Results from America’s Berkeley National Laboratory have cast doubt on the assumption that risk from radiation is always proportional to exposure – a theory that underpins most measures for radiological protection.
Living cells are constantly bombarded by ionizing radiation in various forms and from various sources, all of which have the potential to damage DNA. Unless this damage is corrected by self-repair mechanisms it can result in cell malfunction or the malignancy known as cancer.
These effects have been clearly shown to be statistically likely for high radiation doses, such as those received by Japanese survivors of atomic bombs. What is less well understood and far harder to study are the effects of lower doses of radiation as received from natural sources, medical scans, or to a lesser extent nuclear power operations.
The prevailing method to deal with this area of uncertainty is to extrapolate the observable effects of high doses and assume the same relationship applies to low doses with no observable effect i.e. assume that all levels of exposure come with a commensurate health risk, no matter how small. This approach is used in practice as a basis for the management of occupational and public exposure worldwide.
It is a safe assumption that the amount of DNA damage increases in line with radiation exposure, but Mina Bissell of Berkeley’s life sciences division said today: “Our data show that at lower doses of ionizing radiation, DNA repair mechanisms work much better than at higher doses.” She added that this “casts doubt on the general assumption that any amount of ionizing radiation is harmful and additive.”
The researchers used time-lapse images of cells as they responded to various radiation doses. They were able to see the repair proteins concentrate around parts of DNA that had suffered a double strand break in what are called radiation-induced foci (RIF). Over time the severed ends of DNA strands actually moved within the cell nucleus to gather in larger RIFs known as ‘repair centres’.
Sylvain Costes, who led the study, said that multiple repairs could be taking place simultaneously in the repair centres, leading to more errors in the repaired DNA. He said that at low levels of radiation, such as the natural levels humans experienced throughout evolution, it was “unlikely” that any cell would have to repair more than one double strand break at once.
The study was the first to use time-lapse imagery, which helped it record more RIFs as well as the clustering effect, which begins even before RIFs are formed.
Gerry Thomas, professor of molecular pathology at Imperial College London, told World Nuclear News that while the new theory “makes very good sense,” she would “urge a little caution as this is an in vitro model, and may not be completely representative of tissue response in vivo.”
Nevertheless, said Thomas, “This is very interesting and would probably fit with the findings we have post Chernobyl where most of the exposure to the population was low dose. It may also explain why relatively few patients treated with radiation for cancer go on to get second tumours. In radiotherapy you target the high dose to the tumour, but inevitably the surrounding tissue receives some radiation, but at a much lower dose.”
Costes said the team is now planning to conduct the same experiment with healthy donated cells, rather than immortalized laboratory versions, and to see if the results hold for fibroblast cells as well as the epithelial cells already studied. Another area for research is the clustering of double strand breaks: whether there is a transport mechanism, and whether the repair centres pre-exist.