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Health Risks of Ionizing Radiation: - Clark University

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118 Preconception Exposures<br />

• The biological mechanism seemed unlikely. Doll et<br />

al. (1994) make this point with several arguments<br />

including the fact that radiation damages the<br />

genome randomly, so if preconception radiation<br />

is affecting sperm cells, other heritable diseases<br />

should show an increase along with leukemia.<br />

Evidence for these effects is discussed below.<br />

• There were other possible explanations for the<br />

excess in Seascale. Specifically, the external<br />

dose measurements used by Gardner may have<br />

been correlated with the dose received from<br />

radionuclides in the body (such as uranium,<br />

plutonium and tritium). In this case the internal<br />

dose or the combined external and internal dose<br />

may have been the true cause. Another proposed<br />

explanation for the Seascale cluster was that a high<br />

degree <strong>of</strong> population mixing in the communities<br />

that the workers lived in might have increased the<br />

general exposure to a virus; this virus may have<br />

played a role in the development <strong>of</strong> leukemia.<br />

10.2 Further studies <strong>of</strong> the Gardner hypothesis<br />

in the UK<br />

Both <strong>of</strong> the alternative explanations for the Seascale<br />

cluster were explored in a follow-up cohort study<br />

<strong>of</strong> all 274,170 live births in the county <strong>of</strong> Cumbria<br />

1950-1991 (Dickinson and Parker 2002a). The<br />

new cohort study included three more cases <strong>of</strong><br />

leukemia in the children <strong>of</strong> workers and generally<br />

confirmed the Gardner result (RR 1.9, 1.0-2.2).<br />

Although dose estimates for internal radionuclides<br />

were apparently not available, researchers typically<br />

identify those workers who experienced significant<br />

internal exposures by looking at who was monitored,<br />

assuming that a worker would only be subjected to<br />

monitoring if they were potentially exposed. In the<br />

cohort study Dickinson and Parker found a 3-fold<br />

increase in LNHL risk in the children <strong>of</strong> monitored<br />

workers (controlling for external exposures), but<br />

the result was based on 3 leukemia cases and not<br />

significant (RR 2.9, 0.6-9.8). It is important to note<br />

that monitored workers were shown to have higher<br />

external doses than unmonitored workers (75 mSv<br />

median dose vs 27 mSv); this seems to suggest that<br />

internal and external dose could be correlated. If<br />

true, this would support the idea that the leukemia<br />

cluster might be at least partly attributable to internal<br />

exposures.<br />

Addressing another alternative explanation for the<br />

cluster, population mixing and viruses, Dickinson<br />

and Parker (2002a) found that population mixing<br />

could statistically account for a large part <strong>of</strong> the<br />

leukemia excess in the children <strong>of</strong> Sellafield workers:<br />

The observed excess during 1950-1991 gave a RR<br />

<strong>of</strong> 1.9 (1.0-3.1); this was reduced in the 1969-1991<br />

time window to a RR <strong>of</strong> 1.1 (0.3-2.8) adjusted for<br />

population mixing 1 . On the other hand they showed<br />

a significant preconception radiation dose-response<br />

relationship within the Sellafield cohort that was not<br />

strongly affected by population mixing 2 .<br />

Several other studies have looked at LNHL and<br />

paternal preconception irradiation beyond Sellafield.<br />

One case-control study was based in Scotland (Kinlen<br />

et al. 1993) and found no significant associations<br />

between PPI and LNHL although all odds ratios<br />

calculated by the authors were positive.<br />

The case-control study reported by Roman et al.<br />

(1993) was important because it found a positive<br />

association with relatively low doses. The subjects in<br />

this study lived near the Aldermaston and Burghfield<br />

nuclear weapon plants in England. Although the<br />

fathers who worked at the plant had received less<br />

than 5 mSv <strong>of</strong> external preconception dose there was<br />

a significant LNHL risk associated with exposure to<br />

radiation on the job (RR 9.0, 1.0-107.8).<br />

In a later cohort study <strong>of</strong> UK nuclear workers<br />

Roman et al. (1999) again found an elevated LNHL<br />

rate in children <strong>of</strong> men who were monitored for<br />

radiation (rate ratio 3.0, 0.7-13.0). For those cases<br />

in which dose information was available there were<br />

elevated rates <strong>of</strong> LNHL that became significant for<br />

the highest dose groups 3 . There was also evidence<br />

1 Among children <strong>of</strong> radiation workers born 1969-1991 and aged 0-6 years 63% <strong>of</strong> the cases were estimated to be<br />

attributable to population mixing and 18% were estimated to be attributable to PPI. (Dickinson and Parker 2002b).<br />

2 The rate ratio per 100 mSv was 1.6 (1.0-2.2) before adjusting for population mixing and 1.4 (0.2-3.1) after<br />

adjustment.<br />

3 Leukemia rate ratios were 3.9 (1.0-15.7) for cumulative external doses <strong>of</strong> ≥100 mSv and 5.4 (1.4-20.5)<br />

for doses <strong>of</strong> ≥10 mSv in the 6 months before conception.

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