Age Dependencies in the Modelling of Radiation Carcinogenesis

Models for the dose and age dependence of radiation induced cancer
have been based primarily on the follow-up of the atomic bomb
survivors. Two different concepts have been deduced for leukaemias
and for other cancers. The excess leukaemias appear in a distinct
temporal wave with a maximum 5 to 10 years after radiation
exposure; the distribution is more narrow for younger ages, but
there is little dependence of the total attributable risk on age at
exposure. For other cancers the latent periods are longer and,
according to the current interpretation, the excess rates are then
proportional to the age specific spontaneous rates, so that most
excess cases would arise at old age. The factors of
proportionality, and thus the attributable risks, are assumed to be
markedly higher for young ages at exposure. It is argued here that
there is no firm support for this interpretation. The present
analysis compares the current model for cancers other than
leukaemia to a more meaningful alternative than the so-called
additive model which is usually invoked as a standard of
comparison. The analysis is performed in terms of analytical
expressions, to make the characteristics of the different concepts
more transparent. It is seen that the Japanese data are equally
well fitted by a model that assumes no dependence of sensitivity on
age at exposure but merely accounts for a dependence of the excess
risks on dose and on age attained. This 'age attained model'
corresponds, in essence, to formulations that have been used
earlier for the analysis of lung cancers in uranium miners. The
data up to 1985 for the atomic bomb survivors do not yet permit a
decision between the different models. But the acceptability of the
age attained model shows that age dependencies for leukaemias and
other cancers to be less fundamentally different than commonly
assumed. The age attained model leads to risk projections for young
ages at exposure that are substantially lower than present
estimates. In fact it predicts essentially the same lifetime
attributable risk for exposures at young and intermediate ages;
decreased risks result only for exposures at advanced ages where
the expression periods are already substantially reduced.