Health Risks of Ionizing Radiation: - Clark University

122 Preconception Exposures
Livshits et al. (2001) studied the families of 161
Ukrainian cleanup workers and overall found no
increase in the mutation rate. There was, however,
an apparent nonsignificant increase in mutations in
children conceived within two months of exposure.
Weinberg et al. (2001) studied 41 Ukrainian and
Israeli children who were conceived after their
fathers’ exposures. In this study there was a 7-fold
increase in the mutation being analyzed and the
mutation rate declined with increasing time between
exposure and conception. Kiuru et al. (2003) studied
155 Estonian children born to cleanup workers and
found a nonsignificant increase in mutation rate.
The odds ratio for mutations was almost significant
for cases in which the father was exposed to >20 cSv
(OR 3.0, 0.97-9.30).
Although these results may appear to be in conflict,
they are generally consistent with a scenario in which
the critical exposure is experienced by the father in
the months leading up to conception. This implies
that the sperm-producing cells (spermatogonia)
are not as vulnerable as the developing sperm cells
(spermatocytes). In this case the atomic bomb
survivor data are not very informative because
half of the exposure was maternal and most of the
children were born 10 or more years after exposure.
The chronic exposures of Chernobyl downwinders
and Chernobyl cleanup workers are more likely to
have affected the developing sperm of the exposed
fathers; these studies generally show an increase in
germline mutations.
10.7 Animal evidence
Although we have avoided discussions of animal
studies in the rest of this overview we feel that this
information is important here. Other health effects
discussed in this overview, mainly cancer in the
same individual that is exposed to radiation, have
been accepted as results of radiation exposure
although people continue to debate the nature of the
dose-response relationship. In these cases animal
evidence is not as enlightening as the abundant
human data. With preconception radiation exposure
and heritable effects, however, a debate continues
over whether these effects even exist in humans at
all. Thus it is useful to see if these effects have been
observed in other mammals.
One of the earliest and most frequently cited
animal studies was conducted by Taisei Nomura
(1982). This study involved the exposure of 2,904
parent mice to x-rays. Preconception x-ray exposure
of either parent significantly increased the tumor
rate in the offspring, and this included leukemia.
It appeared from the results that paternal exposure
after the formation of sperm was more likely to
cause this increase than exposure to spermatogonia
(sperm-producing cells). Put another way, exposure
closer to conception was a more clearly defined risk
factor. Mohr et al. (1999) conducted a similar study
and found similar results. Lord and Hoyes (1999)
injected male mice with plutonium-239 three months
before conception, exposed the offspring to gamma
radiation or a chemical carcinogen, and observed
the rate of leukemia. This study demonstrated that
preconception exposure caused the offspring to be
more sensitive to carcinogens that they were exposed
to after birth. Together these and other studies have
provided more evidence that cancer risk can be
increased by preconception exposure in mammals.
Studies that have tried to establish the most sensitive
stage of spermatogenesis for radiation-induced
mutations in mice have produced conflicting results.
Although these have not been resolved, they may
be partly attributable to differences in the strains
of mice used (Niwa 2003). This is important to
consider when drawing inferences for humans from
the mouse studies.
10.8 Discussion
Clearly the Seascale leukemia cluster has received
a lot of attention and analysis, but given the small
number of cases we must be satisfied with likely
explanations rather than answers. There is good
evidence that radiation played a role in creating a
leukemia risk, and both external and internal radiation
should be suspected. In addition, population mixing
is another plausible childhood leukemia risk factor.
Neither of these factors should be ignored and an
interaction between these factors seems plausible
(Little 1995,1999, Wakeford 2002; see also the
discussion of animal evidence above).
The reported doses of radiation involved in these
studies were relatively low; one obvious example
is the LNHL excess with occupational doses below
5 mSv (Roman et al. 1993). Stillbirths among
nuclear workers were almost tripled with maternal