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International variation in radiation dose for computed tomography examinations: prospective cohort study

BMJ 2019; 364 doi: https://doi.org/10.1136/bmj.k4931 (Published 02 January 2019) Cite this as: BMJ 2019;364:k4931

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Unacceptable variation in radiation doses from CT scans

Re: International variation in radiation dose for computed tomography examinations: prospective cohort study

This letter is regarding the article by Smith-Bindman et al. (1) which aimed at determining the patient, institution, and machine characteristics that contribute to variation in radiation doses used for computed tomography (CT). In their prospective cohort study, the authors reported a substantial variation in radiation dose for computed tomography (CT) examinations across patients, institutions, and countries. The carcinogenicity of exposure to low doses of ionizing radiation is addressed by Smith-Bindman et al. by providing evidence that support the so-called linear no-threshold (LNT) model.

Although this paper addresses a challenging issue, relying on the LNT hypothesis to evaluate the radiation risk at low doses and dose rates can be misleading. While the LNT hypothesis assumes detrimental effects arise at the cellular level and are linked to DNA damage, it does not specifically address subsequent DNA repair mechanisms. In particular, some evidence shows that the most effective repair mechanisms can be observed at low doses. Base excision repair (BER), nucleotide excision repair (NER), and mismatch repair are the three fundamental mechanisms associated with DNA repair (2). Substantial evidence shows that radiation-induced DNA damage is significantly less severe than the spontaneous DNA damages that occur from a wide variety of other factors ranging from chemicals, heat, metabolic transients and natural background radiation. It should be noted that less than 0.1% of DNA base changes create a permanent mutation (3). Most are efficiently eliminated by the DNA repair mechanisms. Given this consideration, the frequency of mutations created by exposure to low dose radiation is significantly less than natural mutations. DNA repair and other human body natural defense mechanisms, including the immune system, provide a robust system to protect the body from a wide range of detrimental agents. These repair mechanisms suggest there are flaws in the conclusions of Smith-Bindman et al.

Moreover, reviewing the epidemiological studies shows lack of consistent evidence to support the cancer concerns regarding the exposure to low levels of diagnostic X-rays(4). While, the ICRP-recommended annual effective dose limit for radiation workers is 20 mSv, effective dose in some high background radiation areas is up to 260 mSv/y (13 times higher than the limit for occupational exposures)(5, 6). In spite of this, exposure to these elevated levels of natural radiation has not increased the risk of either acute effects or cancer “Background radiation has never been shown to unequivocally cause acute or latent disease, such as cancer (Hall and Ciaccia 2005)” (7). Moreover, there are reports showing reduced cancer rates in the residents of areas with elevated levels of natural radiation “Reduced cancer occurrence was reported since decades ago for HBRAs (Frigerio et al. 1973, Cohen 1995, Aliyu and Ramli 2015, Mortazavi et al. 2005, Nair et al. 2009, Sun et al. 2000)”(7). Therefore, if exposure of humans to radiation doses of a few hundred mSv per year is detrimental to their health causing increased risk of cancer, it should be evident in these people. In spite of this, nearly all residents still live in their paternal dwellings and there are not consistent reports on any detrimental effects(8, 9).

References:
1. Smith-Bindman R, Wang Y, Chu P, Chung R, Einstein AJ, Balcombe J, et al. International variation in radiation dose for computed tomography examinations: prospective cohort study. Bmj. 2019;2(364).
2. Bruce A, Johnson A, Lewis J, Raff M, Roberts K, Walter P. Molecular Biology of the Cell 5th edn (New York: Garland Science). 2007.
3. McConkey EH. How the human genome works: Jones & Bartlett Learning; 2004.
4. Bevelacqua JJ, Welsh J, Mortazavi SMJ, Doss M. Comments on “Radiation induced breast cancer risk in BRCA mutation carriers from low-dose radiological exposures: a systematic review”. Radioprotection. 2017;53(1):67-8.
5. Ghiassi-Nejad M, Mortazavi SMJ, Cameron JR, Niroomand-Rad A, Karam PA. Very high background radiation areas of Ramsar, Iran: Preliminary biological studies. Health Physics. 2002;82(1):87-93.
6. Mortazavi SMJ, Karam PA. Apparent lack of radiation susceptibility among residents of the high background radiation area in Ramsar, Iran: can we relax our standards? 2005. p. 1141-7.
7. Dobrzyński L, Fornalski KW, Feinendegen LE. Cancer mortality among people living in areas with various levels of natural background radiation. Dose-Response. 2015;13(3):1559325815592391.
8. Mortazavi SMJ, Mozdarani H. Non-linear phenomena in biological findings of the residents of high background radiation areas of Ramsar. International Journal of Radiation Research. 2013;11(1):3-9.
9. Mortazavi SMJ, Mozdarani H. Is it time to shed some light on the black box of health policies regarding the inhabitants of the high background radiation areas of ramsar? International Journal of Radiation Research. 2012;10(3-4):111-6.

Competing interests: No competing interests

11 January 2019
SMJ Mortazavi
Scientist
Fox Chase Cancer Center
333 Cottman Avenue Philadelphia, PA 19111 United States