Radiation biology for pediatric radiologists
Eric Hall2009, Pediatric Radiology
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Abstract
The biological effects of radiation result primarily from damage to DNA. There are three effects of concern to the radiologist that determine the need for radiation protection and the dose principle of ALARA (As Low As Reasonably Achievable). (1) Heritable effects. These were thought to be most important in the 1950s, but concern has declined in recent years. The current ICRP risk estimate is very small at 0.2%/Sv. (2) Effects on the developing embryo and fetus include weight retardation, congenital anomalies, microcephaly and mental retardation. During the sensitive period of 8 to 15 weeks of gestation, the risk estimate for mental retardation is very high at 40%/Sv, but because it is a deterministic effect, there is likely to be a threshold of about 200 mSv. (3) Carcinogenesis is considered to be the most important consequence of low doses of radiation, with a risk of fatal cancer of about 5%/Sv, and is therefore of most concern in radiology. Our knowledge of radiation carcinogenesis comes principally from the 60-year study of the A-bomb survivors. The use of radiation for diagnostic purposes has increased dramatically in recent years. The annual collective population dose has increased by 750% since 1980 to 930,000 person Sv. One of the principal reasons is the burgeoning use of CT scans. In 2006, more than 60 million CT scans were performed in the U.S., with about 6 million of them in children. As a rule of thumb, an abdominal CT scan in a 1-year-old child results in a life-time mortality risk of about one in a thousand. While the risk to the individual is small and acceptable when the scan is clinically justified, even a small risk when multiplied by an increasingly large number is likely to produce a significant public health concern. It is for this reason that every effort should be made to reduce the doses associated with procedures such as CT scans, particularly in children, in the spirit of ALARA.
Figures (15)
![Fig. 1 Direct and indirect actions of radiation. The structure of DNA is shown schematically. In direct action, a secondary electron resulting from absorption of an X-ray photon interacts with the DNA to produce an effect. In indirect action, the secondary electron interacts with, for example, a water molecule to produce a hydroxyl radical (OH:), which in turn produces the damage to the DNA. The DNA helix has a diameter of about 20 A (2 nm). It is estimated that free radicals produced in a cylinder with a diameter double that of the DNA helix can affect the DNA. Indirect action is dominant for sparsely ionizing radiation, such as X-rays. S sugar, P phosphorus, A adenine, T thymine, G guanine, C cytosine (Adapted from [1])](https://figures.academia-assets.com/46913527/figure_001.jpg)
![Fig. 6 Incidence of abnormalities and of prenatal and neonatal death in mice given a dose of 200 rad of X-rays at various times after fertilization. The lower scale consists of Rugh’s estimates of the equivalent stages for the human embryo. (Data from [2]) Congenital abnormalities occur as a consequence of irradiation during organogenesis, which in the human is the period from 10 days to 6 weeks of gestation. Figure 6 illustrates the results of an experiment in which mice were exposed to a large radiation dose at various stages of gestation [2]. During pre-implantation, the principal effect of radiation is death of the newly fertilized egg, i.e. prenatal](https://figures.academia-assets.com/46913527/figure_006.jpg)
![Fig. 7 The frequency of mental retardation as a function of dose among those exposed in utero to atomic-bomb radiation. The data are pooled from Hiroshima and Nagasaki for those exposed at 8 to 15 weeks’ gestational age. The vertical bars represent the 90% confidence intervals. There was not risk at 0 to 8 weeks after conception, and for exposure at later periods during gestation (16+ weeks), the excess is barely significant, even at the higher doses (Adapted from [3])](https://figures.academia-assets.com/46913527/figure_007.jpg)
![Fig. 8 Estimated relative risks for cancer rates in A-bomb survivors during the 1958-1994 follow-up period relative to unexposed individuals. The dashed curve represents + 1 standard error for the smoothed curve. The inset shows data over the whole dose range 0 to 2 Sv (0-200 rem), to which a straight line is fitted, i.e., relative risk is proportional to dose, with no threshold. The main figure is an expanded version of the low-dose region up to 0.5 Sv (500 rem). The straight line is taken from the inset data for the whole dose range. There is a suggestion that low-dose risks are above the line. (Reprinted with permission from [5]) Figure 8 shows the excess relative risk of fatal cancer in the A-bomb survivors as a function of dose [5]. The top line shows the relationship for doses over the whole range of dose up to 2 1/2 Sv. It is evident that the data are fitted quite well by a straight line, i.e. there is a linear relationship between relative risk and dose. The lower line shows in more detail the data up to a dose of 0.5 Sv. There is a suggestion that the data points fall slightly above the straight line extrapolated from high doses, but the differ- ence is barely significant. Figure 9 shows some of the most valuable data gleaned from the A-bomb survivors, namely](https://figures.academia-assets.com/46913527/figure_009.jpg)
![Fig. 10 The attributable lifetime risk from a single small dose of radiation at various ages at the time of exposure. Note the dramatic decrease in radiosensitivity with age. The higher risk for the younger age-groups is not expressed until late in life. These estimates are based on a relative risk model and on a dose and dose-rate effectiveness factor (DDREF) of 2. (Adapted from [6]) the site-specific radiation-induced cancer risk estimates for the principal radiogenic tissues in the body, including the bladder, the breast, lung, thyroid, colon and stomach. Figure 10 [6] shows dramatically the fact that is of considerable interest to the Society of Pediatric Radiolog- ists, namely that lifetime attributable risk of radiation- induced cancer varies dramatically with age at the time of exposure. Although the average risk for the whole population is about 5%/Sv, this rises to 15%/Sv in a young](https://figures.academia-assets.com/46913527/figure_010.jpg)
![Fig. 14 Estimated age-dependent, gender-averaged percentage life- time radiation-attributable cancer risks from a typical single CT scan of the head. The methodology used is summarized in the text. The risks are highly age-dependent, both because the doses are age- dependent and because the risks per unit dose are age-dependent (Adapted from [10]) As arule of thumb, an abdominal CT scan in a 1-year- old child results in a lifetime cancer mortality risk of about one in 1,000. Life is a risky business, and in 1983 the Royal Society published an interesting commentary on risk. It pointed out that risks of one in a million or less tend to be ignored and are quite acceptable in everyday life. This](https://figures.academia-assets.com/46913527/figure_013.jpg)
