Ms. H. O'Leary
Feb. 9, 1994

4. Radiation-lnduced Lung Cancer in Smokers:

There is a large body of published evidence which indicates that bronchial cancer in cigarette smokers--the most common, lethal human cancer--can be attributed to radionuclide "hotspots" in the bronchial epithelium of cigarette smokers. Concentrations of the alpha-particle emitter 210po ranging up to 13 pCi g~ I in the epithelium at bronchial bifurcations of smokers were experimentally observed by Little et al. (New Engl. J. Med. 273, 1343-1351, 1965). The observed hotspot distribution of 210po was attributed to the accumulation of insoluble, 210Pb enriched particles in mainstream cigarette smoke (Martell, 1974, 1975) and confirmed by 210Pb/210Po ratio measurements in epitheliurn tissue (Radford and Martell, 1977). The short-lived decay products of radon-222 and lead-212 in indoor air also contribute to the alpha and beta radiation dose at the bronchial tumor sites of smokers (Martell, 1983, 1987). A list of references for my published papers on radiation-induced bronchial cancer in cigarette smokers is appended. This important hypothesis is further reinforced in a recent study by Martonen et al. (Hlth. Phys. 52, 213-217, 1987).

If it is confirmed that bronchial cancer in smokers is radiation-induced at radionuclide hotspots in small dividing cell populations in the epithelium of smokers, insoluble 210Pb-enriched particles and their decay products are the obvious candidate agents in the etiology of other soft tissue cancers in smokers. Note that cigarette smokers have a higher and earlier incidence of all common human cancers. Uranium miners who smoke cigarettes, exposed to added sources of inhaled radioactivity including high concentrations of 22 'Rn decay products and uranium mineral particles, have a much higher and earlier incidence of lung cancer than that for heavy smoking alone. Similarly, it is to be expected that cigarette smoking plutonium workers are far more susceptible to development of bronchial cancer than are nonsmoking plutonium workers (Gofman, MMA 236, 284286, 1976).

The important possibility that bronchial cancer and other common cancers in cigarette smokers are radiation-induced has not been faulted by the AEC/ERDA/DOE. Instead they try to ignore this disturbing possibility or blame these cancers on proposed chemical carcinogens. The nuclear energy establishment has been much like the tobacco industry. In the face of overwhelming epidemiological evidence to the contrary, the tobacco industry continues to deny the cancer risks and other health consequences of cigarette smoking. Similarly the nuclear establishment has contrived to minimize the contribution of ionizing radiation and has tried to attribute bronchial cancer and other common human cancers to chemical carcinogens. However the cytogenetics of bronchial cancer and other highly malignant human cancers show multiple gross chromosome aberrations which can be readily induced only by external and internal radiation sources. Toxic chemicals and other cell-killing agents and mechanisms play an important role as cofactors and cocarcinogens which speed up the multistage process of malignant transformation and the early onset of malignancy. However the cytognetic evidence clearly implicates radiation interactions in the initiation and progression of malignancy.

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