Speaker: Bernard Le Guen, MD, MSci
Deputy Director CEIDRE Nuclear Engineering Division EDF generation

Abstract Summary:

Ionising rays form part of the environment. Their carcinogenic nature, described as far back as at the start of the 20th century, has since been widely documented. However, the hereditary effects of radiation have never been proven in humans. Regulations governing exposure to low-dose and low dose rate ionising radiation are implicitly based on the principle that there is still a residual risk for humans, whatever the level of exposure. These regulations are based on epidemiological research on the survivors of Hiroshima and Nagasaki. Results are compatible with a linear link between radiation exposure and the excess of solid tumours from exposures of approx. 200 mSv. By conducting retrospective epidemiological studies in work environments, it is possible to directly estimate the cancer risk among workers exposed to low radiation doses. Although it is currently very convenient for risk management, the assumed linearity of the dose/effect relationship has not been verified for all models. More specifically, with regard to low dose rates delivered by low-LET emitters, this hypothesis has been much debated in the light of recent observations.

Ionising radiation can alter any of a cell's molecules, but DNA is the most critical biological target owing to the limited redundancy of genetic information it contains. If DNA is altered, some defects in cellular signalling, as well as in DNA repair and cell cycle control, increase the likelihood of cancer and mutations appearing. Phenomena revealed in the past ten years pertaining to variations in low-dose and high-dose radiosensitivity can not only be explained by variations in the effectiveness of repair or defence systems.

Consequently, recent radiobiological data has shown that the body's defence mechanisms against low and high doses are very different. Today we know that in the event of radiation exposure, if the initial physical phenomena are indeed proportional to the dose, the nature and effectiveness of the triggered defence mechanisms vary according to dose and dose rate. All this data challenges the validity of high-dose effects extrapolated to low doses