alpha-Radiation dose at bronchial bifurcations of smokers from indoor exposure to radon progeny.

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Abstract
Synergistic interactions of indoor radon progeny with the cigarette smoking process were evaluated experimentally. Smoking enhances the air concentration of submicron particles and attached radon decay products. Fractionation in burning cigarettes gives rise to the association of radon progeny with large particles in mainstream cigarette smoke, which are selectively deposited in hot spots at bronchial bifurcations. Because smoke tars are resistant to dissolution in lung fluid, attached radon progeny undergo substantial radioactive decay at bifurcations before clearance. Radon progeny inhaled during normal breathing between cigarettes make an even larger contribution to the .alpha.-radiation dose at bifurcations. Progressive chemical and radiation damage to the epithelium at bifurcations gives rise to prolonged retention of insoluble 210-Pb-enriched smoke particles produced by tobacco trichome combustion. The high incidence of lung cancer in cigarette smokers is attributed to the cumulative .alpha.-radiation dose at bifurcations from indoor radon and thoron progeny-218Po, 214Po, 212Po, and 212Bi.sbd.plus that from 210Po in 210Pb-enriched smoke particles. It is estimated that a carcinogenic .alpha.-radiation dose of 80-100 rads (1 rad = 0.01 J/kg = 0.01 Gy) is delivered to .apprxeq. 107 cells (.apprxeq. 106 cells at individual bifurcations) of most smokers who die of lung cancer.