WAS-1535, There, u? introducing a fictittcusly léree mist of oxposed tissuc, the calculated dose becomes covmensurately smal}. In passing from the real situation in which a hot particle irradiates 10 to 100 alveoli, ‘o the fictional situation in which the jonizing radiation from the hot nsrticle is averaged over 108 alveoli, the dose scale has decreased dy »eughly a factor of &@ million. . Living tissue shows extensive intre-cellular and inter-cellular organization. Several regimes of biological response would be exnected as physical characte.istics of exposure are varied. Carcinogenic response to whole organ exposure by non acute doses of radiation will fall in one of these regimes, and this will be a regime in which there is human experience. Fron the physical characteristics of plutonium aerosols, from the lung deposition experience with aerosols, and from tne lung clearance evperjence with plutcniua particulates, it can be inferred that at Teast one class of parcicles exist which suogect lung tissue to an exposure associated with a different carcinogenic response regime. This is because other biological phenomenon has intervened. For hot particle exposure that phenomencn is mitotic death of cells, 7.e., Toss of the cell's ability to divide. literature on the subject. There is anextensive Radiclogically induced mitotic death is, in fact, the basis for treating malignant tissue with tenizing radiation, and is the cause of most acute syep toms consequent to raagiation exposure. Even though the intercession of extensive mitotic death of cells must eee inovitably piace certain particulate exposures in a different response regime from whole Tung, non acute exposures, a compelling araument might be made that the carcinovenic response in tho forviser case is necessarily