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Health Risks of Ionizing Radiation: - Clark University

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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.

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