Bush__The_Essential_Physics_for_Medical_Imaging - Biomedical ...

older than 55 years of age. The risk estimates for women in the 25-, 35-, and 45-year-old age groups are 0.05%, 0.04%, to 0.02%, respectively, according to theBEIR V report. The data fit a linear dose-response model, with a dose of approximately0.8 Gy (80 rad) required to double the natural incidence of breast cancer.The data from acute and chronic exposure studies indicate that fractionation of thedose reduces the risk of breast cancer induced by low-LET radiation. The latentperiod ranges from 10 to 40 years, with younger women having longer latencies. Incontrast to leukemia, there is no identifiable window of expression; therefore, therisk seems to continue throughout the life of the exposed individual.Improvements in mammography have resulted in a substantial reduction in thedose to the breast. Women participating in large, controlled mammographic screeningstudies have been shown to have a decreased risk of mortality from breast cancer.The American Cancer Society and the American College of Radiology currently recommendannual mammography examination for women beginning at age 40 years.Conclusive evidence of the ability of ionization radiation to produce genetic effectswas first obtained in 1927 with the experimental observations of radiation-inducedgenetic effects in fruit flies. Extensive laboratory investigations since that time (primarilylarge-scale studies in mice) have led scientists to conclude that (a) radiationis a potent mutagenic agent; (b) most mutations are harmful to the organism; (c)radiation does not produce unique mutations; and (d) radiation-induced geneticdamage can theoretically occur (like cancer) from a single mutation and appears tobe linearly related to dose (i.e., linear nonthreshold dose-response model). Althoughgenetic effects were initially thought to be the most significant biologic effect ofionizing radiation, it is clear that, for doses associated with occupational and medicalexposure, the risks are small compared with the spontaneous incidence ofgenetic anomalies and are secondary to their carcinogenic potential.Epidemiologic investigations have failed to demonstrate radiation-induced geneticeffects, although mutations of human cells in culture have been shown. For a givenexposure, the mutation rates found in the progeny of irradiated humans are significantlylower than those previously identified in insect populations. The largestpopulation studied is the atomic-bomb survivors and their progeny. Based on currentrisk estimates, failure to detect an increase in radiation-induced mutations inthis population is not surprising considering how few are predicted in comparisonto the spontaneous incidence. Screening of 28 specific protein loci in the blood of27,000 children of atomic-bomb survivors resulted in only two mutations thatmight have been caused by radiation exposure of the parents.Earlier studies of survivors' children to determine whether radiation exposurecaused an increase in sex-linked lethal genes that would have resulted in increasedprenatal death of males or alteration of the gender birth ratio were negative. Irradiationof human testes has been shown to produce an increase in the incidence oftranslocations, although no additional chromosomal aberrations have been detectedin children of atomic-bomb survivors.