Iodine-131 in thyroids of the meadow vole (Microtus pennsylvanicus) in the vicinity of the Three Mile Island nuclear generating plant.
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Biomedical subjects
Publications and source records attributed to R W Field.
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Lung cancer is the leading cause of cancer death in the United States for both men and women. Although most lung cancer deaths are attributable to tobacco usage, even secondary causes of lung cancer are important because of the magnitude of lung cancer incidence and its poor survival rate. This review summarizes the basic features and major findings from the published U.S. large-scale residential radon case-control studies performed in New Jersey, Iowa, and Missouri (two studies). The methodology from an unpublished study covering Connecticut, Utah, and Southern Idaho is also presented. Overall, the higher categorical risk estimates for these published studies produced a positive association between prolonged radon exposure and lung cancer. Two studies (Missouri-II and Iowa) that incorporated enhanced dose estimates produced the most compelling evidence suggesting an association between prolonged residential radon exposure and lung cancer. The prevailing evidence suggests that the statistically significant findings may be related to improved retrospective radon exposure estimates. The general findings from the U.S. studies, along with extrapolations from radon-exposed underground miners, support the conclusion that after cigarette smoking, prolonged residential radon exposure is the second leading cause of lung cancer in the general population.
Although occupational epidemiological studies and animal experimentation provide strong evidence that radon-222 (222Rn) progeny exposure causes lung cancer, residential epidemiological studies have not confirmed this association. Past residential epidemiological studies have yielded contradictory findings. Exposure misclassification has seriously compromised the ability of these studies to detect whether an association exists between 222Rn exposure and lung cancer. Misclassification of 222Rn exposure has arisen primarily from: 1) detector measurement error; 2) failure to consider temporal and spatial 222Rn variations within a home; 3) missing data from previously occupied homes that currently are inaccessible; 4) failure to link 222Rn concentrations with subject mobility; and 5) measuring 222Rn gas concentration as a surrogate for 222Rn progeny exposure. This paper examines these methodological dosimetry problems and addresses how we are accounting for them in an ongoing, population-based, case-control study of 222Rn and lung cancer in Iowa.