models refer to exposures in units of WLM, we have preserved that formalism in this discussion.
Excess lung cancer in underground miners was evident after exposures to radon decay products of several hundred to several thousand WLM that would equate to long-term exposure to 222Rn in the home at very high concentrations. The health effects of average home concentrations are less certain, and current residential epidemiologic studies are attempting to measure the risk (as discussed later in this chapter). However, risk estimates based on these studies are not currently available.
The exposure assessment for miners was related to the potential energy concentration in air. However, it is the actual bronchial dose that confers the lung cancer risk. Therefore, it is necessary to know whether the bronchial dose in miners per unit PAEC in air in mines yields an equivalent bronchial dose per unit PAEC in homes. If the dose per unit exposure is equal in both situations then the derived miner risk estimates may be applied directly to home exposure.
The projection of risk from the mines to other environments, particularly for domestic exposures and for the entire lifetime, also makes 222 Rn decay product bronchial dosimetry a necessity. That requires not only physical models to evaluate the dose per unit exposure in mines relative to that in other exposure situations but also biological risk models to compare short-term with whole-life exposure. Occupationally exposed miners were exposed for 2 y to about 20 y. As described in the BEIR VI report (National Research Council 1999), there are factors that compensate for differences in exposure conditions between mines and homes, such as unattached fraction and breathing rate. Therefore, the miner risk estimates were used directly to estimate the risk from radon and its decay product exposure in domestic environments (National Research Council 1999).
The alpha dose delivered to target cells in bronchial epithelium arises mainly from the short-lived decay products deposited on the bronchial airway surfaces. The alpha dose from radon gas itself is smaller than that from its decay products because of the location of radon as it decays in the airway; there is a low probability that an alpha particle will interact with a cell. The decay products, however, are on the airway surfaces within about 20 to 30 µm of these target cells, and thus have a higher probability of hitting a target-cell nucleus.
The annual weighted equivalent dose from radon gas decaying in the lung has been calculated by the International Commission on Radiological Protection (ICRP 1981) and the National Council on Radiation Protection and Measurements (NCRP 1987a; 1987b) (see Table 5.1). The gas dose itself is 7 × 10-3 mSv y-1 per Bq m-3 (ICRP 1981) or 5 × 10-3 mSv y-1 per Bq m-3 (NCRP 1987a). The dose from 222Rn gas is lower by about a factor of 10 compared to the bronchial dose from the decay products deposited on the airways.