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|INTRODUCTION In uranium miners, a causal relationship between exposure of the lung to high levels of alpha radiation and the consequential induction of bronchial carcinoma is now well-established (Wagoner, et al., 1965). Quantitation of this cause-effect association presents considerable difficulty, however, as the result of various confounding factors such as the contributing effects of smoking and/or arsenic exposure (Archer, Gillam, and Wagoner, 1976), normal metabolic variability and, perhaps most important of all, the absence of accurate radon/radon daughter exposure data. Estimates of cumulative lung exposures suffer from inaccuracy due to critical factors such as 1) unknown ventilation rates; 2) difficulties in obtaining representative mine air samples; 3) the variable character and magnitudes of the exposure sources; and 4) specific differences in metabolism and job histories that exist among miners. It was with considerable enthusiasm, therefore, that investigators readily embraced the idea of using skeletal burdens of the relatively longlived descendants of radon and its short-lived daughters, i.e., 210 Pb and 210Po (Archer, et al., 1968), to provide a measure of cumulative past exposure wherein the body acts as an integrating dosimeter. Early studies considered excretion rates of 210Pb and 210Po in urine, blood and hair (Sultzer and Hursh, 1954; Black, et al., 1968; Jaworowski, 1965; Bell and Gilliland, 1964) as well as their concentrations in bone samples, if and when they became available (Blanchard, Archer, and Saccomanno, 1969). These methods were ultimately complemented by in vivo, whole-body counting techniques using low background, NaI-Csl(T1) detectors (Eisenbud, et al., 1969). By this latter method, it would be possible to measure the skeletal burden of 210Pb directly, thereby avoiding the many difficulties associated with the relation between nuclide excretion rates and body burden. The rationale was simple; by knowing the skeletal burden of 210Pb it should be possible, by the judicious use of an applicable metabolic model, to estimate the cumulative lung exposure to alpha-emitting radon daughters (Fig. 1). Various models that were consequently constructed, however (Fisher, 1969), all suffered from the same limitation, i.e., the assumption that the source of 210 Pb in the skeleton and the source of lung exposure to the short-lived radon daughters were simply related and, if not, were at [ ] least not too variable (Raabe, 1970). By now, the difficulty with this assumption has been recognized and more sophisticated modeling techniques have been attempted which presumably present a more realistic picture of exposure conditions (Holtzman and Rundo, 1981). There is, nevertheless, the pessimistic view that due to the variety and variability (in time as well as in character) of sources that may exist for the origin of 210Pb in bone, it may [never] be possible to estimate past lung exposures accurately by an indirect, predictive model. For example, the origin of 210 Pb in the skeleton may include such sources as: 1) the decay of short-lived 222Rn daughters, inhaled and ingested; 2) the decay of 222Rn dissolved in body fluids and tissues; 3) directly from 210 Pb present in air, inhaled and ingested; and 4) 210Pb from non-occupational sources, e.g., food, water, smoking and endogenous 226Ra. The contribution of each of these sources may vary depending upon specific site conditions such as ventilation and mining operation. On the other hand, empirical evidence seems to indicate a trend reflecting the simplest of direct|