Synergistic interactions of indoor radon progeny with the cigarette smoking process have been 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 210Pb-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--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 approximately equal to 10(7) cells (approximately equal to 10(6) cells at individual bifurcations) of most smokers who die of lung cancer.
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机译：室内ra气后代与吸烟过程的协同相互作用已通过实验进行了评估。吸烟会提高空气中亚微米级颗粒和附着的ra衰变产物的浓度。燃烧的香烟中的分馏引起ra子后代与主流香烟烟雾中的大颗粒的结合，这些颗粒被选择性地沉积在支气管分叉处的“热点”中。由于烟焦油对肺液中的溶解具有抵抗力，因此附着的ra子后代在清除之前会在分叉处经历大量的放射性衰变。在香烟之间正常呼吸期间吸入的子后代对分叉处的α辐射剂量做出了更大的贡献。分叉处的上皮逐渐受到化学和辐射损伤，从而延长了由烟草三角毛燃烧产生的不溶性210Pb富集烟颗粒的保留时间。吸烟者中肺癌的高发病率归因于室内ra和子后代（218Po，214Po，212Po和212Bi和212Bi）的分叉处累积的α辐射剂量，以及富含210Pb的烟尘颗粒中210Po的分叉辐射剂量。据估计，在单独的分叉处，大约80（10 rads）（1 rad = 0.01 J / kg = 0.01 Gy）的致癌性alpha辐射剂量被传递到大约等于10（7）个细胞（大约等于10（6）个细胞） ）死于肺癌的大多数吸烟者。
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