target afforded by the cell chromosozes. This follaws necessarily from the fact that most alpha interactions with cell chromosomes lead to the subsequent mitctic death of the cell, as Bazendsen hes she (17518) on, Ane production of a malignant cell calls for a sequence of two or more low probability events aad thus cannct be specded up by the applscation of massive alpha doses, but rather onsly by subjecting a much larger number of cells to a limited number of interactions. Additionally, assuming that the tumor risk to the tissue subjected to alpha irradiation {s proportional to Re? (t/t), explained above, it is apparent that the: alpha activity concentration or the activity per particle which is equated to a given tumor risk decreases with increasing time of exposure and also that a given risk can be attributed to smaller cumulative doses when the time of exposure t is appreciably longer than the mean life of the cell, TOs Purch (28) genesis Brues 2”) both peinted out that the two-mutation theories of carcino- (20,22) would imply an exceptionally high effectiveness of widely spaced radiation for tumor production. It is proposed that just such a dose rate reiationship serves to reconcile the observed significant tunor can risk in cigarette smokers with the presence of a persistent lung burden of insoluble smoke particles involving a total of only a few picocuries of a ogy Ne DEage Sehg Se OY ohEe, a: . se, hee et . gb > eG seg 210p. (14) | 3. e > "Hot" Pu0, Particle Risks: If the above tentative conclusions are correct, then the same considerations mus‘ apply in the assessment of tumor risks for hot particles. In this connection a preliminary considera- tion of the influence of specific alpha activity and particle size of the hot - alpha emitting particles is in order. Raabe et ar, (29) report an apparent rate of dissolution of *7°PUC, in ling fluid which is two orders of magnitude higher than that observed for **°Pu0, particles. Such a dramatic difference in the chemical behavior