Radon exposure limits are given in terms of radon gas concentration in the air. However, in the calculation of radon dose to the lung, the radon equilibrium equivalent concentration is used. The measured equilibrium factor times the measured radon gas concentration estimates the equilibrium equivalent concentration. Therefore, the equilibrium factor is an important factor in radon dose calculations. A review of published measurements of equilibrium factors shows a range of values reported in studies from more than 20 countries, measured in indoor residential, indoor public, and outdoor environments. Values for ²²²Rn are reported and discussed here, with special attention paid to results from India and China, where measured equilibrium factors are reported for hundreds and thousands of households, respectively. The wide range of equilibrium factors suggests that location-specific values are more appropriate than a worldwide average value in the calculation of lung bronchial dose.

An epidemiologic study of childhood leukemia in Denmark (2,400 cases; 6,697 controls) from 1968 to 1994 suggested a weak, but statistically significant, association of residential radon exposure and acute childhood lymphoblastic leukemia (ALL). The Danish study estimated a relative risk (RR) = 1.56 (95% CI, 1.05–2.30) for a cumulative exposure of 1,000 Bq m⁻³ y. For an exposure duration of 10 y their RR corresponds to a radon concentration of 100 Bq m⁻³. There are two dose pathways of interest where alpha particles could damage potential stem cells for ALL. One is the alpha dose to bone marrow, and two is the dose to bronchial mucosa where an abundance of circulating lymphocytes is found. Compared with an exposure of about 1 mSv y⁻¹ from natural external background, radon and decay products contribute an additional 10 to 60% to the bone marrow equivalent dose. The other pathway for exposure of T (or B) lymphocytes is within the tracheobronchial epithelium (BE). Inhaled radon decay products deposit on the relatively small area of airway surfaces and deliver a significant dose to the nearby basal or mucous cells implicated in human lung cancer. Lymphocytes are co-located with basal cells and are half as abundant. Using a 10-y exposure to 100 Bq m⁻³, our dose estimates suggest that the equivalent dose to these lymphocytes could approach 1 Sv. The relatively high dose estimate to lymphocytes circulating through the BE, potential precursor cells for ALL, provides a dose pathway for an association.

A miniature four-chamber alpha track detector was developed that measures both (222)Rn (radon) and (220)Rn (thoron), in duplicate. Using this detector and the previous long-term measurements of the (220)Rn decay products (212)Pb, and (212)Bi, an equilibrium factor, F(eq), is derived for both outdoor and indoor (220)Rn environments (0.004±0.001 outdoors and 0.04±0.01 indoors). The lung airway dose can then be calculated from a dose factor from UNSCEAR that requires the equilibrium equivalent thoron concentration (EEC), i.e. the product of F(eq) and the (220)Rn gas concentration. The lung dose from thoron in domestic or occupational surveys is often overlooked. The values of F(eq) for thoron in several published studies are in general agreement with the values reported here. Thus, a long-term alpha track measurement of thoron multiplied by an appropriate indoor or outdoor equilibrium factor yields the EEC, which can be used to assess bronchial lung dose.

A roundtable discussion was made at the end of the workshop. All the presentations were summarised in this discussion. It involved measurement techniques, quality assurance and dose assessment and health effects of thoron and its progeny. In particular, major epidemiological studies may be affected by thoron interference in radon measurements. Since their data are not sufficient when compared with that of radon, further efforts in thoron studies will be needed.

Guidelines for occupational exposure to radiation are based on annual absorbed or effective dose. Guidelines for ²²²Rn exposure are currently based on air concentrations of ²²²Rn or decay products. Models of bronchial dose from decay product exposure are based on calculations that have five major parameters with parameter variabilities ranging from 20 to 50%. Many countries currently use the ICRP dose conversion convention, which is a ratio of lifetime ²²²Rn lung cancer risk to lifetime atomic bomb dose risk. The results of ongoing epidemiology changed both lifetime risk values, and the dose conversion convention has increased by a factor of 2. Therefore, the current dose conversion convention risk ratio is to be replaced by biokinetic dosimetric models. The main effect of variability in the value of ²²²Rn dose factors on industry is that the workplace atmosphere must be characterized accurately, and at present, this is not possible. A history of the dose factor models is central to factor development. The values of the dose model parameters are described illustrating the difficulty in calculation of a dose factor with universal applicability. The objective is to show the range of each parameter and the effect of the dose factor used when reporting occupational or residential bronchial dose.