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. 2023 Jul 6;25(7):1368-1376.
doi: 10.1093/neuonc/noad012.

Computed tomography scan radiation and brain cancer incidence

Nicolas R Smoll  1 , Zoe Brady  1   2 , Katrina J Scurrah  1 , Choonsik Lee  3 , Amy Berrington de González  3 , John D Mathews  1
Affiliations

Computed tomography scan radiation and brain cancer incidence

Nicolas R Smoll et al. Neuro Oncol. .

Abstract

Background: Computed tomography (CT) scans make substantial contributions to low-dose ionizing radiation exposures, raising concerns about excess cancers caused by diagnostic radiation.

Methods: Deidentified medicare records for all Australians aged 0-19 years between 1985-2005 were linked to national death and cancer registrations to 2012. The National Cancer Institute CT program was used to estimate radiation doses to the brain from CT exposures in 1985-2005, Poisson regression was used to model the dependence of brain cancer incidence on brain radiation dose, which lagged by 2 years to minimize reverse causation bias.

Results: Of 10 524 842 young Australians, 611 544 were CT-exposed before the age of 20 years, with a mean cumulative brain dose of 44 milligrays (mGy) at an average follow-up of 13.5 years after the 2-year lag period. 4472 were diagnosed with brain cancer, of whom only 237 had been CT-exposed. Brain cancer incidence increased with radiation dose to the brain, with an excess relative risk of 0.8 (95% CI 0.57-1.06) per 100 mGy. Approximately 6391 (95% CI 5255, 8155) persons would need to be exposed to cause 1 extra brain cancer.

Conclusions: For brain tumors that follow CT exposures in childhood by more than 2 years, we estimate that 40% (95% CI 29%-50%) are attributable to CT Radiation and not due to reverse causation. However, because of relatively low rates of CT exposure in Australia, only 3.7% (95% CI 2.3%-5.4%) of all brain cancers are attributable to CT scans. The population-attributable fraction will be greater in countries with higher rates of pediatric scanning.

Keywords: Brain cancer; CT Scans; Radiation Epidemiology; low-dose radiation; reverse causation.

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Conflict of interest statement

All authors declare that they have no conflicts of interest.

Figures

Figure 1.
Figure 1.
Categorization of person-years into unexposed and exposed, with cumulative dose estimation. Exposure lagging affects the transfer date; the date of the first scan plus the lag period gives the transfer date. Induction is the period prior to cancer initiation. The hypothetical latent period (LP) is the period between initiation and the first symptoms of cancer. The pre-diagnostic symptomatic interval (PSI) is the period between the first symptom and the formal diagnosis of cancer. CT1 and CT2 represent potentially causal scans, while CT3 represents a reverse causation scan which is not included in the total dose calculation. The dose from CT1 was 48 mGy and that from CT2 was 50 mGy, giving a total cumulative dose of 98 mGy.
Figure 2.
Figure 2.
Excess relative risk /100 mGy, with 95% confidence intervals, by lag period. The substantial decline at lags of one and 2 years is likely attributable to reverse causation, whereas the slower decline at longer lags is attributable to effect modification (see text).
See this image and copyright information in PMC

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