Health Risks of Ionizing Radiation: - Clark University

52 Atomic Bomb Survivors
of the 8 th week to the end of the 15 th week after
conception; within this period the dose response for
mental retardation can be described as linear with
an apparent ERR of 43/Gy 14 . In a later review Otake
and Schull (1998) expanded these observations to
include impaired school performance and decreased
IQ, both outcomes related to dose and restricted to
the gestational period of 8-25 weeks.
Delongchamp et al. (1997) found that there was
a significantly elevated risk of cancer mortality for
those exposed in utero with an ERR of 3/Sv (90% CI
0.6-7.2) based on 8 cases. The risk of childhood cancer
could not be easily observed in this cohort; based on
1 case the ERR estimate was 23/Sv (1.7-88). This is
very uncertain but consistent with the estimated doseresponse
pattern of childhood cancer after prenatal
x-rays (51/Gy, 28-76; Wakeford and Little 2003).
4.7 Discussion
Age, time and gender. It is clear from the above
discussion that age and gender play critical roles in
the patterns of risk associated with exposure to the
atomic bombs. Generally, relative risks are higher for
younger ages at exposure and for females. Preston
(2000) summarizes the influence of age and gender
in the RERF analyses. Time can be a complicated
confounding variable because it can be represented
in different ways. Age at exposure is one way, and
another is time since exposure. Different models
make use of one or both of these factors. Pierce and
Mendelsohn (1999) have argued that attained age,
the age of subjects at the time of diagnosis or death,
is the best way to model the effect of time on solid
cancer incidence. They found that excess relative
risk decreases throughout life in proportion to 1/age.
Although these alternative models are interesting,
it may be the case that several models fit the data
equally well. Heidenreich et al. (2002) have argued
that the atomic bomb survivors, despite being the
standard reference cohort, may not be sufficiently
large to illuminate the fine points of the cancer
response to radiation.
What we can say with little doubt is that
childhood exposure presents more of a risk than adult
exposures. This is mechanistically reasonable since
the tissues in a child’s body are growing rapidly.
The ERR of solid cancer mortality was ~1.9 per Sv
after exposure in infancy according to Preston et al.
(2003), compared to 0.47 per Sv after exposure at
age 30. The risks of solid cancer incidence followed
a similar pattern, and this was true of several types,
notably thyroid cancer (see Figures 4-1 and 4-2).
Leukemia risk follows a more complicated pattern
and only ALL shows a clear effect of age at exposure,
with childhood exposures carrying a higher risk.
Leukemia, however, has a very short latent period
of as few as 2 years and follow-up of the LSS cohort
began 5 years after the bombings. A number of
cases are therefore not included in these analyses;
inclusion of these cases might have increases the
estimated leukemia risk and might have shed more
light on the effects of age at exposure (Preston et al.
1994).
Some major confounders can be addressed in this
cohort. Pierce et al. (2003), for example, considered
the effect of smoking on lung cancer incidence rates
in the a-bomb cohorts. The authors analyzed the
smoking histories of 45,113 members of the LSS
cohort and found that smoking and radiation are
likely additive in effect and are almost certainly not
multiplicative.
Dose-response curves. The atomic bomb
survivor data have been analyzed many times to
examine dose-response patterns in detail. This
research has consistently found no evidence of a
threshold dose below which there is no cancer risk
(Thompson et al. 1994, Pierce et al. 1996, Preston et
al. 1994, 2003a, 2003b, Little and Muirhead 1997).
The linear dose-response model has been
commonly applied to solid cancer incidence and
mortality data because it is simple and intuitive and
because it fits the data better than a linear-quadratic
or some other upward-turning curve. Some detail
is obscured by a simple linear model, however. At
doses above a few Gy the estimated ERR per dose
begins to plateau; these doses are approaching the
acutely lethal dose range and the dynamics of the
biological response are very different from lowdose
scenarios. At low doses, as we mentioned
above, a simple linear model might underestimate
the true risk. The ERR for solid cancer mortality, for
14 The dose-response was described in the text as having a linear increase in frequency of 0.44 per Gy (0.26-0.62) and
a background frequency of 0.01.