Health Risks of Ionizing Radiation: - Clark University

adon (Lubin et al. 1997). These results have since
been confirmed in two other large pooled analyses
of North American and European studies (Krewski
et al. 2005, Darby et al. 2005).
Our appendix on preconceptional exposures
is a less formal meta-analysis. It suggests that
preconceptional exposure of fathers, particularly in a
relatively small window of time prior to conception,
can lead to a cancer risk in the children that are
conceived. We can statistically demonstrate that this
is likely to be true. We can also respond to some
skepticism from the scientific community--atomic
bomb survivors might not be informative on this
issue, for example, so we shouldn’t consider a lack
of evidence from this cohort to be crucial. We should
be open to the abundant evidence that animal studies
bring to this issue (this issue is discussed further in
section 10 and in appendix C).
These are just a couple of illustrations; any
particular topic in this overview could be explored
further with varying degrees of effort. We find that if
we consider an issue carefully and comprehensively
we can come to a very different conclusion than
those who look at a few study results individually
or who are constrained by a preconceived judgment.
It is very important to keep an open mind. With that
perspective we should return one last time to the
idea of a threshold.
What if there is a threshold dose? It is
impossible to completely rule out the possibility.
We find it hard to justify a threshold of 0.1 Sv but
maybe a much lower threshold exists. It could
be, for example, that damage caused by a small
amount of radiation, maybe 0.001 Sv, is perfectly
repaired with no long-term consequences. This is of
course a possibility, although evidence from other
fields of study tends to stack up against it 16 . Land
(2002) published an interesting illustration of the
implications of the possibility of a threshold on risk
Discussion 173
estimates. Instead of choosing one model or the
other, Land created a hypothetical dose-response
relationship by combining a linear no-threshold
model with a threshold-type model, allowing each
model to have a weight equal to the probability of
it being correct. Not surprisingly, the estimated risk
decreases as we increase the likelihood of a threshold.
But the risk estimate is uncertain; there is an upper
confidence limit on our estimated risk and this is
the more important value for purposes of radiation
protection. Land shows that this confidence limit
is only affected by a threshold likelihood greater
than ~80%. We can’t easily quantify the likelihood
of a threshold, but we can look at other, biological
observations get a rough idea; it would be very hard
to argue that the likelihood could be this high.
Some biological phenomena, such as the
adaptive response 17 , suggest possible threshold doses
and even lend support to a theory of hormesis. Other
biological phenomena that have been observed at
low doses include the bystander effect and genomic
instability (see for example Morgan 2003). These
observations suggest that radiation can hit a cell
and cause effects in descendents of the hit cell or in
cells surrounding the hit cell. Based on these types
of effects, which only appear to be significant at
low doses, we might expect a dose-response curve
that has a low-dose region where the linear model
would underestimate the true risk. This type of doseresponse
is suggested in the atomic bomb survivor
data as shown in Figure 13-1; here we see that the
estimate of the ERR/Sv at low doses tends to be
higher than it is over the whole range of doses.
Biological observations at low doses therefore
present mechanisms that pull in two directions,
potentially reducing and enhancing low-dose risk
at the same time 18 . Brenner et al. (2003) wrote a
very good review of the state of low-dose radiation
risk research that considered evidence from both
16 For example, it has been shown that a single track of radiation can damage DNA and that DNA repair mechanisms
such as non-homologous end-joining do not work perfectly. Thus any amount of radiation could theoretically
cause a cancer-initiating mutation. Land (2002), Upton (2003) and Brenner et al. (2003), among others, consider
epidemiological evidence in light of biological considerations.
17 Adaptive response refers to experiments where cells are exposed to a small dose of radiation followed by a large
dose. In some cases the small dose appears to reduce the effects of the larger dose. It has been suggested that the
small dose might induce DNA repair mechanisms so that the cell is then better equipped to deal with the large
dose.
18 This puzzle was recently the subject of a special issue of Mutation Research (volume 568, 2004).