Radon daughter exposure and lung cancer.

What Agricola and Paracelsus described in the sixteenth century as "pulmonary consumption" among miners were probably the first case reports on lung cancer due to exposure to radon, an exposure that, today, is a matter of concern not only to miners but also in some countries to the general population. Radon, discovered by Rutherford in 1899, is a noble gas created by the decay of radium-226 in the uranium decay chain. When radon decays in the air, its short lived radioactive daughters (isotopes of polonium, bismuth, and lead) tend to attach to surfaces and to aerosol particles such as dust and cigarette smoke. Hence, through inhalation of radon daughters (and to a minor degree radon) the epithelium is radiated. Although radon daughters give off alpha, beta, and gamma radiation, it is the alpha radiation that delivers the significant dose to the tracheal and bronchial epithelium. The basal stem cells of the respiratory epithelium are considered to be those predominantly at risk after the inhalation of radon daughters. The acute toxicity of radon was established in the early twentieth century and later studies showed that exposure to radon could induce lung tumours, both benign and malignant, and other cancers in experimental animals. A dose response relationship was established showing that the efficiency of radon and radon daughter exposure increased as cumulative exposure decreased. Radium in the ground is the major source of radon outdoors but other sources contribute both outdoors and indoors-for example, natural gas, building materials, and ground water, especially from deep wells. The concentration of radioactivity in the ground varies considerably and the emanation of radon may show great differences within the same area. Radon is carried into the mines, particularly through deep underground water streams, but will also diffuse out of the rocks and from crushed ore; the miner gets exposed from breathing the mine atmosphere. Exposure to the general population occurs from indoor radon concentrations built up from the leakage of radon into houses from the geological materials in the ground and walls. The concentrations of radon and its daughters are heavily influenced by ventilation and by the presence of aerosols. In 1879 Herting and Hesse reported the neoplastic nature of the lung disease among the miners in Schneeberg in Germany. Later, similar findings were reported from Joachimsthal in Czechoslovakia. For several decades the high mortality from lung cancer among these miners was thought of as a rare example of radiation induced occupational lung cancer. Today, however, several groups of miners have been shown to have a high incidence of lung cancer and with a few exceptions, coal mining and potash mining, for example, it seems as if underground mining involves an appreciable excess risk of lung cancer due to exposure to radon and its daughters. In various epidemiological studies the relative risk estimates are between four and 21, suggesting that about 70-90% of the lung cancers among underground miners might be due to occupational exposure to radon and its daughters. Although the environment in the mines may have a modifying effect on the lung cancer rate, there is an acceptable agreement in the risk estimates, when different mining populations are compared, the excess of lung cancer being closely related to the cumulative radiation dose. In the early studies of United States uranium miners almost every miner with lung cancer was a smoker and there was clearly a multiplicative interaction between smoking and radon daughter exposure. Consequently, smoking was thought to be the major contributor to the risk of lung cancer. This pattern remained in a follow up of these miners until December 1977,' suggsting that only a small fraction of lung cancer in non-smokers was due to radon daughter exposure. Other studies, however, showed an additive effect between smoking and radon daughter exposure.2 In some studies the average latent period from start of mining until death from lung cancer was about 3-12 years shorter in smokers than in nonsmokers. This could indicate that the major effects of tobacco smoke are exerted in the later phases of cancer development and may be those of a promoter, radiation acting in the early stages as an initiator. There is experimental work supporting this view, which also gains support from the experience that the risk of lung cancer in ex-smokers, 10-15 years after cessation of smoking, is only slightly greater than that of non-smokers. This would lead to an expectation of a multiplicative effect between radon daughter exposure and smoking, as also seen in some studies of miners. Under certain circumstances, however, smoking may influence mucous secretion and cause hyperplasia of the epithelium in the respiratory tract,