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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.

Energy deposition and cellular radiation effects arising from the interaction of single 218Po and 214Po alpha particles with basal and secretory cell nuclei were simulated for different target cell depths in the bronchial epithelium of human airway generations 2, 4, 6, and 10. To relate the random chord lengths of alpha particle tracks through spherical cell nuclei to the resulting biological endpoints, probabilities per unit track length for different cellular radiation effects as functions of LET were derived from in vitro experiments. The radiobiological data employed in the present study were inactivation and mutation (mutant frequency at the HPRT gene) in V79 Chinese hamster cells and inactivation and transformation in C3H 10T1/2 cells. Based on computed LET spectra and relative frequencies of target cells, probabilities for transformation, mutation, and cell killing in basal and secretory cells were computed for a lifetime exposure of 20 WLM. While predicted transformation probabilities were about two orders of magnitude higher than mutation probabilities, they were still about two orders of magnitude lower than inactivation probabilities. Furthermore transformation probabilities for basal cells are generally higher than those for secretory cells, and 214Po alpha particles are primarily responsible for transformations in bronchial target cells.

According to the theory and idea of Hopke et al., a bronchial dosimeter consisting of multiple metal screens has been developed to measure the deposition fractions of radon and thoron progeny in the nasal (N) and tracheobronchial (T-B) regions of the human respiratory tract and to give the dose conversion factors in the T-B region in units of mGy WLM(-1) and mSv y(-1) per Bq m(-3). Different air treatments have been performed in a closed laboratory, which include the use of air conditioning and the application of positive and negative ions for the investigation of the change of the dose conversion factors. At the same time, the radon and thoron gas concentrations have also been measured in the laboratory by active sampling using newly designed activated charcoal canisters connected in series with the bronchial dosimeter for the calculation of the resulted annual effective dose under different air treatments. It is observed that the calculated dose conversion factors derived from the bronchial dosimeter have large discrepancies with those computed using existing lung models. It has also been found that the application of negative ions cannot reduce the annual effective dose in the T-B region; the application of positive ions can lead to a reduction, but not as much as the use of air conditioning. The mitigation of radon effects by air conditioning demonstrated using the bronchial dosimeter is more prominent than that shown by using lung models.

A dosimeter for radon progeny has been proposed consisting of a single sampler with one 400-mesh wire screen and one filter, which is considered as a model for a portable bronchial dosimeter. During the sampling, air is drawn through the screen and the filter at a face velocity of 12.0 cm s(-1). After sampling, measurements of the screen and the filter are made at the same time through gross alpha counting. The annual effective dose (E, in mSv y(-1)) is calculated employing the exposure to radon progenies in the tracheobronchial (T-B) region. The dosimeter can be used in conjunction with an activated charcoal canister for the measurement of the radon gas concentration to yield the effective dose conversion factor (DCF, in mSv y(-1) per Bq m(-3)). These have laid the foundation to the design of a portable bronchial dosimeter. The validity of the dosimeter has been tested through measurements of annual effective dose and the effective dose conversion factor in different environments.

A series of experiments was performed to determine deposition efficiencies of four sizes of radiolabeled monodisperse particles in custom-made hollow tracheobronchial models. The particles had geometric diameters of about 1, 5, 10, and 15 microm. The tracheobronchial models, consisting of a trachea and two or more additional generations, had dimensions representative of a typical adult, a 7-y-old child, and a 4-y-old child; the child-size models were appropriately scaled-down replicas of the adult-size model. Each deposition experiment was conducted using a steady inspiratory airflow representative of low physical activity for the appropriate age of individual: 20 L min(-1) for the adult; 9 L min(-1) for the 7-y-old; 5.5 L min(-1) for the 4-y-old. The results indicate that deposition efficiency of the particles increased substantially (up to 35 times) in all three models as particle diameter increased from 1-15 microm, undoubtedly as a result of particle impaction and sedimentation-related phenomena. An analysis of variance demonstrated the occurrence of statistically-significant (p < 0.05) main effects of hollow model size and particle size; the interaction between the two parameters was also significant. In general, deposition efficiencies of the various sizes of particles were greater in the child-size models than in the adult-size model; this effect may have risk assessment implications. In addition, the results obtained experimentally agreed more closely with those predicted using a radiation-protection mathematical particle deposition formulation as the particle size increased for each of the sizes of models.

The alpha-activity on the bronchial airways has been calculated for 222Rn daughter exposures producing observable excess bronchogenic lung cancer in underground miners. The activity distribution of aerosol particles with attached 222Rn daughters on the bronchial tree is truly diffuse because of the short half-life of the daughters and the large number of particles in the ambient aerosol. From the bronchial airway activity and the minor epidemiology, it can be shown that it requires, on average, 4 X 10(9) stem cells in bronchial epithelium to be hit in order to produce an observed lung cancer. For very high 222Rn daughter exposures of miners, multiply hit cells are highly probable; yet the lung cancer response is lower per unit exposure at high exposures than for mining exposures--near those sustained in the environment probably due to stem cell death. A knowledge of the number of multiply hit cells in miners permits some infererences to be made about the effectiveness of particulate versus diffusely distributed alpha emitters in the lung, namely, that particulates should not be significantly more effective in lung cancer induction than a diffuse distribution.