nor were the measurement at these sites necessarily representative of average ambient radon concentrations in each state. But the EPA data set is the only one with a fully national extent. The committee does not believe that the data are sufficiently representative to provide a population-weighted annual average ambient radon concentration. An unweighted arithmetic mean radon concentration of 15 Bq m-3, with a standard error of 0.3 Bq m-3 was calculated based on the EPA data set, and the committee recommends use of this value as the best available national ambient average concentration. After reviewing all the other ambient radon concentration data that are available from other specific sites, the committee concluded that the national average ambient radon concentration would lie between 14 and 16 Bq m-3.
The transfer coefficient is the average fraction of the initial average radon concentration in water that is contributed to the indoor airborne radon concentration. The average transfer coefficient estimated by a model and the average estimated from measurement data are in reasonable agreement. The average of the measurements was 0.9 × 10-4 with a standard error of 0.1 × 10-4, and the model's average was either 0.9 × 10-4 or 1.2 × 10-4 depending on the choice of input parameter values. Having considered the problems with both the measurements of the transfer coefficient and the measurements that are the input values into the model, the committee concludes that the transfer coefficient is between 0.8 × 10-4 and 1.2 × 10-4 and recommends that EPA continue to use 1.0 × 10-4 as the best central estimate of the transfer coefficient that can now be obtained.
The biologic effects of radon exposure under the low exposure conditions found in domestic environments are postulated to be initiated by the passage of single alpha particles with very high linear energy transfer. The alpha-particle tracks produce multiple sites of DNA damage that result in deletions and rearrangements of chromosomal regions and lead to the genetic instabilities implicated in tumor progression. Because low exposure conditions involve cells exposed to single tracks, variations in exposure translate into variations in the number of exposed cells, rather than in the amount of damage per cell. This mechanistic interpretation is consistent with a linear, no-threshold relationship between high-linear energy transfer (high-LET) radiation exposure and cancer risk, as was adopted by the BEIR VI committee. However, quantitative estimation of cancer risk requires assumptions about the probability of an exposed cell becoming transformed and the latent period before malignant transformation is complete. When these values are known for singly hit