Carcinogenic Effects Of Radiation Research Articles

Thyroid Cancer in Regions Most Contaminated after the Chernobyl Disaster.

Exposure to ionizing radiation, especially during childhood, is a well-established risk factor for thyroid cancer. Following the 1986 Chernobyl nuclear power plant accident the total number of cases of thyroid cancer registered between 1991 and 2015 in males and females who were less than 18 years old exceeded 19,000 (in Belarus and Ukraine, and in the most contaminated oblasts of the Russian Federation). However, as indicated by the United Nations Scientific Committee on the Effects of Atomic Radiation the fraction of the incidence of thyroid cancer attributable to radiation exposure among the non-evacuated residents of the contaminated regions of Belarus, Ukraine and Russia is of the order of 0.25. Apparently, the increased registration of thyroid neoplasms in the parts of these countries is a classical 'screening effect', i.e., massive diagnostic examinations of the risk-aware populations performed with modern eqipment resulting in detection of many occult neoplasms (incidentalomas). Moreover, one type of thyroid cancer previously called 'encapsulated follicular variant of papillary thyroid carcinoma' is non-invasive and instead of 'carcinoma' should now be recognized as 'noninvasive follicular thyroid neoplasm with papillary-like nuclear features.' Other potential causes of overdiagnosing of thyroid tumors include increase of the spontaneous incidence rate of this disease with age, iodine deficiency among children from Belarus, Russia and Ukraine, and/or consumption by these children of drinking water containing high levels of nitrates that likely coincides with the carcinogenic effect of radiation on the thyroid gland.

More Evidence That Low-Dose Ionizing Radiation Is Associated with Increased Cancer

Concerns about the carcinogenic effects of radiation are largely based on data from atomic bomb survivors, and the effects of ionizing radiation used

A Mechanistic Model for Medulloblastoma Induction in Mice

Medulloblastomas in Patched heterozygous mice (Ptc1(+/-) mice) are induced with high probability by ionizing radiation applied in the immediate post-natal period. A mathematical model is described here that accommodates the dependence of the medulloblastoma incidence on dose, age at exposure and age. The model assumes that the first step in the development of the cancer is already present in all cells of the patched mouse due to germ-line inactivation of one allele of the patched tumor suppressor gene. The subsequent rate-limiting step is dependent linearly on dose at least up to 3 Gy. The observed strong decrease in carcinogenic effect of radiation between exposure on day 1 and day 10 is described by a physiological elimination of target cells during post-natal maturation of the brain. A single malignant cell develops into a tumor following a gamma-distribution with mean of about 160 days. The multiplicity of medulloblastomas is predicted.

Assessment of the risk for developing a second malignancy from scattered and secondary radiation in radiation therapy.

With the average age of radiation therapy patients decreasing and the advent of more complex treatment options comes the concern that the incidences of radiation-induced cancer might increase in the future. The carcinogenic effects of radiation are not well understood for the entire dose range experienced in radiation therapy. Longer epidemiologic studies are needed to improve current risk models and reduce uncertainties of current risk model parameters. On the other hand, risk estimations are needed today to judge the risks versus benefits of modern radiation therapy techniques. This paper describes the current state-of-the-art in risk modeling for radiation-induced malignancies in radiation therapy, distinguishing between two volumes: first, the organs within the main radiation field receiving low or intermediate doses (typically between 0.1 and 50 Gy); and second, the organs far away from the treatment volume receiving low doses mainly due to scattered and secondary radiation (typically below 0.1 Gy). The dosimetry as well as the risk model formalisms are outlined. Furthermore, example calculations and results are presented for intensity-modulated photon therapy versus proton therapy.

COMMUNICATION OF BENEFITS AND RISKS OF MEDICAL RADIATION: A HISTORICAL PERSPECTIVE

X-rays were discovered by Wilhelm Röntgen in 1895. Within one year, benefits of x-rays, such as visualization of fractures, and detriments, such as x-ray dermatitis, were recognized. Nobel Laureates Pierre and Marie Sklodowska Curie discovered the radioactive element radium in 1898, and a year later the application of radiation to cure cancer was reported. A significant price was paid for this: Marie Curie died of aplastic anemia related to her radiation exposure, and her daughter Irene Joliot Curie, Nobelist for radiochemical research, died of radiation-induced leukemia. Internationally developed radiation protection recommendations were formalized starting in the late 1920s. The increasing use of ionizing radiation in medical diagnosis and radiation therapy has brought significant societal benefits. Known risks of therapeutic radiation include coronary artery disease and secondary malignancy. However, recently concerns have been raised of possible very small but incremental increases in malignancies due to diagnostic medical radiation. Patients are largely unaware of, and referring physicians and even radiologists often underestimate, the carcinogenic effects of radiation. There is a need to determine the appropriateness of imaging tests that use ionizing radiation prior to performance; optimize imaging protocols to reduce unnecessary radiation; include patients in the decision process and encourage and enable them to track their radiation exposure; and promote education about medical radiation to patients, referring physicians, radiologists, and members of the public. The basic radiation protection principles of justification, optimization, and application of dose limits still pertain.

Effects of Low Doses of Radiation: Joint Statement from the Following Participants at the 15th Pacific Basin Nuclear Conference, Sessions Held in Sydney, Australia, Wednesday 18 October 2006

Effects of Low Doses of Radiation: Joint Statement from the Following Participants at the 15^th Pacific Basin Nuclear Conference, Sessions Held in Sydney, Australia, Wednesday 18 October 2006

Occupational exposure, epidemiology and compensation

The data summarized in this section are taken mainly from the 2000 Report of the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR), and generally refer to occupational exposures assessed to have been experienced during the earlyand mid-1990s [1]. Occupational exposures in the United Kingdom from 1998 to 2003 have been reviewed recently by the Radiation Protection Division of the Health Protection Agency [2]. Soon after its discovery by Roentgen in 1895, ionizing radiation was exploited in medicine as a diagnostic and therapeutic tool, leading to the inadvertent exposure of medical staff. In the early years of the 20th century, exposures to medical personnel tended to be large, sometimes leading to deterministic effects such as epilation and skin burns. The first substantial epidemiological evidence for the carcinogenic effects of radiation was obtained from observations on radiologists. The use of radiation in medicine grew throughout the last century and currently includes a variety of diagnostic techniques (e.g. fluoroscopy and cardiac catheterization), dental radiography, radionuclides used for organ imaging in nuclear medicine, radiotherapy and other uses such as biomedical research. Initially, it was X-rays that were employed, but techniques became more sophisticated such that other radiations [e.g. densely ionizing alpha particles (He) and neutrons] were introduced. Medical workers now constitute the largest group occupationally exposed to man-made sources of radiation: throughout the world, 2.5 million medical workers are monitored for exposure to radiation (the majority of these being employed in the countries of the Organization for Economic Cooperation and Development), leading to an average annual collective effective dose of 1000 person.Sv. In contrast to the high-level exposures experienced by early medical workers, the reported annual occupational doses in excess of 15 mSv are now rare. The industrial use of radiation is multifarious and includes radiography, irradiation (e.g. the sterilization of medical products), luminizing, radionuclide production and distribution, well logging and accelerator operation. Some 0.75 million workers are monitored for exposure, leading to an average annual collective effective dose of 400 person.Sv. Although individual doses are generally small, a few workers (such as those involved in site radiography) receive annual doses in excess of 15 mSv, and occasionally serious over-exposures are reported. The luminizing of dials with radium-based paint in the first half of the last century led to accidental ingestion of the paint and, particularly in the United States, high intakes of radium. Occupational exposure also occurs in educational establishments ( 0.33 million monitored workers worldwide) and in veterinary medicine ( 50 000 radiation workers), leading to average annual collective effective doses of 30 person.Sv and 10 person.Sv, respectively. The discovery of neutron-induced nuclear fission in the 1930s led to the development of the nuclear weapons and power industries in the second half of the 20th century and consequent occupational exposure to natural and man-made sources of radiation. Workers in these industries are involved in mining and processing of uranium, nuclear fuel production, reactor operation, irradiated fuel reprocessing and product and waste management. Additional occupational exposures occur in research and development activities and in production and testing of nuclear weapons. The exposure of workers at the Mayak facility in the Southern Urals to external sources of gamma and neutron radiation and to alphaemitting plutonium before 1959 were very high, occasionally sufficiently so to produce deterministic effects. The total number of monitored workers in the commercial nuclear fuel cycle is 0.8 million and the average annual collective effective dose is 1500 person.Sv. Accurate figures for the defence industry are difficult to come by, but the annual collective effective dose worldwide is likely to be in the range of 100–300 person.Sv. By far, the largest source of occupational exposure is naturally occurring radiation. The excess risk of lung Correspondence to: Richard Wakeford, 6 Bourne Street, Wilmslow, Cheshire SK9 5HD, UK. Formerly: British Nuclear Fuels plc, 1100 Daresbury Park, Warrington WA4 4GQ, UK. e-mail: richard.wakeford@Gmail.com

Radiation doses in pediatric radiology: influence of regulations and standards

The benefits of x-ray examinations contribute to the quality of modern medicine; however the risk of using x-rays, a carcinogen, has always been a concern. This concern is heightened for pediatric patients, who have a much greater sensitivity to the carcinogenic effects of radiation than adults. The principle of as low as reasonably achievable, or ALARA, is essential for minimizing the radiation dose patients receive, especially for pediatric patients. In order to keep radiation doses ALARA, one must know the dose patients receive. The determination of radiation dose in a standard way is therefore necessary so that these doses can be compared with practice, and for meaningful comparison against voluntary standards. In extreme situations, where public health needs may require mandatory standards, or regulations, the quantitative measurement and calculation of radiation dose becomes essential. How some radiation dose metrics and standards have evolved, including the value of different metrics such as entrance air kerma, organ dose, and effective dose will be presented. Recent pediatric x-ray studies, whether or not dedicated pediatric equipment is necessary, and recent initiatives by the Food and Drug Administration for pediatric population will be discussed.

Ionizing radiation and cancer risk: evidence from epidemiology.

Ron, E. Ionizing Radiation and Cancer Risk: Evidence from Epidemiology. Radiat. Res. 150 (Suppl.), S30-S41 (1998). Epidemiological studies provide the primary data on the carcinogenic effects of radiation in humans. Much of what is known has come from studies of the atomic bomb survivors, and to a lesser extent from patients receiving radiotherapy. These studies demonstrate that exposure to moderate to high doses of radiation increases the risk of cancer in most organs. For all solid cancers combined, cancers of the thyroid, breast and lung, and leukemia, risk estimates are fairly precise, and associations have been found at relatively low doses (<0.2 Gy). Associations between radiation and cancers of the salivary glands, stomach, colon, bladder, ovary, central nervous system and skin have also been reported, but the relationships are not as well quantified. Associations between radiation and cancers of the liver and esophagus, and to a lesser extent multiple myeloma and nonHodgkin's lymphoma, have been reported in a few studies, but results are inconsistent. Chronic lymphocytic leukemia, Hodgkin's disease, and cancers of the pancreas, prostate, testis and cervix have rarely been linked to radiation exposure. A linear no-threshold model adequately describes the dose-response relationship for solid cancers, although at extremely high doses the risk appears to flatten out. Because few populations have been followed until the end of life, the temporal patterns of risk are not completely known. An increased risk, however, does continue for several decades. In contrast, radiation-related leukemias begin to occur shortly (2-3 years) after exposure and, at least in the A-bomb survivors, a linear-quadratic dose response seems to fit the data better than a pure linear model. Radiation does not act entirely in isolation. It can interact with other carcinogens, e.g. tobacco or chemotherapeutic agents, and with host factors such as age at exposure, gender or reproductive history. Interactions with medical interventions or with certain heritable mutations have also been suggested. While the studies of high-dose exposures are essential for understanding the overall biological consequences of radiation exposure, the public is more concerned about the long-term health effects from protracted exposures at low doses. Unfortunately, the inherent limitations of epidemiology make it extremely difficult to directly quantify health risks from these exposures. While most epidemiological data are compatible with linear extrapolations from exposures at high doses or high dose rates, they cannot entirely exclude other possibilities. As the field of epidemiology advances, understanding more about the health effects of prolonged and low-dose exposures will be the next

Radiation Hormesis: Data and Interpretations

Although the biological effects of large doses of ionizing radiation are predominantly harmful, low-to-intermediate doses have been observed to enhance growth and survival, augment the immune response, and increase resistance to the mutagenic and clastogenic effects of further irradiation in plants, bacteria, insects, and mammals. The existence of these stimulatory, or “adaptive”, responses implies that the dose-response relationships for genetic and carcinogenic effects of radiation may be similarly biphasic, or hormetic, in nature, a possibility with far-reaching implications for radiation protection. As yet, however, the extent to which such responses may actually reduce the risks attributable to low-level irradiation remains to be determined, pending further elucidation of the relevant dose-response relationships and the apparent lack of responsiveness in some individuals. Therefore, further research is needed to resolve this question.

Post-irradiation osteosarcoma : A case report

Radiotherapy can induce a malignancy at a latter time. A case ofsecondary osteosarcoma in the clavicula coused by radiotherapy 16 years earlier is reporled. The carcinogenic effect of radiation is a well-known fact. Radiotherapy is used in the management of cancer, and at a latter time may contribute to the development of a secondary malignancy which differ from the primary one. The frequency of malignancy attributed to radiation is very low preceded by a long latent period, so that the incidence is usually published as case reports.l Here we present a case of osteosarcoma of the clavicle, secondary to radiotherapy administered for a malig- nancy in the nasopharyngeal area, 16 years before.

Ionizing Radiation and Cancer Risk: Evidence from Epidemiology

Epidemiological studies provide the primary data on the carcinogenic effects of radiation in humans. Much of what is known has come from studies of the atomic bomb survivors, and to a lesser extent from patients receiving radiotherapy. These studies demonstrate that exposure to moderate to high doses of radiation increases the risk of cancer in most organs. For all solid cancers combined, cancers of the thyroid, breast and lung, and leukemia, risk estimates are fairly precise, and associations have been found at relatively low doses (<0.2 Gy). Associations between radiation and cancers of the salivary glands, stomach, colon, bladder, ovary, central nervous system and skin have also been reported, but the relationships are not as well quantified. Associations between radiation and cancers of the liver and esophagus, and to a lesser extent multiple myeloma and non-Hodgkin's lymphoma, have been reported in a few studies, but results are inconsistent. Chronic lymphocytic leukemia, Hodgkin's disease, and cancers of the pancreas, prostate, testis and cervix have rarely been linked to radiation exposure. A linear no-threshold model adequately describes the dose-response relationship for solid cancers, although at extremely high doses the risk appears to flatten out. Because few populations have been followed until the end of life, the temporal patterns of risk are not completely known. An increased risk, however, does continue for several decades. In contrast, radiation-related leukemias begin to occur shortly (2-3 years) after exposure and, at least in the A-bomb survivors, a linear-quadratic dose response seems to fit the data better than a pure linear model. Radiation does not act entirely in isolation. It can interact with other carcinogens, e.g. tobacco or chemotherapeutic agents, and with host factors such as age at exposure, gender or reproductive history. Interactions with medical interventions or with certain heritable mutations have also been suggested. While the studies of high-dose exposures are essential for understanding the overall biological consequences of radiation exposure, the public is more concerned about the long-term health effects from protracted exposures at low doses. Unfortunately, the inherent limitations of epidemiology make it extremely difficult to directly quantify health risks from these exposures. While most epidemiological data are compatible with linear extrapolations from exposures at high doses or high dose rates, they cannot entirely exclude other possibilities. As the field of epidemiology advances, understanding more about the health effects of prolonged and low-dose exposures will be the next challenge.

Special susceptibility of the child to certain radiation-induced cancers.

The carcinogenic effects of exposure to ionizing radiation vary markedly with age, as revealed by studies of Japanese atomic bomb survivors and of Marshall Islanders exposed to fallout from U.S. nuclear weapons tests in the South Pacific in 1954. An increase in cancers of adulthood after intrauterine exposure, as reported in 1988, has not been sustained. After childhood exposure, increases in leukemia, breast cancer, and thyroid cancer are well established. The carcinogenic effects of radiation on the young have been reported after intrauterine exposures and after exposures during childhood. Cancers with short latent periods such as leukemia occur during childhood, but those with long latent periods such as breast cancer occur in adulthood.

Claim That Medical X-rays Caused Most US Breast Cancers Found Incredible

A RESPECTED authority on the biological effects of ionizing radiation has just published a book claiming that the vast majority of breast cancers in the United States were caused by the high doses of medical x-rays that women often received in the decades before the carcinogenic effects of radiation were recognized. The book, which is based on one man's study of the medical literature going back to 1910, concludes that medical x-rays are responsible for at least 62%, and probably more than 75%, of the approximately 182 000 cases of breast cancer diagnosed each year in the United States. However, the study, which has not been peer reviewed, is not persuading leading cancer and radiation experts, who say there are major problems with some of the assumptions and conclusions of its author, John W. Gofman, MD, PhD, professor emeritus of molecular and cell biology at the University of California, Berkeley.

Incidence of second cancers in patients treated for Hodgkin's disease.

Numerous studies of treatment for Hodgkin's disease have demonstrated large increases in the incidence of leukemia in the early years following chemotherapy, although the duration of effect and the specific agents involved are not well understood. Also, some, but not all, studies have indicated that the incidence of certain solid tumors increases following treatment for Hodgkin's disease. We studied the association between treatment for Hodgkin's disease and the incidence of second cancers. We conducted a study within a cohort that included 10,472 patients from 14 cancer centers in the United States and Canada who were first diagnosed as having Hodgkin's disease at some point from 1940 through 1987. Discounting the 1st year after diagnosis, the average length of follow-up was 7.1 years per subject. We observed 122 leukemias and 438 solid tumors. The relative risk (RR) of leukemia following chemotherapy, compared with no chemotherapy, was 14 (95% confidence interval [CI] = 5.6-35). Increased risks of leukemia were observed after treatment with chlorambucil (RR = 2.0; 95% CI = 1.1-3.6), procarbazine (RR = 4.9; 95% CI = 2.6-9.1), vinblastine (RR = 1.7; 95% CI = 1.1-2.8), and a group of rarely used drugs that included methotrexate, vindesine, etoposide, and 22 others (RR = 3.8; 95% CI = 1.9-7.4). RRs were also estimated for various combinations of drugs, including MOPP (mechlorethamine, vincristine, procarbazine, and prednisone) (RR = 5.9; 95% CI = 2.9-12) and ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine) (RR = 1.5; 95% CI = 0.7-3.4). The RR of leukemia associated with splenectomy was 1.6 (95% CI = 1.0-2.5). The RR of solid tumors following chemotherapy was 1.4 (95% CI = 1.1-1.8). For the group of rarely used drugs, the RR of solid tumors was 3.1 (95% CI = 1.7-5.8). Chemotherapy was associated with an increased risk of cancers of the bones, joints, articular cartilage, and soft tissues (RR = 6.0; 95% CI = 1.7-20), and cancers of the female genital system (RR = 1.8; 95% CI = 1.1-3.2). In patients followed for 10 or more years after radiotherapy, increased risks were found for cancers of the respiratory system and intrathoracic organs (RR = 2.7; 95% CI = 1.1-6.8) and for cancers of the female genital system (RR = 2.4; 95% CI = 1.1-5.4). Procarbazine, chlorambucil, and vinblastine are associated with increased leukemia risk. Combination drug regimens have leukemogenic effects estimated as the product of RRs for individual drugs. Chemotherapy and radiotherapy increase the risk of selected solid tumors, and the effect of chemotherapy on solid tumor risk is weaker than the leukemogenic effect. Without doubt, the benefits of treatment of Hodgkin's disease outweigh the risk of a subsequent malignancy, but data on the carcinogenic effects of radiation and drugs beyond 10 years after treatment continue to be sparse, and future analyses should be directed at long-term survivors.

Cellular, Molecular, and Carcinogenic Effects of Radiation

(1) The biologic effects of ionizing radiation at the cellular and molecular levels differ from those of many chemical agents. Radiation is a classic genotoxic agent. The important DNA lesion with respect to its cytotoxic and mutagenic effects appears to be the DNA double strand break, whereas chemotherapeutic alkylating agents induce primarily base damage from adduct formation and cross-linking. Radiation-induced mutations result primarily from large-scale structural changes in DNA as a result of mechanisms such as chromosomal deletions, rearrangements, and homologous recombination, rather than point mutation as generally observed with alkylating agents. Finally, radiation is highly cytotoxic; a significantly increased frequency of specific gene mutations is usually observed only following doses that produce significant cell killing. (2) Radiation may not be a very potent inducer of second malignant tumors, at least in most cases. This prediction is derived from the localized nature of the exposure during clinical radiotherapy, in which the dose to normal tissues is minimized, and from the fact that radiation tends to be cytotoxic rather than mutagenic. The very high doses employed in curative radiotherapy may thus kill potentially transformed cells in the field. An exception to this general prediction may be Hodgkin's disease, in which a relatively large volume of tissue is treated with lower total radiation doses. (3) We have a firm scientific basis on which to predict the carcinogenic effects of radiation at many tissue sites, owing to extensive quantitative epidemiologic data in human populations. Unlike for chemical agents, radiation can be easily detected, and the absorbed dose to critical tissues is precisely measured. Thus, we know about the sensitivity of many target tissues to radiation-induced cancer. (4) A number of factors can modify the carcinogenic effects of radiation. It is likely that important interactive effects will occur between radiation and chemotherapeutic alkylating agents, which may depend upon the timing and order of the treatments as well as the particular agent(s) employed. (5) Genetic predisposition to radiation-induced cancer may be a confounding factor in the prediction of its effects in any given individual.

The health effects of low-level ionizing radiation.

Within months after Roentgen's discovery of the x-ray in 1895, bums of the skin and other acute injuries were encountered in pioneer radiation workers ( 12, 27), thus prompting efforts to reduce the levels of occupational exposure. In subsequent years, as the thresholds for different types of reactions gradual­ ly became better known, the exposure limits for radiation workers underwent a series of further reductions (82, 83). As a result, protection standards ultimately evolved that now suffice to prevent gross damage of tissue, barring radiation accidents (37). Although today's protection standards are adequate to prevent gross injury, they are not presumed to protect completely against the mutagenic and carcinogenic effects of radiation, which may have no thresholds (57, 87). The concept that the mutagenic effects of radiation might have no threshold dates from the 1940s, when classical experiments on the fruitfly suggested that the frequency of mutations increases in proportion to the dose of x-rays, without a threshold (54). In the 1950s , apprehension that future generations might suffer genetic harm from the global increases in environmental radia­ tion caused by atmospheric testing of nuclear weapons prompted national (55) and international (94) assessments of the risks, which have been periodically updated (87, 89-93). Concern about the hazards associated with low-level irradiation was further

Air Reduction for Intussusception in Infancy and Childhood:Ultrasonographic Diagnosis and Management Without X-Ray Exposure

For the treatment of uncomplicated intussusception in infants and children, we attempted air reduction without x-ray study to avoid the genetic and carcinogenic effects of radiation. Intussusception could generally be diagnosed by ultrasonography in addition to the history and typical clinical signs without using a barium enema. The success of reduction could also be safely evaluated from the disappearance of both the characteristic sonographic target sign and the abdominal palpable mass, and improvement in the general condition 2 or 3 hours after completing this procedure. This simple, cheap and clean reduction method was applied to 127 patients under strict indications and sedation with diazepam. The successful reduction rate was high (90.6%) and equal to that by hydrostatic reduction. Accordingly, this procedure appears to be safely applicable to the management of uncomplicated intussusception in infancy and childhood.

Cancer induction and non-stochastic effects.

The mechanisms of carcinogenesis are not known in detail, but there is strong evidence that cancer usually arises from a single transformed cell. Hence, although the process of carcinogenesis appears to require a multiplicity of changes in the affected cancer-forming cell, such as may be associated with successive stages of tumour initiation, tumour promotion, and tumour progression, only one such change induced by radiation in an appropriate cell may be conceived to increase the probability of neoplasia in a suitably susceptible individual. For this reason, carcinogenic effects of radiation, like mutagenic effects of radiation, are considered for purposes of radiological protection to have no threshold and to behave as stochastic phenomena. In contrast, certain other effects of radiation, such as cataract of the lens, infertility, and depression of the bone marrow, require the killing of many cells in the affected organs. Thus, they vary in severity with the extent of cell loss and have thresholds of detectability which depend on the sensitivity with which the consequences of cell loss can be measured.

Health effects of low level radiation: Carcinogenesis, teratogenesis, and mutagenesis

The carcinogenic effects of radiation have been demonstrated at high dose levels. At low dose levels, such as those encountered in medical diagnosis, the magnitude of the effect is more difficult to quantify. Three reasons for this difficulty are (1) the effects in human populations are small compared with the natural incidence of cancer in the populations; (2) it is difficult to transfer results obtained in animal studies to the human experience; and (3) the effects of latency period and plateau increase the complexity of population studies. In spite of these difficulties, epidemiologic studies of human populations exposed to low levels of radiation still play a valuable role in the determination of radiation carcinogenecity. They serve to provide upper estimates of risk and to rule out the appearance of new effects that may be masked by the effects of high doses. While there is evidence for mutagenic effects of radiation in experimental animals, no conclusive human data exist at the present. It is not possible to rule out the presence of genetic effects of radiation in humans, however, because many problems exist with regard to the epidemiologic detection of small effects when the natural incidence is relatively large. In animals, subtle effects (eg, a decrease in the probability of survival from egg to adult) may occur with greater frequency than more dramatic disorders in irradiated populations. However, these types of genetic abnormalities are difficult to quantitate. Current risk estimates are based primarily upon data pertaining to dominant mutations in rodents. Some specific locus studies also permit identification of recessive mutation rates. The embryo and fetus are considered to be at greater risk for adverse effects of radiation than is the adult. This sensitivity was predicted in 1906 by the law of Bergonie and Tribondeau and has been demonstrated in human and animal populations. At high dose levels (above 15 rem), the effects of radiation depend upon the gestational stage at which irradiation occurs. Prior to the second week, the predominant effect is preimplantation death, while during the period of major organogenesis (second to sixth week), growth retardation and CNS abnormalities may be produced. These effects have not been demonstrated with a high degree of statistical significance at low dose levels (below 15 rem) and are not considered to present a serious hazard for patients undergoing radiologic exams.