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ECRR 2003 Recommendations of the European Committee on Radiation Risk
The Health Effects of Ionising Radiation Exposure at Low Doses for
Radiation Protection Purposes. Regulators' Edition.
Executive Summary
This report outlines the committee's findings regarding the effects
on human health of exposure to ionising radiation and presents a new
model for assessing these risks. It is intended for decision-makers and
others who are interested in this area and aims to provide a concise
description of the model developed by the committee and the evidence on
which it depends. The development of the model begins with an analysis
of the present risk model of the International Commission on
Radiological Protection (ICRP) which is the basis of and dominates all
present radiation risk legislation. The committee regards this ICRP
model as essentially flawed as regards its application to exposure to
internal radioisotopes but for pragmatic reasons to do with the
existence of historical exposure data has agreed to adjust for the
errors in the ICRP model by defining isotope and exposure specific
weighting factors for internal exposures so that the calculation of
effective dose (in Sieverts) remains. Thus, with the new system, the
overall risk factors for fatal cancer published by ICRP and other risk
agencies may be used largely unchanged and legislation based upon these
may also be used unchanged. It is the calculation of the dose which is
altered by the committee's model.
1. The European Committee on Radiation Risk arose out of criticisms
of the risk models of the ICRP which were explicitly identified at the
European Parliament STOA workshop in February 1998; subsequently it was
agreed that an alternative view should be sought regarding the health
effects of low level radiation. The committee consists of scientists and
risk specialists from within Europe but takes evidence and advice from
scientists and experts based in other countries.
2. The report begins by identifying the existence of a dissonance
between the risk models of the ICRP and epidemiological evidence of
increased risk of illness, particularly cancer and leukaemia, in
populations exposed to internal radioactive isotopes from anthropogenic
sources. The committee addresses the basis in scientific philosophy of
the ICRP risk model as applied to such risks and concludes that ICRP
models have not arisen out of accepted scientific method. Specifically,
ICRP has applied the results of external acute radiation exposure to
internal chronic exposures from point sources and has relied mainly on
physical models for radiation action to support this. However, these are
averaging models and cannot apply to the probabilistic exposures which
occur at the cell level. A cell is either hit or not hit; minimum impact
is that of a hit and impact increases in multiples of this mimimum
impact, spread over time. Thus the committee concludes that the
epidemiological evidence of internal exposures must take precedence over
mechanistic theory-based models in assessing radiation risk from
internal sources.
3. The committee examines the ethical basis of principles implicit in
the ICRP models and hence in legislation based on them. The committee
concludes that the ICRP justifications are based on outmoded
philosophical reasoning, specifically the averaging cost-benefit
calculations of utilitarianism. Utilitarianism has long been discarded
as a foundation for ethical justification of practice owing to its
inability to distinguish between just and unjust societies and
conditions. It may, for example, be used to underpin a slave society,
since it is only the overall benefit which is calculated, and not
individual benefit. The committee suggests that rights-based
philosophies such as Rawls Theory of Justice or considerations based on
the UN Declaration of Human Rights should be applied to the question of
avoidable radiation exposures to members of the public resulting from
practice. The committee concludes that releases of radioactivity without
consent can not be justified ethically since the smallest dose has a
finite, if small, probability of fatal harm. In the event that such
exposures are permitted, the committee emphasises that the calculation
of 'collective dose' should be employed for all practices and time
scales of interest so that overall harm may be integrated over the
populations.
4. The committee believes that it is not possible accurately to
determine 'radiation dose to populations' owing to the problems of
averaging over exposure types, cells and individuals and that each
exposure should be addressed in terms of its effects at the cell or
molecular level. However, in practice, this is not possible and so the
committee has developed a model which extends that of the ICRP by the
inclusion of two new weighting factors in the calculation of effective
dose. These are biological and biophysical weighting factors and they
address the problem of ionisation density or fractionation in time and
space at the cell level arising from internal point sources. In effect,
they are extensions of the ICRP's use of radiation weighting factors
employed to adjust for differences in ionisation density resulting from
different quality radiations (e.g. alpha-, beta and gamma).
5. The committee reviews sources of radiation exposure and recommends
caution in attempting to gauge the effects of novel exposures by
comparison with exposures to natural radiation. Novel exposures include
internal exposures to artificial isotopes like Strontium-90 and
Plutonium-239 but also include micrometer range aggregates of isotopes
(hot particles) which may consist of entirely man-made isotopes (e.g.
plutonium) or altered forms of natural isotopes (e.g. depleted uranium).
Such comparisons are presently made on the basis of the ICRP concept of
'absorbed dose' which does not accurately assess the consequence for
harm at the cell level. Comparisons between external and internal
radiation exposures may also result in underestimates of risk since the
effects at the cell level may be quantitatively very different.
6. The committee argues that recent discoveries in biology, genetics
and cancer research suggest that the ICRP target model of cellular DNA
is not a good basis for the analysis of risk and that such physical
models of radiation action cannot take precedence over epidemiological
studies of exposed populations. Recent results suggest that very little
is known about the mechanisms leading from cell impact to clinical
disease. The committee reviews the basis of epidemiological studies of
exposure and points out that many examples of clear evidence of harm
following exposure have been discounted by ICRP on the basis of invalid
physical models of radiation action. The committee re-instates such
studies as a basis for its estimates of radiation risk. Thus the
100-fold discrepancy between the ICRP model's predictions and the
observed cases in the Sellafield childhood leukemia cluster becomes an
estimator of risk for childhood leukemia following such exposure. The
factor is thus incorporated by the committee into the calculation of
harm from internal exposure of specific types through its inclusion in
the weighting factors used to calculate the 'effective dose' to the
children in Sieverts.
7. The committee reviews the models of radiation action at the cell
level and concludes that the 'linear no threshold' model of the ICRP is
unlikely to represent the response of the organism to increasing
exposure except for external irradiation and for certain end points in
the moderately high dose region. Extrapolations from the Hiroshima
lifespan studies can only reflect risk for similar exposures i.e. high
dose acute exposures. For low dose exposures the committee concludes,
from a review of published work, that health effects relative to the
radiation dose are proportionately higher at low doses and that there
may be a biphasic dose response from many of these exposures owing to
inducible cell repair and the existence of high-sensitivity phase
(replicating) cells. Such dose-response relationships may confound the
assessment of epidemiological data and the committee points out that the
lack of a linear response in the results of epidemiological studies
should not be used as an argument against causation.
8. In further considering mechanisms of harm, the committee concludes
that the ICRP model of radiation risk and its averaging methods exclude
effects which result from anisotropy of dose both in space and in time.
Thus the ICRP model ignores both high doses to local tissue caused by
internal hot particles, and sequential hits to cells causing replication
induction and interception (second event), and merely averages all these
high risk situations over large tissue mass. For these reasons, the
committee concludes that the unadjusted 'absorbed dose' used by ICRP as
a basis of risk calculations is flawed, and has replaced it with an
adjusted 'absorbed dose' which used enhancement weightings based on the
biophysical and biological aspects of the specific exposure. In
addition, the committee draws attention to risks from transmutation from
certain elements, notably Carbon-14 and Tritium, and have weighted such
exposures accordingly. Weightings are also given to radioactive versions
of elements which have a particular biochemical affinity for DNA e.g.
Strontium and Barium and to certain Auger emitters.
9. The committee reviews the evidence which links radiation exposure
to illness on the basis that similar exposures define the risks of such
exposures. Thus the committee considers all the reports of associations
between exposure and ill health, from the A-bomb studies to weapons
fallout exposures, through nuclear site downwinders, nuclear workers,
reprocessing plants, natural background studies and nuclear accidents.
The committee draws particular attention to two recent sets of exposure
studies which show unequivocal evidence of harm from internal
irradiation at low dose. These are the studies of infant leukemia
following Chernobyl, and the observation of increased minisatellite DNA
mutations following Chernobyl. Both of these sets of studies falsify the
ICRP risk models by factors of between 100 and 1000. The committee uses
evidence of risk from exposures to internal and external radiation to
set the weightings for the calculation of dose in a model which may be
applied across all exposure types to estimate health outcomes. Unlike
the ICRP the committee extends the analysis from fatal cancer to infant
mortality and other causes of ill health including non-specific general
health detriment.
10. The committee concludes that the present cancer epidemic is a
consequence of exposures to global atmospheric weapons fallout in the
period 1959-63 and that more recent releases of radioisotopes to the
environment from the operation of the nuclear fuel cycle will result in
significant increases in cancer and other types of ill health.
11. Using both the ECRR's new model and that of the ICRP the
committee calculates the total number of deaths resulting from the
nuclear project since 1945. The ICRP calculation, based on figures for
doses to populations up to 1989 given by the United Nations, results in
1,173,600 deaths from cancer. The ECRR model predicts 61,600,000 deaths
from cancer, 1,600,000 infant deaths and 1,900,000 foetal deaths. In
addition, the ECRR predict a 10% loss of life quality integrated over
all diseases and conditions in those who were exposed over the period of
global weapons fallout.
12. The committee lists its recommendations. The total maximum
permissible dose to members of the public arising from all human
practices should not be more than 0.1mSv, with a value of 5mSv for
nuclear workers. This would severely curtail the operation of nuclear
power stations and reprocessing plants, and this reflects the
committee's belief that nuclear power is a costly way of producing
energy when human health deficits are included in the overall
assessment. All new practices must be justified in such a way that the
rights of all individuals are considered. Radiation exposures must be
kept as low as reasonably achievable using best available technology.
Finally, the environmental consequences of radioactive discharges must
be assessed in relation to the total environment, including both direct
and indirect effects on all living systems. |