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1. Introduction
The damaging effects of ionising radiation on tissues in the body have been known for about 100 years. This knowledge was followed by evidence that high doses of radiation can cause cancer. These carcinogenic effects have been studied most closely by following the health (epidemiological study) of radiation-exposed survivors of the 1945 atomic (A-) bomb explosions in Japan. These A-bomb studies provide much of the information available on the radiation dose-response of risk of leukaemia and solid tumours although further knowledge has come from other investigations of people exposed to radiation accidentally, in their work or through medical procedures. In addition, such studies have provided evidence on the more general aspects of radiation induced tissue injury and how it may be assessed and treated. Specific forms of non-cancer effects in tissues have also been considered, including effects on brain development following pre-natal exposures and damage to germ cells in reproductive organs which can result in heritable disease.
The achievement of an acceptable balance between the detrimental effects of radiation and its benefits to society requires a scientifically robust and acceptable system of radiation protection that is applicable to public and occupational exposures. The radiation doses that apply to these exposures are invariably below a level where direct epidemiological study can inform on cancer risks.
At these low doses received at low dose rates the risks are very small when compared with the 20-25% chance of a typical individual developing fatal cancer from other causes. Nevertheless, for protection purposes, it is important to improve judgements on how the cancer risks known to apply at moderate to high doses may be projected downwards to these low doses and dose rates. To achieve this it is important to extend knowledge of the mechanisms through which radiation damage to cells in tissues allows a small number to enter a multi-stage process of mal-development which can lead to cancer (see note 3); this process can take tens of years to complete. Stated in a simple way, with good knowledge of the biology of radiation action within the cancer process it will be possible to construct well-founded mathematical models to describe radiation risk at the low doses that are most relevant to human exposures. These biologically validated models will be of substantial value in developing firm views on whether radiation risk increases as a simple function of dose (e.g. a linear dose-response) or alternatively whether there is a true low dose threshold where risk may be discounted.
An additional fundamental issue that has come to the fore in recent years is the question of variation in inter-individual risk due to the effects of genetic make-up on radiation response. A few rare genetic disorders that may substantially influence radiation risk are known but it is believed that more common genetic factors currently escape detection because their effects are relatively weak. An understanding of such common genetic factors will aid judgements on how radiation risks are distributed in the population and whether certain genetic sub-groups are under-protected.
For some time the Commission has recognised the importance of obtaining this fundamental information and to couple it with epidemiological findings. Also, rapid advances in modern biology, genetics and medicine are providing the background knowledge and tools to seek answers to these outstanding questions in radiation protection (see note 2). The research that the Commission has identified and supported in these areas has made important progress during the 4th and 5th Framework Programmes (FP). The research strategies and scientific progress of these programmes are summarised in the following sections of this website together with a view of how work may be extended within the 6th FP. |
