I have a question regarding the dose-response curve presented in the LSS (Life Span Study) versus the dose-response curve in International Commission on Radiological Protection (ICRP) Recommendation 103. In the LSS (Preston 2007), the incidence of solid cancer versus dose curve is presented in terms of weighted colon dose. However, in ICRP 103, the incidence of solid cancer versus dose is presented in terms of Sv (total effective dose). How does ICRP convert the weighted colon dose to the effective dose?

ICRP lists
recommended tissue weighting factors to be used in consideration of stochastic
effects and determination of effective dose. The tissue weighting factor is a
relative measure of the risk of certain serious stochastic effects that might
result from irradiation of that specific tissue. The sum of all the tissue
weighting factors used in effective dose determinations is 1.0. The effective
dose, as you likely know, is determined by multiplying the equivalent dose (for
beta radiation, gamma radiation, and x rays, the equivalent dose is numerically
equal to the absorbed dose) to each significantly irradiated tissue by its
respective tissue weighting factor and then summing up all such products to
obtain effective dose. If only a single organ is irradiated, the effective dose
would be the equivalent dose to that organ multiplied by its tissue weighting
factor.

ICRP lists
tissue weighting factors in Table 3, page 65, of Publication 103, which you
cite. Individual tissue weighting factor values range from 0.01 to 0.12. For
the colon, the ICRP-recommended tissue weighting factor is 0.12. Thus, the
equivalent dose to the colon would be multiplied by this factor to obtain the
contribution of the colon dose to effective dose. Thus, under current
recommendations, if the colon received an absorbed dose of 1.0 Gy from gamma rays,
the equivalent dose to the colon would be 1.0 Sv, and the contribution to the
effective dose would be 0.12 Sv. Under earlier recommendations of the ICRP
(ICRP Publication 60), the colon was among remainder tissues and the default weighting
factor was 0.06 compared to the current value of 0.12. Use of the older factor
would have reduced the effective dose component from the colon by a factor of
two compared to the value calculated using the current weighting factor.

Keep in mind
that the quantity effective dose is used in radiation protection when attempting
to assess the overall potential stochastic risk associated with radiation
exposure. It is not intended for use in judging the impact of dose on
individual organs or tissues. Since Dale Preston and colleagues were concerned with
individual organs for purposes of assessing risk of radiation-induced cancer in
those organs, such doses would presumably have been reported as absorbed doses
or kerma. When weighted organ doses are used in investigations of cancer
incidence, the weighting usually refers to multiplying the absorbed dose,
generally expressed in grays (Gy), from a given radiation type by an
appropriate radiation weighting factor to convert to equivalent dose, usually
expressed in sieverts (Sv). The population of exposed survivors from the World War
II bombings of Japan was exposed to gamma radiation and, in part, neutron
radiation, and the radiation weighting factor has often been taken as 1.0 for
the gamma radiation and 10 for the neutron radiation.

I looked at
the figures in the cited Preston publication
and noticed that the cancer response plots are in fact shown with excess
relative risk plotted against weighted organ dose in Gy, the unit of absorbed
dose or kerma. If the radiation weighting factors had been applied, I would have
expected the dose unit to be Sv, representative of equivalent dose. I do not
currently have access to the text of the publication, so I can not say for
certain what the dose weighting refers to, but the weighting would not have
anything to do with the tissue weighting factors used to estimate stochastic
impact, as when effective dose is determined. If you require more specific
information about the dose weighting process used by Preston and colleagues, I suggest
that you attempt to contact one of the authors. Good luck.

George
Chabot,
PhD, CHP

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