Occupational Intakes of Radionuclides Part 1 - ICRP

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DRAFT REPORT FOR CONSULTATION
3.5.4 Treatment of radioactive progeny produced in systemic
compartments
(226) In Publication 30 (1979) and Publication 68 (1994b) the general assumption
was made that chain members produced in systemic compartments following intake
of a parent radionuclide adopt the biokinetics of the parent. This is referred to as the
assumption of ‘shared kinetics’. The alternate assumption of ‘independent kinetics’ of
chain members was made in Publication 68 when the parent was an isotope of lead,
radium, thorium, and uranium, and also for iodine progeny of tellurium and for noble
gas isotopes arising in various chains. The implementation of independent kinetics of
progeny was based on a general pattern of behaviour of systemically produced
progeny radionuclides suggested by a review of experimental and occupational
studies (Leggett, 1985). That is, the data suggested that most radioactive progeny
produced in soft tissue or bone surface tended to migrate from the parent and begin to
follow their characteristic biological behavior, while radionuclides produced in bone
volume tended to remain with the parent radionuclide in bone over the period of
observation.
(227) The assumption of independent kinetics is generally applied here to progeny
radionuclides produced in systemic compartments or absorbed to blood after
production in the respiratory or alimentary tract. The basic assumption is that a
progeny radionuclide will follow its characteristic behaviour after it first reaches
blood. The rate at which a progeny radionuclide is estimated to migrate from its place
of birth to blood is based on reported data where available. In the absence of specific
information the default assumption is that the progeny radionuclide immediately
begins to follow its characteristic behaviour from the time of birth. The
implementation of this default assumption is essentially a matter of assigning progeny
atoms produced by decay of the preceding chain member(s) to appropriate
compartments of the progeny radionuclide’s characteristic biokinetic model, which
predicts the subsequent fate of these atoms. This is not always a straightforward
exercise due to structural differences in the systemic models for many parent and
progeny combinations. For example, a radionuclide may be born in an explicitly
designated tissue T in the parent’s model that is not an explicitly designated tissue in
the progeny radionuclide’s characteristic model. When this happens, the rate of
removal of the progeny radionuclide from T and the destination of the removed
activity must be defined before the model can be solved. For a number of chains
addressed in this series of reports, this problem has been resolved by expanding the
chain members’ characteristic models to include all explicitly designated tissues in
the models for preceding chain members, based on available biokinetic data on the
progeny radionuclide and its chemical or physiological analogues. An alternate
‘automated’ default treatment of this problem and other issues regarding differences
in model structures for parent and progeny radionuclides is described in Section 3.7.2,
which addresses the contribution of radioactive progeny to dose.
(228) Even if the progeny radionuclide is produced in a tissue that is an explicitly
designated source organ in the progeny radionuclide’s characteristic model,
implementation of the default treatment of independent kinetics becomes somewhat
arbitrary if the progeny radionuclide’s model divides the tissue into compartments
that are not identifiable with compartments in the parent’s model. For example,
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