Suchergebnisse

The presence of environmental tobacco smoke (ETS)in homes has been implicated in the causation of lung cancer. While of interest in its own right, ETS also influences the risk imposed by radon and its decay products. The interaction between radon progeny and ETS alters the exposure, intake, uptake, biokinetics, dosimetry, and radiobiology of those progeny. The present paper details model predictions of the various influences of ETS on these factors in the U.S. population and provides estimates of the resulting change in the risk from average levels of radon progeny. It is predicted that the presence of ETS produces a very small (perhaps unmeasurable)increase in the risk of radiation‐induced tracheobronchial cancer in homes with initially very high particle concentrations for both active and never‐smokers, but significantly lowers the risk in homes with initially lower particle concentrations for both groups when generation 4 of the lung is considered the target site. For generation 16, the presence of ETS generally increases the radon‐induced risk of lung cancer, although the increase should be unmeasurable at high initial particle concentrations. The net effect of ETS on human health is suggested to be a complicated function of the initial housing conditions, the concentration of particles introduced by smoking, the target generation considered, and the smoking status of exposed populations. This situation precludes any simple statements concerning the role of ETS in governing the incidence of lung cancer in a population.

A model of the biokinetics of radon in the human body following ingestion is developed from existing data. Calculations of the probability of cancer fatality from use of radon‐laden water in the home then are presented. The pathways of emanation and ingestion are examined and shown to lead to roughly equal risks. The probability of fatal cancer resulting from lifetime use of water at a radon concentration of 1 pCi/L is shown to be 1 × 10−6, with a reasonable range between 2 × 10−7 and 5 × 10−6. The allowed concentration consistent with an excess risk of 10−4 then is approximately 100 pCi/L, which is exceeded in a significant fraction of U.S. water supplies. The lifetime number of premature deaths due to waterborne radon in the U.S. is estimated to lie between 5000 and 125,000, with a best estimate of 25,000.

This article considers the role of scientific rationality in understanding statements of risk produced by a scientific community. An argument is advanced that, while scientific rationality does impose constraints on valid scientific justifications for restrictions on products and practices, it also provides flexibility in the judgments needed to both develop and apply characterizations of risk. The implications of this flexibility for the understanding of risk estimates in WTO and NAFTA deliberations are explored, with the goal of finding an intermediate ground between the view that science unambiguously justifies or rejects a policy, and the view that science is yet another cultural tool that can be manipulated in support of any decision. The result is a proposal for a dialogical view of scientific rationality in which risk estimates are depicted as confidence distributions that follow from a structured dialogue of scientific panels focused on judgments of evidence, evidential reasoning, and epistemic analysis.