1146 RADIATION BIOLOGY 



this subject are those of Brues (1951) and several chapters in "Medical 

 Physics," of Glasser (1950). In locating and interpreting the enormous 

 literature we have made much use of these publications. 



The induction of neoplasia by ionizing radiations was noted accidentally 

 soon after discovery of X radiation and radioactive substances and the 

 clinical observations were soon verified by experimental studies in 

 animals. Exposure to ionizing radiations arose as a new industrial and 

 medical hazard and also as a tool of experimental carcinogenesis and 

 cancer therapy. The artificial production of radioactive substances has 

 increased tremendously the potentialities of application of ionizing radia- 

 tions to varied fields of science and industry, but accidental or incidental 

 exposure to large quantities of radiation has also greatly multiplied the 

 hazards of neoplasia induction. 



The use of ionizing radiations in science and industry is now in rapid 

 ascendency; knowledge of the carcinogenic potencies of radioactive sub- 

 stances is still much limited. The present review aims to survey the pub- 

 lished observations and to point to deficiencies of knowledge concerning 

 carcinogenesis by ionizing radiations. 



PHYSICAL ASPECTS OF CARCINOGENESIS BY IONIZING RADIATIONS 



The interaction of ionizing radiations with biologic matter is discussed 

 and the term of specific ionization or linear energy transfer is defined in 

 other chapters. The specific ionization in biologic matter varies from a 

 theoretical 6.3 ion pairs per micron (Gray, 1946) approached by the X 

 radiation in the multimillion-volt range to several thousand for the a par- 

 ticles and many thousand for the heavy fission particles. This difference 

 in specific ionization causes marked quantitative differences in the 

 biologic effects on small biologic entities. Similar quantitative differ- 

 ences may not exist as concerns the acute lethal syndrome in animals. 

 When calculated for the same absorbed energy with equal dose rates, the 

 30-day LD 50 for mice is approximately the same after X irradiation as 

 after internal a irradiation from intravenously injected radon in equi- 

 librium with its short-lived decay products (Hollcroft and Lorenz, 1952). 

 The slight difference observed might be explained by the nonuniformity 

 in distribution of the a emitters. On the other hand, Zirkle (Chap. 6) 

 has shown that cyclotron neutrons are approximately five times and 

 X radiation 1.5 times as effective as y radiation in killing mice (30-day 

 LD 50 ). The application of such findings to radiation carcinogenesis is, 

 however, merely speculative. The scant data in the literature (Henshaw 

 et at., 1947, and Upton and Furth, 1951, unpublished data) indicate no 

 marked differences in tumor induction by neutrons as compared to X 

 or 7 radiation. 



The following generalizations apply to the process of carcinogenesis: 

 If the tumor induction is caused by a direct action of the radiation on 



