Carcinogenic risk from hot particle exposures - has ICRP got it right?

Abstract

The argument has become very familiar - that radionuclides introduced into the environment from nuclear installations, fall-out from weapons testing, or whatever source, are responsible for substantial increases in cancer rates, and, because current risk estimates do not support this conclusion, they must be very wrong. It is argued that there must be some way in which low levels of artificial radionuclides, levels that result in tissue doses lower than from naturally-occurring radionuclides, pose a risk that is yet to be appreciated. One obvious problem with current risk estimates, it is suggested, is the simplistic averaging of doses from hot particles - see, for example, the home page of the Low Level Radiation Campaign website (www.llrc.org).It is true that the most widely used estimates of dose and carcinogenic risk from incorporated radionuclides, provided by the International Commission on Radiological Protection (ICRP), are based on calculations of average dose. Dose estimates do consider, however, the distribution of target cells within tissues. Doses to the respiratory tract from inhaled radionuclides take account of the position of target cells for the induction of different lung cancer types in the bronchial and bronchiolar airways (ICRP 1994). Similarly, the distribution of target cells in skeletal tissues is taken into account in estimates of risk of bone cancer and leukaemia (ICRP 1979, Goessner et al 2000). In other cases, the liver for example, the assumption is made that target cells are distributed throughout the whole organ. Thus, the target tissue volume can vary from a single layer of cells to a whole organ. But, having considered the available animal and human data on hot particle effects, ICRP concluded that risk should be estimated on the basis of average dose within the target tissue (ICRP 1980, 1991). Claims that dose from hot particles can be orders of magnitude more carcinogenic than dose delivered uniformly were judged to be poorly founded.Charles and Mill (pages 5-28 of this issue) have provided a review of in vitro and in vivo experimental studies and epidemiolocal evidence relevant to the hot particle question. Most information comes from animal studies but with support from recent in vitro studies. Charles and Mill conclude that ICRP dose averaging is likely to provide a reasonable estimate of carcinogenic risk, within a factor of ±3. The evidence includes a quite surprising concordance of risk estimates for radiation-induced lung cancer from three sources: Russian Mayak workers exposed to plutonium-239, mainly by inhalation, underground miners exposed to radon-222 and its progeny, and Japanese atomic bomb survivors exposed to external radiation. Taking account of differences in relative biological effectiveness of alpha particles and low LET radiations, the risk estimates derived were similar despite differences including the time-course of dose delivery and the heterogeneity of energy deposition from plutonium-239 oxide particle...