This would require an international study involving tens of thousands of people, supposing that it would be possible to monitor such a population throughout their entire lives. Today, is not possible to come to a conclusion as the existence, or not, of a dose threshold below which there would be no effect related to the exposure to ionising radiation. For the purpose of managing risks and protection, there is an international consensus to consider, out of prudence, that any exposure to ionising radiation at any level can possibly result in an effect, even weak, across a population group. For exposures to weak doses, where a true risk has been neither proven nor disproven, the probability of developing stochastic effects is, by agreement, considered as being proportional with the dose received. The quantification of the relation between the dose and the effect is, in this context, established by extrapolating from what has been observed with higher doses.
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