Effective doses and risks from medical diagnostic x-ray examinations for male and female patients from childhood to old age

The UK Ionising Radiation (Medical Exposure) Regulations (DHSC 2018), and equivalent legislation in other countries, require the justification of all medical exposures to ionising radiation, taking account of the characteristics of the individual patient, to demonstrate that the clinical benefits of exposure outweigh any risks. Effective dose, E, is commonly and increasingly used in medical practice as a measure of risk to health from radiation exposure, although it was not designed for this application. The primary purpose of effective dose, as defined by the International Commission on Radiological Protection (ICRP 2007), has been the quantification of radiation exposures of workers and members of the public in order to demonstrate compliance with dose limits and to optimise protection against stochastic health effects following low-level exposure (i.e. low doses or low dose-rates), principally cancer (ICRP 1991, 2007, 2021, 2022). For this purpose, the requirement has been for a single quantity appropriately representing the (weighted) summation of organ/tissue-specific absorbed doses from each source of radiation, which is applicable to all workers or all members of the public.

In its application in medicine in the justification of procedures for individual patients, and the understanding and communication of risks, the use of effective dose has two main deficiencies.

The first shortcoming is that the calculation of effective dose involves sex-averaging of organ/tissue doses calculated using male and female reference phantoms of the human body. The use of reference phantoms is a positive step in the provision by ICRP of reference effective dose coefficients, but these calculations do not take account of differences between individuals in body and organ/tissue masses and dimensions. Sex-averaging of organ/tissue doses is also clearly not intended to provide estimates of dose to specific individuals. Second, effective dose is calculated using tissue weighting factors based on sex- and age-at-exposure-averaged risks of cancer and heritable effects. These stochastic risks, as well as being sex- and age-averaged, are calculated using cancer incidence risk estimates that are averaged over two fixed composite (Asian and Euro-American) populations, as representing the global population. The values obtained do not apply to any one particular population group and also, importantly, do not show recognised differences in risks between males and females and by age-at-exposure (ICRP 2021).

This paper applies the cancer risk models used by ICRP (2007) to calculate stochastic detriment values following low-level exposure to radiation, but presents lifetime excess cancer incidence predictions to show the differences in risk estimates between males and females, between children and adults as a function of age-at-exposure, and between the two composite populations. Cancer risks are estimated for a range of diagnostic x-ray examinations and expressed as lifetime excess cancer incidence risk per effective dose for each procedure, using organ/tissue-specific risk models and organ/tissue-specific absorbed doses. Diagnostic procedures target specific organs/tissues and hence result in a highly heterogeneous distribution of absorbed doses between organs/tissues. The total risk resulting from the exposure depends on the sensitivity of the organs/tissues receiving the highest doses, and this sensitivity will vary with sex, age-at-exposure and population group.

2.1. ICRP risk models

The cancer risk models developed by ICRP for application in its 2007 Recommendations are based primarily on cancer incidence data from the life span study (LSS) of the Japanese atomic bomb survivors, with follow up from 1958 to 1998 for solid cancers and from 1950 to 2000 for leukaemia (ICRP 2007, 2022, Cléro et al 2019, 2022, Ban et al 2022). Models based on the excess absolute risk (EAR, the additional risk due to the exposure) and excess relative risk (ERR, the proportional increase in risk compared to the background risk) were developed that related EAR and ERR to organ/tissue-specific absorbed dose using the DS02 dosimetry system for the following ten specific organs/tissues: female breast, lung, stomach, colon, red bone marrow (RBM), bladder, liver, thyroid, oesophagus and ovary. The nominal risk estimates from the 1990 Recommendations (ICRP 1991) were used for bone and (non-melanoma) skin cancers because LSS data for these cancers offered only a limited opportunity for the derivation of risk models (ICRP 2007, 2022, Cléro et al 2019, Ban et al 2022). EAR and ERR models were developed from the LSS incidence data for the remaining solid cancers considered as a single group; risk estimates were not derived for the lymphomas or multiple myeloma, for which evidence of any radiation-related risk is limited. For solid cancers, the models are linear, no-threshold dose-responses, allowing for risk modification by sex, age-at-exposure and attained age. For leukaemia following irradiation of RBM, ICRP (2007) used an EAR model with an explicit linear-quadratic dose-response that allowed for the modifying effects of sex, age-at-exposure and time-since-exposure, similar to that described by Preston et al (1994); ERR estimates were derived from this EAR model using the LSS background leukaemia incidence rates (Cléro et al 2019, 2022, ICRP 2022, Ban et al 2022). Minimum latency periods were set at two years for leukaemia and five years for solid cancers (Cléro et al 2019) (although it later transpired that the latency period used for leukaemia was actually five years (Cléro et al 2022)).

EAR and ERR models lead to similar predictions of the excess risks of cancer in the population that was used to derive the risk models, but they can lead to markedly different excess risk estimates when applied to other populations with different baseline cancer rates. ICRP (2007) used baseline cancer incidence rates for two fixed composite populations (based on populations with well-established cancer registries) defined by averaging, respectively, Asian (Shanghai, Osaka, Hiroshima and Nagasaki) and Euro-American (Sweden, UK and USA) populations for specific periods; leukaemia baseline incidence rates excluded chronic lymphocytic leukaemia (CLL, now considered to be a form of non-Hodgkin lymphoma) (Cléro et al 2019). Age-averaged lifetime cancer incidence risks were calculated for each composite population and sex by applying the EAR and ERR models to the databases using a single dose of 100 mGy of low-LET radiation delivered to each organ/tissue, and a weighted average of the model estimates was then computed. The relative weights given to the EAR and ERR models varied for the different cancer sites, based on judgements concerning their relative applicability for risk transfer, as follows: EAR:ERR of 0.0:1.0 for thyroid and skin, 1.0:0.0 for breast and bone, 0.7:0.3 for lung, and 0.5:0.5 for all other cancers. For solid cancers, ICRP (2007) applied a dose and dose rate effectiveness factor (DDREF) of 2 to reduce risk estimates for normal applications at low doses (<∼100 mGy) or low dose rates (<∼5 mGy h−1) 4 to organs and tissues, but no DDREF was used for leukaemia. The resulting lifetime risk estimates were further averaged over composite population and sex to produce final nominal risk coefficients consisting of sex-, age-, population- and model-averaged (weighted as appropriate) lifetime excess absolute risks of cancer incidence (LEAR, the EAR of cancer incidence over the remaining lifetime) per Gy for the ten sites, and one grouping of sites (other solid), of cancer; nominal risk coefficients were additionally presented for bone and skin cancers (ICRP 2007). Details may be found in Cléro et al (2019, 2022), Ban et al (2022) and ICRP Publication 152 (ICRP 2022). ICRP (2007) defines 'nominal' in this context as 'sex-averaged and age-at-exposure-averaged lifetime risk estimates for a representative population'.

Detriment (to health) was calculated by ICRP (2007) from these values of the nominal LEAR of cancer incidence per Gy by adjusting for severity of each cancer type, applying weighting factors for lethality, morbidity associated with non-fatal cancers, and years of life lost. As discussed by Cléro et al (2019), Ban et al (2022) and ICRP (2022), these severity weighting factors were broad evaluations of available data, which involved expert judgement in interpreting limited data for the purpose of these adjustments; for example, lethality fractions were those that had been used for the ICRP 1990 Recommendations (ICRP 1991) and did not vary between the sexes or change when children and the elderly were removed from the age-at-exposure averaging (ICRP 2007). Total cancer detriment was obtained by summing the detriment values for each cancer site. Estimated risks of heritable effects from irradiation of the gonads, derived from animal experiments and knowledge of human genetics, were similarly averaged to derive a nominal value of LEAR per Gy, which was severity weighted to provide a detriment value that was then added to the cancer detriment to provide the overall detriment for stochastic health effects. Tissue weighting factors, wT, are simplified values chosen to represent relative detriment from each organ/tissue when averaged over both sexes and all ages. For simplicity, only four different values of wT are used: 0.12, 0.06, 0.04 and 0.01, and ΣwT = 1 when summed over all tissues.

Note that, while nominal risk coefficients are calculated as LEAR per Gy absorbed dose to organs/tissues for the effect resulting from this irradiation, the nominal risk coefficients presented by ICRP (2007) are expressed as LEAR per Sv effective dose by convention as the basis for the use of this protection quantity. Similarly, the detriment is expressed per effective dose. Two overall detriment values were presented in ICRP Publication 103: 5.7 × 10−2 Sv−1 effective dose for the whole population (both sexes, all ages), and 4.2 × 10−2 Sv−1 effective dose for a working age population (both sexes and 18–64 yr age-at-exposure). Cancer detriment, for a uniform exposure, dominates at 5.5 × 10−2 Sv−1 and 4.1 × 10−2 Sv−1, respectively.

2.2. Application of ICRP models

Wall et al (2011) constructed 11 cancer EAR and ERR models from the appropriate LSS cancer incidence data, following the methodology described in ICRP Publication 103 (ICRP 2007) as closely as possible, although later information on this methodology has revealed various aspects of the description provided in Publication 103 that require revision (Cléro et al 2019, 2022, ICRP 2022, Ban et al 2022). The LEAR of cancer incidence estimates were calculated for each organ/tissue receiving a uniform absorbed dose of 10 mGy of low-LET radiation. Comparison of the results of applying the models of Wall et al (2011) with equivalent results presented in Publication 103 show good agreement for most cancer types. However, discrepancies were observed for thyroid cancer (−42%) and leukaemia (+50%), and less so for female breast cancer (−13%), which were largely unexplained (Wall et al 2011), although the differences have, at least in part, been clarified by further elucidation of what was done to derive the ICRP models (Cléro et al 2019, 2022, ICRP 2022, Ban et al 2022). Despite these differences, the overall LEAR of cancer incidence (excluding bone and skin cancers) was calculated by Wall et al (2011) as 665 × 10−4 Gy−1, (i.e. 665 cases per 10 000 persons per Gy) compared with a value of 688 × 10−4 Gy−1 presented in Publication 103 (ICRP 2007), results that are within 3% of each other, which is good overall agreement.

In ICRP Publication 103 (ICRP 2007, Cléro et al 2019) LEAR estimates of cancer incidence were calculated using the measure, risk of exposure-induced cancer (REIC) (Thomas et al 1992), which was also the measure used by Wall et al (2011). ICRP Publication 147 (ICRP 2021) presented results for the LEAR of cancer incidence measured as the lifetime attributable risk (LAR), and LAR is also used in this paper, although the difference between the REIC and LAR estimates are generally small, as noted later.

Table 1 shows results obtained for lifetime EARs of cancer incidence calculated as LAR, considering 11 different cancer types: female breast, lung, stomach, colon, bladder, liver, thyroid, oesophagus, ovary, non-CLL leukaemia, and all other solid cancer sites as a single grouping, excluding skin and bone cancers. The cumulative EAR of cancer incidence per organ/tissue absorbed dose up to an attained age of 100 years was calculated separately for males and females and by category of age-at-exposure (ten age-at-exposure 10 yr groups, from 0–9 yr to 90–99 yr). Calculations were performed for the ICRP Euro-American composite population. The equivalent results using REIC as a measure of LEAR are shown in table S1, and are similar to those shown in table 1.

Table 1. Estimates of lifetime attributable risk (LAR) of cancer incidence per organ/tissue absorbed dose (×10−4 Gy−1) from uniform whole-body exposure to low-LET radiation for the ICRP (2007) Euro-American composite population, by organ/tissue, sex and age-at-exposure using ICRP (2007) risk models (adapted, with permission, from ICRP Publication 147 (ICRP 2021), table 2.4). Cancer incidence excludes cancers of the skin and bone. Calculations performed with a uniform whole-body dose of 10 mGy of low-LET radiation.

 Lifetime attributable risk (LAR) of cancer incidence per organ/tissue absorbed dose (×10−4 Gy−1)a Age at exposure (years)Organ/tissue0–910–1920–2930–3940–4950–5960–6970–7980–8990–99 Males Lung7070708080806040203Stomach100806040302010520Colon160130110806040201040RBM13013080707040301072Bladder908070605030201051Liver6050403020106310Thyroid402063100000Oesophagus10101010101010851Other solid4903202401409050301030 All above organs/tissues 1150 880 680 500 400 290 190 100 40 8 Females Breast670410250150804020720Lung150160170180190190160110506Stomach170130100705030201050Colon80705040302010830RBM505050405030201041Bladder8070605040403020101Liver30202010964210Thyroid190803010410000Oesophagus1010101010202020203Ovary6040302020106310Other solid3702501701208050301050 All above organs/tissues 1850 1300 940 710 570 440 320 210 100 10

RBM = Red bone marrow.Risks are calculated using EAR and ERR models and applying a DDREF of 2 for all cancer types other than leukaemia, and with ERR/EAR weightings of 1/0 for thyroid, 0.3/0.7 for lung, 0/1 for breast, 0.5/0.5 for all other cancers. Minimum latency periods applied were two years for leukaemia and five years for solid cancers. a cases per 10 000 persons per Gy.

The LAR values presented in table 1 show, when taking the 30–39 yr age-at-exposure group as a reference, LAR estimates about two to three times higher in the youngest group (0–9 yr at exposure) and about two to three times lower at an age-at-exposure of 60–69 yr. A very similar pattern of results is obtained using the ICRP Asian composite population, as illustrated in figure 1, which shows the variation of the LAR of cancer incidence by sex and age-at-exposure for Euro-American and Asian composite populations.

Figure 1. Variation of the lifetime attributable risk (LAR) of cancer incidence (×10−4 Gy−1) with sex, age-at-exposure and ICRP (2007) Asian and Euro-American composite population following a uniform absorbed dose of 10 mGy of low-LET radiation to all organs/tissues of the body. Cancer incidence excludes cancers of the skin and bone. Plots are based, with permission, upon results presented in ICRP Publication 147 ((ICRP 2021), tables 2.4 and 2.5) using the risk models and associated assumptions of ICRP Publication 103 (ICRP 2007).

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However, the results show substantial differences between cancer types (table 1), as illustrated in figure 2 for lung and thyroid cancers. While the LAR of cancer incidence values for most cancer types are greatest at younger ages at exposure, this tendency is more pronounced for some (e.g. thyroid cancer) than others (e.g. oesophageal cancer); lung cancer is a notable exception for which risks peak for exposures in middle age (UNSCEAR 2013, Cahoon et al 2017). Because of these variations, the contribution of the different cancer types to overall lifetime risk varies substantially with age-at-exposure as well as between males and females, and the sex-specific differences in LAR estimates are particularly notable for lung and thyroid cancers. Note that variations with age-at-exposure reflect cumulative lifetime risks of cancer incidence, so that reduction of risk with increasing age-at-exposure reflects mainly the reduction in remaining lifetime after exposure during which the risk may be expressed rather than a variation of sensitivity with age-at-exposure, although the latter variation also plays a role, especially in combination with a decrease in risk with time-since-exposure (UNSCEAR 2013).

Figure 2. Lifetime attributable risk (LAR) of cancer incidence per organ/tissue absorbed dose (×10−4 Gy−1) from uniform exposure to low-LET radiation for the ICRP (2007) Euro-American composite population for lung and thyroid cancer incidence for females and males by age-at-exposure (from table 1). Calculations performed with the ICRP (2007) risk models and organ/tissue doses of 10 mGy. Adapted, with permission, from ICRP Publication 147 (ICRP 2021), figure 2.1.

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Effective dose, as currently defined, is calculated in reference male and female phantoms of specific ages: newborn, ages 1, 5, 10 and 15 yr, and adult (ICRP 2007, 2020, 2021). Absorbed doses and equivalent doses to organs and tissues are calculated separately for males and females and then sex-averaged for the calculation of effective dose. The final stage in the calculation of effective dose, E, is the weighted averaging of organ/tissue equivalent doses: $E = \mathop \sum \nolimits_} }}}}$, where HT is the equivalent dose to tissue T and wT is the corresponding tissue weighting factor. Effective dose calculated with each of the phantom male and female combinations relates to the two stochastic detriment values of 574 × 10−4 Sv−1 effective dose for the whole population and 422 × 10−4 Sv−1 effective dose for a working-age population (age-at-exposure, 18–64 yr).

While effective dose can be used to represent the overall dose received by a particular person from a particular exposure, which can be used for the purposes of radiological protection as intended by ICRP (2007), it clearly does not provide a measure that is specific to that individual, either in terms of total (whole-body) dose or of the related total risk. Nonetheless, effective dose is the reported quantity that allows comparisons of doses from different procedures in different clinical settings. The relationship between effective dose and risks and the quantification of risks using organ/tissue absorbed doses is discussed in other sections of this paper.

Effective dose from medical procedures is calculated using dose coefficients that relate measurable quantities to the protection quantity. ICRP has published dose coefficients for diagnostic procedures in nuclear medicine, but has not yet provided such reference dose coefficients for diagnostic x-ray imaging procedures. However, dose coefficients are available from published studies for the calculation of organ/tissue doses and effective doses from entrance surface air kerma (Ke) or kerma-area product (PKA) for radiography and fluoroscopy (Jones and Wall 1985, Hart et al 1994, Ranniko et al 1997, Kramer et al 2004), or the dose-length product (DLP) for computed tomography (CT) (Lee et al 2011, 2012, Wall et al 2011, Ding et al 2015, Shrimpton et al 2016).

Table 2 provides illustrative examples of effective dose estimates for diagnostic procedures. The highest effective doses for radiographic examinations are in the range of 0.1–1 mSv, while others are substantially lower. For example, table 3 summarises results from a review by Wall et al (2011) in which effective dose was calculated using ICRP (2007) methodology, showing that doses from radiographic procedures ranged from 0.1 µSv (knee, foot) to 0.4 mSv (lumbar spine, thoracic spine). Effective doses from examinations involving fluoroscopy and radiography were in the range of 1–4 mSv.

Table 2. Examples of typical effective doses (mSv) for adults in three countries for some common diagnostic x-ray examinations (adapted, with permission, from ICRP Publication 147, ICRP (2021), table 5.1).

Diagnostic procedureEffective dose (mSv)UKaUSAbRussian FederationcRadiography   Chest PA0.010.030.1Chest Lat0.040.070.18Lumbar spine AP0.392.00.6Lumbar spine Lat0.21—0.6Abdomen AP0.430.61.0Pelvis AP0.280.40.7Interventional   Coronary angiography3.91515Femoral angiography2.375–10Computed tomography   CT Head1.81.61.8CT Chest146.16.3CT Abdomen16—9CT Abdomen + Pelvis137.7 CT Chest + Abdomen + Pelvis191225Nuclear Medicine   Bone scan: 99mTc343PET whole-body tumour imaging (18F FDG)d7.6135

PA: postero-anterior; AP: antero-posterior; Lat: lateral; PET: positron emission tomography; FDG: fluorodeoxyglucose. a Wall et al (2011); Shrimpton et al (2016); ARSAC (2020). b Mettler et al (2008); Smith-Bindman et al (2015); Alessio et al (2015); Becker et al (2016); Kanal et al (2017); NCRP (2019). c Chipiga and Bernhardsson (2016); Vodovatov et al (2017); Zvonova et al (2015); Balonov et al (2018). d Doses are for PET tumour imaging from 18F only and do not include CT which is frequently performed with PET.

Table 3. Typical values of effective dose for adult patients from x-ray examinations involving radiography alone and with fluoroscopy. Adapted from Wall et al (2011), tables 7, 11 and 14, by kind permission of UK Health Security Agency.

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