R.K. Sachs.
International Journal of Radiation Biology, 75: 1335, 1999.
Review of: Radiation Protection Dosimetry: A Radical Reappraisal.
J.A. Simmons and D.E. Watt.
(Medical Physics Publishing, Madison). 140 pp.
ISBN 0-944838-87-1.
The core of this short book is chapter 5, which
extends biophysical modeling results originated
in the 1980's. Evidence is presented that a main
determinant of charged particle effectiveness for killing
mammalian cells is lambda, the mean free path for linear
primary ionization, essentially the average
distance between energy deposition events along the primary track.
For many different radiations, maximum
effectiveness as the energy varies
is found for lambda approximately 1.8 nm, a value
the authors interpret geometrically, in terms of DNA double strand
breaks (DSBs). They suggest that delta ray action
rarely produces DSBs at locations away from a primary ion
track, and that the average energy per delta ray
has little biological importance. They argue that
therefore two energy-based quantities, LET and dose,
should be replaced by #lambda# and particle flux in
biophysical analyses and, in a radical reappraisal of
radiation protection methodology,
weighting factors should be replaced by bioeffect cross sections.
Earlier chapters emphasize historical aspects
of radiation protection. In chapter 4 the authors survey other
biophysical models that are related to their own.
It is very useful to have various models thus interconnected.
However, the model descriptions are introductory rather than
definitive, and the reader may be perplexed by discrepancies
between equations and text unless the original papers are consulted.
Chapter 6 briefly describes an over-all model of radiation
damage, with most
endpoints taken to be directly proportional to the number
of unrepaired DSBs. For example,
the authors analyze dose-response relations and dose-rate effects
for cell inactivation, assuming one-track action,
linear first-order DSB repair, variation of radiosensitivity
during the cell cycle, and DSB fixation at an M
checkpoint. The treatment has a number of quite
puzzling features. For example, the authors
state that, in the case of acute irradiation,
linear log-survival holds for synchronized cells
(i.e. no shoulder, even at low LET), and also holds
for asynchronous cells (i.e. cell population heterogeneity in
radioresponse does not lead to resistant tails).
The authors strongly oppose linear no-threshold extrapolations
in risk assessment, and they survey some of the relevant
epidemiological literature on carcinogenesis. They
state that their approach,
replacing dose by fluence, would "effectively remove" the
linear no-threshold hypothesis, but do not adequately explain why.
In all, this is an interesting, highly individualistic book
well worth reading.