Rad is the old and still used unit of absorbed dose. One gray is equivalent to rads. Equal doses of all types of ionizing radiation are not equally harmful to human tissue.
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Alpha particles produce greater harm than do beta particles, gamma rays and X-rays for a given absorbed dose, so 1 Gy of alpha radiation is more harmful than 1 Gy of beta radiation. To account for the way in which different types of radiation cause harm in tissue or an organ, radiation dose is expressed as equivalent dose in units of sievert Sv.
The dose in Sv is equal to the total external and internal "absorbed doses" multiplied by a "radiation weighting factor" W R - see Table 2 below and is important when measuring occupational exposures. Before, this weighting factor was referred to as Quality Factor QF. Equivalent dose is often referred to simply as "dose" in every day use of radiation terminology.
The old unit of "dose equivalent" or "dose" was rem. When a radioactive material gets in the body by inhalation or ingestion, the radiation dose constantly accumulates in an organ or a tissue. The total dose accumulated during the 50 years following the intake is called the committed dose. The quantity of committed dose depends on the amount of ingested radioactive material and the time it stays inside the body. The effective dose is the sum of weighted equivalent doses in all the organs and tissues of the body. Effective dose is measured in sieverts Sv.
Tissue weighting factors Table 4 represent relative sensitivity of organs for developing cancer. In Canada, the Radiation Protection Regulations set radiation exposure limits for the public and nuclear energy workers. The annual effective dose limit is 1mSv for the Canadian public. Based on information from regular monitoring of the most exposed workers, such as a radiographer, shows that the average annual doses are 5 mSv per year.
The main ways to control radiation exposure include engineering controls, administrative controls and personal protective equipment. Examples of these controls include:. Approximately forty-four 44 percent of monitored workers worldwide are exposed to artificial sources of radiation. Of those workers exposed to artificial sources, seventy-five percent work in the medical sector.
Table 5 shows trends in global radiological exposure of workers since the s. The effects of being exposed to large doses of radiation at one time acute exposure vary with the dose. Here are some examples:. In underground uranium mines, as well in some other mines, radiation exposure occurs mainly due to airborne radon gas and its solid short-lived decay products, called radon daughters or radon progeny. Radon daughters enter the body with the inhaled air. The alpha particle dose to the lungs depends on the concentration of radon gas and radon daughters in the air.
Such estimates of cancer and genetically heritable risk from x-ray exposure have a broad range of statistical uncertainty, and there is some scientific controversy regarding the effects from very low doses and dose rates as discussed below. To date, there is no evidence of genetically heritable risk in humans from exposure to x-rays. Under some rare circumstances of prolonged, high-dose exposure, x-rays can cause other adverse health effects, such as skin erythema reddening , skin tissue injury, and birth defects following in-utero exposure.
Because of the rapidly growing use of pediatric CT and the potential for increased radiation exposure to children undergoing these scans, special considerations should be applied when using pediatric CT. Among children who have undergone CT scans, approximately one-third have had at least three scans.
The quantity most relevant for assessing the risk of cancer detriment from a CT procedure is the "effective dose". The unit of measurement for effective dose is millisieverts abbreviated mSv. Effective dose allows for comparison of the risk estimates associated with partial or whole-body radiation exposures. It also incorporates the different radiation sensitivities of the various organs in the body. Radiation dose from CT procedures varies from patient to patient. The particular radiation dose will depend on the size of the body part examined, the type of procedure, and the type of CT equipment and its operation.
Typical values cited for radiation dose should be considered as estimates that cannot be precisely associated with any individual patient, examination, or type of CT system. The actual dose from a procedure could be two or three times larger or smaller than the estimates. Limitation of Exposure to Ionizing Radiation.
Because essentially no data from human populations are available to allow investigators to make direct estimates of risk from exposure to these types of radiation, or which address the factors influencing sources of uncertainty in risk estimation, such estimates are heavily dependent on data from other studies. Hence, both an adequate understanding of the relationships between RBE and particle type and energy, as well as information on dose response and dose rate effects derived from experimental studies are essential to understanding the cancer risks associated with deep-space travel.
Existing experimental data are inadequate. Even in animal systems, data on tumor induction following exposure to protons and heavy ions are sparse. Critical data on cellular responses to irradiation, required to support the use of laboratory animal tumor data for estimating risks to humans, are also lacking in many instances. Cell survival studies, while not directly applicable to estimation of cancer risks, do permit comparisons of the effectiveness of different types and levels of radiation and determination of the repairability of induced DNA damage.
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Cellular studies of the induction of somatic mutations and chromosomal aberrations provide data that can be linked fairly directly to carcinogenic effects. Such studies, particularly in human cell systems, are important for understanding possible mechanisms of carcinogenicity and in the appropriate application of animal data to the estimation of risks to humans.
As described in Chapter 1 , data for tumor induction following proton irradiation are available for only a few tumor types following acute exposure. The limited dose-response data that can be obtained from these studies suggest similarities to responses that would be seen after gamma ray irradiation. Cellular studies have been conducted using protons of different energies to examine cell survival and induction of chromosomal aberrations.
While most data tend to support the view that the risks for carcinogenic effects, as a result of irradiation by high-energy protons, will be similar to those for low-LET radiation, additional studies of protons in the. The purpose of such experiments would be to determine whether biological effects of exposure to these higher-energy protons are qualitatively similar to those seen with exposure to low-LET radiation and to determine whether repair of proton-induced DNA damage can be observed. Information on tumor induction following exposure to heavy ions is also limited.
Burns et al. However, because of the dominance of the dose-squared term concave upward in the low-LET dose response, the data do not allow for the estimation of a single RBE value that could be used in the determination of an appropriate weighting factor that is independent of dose. As stated previously, the determination of appropriate quality factors requires information on the relationship between LET and RBE for tumor induction.
The only systematic study of such relationships was conducted for the Harderian gland in mice. While not able to be used directly for the derivation of quality factors, studies of cells have provided evidence that for high-LET radiation, linear dose-response relationships are only slightly influenced by fractionation or protraction. Conclusions The present state of knowledge regarding cancer induction by irradiation, as described above, requires that additional research be directed in two areas. First, a pragmatic set of studies is needed to provide data necessary for the determination of appropriate quality factors that should be used in making risk calculations.
These should be systematic studies of RBE as a function of particle type and energy for a select number of heavy ions and for protons using well-defined animal models for tumorigenesis. In addition, information on dose rate and fractionation effects for protons is also needed. Improvements in risk estimates beyond those attainable with these data require a more complete understanding of the mechanisms of tumor induction and of principles that will aid in using data, from experimental systems subjected to relatively high radiation doses, to estimate effects on humans exposed to low, protracted doses and in estimating risks across populations.
These kinds of studies will require the development and exploration of new model systems and the application of developing technologies in cell and molecular biology. Outside Earth's magnetic field, the fluence rates of the GCR are at the maximum during solar minimum: about 4 protons per cm -2 s -1 , 0. The number of particles traversing cell nuclei depends, of course, on the size of the nucleus Figure 2.
Errors are estimated from total number of tumors. Extrapolations of rat skin tumor incidence: Dose, fractionation and linear energy transfer. Baverstock and J. Stather, eds. Taylor and Francis, London. Reprinted with permission from Taylor and Francis. The dependence of size of the nuclei of neurons on the probability of traversal of heavy charged particles in space.
The effect of space radiation on the nervous system. Space Res. Certainly, animals in experiments have been exposed to higher fluence rates than are likely to be encountered in space—and have not shown clinically detectable changes in the CNS. The main concern, however, is about HZE particles, particularly iron ions. The axons and dendrites of neurons are very radioresistant, and the cell nuclei, which do not undergo division in adult life, appear to be very resistant as well. They are not lost after irradiation in mitosis, as is usually the case with proliferating cells.
What is inadequately known is whether any functional capability is diminished and, in particular, whether effects such as decreased DNA repair occur late in life long after exposure. Lack of Data for Estimating Risks The reason for concern regarding the CNS is due to the fact that it cannot be stated with confidence what late effects, if any, might occur in the CNS of humans exposed to the various types of radiation in space such as heavy ions and secondaries of the more prevalent protons.
There is evidence that in photoreceptors iron ions cause an increased loss of DNA. Before investigators can conclude that the risks of late effects to the CNS are so improbable that they are not of concern, there have to be some data for relevant end points and doses.
Relative Radiation Sensitivities of Human Organ Systems
Effects of HZE Particles The concern about HZE particles is that the energy deposition may be significantly different from that of radiation qualities for which we have some radiobiological understanding. One particle of very high Z and energy can traverse a number of contiguous cells. There is very dense ionization in the inner part or core of the particle track, with secondary particles and delta rays extending to neighboring cells.
Although this pattern of potential damage raised concerns many years ago about the possibility of microlesions, the concerns have not yet been answered satisfactorily. While the lack of a solution to these concerns may seem surprising, the existence of the HZE particle component has been known only since , and biological research using heavy ions has been restricted to a very small number of centers in the world with suitable accelerators.
Furthermore, the critical experiments have proven difficult to carry out. The effects of HZE particles on the CNS include 1 cellular effects, including biochemical changes; 2 functional changes; and 3 late effects, especially DNA repair deficiencies. Cellular Effects High doses of low-LET radiation cause cellular changes and degeneration in neuronal tissues. Heavy ions are more effective in causing cellular damage, and the effects appear earlier than those appearing after exposure to low-LET radiation.
In studies of the forebrain of rabbits, damage could be detected after exposure to 0. For example, what is the effect of various radiation fluences on the centers in the floor of the fourth ventricle, the site of a number of centers including the cardiac and respiratory centers, in which there are closely packed neuron cell bodies? If traversal of neurons by the various HZE particles in the GCR does in fact result in early- or late-occurring damage, the fourth ventricle is an area of the brain that could be at risk there are also others. This example indicates how little we know about the potential effects of radiation on the CNS.
Without such information it is impossible to assess the potential risk of clinically important damage to the CNS that might result from crew members' exposure to radiation during long-duration missions in deep space. Doses in the range of 0. Taste aversion has long been used as a test of behavioral and other changes induced by irradiation, and studies indicate that iron ions are more effective than lower-LET radiation in altering this particular type of behavior. Late Effects, Especially Repair Deficiencies Because many of the experiments concerning heavy ions have been associated with end points relevant to radiotherapy, questions about the effects on nonrenewing cell systems, especially the CNS, have remained unanswered.
Differentiated cells such as those in the CNS or the liver can incur relatively large doses of radiation of different qualities and still retain their function. What is not known is whether untoward effects may appear later. The integrity of the transcribing regions of the genome must be reserved to ensure the fidelity of the RNA transcripts and also of the proteins, translated from RNA, that are necessary for the correct functioning of cells. Changes with age in the retinal DNA of rabbits after irradiation have been studied by Lett and his coworkers.
The age at which secondary changes in the DNA of the photoreceptor occurred decreased with an increase in the LET of the radiation. The secondary changes in the DNA occurred earlier and were more marked with iron ions than with other heavy charged particles or with photons. Significant effects were noted after exposure at 2 to 3 Gy of iron ion radiation. If it is assumed that the photoreceptors are a reasonable surrogate for neurons in the CNS, then the above results suggest that it is necessary to obtain adequate dose-response data using the most sensitive techniques for detecting DNA damage.
Furthermore, it is mandatory to determine whether or not breakdown of DNA, which is an indication of impending cell death, occurs many years after exposure to radiation. As yet, there are no complete data for RBE-LET relationships for the relevant end points for assessing the risk of radiation-induced damage. Cataracts are considered a hazard of exposure to radiation, and limits for exposure are set for terrestrial workers who deal with radiation sources.
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The limits are based on estimates from studies of humans exposed to low-LET radiation. There is considered to be a threshold dose below which lenticular opacities of clinical importance do not occur. For this reason, cataract induction is considered a deterministic effect. However, the threshold is more a matter of the level of detection capable of detecting the beginning of cataractogenesis, and the most likely mechanism is consistent with a stochastic effect.
Assessing the risk of cataractogenesis from irradiation in space, in particular in deep-space missions, requires a knowledge of the associated RBE values of the various types of radiation. There are no data for induction of cataracts in humans exposed to HZE particles, and only sparse data for induction by protons. Thus, reliance on data from animal experiments is necessary. The sensitivity of the lens of different species varies by more than an order of magnitude, decreasing with increasing size.
In humans, a threshold dose for low-LET radiation of about 2. For the atomic bomb survivors, a somewhat lower threshold dose, 1. Data from patients receiving radiotherapy or irradiation prior to bone marrow transplantation suggest a significant decrease, perhaps on the order of fivefold, in cataractogenic effects compared with the number induced by single high-dose-rate exposures. On the basis of experiments with rats, 69 no such sparing would be predicted for the effects of exposure to very high LET radiation.
Evidence from studies on monkeys indicates that the cataractogenic effect of protons will not be very different from that of gamma rays. The estimates of the risk of cataract induction from exposure to heavy ions are somewhat disparate, 71 , 72 and until more definitive estimates are in hand, relatively high RBE values should be used in calculating the equivalent doses for estimating risk. The great majority of data on the assessment of genetic or heritable effects in human populations following exposure to radiation has come from studies of the atomic bomb survivors.
The following end points have been assessed: untoward pregnancy outcomes major congenital malformation, stillbirth, neonatal death ; sex of child; tumors with onset prior to the age of 20; death of liveborn infants through an average age of There were no significant increases in any of these indicators from a combined parental gonadal equivalent dose of 0. A recent study by Kodaira et al. A similar result was reported by Satoh et al. UNSCEAR 76 made estimates of the unirradiated background incidence of mutational effects per generation for the end points studied on the acutely exposed Japanese population.
Allowing for chronic exposure, a gonadal dose reduction factor was applied to give a minimal estimated doubling dose of 4 Sv for genetic effects.
Hence the actual increase above background in heritable effects per locus, depending on the particular locus, and the risk of heritable effects to individuals engaged in extended space travel will be low. In addition, because the number of individuals who might be exposed to ionizing radiation during long-range spaceflight will represent a very small fraction of the population, any genetic risk to the human gene pool would be negligible. The rapid increase in knowledge of the mechanisms of tumor induction and heritable effects has led to a clear appreciation of the potential for a genetic predisposition to the induction of cancer by exogenous agents and endogenous processes and to induction of heritable changes.
Such a predisposition might be specific for a single agent such as ionizing radiation e. Given that within the normal human population a range of risk exists for induction of cancer, it is difficult at this time to assign a value for increased risk owing to a single genetic susceptibility. In general, most of the genetic susceptibility or sensitivity factors that are common in the population tend to increase relative risk by small amounts.
Those conferring high relative risk are present at a low frequency. The latter is particularly true for susceptibility for which background frequencies of cancer are high. It has become increasingly apparent that the sensitivity of cells to radiation is controlled in part by the relationship of DNA repair kinetics to cell cycle progression. The quintessential example is the gene p53, which is involved in cell cycle control at the G 1 checkpoint, the time point in the cell cycle at which DNA synthesis begins, and in the repair of DNA damage either directly or indirectly.
The question of interest then is, What kinds of genotypes might elicit increases in sensitivity to radiation? For example, it is apparent that control of the cell cycle is a very complex process involving in part the interactions of cyclins, cyclin-dependent kinases, and cyclin-dependent kinase inhibitors. Alterations in any of these components could lead to abrogation in the cell cycle control, which would lead to abnormal responses to DNA damage and an increased sensitivity to genetic alteration.
It remains of considerable importance to understand the mechanisms of genetic instability arising from abrogation of control at checkpoints in the cell cycle, and to determine the effects these mechanisms can have on radiosensitivity. Work in this area by the wider community of cancer investigators would lead to understanding of the role of genetic instability in cancer predisposition, and to development of assays for detecting individuals at increased risk.
While there will be a range of genotypes among individuals selected for long-range spaceflight, there is a very low probability that there will be highly sensitive individuals in the group. Very specific genotypes, such as those giving rise to ataxia telangiectasia and Li-Fraumeni syndrome, are obvious phenotypically, and such individuals would not constitute part of the selection pool.
More subtle individual differences in sensitivity to ionizing radiation would not be detectable phenotypically. It could be argued that a radiosensitivity assay G 2 sensitivity such as that described by Scott et al. However, such an assay is not, at present, directly predictive of an increased sensitivity to an adverse health outcome.
Hence, it is appreciated by cancer investigators that a more complete assessment of the G 2 sensitivity assay needs to be conducted in order to establish its range of sensitivity and possible predictive capability for cancer or heritable effects. The repair mechanisms utilized by the human body after exposure to radiation are an important part of any discussion of radiation effects, and the repair of damage to DNA is of obvious interest when considering late effects such as cancer.
It has been known for a number of years that sophisticated and complex cellular processes exist for repairing all types of DNA damage: single-strand breaks, double-strand breaks, and a wide variety of types of base damage, all of which can result from exposure to radiation. In the past 5 years, the repair processes for handling DNA damage have been largely characterized at the molecular level, and their complexity has been established. It is interesting to note that several of the repair processes are modifications of the functions of other cellular housekeeping proteins, such as transcription complexes or cell cycle control genes.
The very specific incisions required for removal of DNA damage are produced by enzymes of this complex. Reviews by Wood et al. While the actual process of excising damaged nucleotides by NER is quite well worked out, the cellular control and damage recognition processes are still the subject of extensive research efforts. More recently, an understanding of repair of DNA damage induced by ionizing radiation has emerged. Two recent reviews, one on the repair of oxidative damage 86 and a second on double-strand break repair, 87 describe the current level of knowledge.
The enzymology of repair of some damaged bases and sugars has been quite thoroughly described in bacterial systems and to a lesser extent in S. In broad terms, the process of base and sugar damage repair involves damage recognition, base excision of purine or pyrimidines, site incision, and fragment release. Clearly, variations in efficiency among cell types or species, or within a population, can occur at any one of these steps, each of which is under genetic control.
Books by John T. Lett (Author of Advances in Radiation Biology, Volume 4)
At this time, however, no human syndrome has been identified that results in a sensitivity to ionizing radiation attributable to a deficiency in the repair of oxidative damage. The understanding of the mechanism of repair of DNA double-strand breaks has taken several significant steps forward recently. Studies have demonstrated that there is a close association between the repair of site-specific double-strand breaks introduced during V D J recombination and those generated by DNA-damaging agents.
It has been shown that several radiosensitive mammalian mutants are defective in Ku80, that cells from severe combined immunodeficient scid mice have a DNA repair defect, and that additional radiosensitive cell lines have a deficiency in DNA-PK cs. It has been suggested that there could be a link between double-strand break repair machinery and transcription, as has been described for NER. To date, no human syndromes that are characterized by defects in DNA-PK have been identified, although the DNA-PK cs gene maps to the same human chromosome region as the one for the human gene that complements scid.
A good deal has been learned about repair mechanisms by studying the human syndrome ataxia telangiectasia AT , which is characterized by a sensitivity to cell killing and mutation induction in cells in vitro as a result of exposure to low-LET x rays, and, in some cases, by a loss of x-ray-induced inhibition of initiation of DNA synthesis. It was presumed by investigators that these phenotypes were the consequence of a DNA repair defect, and that different steps or components were controlled by genes in the four different complementation groups, all of which map to a single chromosome region.
However, the recent cloning of the AT mutated gene ATM 97 and additional characterization of homologous genes in yeast 98 , 99 have shown that the defect in AT cells is not the result of a repair defect but results from an altered cell cycle control, and perhaps an inability to activate damage-inducible DNA repair. The radiosensitivity and cancer susceptibility of ATM homozygotes are well established and very clear-cut. On the other hand, whether or not there is increased sensitivity in ATM heterozygotes is less clear. It has been reported that there is an increased breast cancer risk for ATM heterozygotes, although this remains equivocal.
Recently, Scott et al. Thus, heterozygosity for DNA repair genes, where the phenotype is not immediately apparent, could be a marker for susceptibility to cancer, particularly following exposure to ionizing radiation. It is expected that screening for ATM heterozygosity will soon be possible based on recent reports of the genomic organization and gene sequence. A growing understanding of the various mechanisms of repair of ionizing radiation-induced DNA damage, and of the effects of mutations in genes involved in the repair itself or in its control, is likely to greatly aid in predicting the risk of adverse biological effects arising from exposure to radiation, and eventually in identifying individuals at increased risk.
Over many years, NASA maintained only a very small radiation health program because of the responsibility, mandated to the Department of Energy DOE and its predecessors, for radiation studies. Recently, the funding for NASA radiation research has increased. However, although the percentage increase in funding has been large, the budget in years past was small. Moreover, DOE has significantly reduced its funding for radiation studies in the last few years. Major radiation and animal facilities have been closed, including the high-LET radiation sources for experimental studies at Oak Ridge and Argonne national laboratories.
DOE funding of the important facility at Columbia University has been terminated, and the future of the radiation facilities at the Armed Forces Radiobiology Research Institute is now threatened. BEVALAC, the only facility in the United States that was producing beams of heavy ion spectra of energy and LET suitable for cellular and animal studies, as well as for investigations of fragmentation and aspects important for dosimetry, was closed by DOE in As noted by several previous advisory groups see, for example, Appendix D , this closure has had very serious consequences for efforts to estimate risks from exposure to radiation in deep space.
Two accelerators, one in Germany and one in Japan, have been developed for heavy ion radiotherapy see Appendix C and could be of use in the NASA program. There is no question that international collaboration involving accelerators with guarantees of appropriate particles and beam time , personnel to operate and use the facilities , and the necessary financial commitments would be of help in carrying out the priority experiments outlined in Chapter 4.
The present U. At this rate of utilization, it would take more than 20 years to obtain the physical and biological data needed to make rational decisions about the shielding needed to protect space crews from the biological effects of radiation in space see Chapter 4. Collaborative efforts cannot involve transfer of animals among international sites because of strict national quarantine restrictions aimed at reducing the spread of potentially hazardous microorganisms and viruses.
Moreover, the travel of animals over a number of time zones would force a resetting of their biological clocks, during which time they would be physiologically and psychologically altered and not useful for controlled experiments. Hence, a requirement for international efforts is the establishment of identical animal colonies at international sites so as to eliminate scientific and legalistic impediments and any effects of biological variability in experimental results.
All animal colonies, for example, would have to conform to international accreditation standards, and animal experiments would have to be approved by local institutional review boards and by the board of a collaborating investigator's institution. Lemaignen, L. Document No. DDT Simonsen, L. Temporal analysis of the October proton flare using computerized anatomical models. Curtis, S. Risk cross sections and their application to risk estimation in the galactic cosmic-ray environment. Badhwar, G. Galactic cosmic radiation model and its applications.
Guidance on Radiation Received in Space Activities. Conklin, J.