Health Risks of Ionizing Radiation: - Clark University
Health Risks of Ionizing Radiation: - Clark University
Health Risks of Ionizing Radiation: - Clark University
Create successful ePaper yourself
Turn your PDF publications into a flip-book with our unique Google optimized e-Paper software.
Radiotherapy for childhood cancer. Tucker et<br />
al. (1987), investigating leukemia after childhood<br />
cancer therapy, found an excess associated with<br />
alkylating agents but not radiation therapy. Garwitz et<br />
al. (2000), on the other hand, concluded that radiation<br />
was the most important treatment-related risk factor<br />
for the development <strong>of</strong> a second malignant neoplasm<br />
in children who were exposed under the age <strong>of</strong> 20<br />
for a first malignant neoplasm. The irradiated group<br />
had a RR <strong>of</strong> 4.3. Chemotherapy appeared to play<br />
only an accessory role <strong>of</strong> potentiating the effects <strong>of</strong><br />
radiotherapy. Loning et al. (2000) found that children<br />
that received cranial radiation for the treatment <strong>of</strong><br />
acute lymphoblastic leukemia had a higher risk<br />
for developing secondary neoplasms. The risk <strong>of</strong><br />
thyroid cancer was specifically investigated by de<br />
Vathaire et al. (1999b). Cases where the first cancer<br />
had been thyroid cancer were excluded from this<br />
cohort <strong>of</strong> French and English children. The mean<br />
thyroid dose was quite high (7 Gy), and although<br />
the estimated risk was unusually high, suggesting<br />
a predisposition to cancer, the dose-response<br />
relationship within the cohort was consistent with<br />
radiation-induced thyroid cancer patterns in other<br />
cohorts 31 . Acharya et al. (2003) looked at 33 cases <strong>of</strong><br />
thyroid neoplasms in cancer survivors who had been<br />
treated with radiation. Thirteen <strong>of</strong> these neoplasms<br />
were malignant, more than would be expected based<br />
on a 5% malignancy rate in the general population.<br />
Again, doses had been quite high (10-42 Gy) and<br />
these patients were possibly predisposed to cancer.<br />
Wong et al. (1997) examined retinoblastoma 32<br />
patients; these patients are expected to have a<br />
strong genetic predisposition to cancer. The authors<br />
demonstrated a much higher risk in patients whose<br />
primary cancer was hereditary, as expected, but also<br />
demonstrated a dose-response trend for sarcomas <strong>of</strong><br />
bone and s<strong>of</strong>t tissue 33 . The OR for any second cancer<br />
Medical Exposures 29<br />
among nonhereditary retinoblastoma patients was<br />
1.6 (0.7-3.1).<br />
3.5 In utero exposures<br />
Studies <strong>of</strong> prenatal exposure to radiation, mainly<br />
through obstetric x-rays, have clearly demonstrated<br />
risks at relatively low doses. Alice Stewart and<br />
others published results linking prenatal exposure<br />
and childhood cancer in the 1950s (Stewart et al<br />
1956, 1958), and this study grew into the Oxford<br />
Survey <strong>of</strong> Childhood Cancers (OSCC). Although the<br />
OSCC contains the majority <strong>of</strong> the data pertaining<br />
to this association, other studies have generated<br />
consistent results. One <strong>of</strong> the challenges in analyzing<br />
these data is the lack <strong>of</strong> good dose information; the<br />
average dose <strong>of</strong> an x-ray exam has declined over<br />
the years and precise estimates <strong>of</strong> dose per exam<br />
are not available 34 . The studies discussed below<br />
have attempted to make reasonable inferences about<br />
dose and apply them to observed childhood cancer<br />
outcomes.<br />
The OSCC grew to include all childhood cancers<br />
in Great Britain and in 1981 consisted <strong>of</strong> 15,276 casecontrol<br />
pairs. Initial observations found increased<br />
risks <strong>of</strong> childhood leukemia (RR 1.92, 1.12-3.28)<br />
and other childhood cancers (RR 2.28, 1.31-3.97)<br />
after prenatal x-rays <strong>of</strong> the mother’s abdominal area<br />
(Stewart et al. 1956, Doll and Wakeford 1997). As<br />
prenatal exposure has decreased, so has the estimated<br />
risk. Knox et al. (1987) estimated an average relative<br />
risk <strong>of</strong> 1.94 over the period 1953-79. This analysis<br />
also suggested that the relative risk was highest for<br />
cancers at age 4-7. Gilman et al (1988) also looked<br />
at the OSCC and argued that the timing <strong>of</strong> the<br />
exposure in the pregnancy was more important than<br />
the dose in increasing cancer risk. Specifically, these<br />
authors found that x-rays taken in the first trimester<br />
31 With a dose <strong>of</strong> 0.5 Gy the SIR was 35 (90% CI 10-87). The ERR was stated to be between 4 and 8 per Gy; this can<br />
be compared to the estimate from Ron et al. (1995) <strong>of</strong> 7.7/Gy<br />
32 Retinoblastoma is a cancer <strong>of</strong> the eye that typically affects young children and is largely hereditary.<br />
33 The odds ratios for sarcomas (1.9, 3.7, 4.5, 10.7) increased with median dose (7, 20, 40, 98 Gy) compared to the 0-5<br />
Gy dose group.<br />
34 Knox et al. (1987) cite the National Radiological Protection Board estimate that the mean fetal gonadal dose per<br />
exposure in 1977 was 3.5 mGy. The United Nations Scientific Committee on the Effects <strong>of</strong> Atomic <strong>Radiation</strong><br />
estimated that the mean fetal dose per film was 18.0 mGy between 1947 and 1950 and 5.0 mGy between 1958 and<br />
1960. Mole (1990) used an estimated mean dose <strong>of</strong> 6 mGy for the period 1958-61.