Health Risks of Ionizing Radiation: - Clark University
Health Risks of Ionizing Radiation: - Clark University
Health Risks of Ionizing Radiation: - Clark University
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28 Medical Exposures<br />
(2.1-28.7). This paper is discussed in greater detail<br />
in appendix B.<br />
3.4 Radiotherapy for cancer<br />
<strong>Radiation</strong> is an important cancer therapy tool.<br />
Although the benefits <strong>of</strong> radiation therapy obviously<br />
outweigh the risks in many cases, researchers<br />
and doctors have long been concerned about the<br />
possibility <strong>of</strong> second cancers in cancer patients.<br />
Two types <strong>of</strong> potential risk factors converge in these<br />
patients; genetic or environmental predisposition<br />
to cancer, demonstrated by the first cancer, and the<br />
therapy, either chemotherapy or radiation. These<br />
factors make information about cancer patients a hard<br />
body <strong>of</strong> evidence to compare with other studies. The<br />
underlying genetic cancer risk can be accounted for,<br />
to some degree, by focusing exclusively on cancer<br />
patients and assessing the dose-response patterns or<br />
using cancer patients not treated with radiation as<br />
controls. Doses are typically very high, so we do not<br />
go into these studies in depth and only discuss a few<br />
representative papers. Little et al. (1999) provide<br />
a comprehensive review <strong>of</strong> the field in relation to<br />
atomic bomb survivor-based risk estimates 28 .<br />
Boice et al. (1987, 1988) have studied radiation<br />
treatment for cancer <strong>of</strong> the cervix using casecontrol<br />
methods. Doses to bone marrow were on the<br />
order <strong>of</strong> several Gy from this procedure. The 1987<br />
paper focused on leukemia and found a marginally<br />
significant doubling <strong>of</strong> risk (RR 2.0, 90% CI 1.0-<br />
4.2). The risk appeared to increase with dose up<br />
to about 4 Gy and the authors fit the data with a<br />
linear-exponential model with compartmentalized<br />
dose estimates (see Weiss et al. 1995, above). In this<br />
case the linear estimate <strong>of</strong> ERR was 0.88/Gy 29 . The<br />
1988 paper focused on second cancers generally.<br />
Tissues close to the cervix received doses ranging<br />
as high as 200 Gy or more; cell killing is an obvious<br />
consideration in these cases. The incidence <strong>of</strong><br />
cancers <strong>of</strong> the rectum, bladder, and genital organs<br />
was significantly increased. The thyroid received an<br />
average dose <strong>of</strong> 0.11 Gy and showed a nonsignificant<br />
tw<strong>of</strong>old increase in cancer risk (RR 2.35, 0.6-8.7).<br />
Travis et al. (2000) examined men who had<br />
been treated for testicular cancer with radiation to<br />
see if they had an increased incidence <strong>of</strong> leukemia.<br />
The mean bone marrow dose in this cohort was 12.6<br />
Gy. Patients who had been treated with radiation and<br />
not chemotherapy were found to have a threefold<br />
leukemia risk (RR 3.1, 0.7-22) compared to patients<br />
who had not received radiation or chemotherapy.<br />
Risk appeared to be significantly related to dose<br />
although the relationship was not quantified.<br />
Gilbert et al. (2003) investigated the lung cancer<br />
risk among Hodgkin’s disease patients. This study<br />
benefited from estimates <strong>of</strong> radiation dose for<br />
specific locations <strong>of</strong> the lung where cancer later<br />
developed. The authors were also able to control for<br />
chemotherapy treatments and smoking. There was a<br />
significant dose-response relationship in this cohort<br />
(ERR 0.15/Gy, 0.06-0.39) and even though most<br />
doses were above 30 Gy there was little evidence<br />
for departure from linearity, indicating similar doseresponse<br />
relationships for lower doses 30 . It was<br />
found that the interaction between chemotherapy<br />
and radiation was almost exactly additive while the<br />
interaction between radiotherapy and tobacco use<br />
seemed to be multiplicative. Hancock et al. (1993)<br />
found that women who were treated for Hodgkin’s<br />
disease had an increased risk <strong>of</strong> breast cancer<br />
incidence and mortality (incidence RR 4.1, 2.5-5.7);<br />
this risk was particularly evident in women who<br />
had been treated before the age <strong>of</strong> 15 (incidence RR<br />
136, 34-371). Most tumors arose in tissues receiving<br />
~44 Gy. These authors also found evidence for an<br />
increased incidence <strong>of</strong> thyroid disease in this cohort<br />
(thyroid cancer RR 15.6, 6.3-32.5; Hancock et al.<br />
1991).<br />
28 They found that in almost all cases the atomic bomb survivor-based risk estimates were higher. The authors<br />
speculated that cell sterilization from the scheduled high doses <strong>of</strong> the medical exposure were largely responsible for<br />
the difference.<br />
29 This is substantially lower than the estimated ERR <strong>of</strong> 5.18/Gy (0.81-23.63) from the ankylosing spondylitis cohort<br />
(Weiss et al. 1995).<br />
30 The lung cancer incidence pattern in the atomic bomb survivors showed a higher ERR <strong>of</strong> 0.95/Gy (0.60-1.36;<br />
Thompson et al. 1994). Doses among atomic bomb survivors were acute, single doses about 100 times lower than<br />
the fractionated doses in these Hodgkin’s disease patients.