Search

Studies of miners provide the basis for public health efforts to reduce residential radon progeny exposure. Because the preponderance of households do not have members who smoke indoors, studies of non-smoking miners contribute essential data for risk assessments for residential radon progeny exposure. We studied a cohort of 2,209 never-smokers who were underground uranium miners employed in the western U.S. from 1956 to the early 1990's and who participated in a screening program for lung cancer conducted by Saccomanno and colleagues. After determining the vital status and cause of death in the cohort, we conducted a nested case-control study of 55 lung cancer deaths in males and 3 age-matched controls for each case. The relative risk of lung cancer was 29.2 (95% CI 5.1, 167.2) for miners with greater than 1,450 WLM compared with those exposed to less than 80 WLM. Temporal factors affected risk, including average dose rate, which was inversely associated with lung cancer risk, and the length of time since last exposure, which was directly associated with decreased risk. As in studies of non-smokers and smokers combined, the exposure response relationship in never-smokers was consistent with a decreased slope at higher WLM, which resulted, in part, from an inverse dose rate effect.

Many uranium miners have been disabled by and died of pulmonary fibrosis that was not recognized as an occupational disease. A review of animal studies, complications from whole body irradiation, pulmonary function, and mortality studies of uranium miners led us to suspect radiation-induced chronic diffuse interstitial fibrosis in miners who had inhaled excessive radon progeny. A selected group of uranium miners (22) with severe respiratory disease (but no rounded nodules in chest films) were studied. Lung tissue from five disclosed severe diffuse interstitial fibrosis, with "honeycomb lung" in all. Some also had small anthrasilicotic nodules and birefringent crystals. Although quartz crystals probably contributed, we concluded that the predominant injurious agent in these cases was alpha particles from radon progeny. This disease, after a long latent period, usually results in pulmonary hypertension, shortness of breath, and death by cardiopulmonary failure.

All underground mines have higher radon levels than are found in surface air. Ventilation is the primary method of controlling radon levels. Fourteen cohort and seven case-control studies done on underground miners are reviewed; they include many types of ore. Only five of the studies deal with more than 100 lung cancer deaths. Variations in the attributable risk are given. Some generalizations can be drawn from these studies: the longer the follow-up, the greater is the attributable risk, even though the relative risk is reasonably constant. The induction-latent period is quite variable but is shortened by high exposure rates, by cigarette smoking, and by increasing age at start of mining. The predominant histological type of lung cancer among miners changed from small-cell undifferentiated for short follow-up time to epidermoid after long follow-up times. With short follow-up time, a multiplicative interaction between smoking and radiation was indicated, but, with long follow-up time, the two factors appear to be simply additive. This difference is probably due to the shortened latent period among cigarette smokers, not to synergism.

There are substantial animal and epidemiological data related to cigarette smoking and lung cancer among miners exposed to elevated levels of radon daughters that appears to be in disagreement. An hypothesis is advanced that explains most of this disagreement as being derived from temporal differences of cancer expression. The hypothesis is that a given radiation exposure induced a finite number of lung cancers, which have shorter latent periods due to the cancer promotion activity of smoke among cigarette smokers. According to this hypothesis, the life-shortening effect is greater among smoking miners than nonsmoking miners, and the ultimate number of lung cancers among smoking miners will be only a little larger than among nonsmokers. The greater number will derive from the additive effect of radiation and smoking, plus the greater force of competing causes of death among elderly nonsmokers.

Mortality of uranium miners from both lung cancer and other respiratory diseases is strongly dependent on exposure to radon daughters, cigarette smoking and height. Lung cancer among 15 different mining groups (uranium, iron, lead, zinc) was analyzed to determine what factors influence incidence and the induction-latent period. At low exposure or exposure rates, alpha radiation is more efficient in inducing lung cancer, producing an upward convex exposure-response curve. The induction-latent period is shortened by increased age at start of mining, by cigarette smoking and by high exposure rates. For a follow-up period of 20 to 25 years, the incidence increases with age at start of mining, with magnitude of exposure and with amount of cigarette smoking. Instead of extrapolating downward from high exposures to estimate risk at low levels, it is suggested that it might be more appropriate to use cancer rates associated with background radiation as the lowest point on the exposure-response curve. Although health risks are much greater in uranium mines than mills, there is some health risk in the mills from long-lived radioactive materials.

A mortality analysis of a group of white and Indian uranium miners was done by a life-table method. A significant excess of respiratory cancer among both whites and Indians was found. Nonmalignant respiratory disease deaths among the whites are approaching cancer in importance as a cause of death, probably as a result of diffuse parenchymal radiation damage. Exposure-response curves for nonsmokers are linear for both respiratory cancer and "other respiratory disease." Cigaret smoking elevates and distorts that curve. Light cigaret smokers appear to be most vulnerable to lung parenchymal damage. The predominant histologic cancer among nonsmokers is small-cell undifferntiated, just as it is among cigaret smokers.