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...