atinon Preteen Dein Wal. 23 Nod pp. 10-187 (oa Nuclear Technlogy Publishing THE RADIOLOGICAL SIGNIFICANCE OF BETA EMITTING HOT PARTICLES RELEASED FROM THE CHERNOBYL NUCLEAR POWER PLANT W. Hofmannt*, D. J. Crawford-Brownt and T. B. Martonen$ +Center for Extrapolation Modeling, Duke University Medical Center Durham, NC 27710, USA Department of Environmental Sciences and Engineering School of Public Health, University of North Carolina Chapel Hill, NC 27514, USA SToxicology Branch, Health Effects Research Laboratory US Environmental Protection Agency, Research Triangle Park, NC 27711, USA Received September 21 1987, Revised February 3 1988, Accepted April 8 1988 Abstract — In order to assess radiological hazards associated with inhalation of beta emitting hot particies detected in fall out from the Chernobyl incident, radiation doses and lung cancer risk are calculated for a hot particle composed entirely of "Ru, Lung cancer risk estinates are based upon an initition-promotion model of carcinogenesis. In the immediate vicinity of a hot particle, calculations indicate that doses may be extremely high, so that all cells are killed and no tumour will arise. At intermediate distances, however. the probability for lung cancer induction exhibits a distinct maximum, Risk enhancement factors, computed relative to a uniform radionuclide distribution of equal activity, are highest for intermediate activities and hot particles moving in the lung. While the risk from inhalation of "Ru hot particles might, indeed, exceed that from all other exposure pathways of the Chernobyl fall-out, it still les within normal fuctuations of radon progeny induced lung cancer risk. INTRODUCTION Hot particles of beta emitting radionuclides have been detected in the fall-out originating from the Chernobyl reactor accident, varying considerably in radionuclide composition ‘and activity. The first measurements of hot particle activities conducted immediately after the nuclear accident have been reported by Devell et aX” who presented information on three selected hot particles. One of the particles contained mainly "Ru (10,000 Bq), while another particle was composed almost entirely of “Ba and "La (2400 Bq). Other radionuclides detected in these hot particles were "'Cr (1700 Bq), *Mo"Te(1600 Bq), “Ru (2800 Bq), and smaller activities of "Te, *Zr-°Nb, "'Ce, and “Ce. All three hot particles, however, varied significantly in their nuclide composition aad total activity, with totals ranging from 2740 to 18,280 Bq, Electron microscopy revealed nearly spherical shapes with geometric diameters of ~ 1 am. After the radioactive cloud had moved on to Central and Western Europe, hot particles were also measuted in other countries. Results of measurements in Hungary for the period April 29 through May 8, 1986, indicated much smaller activities”. The total activities of 15 hot particles reportedly ranged from 25 to 617 Bq, consisting of * Permanent Address: ion of Biophysics, University of Salzburg, A-5020 Salzburg, Austria. Zr 95Nb, MRu, Ru, Ba-"La, “1Ce, and “Ce in significantly varying compositions. The nuclides with the highest activities were Ru (455 Bq), “Ba (147 Bq), "Ru (110 Bq), and °°Nb (91 Bq). Hot particles found in Bulgaria had a mean activity of 260 Bq. with a maximum of 1500 Bq. The highest activities were associated with ™Ru and Ru, but 8Z1-Nb, Ce, and ‘Ce nuclides have also been detected. Geometric particle sizes were in the range of 0.5 to 3 um, exhibiting. however, very ircegular shapes. In all these measurements, the contribution from alpha emitters, mainly “Cm, was less than 1% of, the beta activities. Also, the activities of iodine and caesium isotopes, which constitute the most significant portions of the fall-out doses via inhalation and ingestion, were small compared with the other beta activities in the particles. INHALATION OF HOT PARTICLES “The radionuclide most frequently found in ail hot particles is “Ru, with an average activity of about 300 Bq per particle". The half-life of ‘“Ru is 39.3 Disclaimer” The research deseribed in this article has been reviewed by the Health Effects Research Laboratory, U.S. Environmental Protection Agency. and approved for publication. Approval does not signify that the contents necessarily reflect the views and polices of the Agency nor does mention of the trade names or Eommercial products consitute endorsement for recommendation for use 149W. HOFMANN, D. J. CRAWFORD-BROWN and T. B, MARTONEN days, and it decays primarily by emission of a beta particle with maximum energy 0.212 MeV (89%) and average energy 0.062 MeV), In our consideration of the radiological risk associated with inhalation of hot particles we use a hot particle composed entirely of '“Ru, with an activity of 300 Bq and a geometric diameter of 1 um. This particle will be compared with 30 Bq and 3000 Bg particles, reflecting the observed broad range of activities Similar results will be obtained for other B emitting radionuclides of comparable, half-life and energy, such as Zr, "Nb, “Ba and "Ce. Published data on the concentration of hot particles in ambient air during the time of the passage of the radioactive cloud are very limited Balashazy et af reported that the average hot Particle concentration in Budapest during the period 29 April - 8 May 1986, was 5 x 10" m™. Under the assumption that the total "Ru activity in air consists entirely of hot particles, Burkart used data obtained in Switzerland to derive an upper estimate of 5 x 104 m® for 10 kBq particles with 2 um diameter. and $ x 107 m for 100 Bq particles with 0.43 yum diameter. Using the same relative activity fractions for the two particle sizes for total activity measurements in Bulgaria, plus additional data on the hot particle concentrations on the ground", we estimate an average atmospheric hot particle concentration of about 1 x 10° m® for Bulgaria over a period of approximately one week. ‘Thus, measured and estimated hot particle concentrations range from 5 x 10° to 5 x 107 m?. From these data, we derive an average hot particle concentration of 1 x 10°? m* and will use this value in our subsequent analysis. The reader must note that this assumed concentration is an average of the few published studies and is only coincidentally ‘equal to the value measured in Bulgaria In ot simulation, assuming a respiratory minute volume of 15 J.min"! as an average value for resting and light activity breathing over @ whole day”, and an exposure time of onc week, 0.15 particles will be inhaled per exposed individual. For a J wm particle the probability for deposition in the pulmonary region is about 20% (note: tracheobronchial deposition will be neglected here because mucociliary clearance will be relatively fast compared with the long half-life of "'Ru of 39.3 days). Thus a mean value of 0,03 particles per person will be deposited in the respiratory tract, or 1 person out of 33 will deposit one hot particle. ‘Applying Poisson statistics, the probability for inhaling and depositing two particles is 4 x 10, and 4 x 10° for three hot particles. Thus higher hot particle concentrations in ambient air will increase the number of individuals inhaling a hot particle, but ‘not the number of inhaled particles per person. "Ru in the oxide form® is considered an insoluble particle", Bailey and Fry" report a two clearance phase mechanism for insoluble particles in the pulmonary region, having half-lives of 26 and 575 days. The very long (575 days) balf- time dominates retention, with 90% of the activity going into this compartment. For our calculations ‘we assume that a hot particle, once deposited, will be retained in the decp lung for 1 year. Thus, the cumulative activity of a 300 Bq “Ru hot particle integrated over one year is 17.1 KBq.day. DOSIMETRY AND RISK ASSESSMENT Now, we shall address the question: what is the lung cancer risk for an individual subsequent to inhalation of such a hot particle? A review of information concerning the decay of Ru indicates that “Ru decays into Rh” (97%) by emission of thice betas, with maximum energies of 0.10 MeV (7%), 0.212 MeV (89%), and 0.71 MeV (3%). while only 0.3% decay directly into the stable "Rh. For thesc betas we use an average energy of 0.062 MeV. All excited energy levels of T™Rh decay through emission of several gammas into the metastable “™“Rh®, and further, with a half- life of 57 min, into the Rh ground state by emitting an internal conversion electron of 0.0398 MeV energy. Thus the dose to the surrounding tissue from a decaying “Ru nuclide is delivered by (@ betas, (ii) conversion electrons, and (iii) gamma rays. Inhalation of a ‘Ru hot particle results in an average lung dose of 3.2 x 10° (30 Bg), 3.2 x 107 (00 Ba), and 3.2 x 10" (3000 Bq) mGy.y, respectively’, These doses are far below the maximum permissible doses to the general public of 5 mGy.y" (1/10 of the annual limit for radiation workers) or 1.67 mGy.y" (1/30), as is the current practice in most countries. Recently, however, Hohenemser et al question whether a hot “Ru particle is more carcinogenic than uniformly distributed nuclides of the same total activity. ‘The term ‘hot particle’ is usually used in the context of alpha emitting radionuclides, especially plutonium. Tamplin and Cochran? initiated the controversy about hot particles by contending that inhalation of hot particles containing a certain amount of alpha emitters represents a lung cancer risk which is substantially higher than if the same amount of radionuclides were distributed among smaller sources in the lung. Subsequently, the hot particle issue has been addressed by numerous scientists and scientific bodies who have concluded that a hot particle effect with regard to lung cancer has not been demonstrated in either humans or laboratory animals"), However, the finding that lung cancer risk per unit dose in experimental animals for insoluble transuranics is two to three 150BETA HOT PARTICLE DOSIMETRY times that for soluble transuranics could be interpreted as a hot particle effect’ (although other interpretations, such as dose rate, might be invoked). No comparable imental information, however, can be found in the literature for hot beta emitting particles. Coggle et af" have conducted experiments in which mice were irradiated with X rays. either uniformly or non-uniformly microbeams. These experimental conditions are similar to those in the present paper in that the radiation was low LET and microbeams were of 1 mm diameter (Similar in scale to the irradiated zone surrounding the "Ru particles). Their experimental results suggest that the lungs were slightly less sensitive to lung cancer induction when 20% of the lung was irradiated with mictobeams as opposed to uniform irradiation, with the average absorbed dose being the same in both cases. The model developed in the present paper will be applied to their data and discussed in a later section. Recently, Hofmann and Martonen'"” studied theoretically the carcinogenic potential of thot spots’ of alpha emitting radon progeny at bronchial airway bifurcations. The term ‘hot spot’ for radon progeny indicates that activity is not concentrated in @ single particle, but remains highly localised. In addition, the activities involved are much smaller than for a typical hot particle. Consistent with the aforementioned experimental results, lung cancer risk associated with a single ‘hot spot’ which delivers an average dose, D, at sufficiently high doses (greater than 1 Gy) was predicted to be smaller than that for uniformly distributed nuclides at the same dose, but higher at sufficiently small activities (producing less than 0.05 Gy). Similar results, i.e. lower predicted risk at high activities but higher risk at low activities, have been reported by Mayneord and Clarke" for Pu. Moreover, Mayneord and Clarke st beta emitting hot particles (*Rb, *S), finding the same tendency as has been observed for alpha emitters. Thus theoretical models predict a reduced risk at a given dose for high activities relative to uniform distribution, consistent with the _limited experimental evidence, but an increased risk at low activities. ‘We shall, therefore, seek to estimate the lung cancer risk of a Ru hot particle for three different activities, i.e. 30, 300, and 3000 Bq. This range of activities is similar to the range of measured activities reported earlier. Before proceeding to the development of a predictive model, 2 few words are needed concerning the evidential support for the model. Such support may be found in two primary forms: (i) evidence that the axioms of the model are correct, and (ii) evidence that the composite model correctly predicts the results of dose-response studies for hot particles. Unfortunately, the latter form of evidence is not available at present in the desired form. Instead, some loosely related observations are available, and these will be described inthe discussion section. Our model has to rely, therefore, mainly ‘on the first form of evidence. Despite the lack of appropriate data for model validation, however, the assessment of health effects of the Chernobyl fall-out warrants the application of this predictive model in the absence of any other information. It is assumed that any predictive model for radiation induced cancer must account for three properties of radiation. First is the ability of radiation to kill cells, which has been described mathematically by an exponential dose-response function with an exponent linear-quadratic in dose. Second is the ability of radiation to transform cells into (at least) a precancerous state. The probability of a cell being transformed, while at the same time surviving irradiation, then may be given as the product of the two terms discussed above, as suggested in the BEIR-III Report” ‘The probability that a given cell will survive and be transformed when receiving a dose D then can be represented by the general form of an incidence function?” as Pum = (@D + BD*) exp [-(yD + 6D7)] where a and fi are sensitivity parameter transformation, and y and 5 ate sensitivity parameters for cell killing. Since we are not aware of published data describing the transformation function for beta emitters in lung tissue, a ratio of aif = { Gy, as found in many radiobiological studies concerning the action of low LET radiations on cells", will be assumed here. For cell killing, we shall use two different sets of data reflecting the effect of tissue sensitivity variations, as suggested by Mayneord and Clarke": (iy = 3 x 107 Gy! and 8 = 1 x 10" Gy, derived from the leukaemia incidence in atomic bomb survivors™, and (ii) ¥ = 5.3 x 107 Gy" and 6 = 1.9 x 107 Gy®, derived from survival studies of V79 Chinese ‘hamster cells), The choice to test modet predictions under two sets of assumptions about cell killing parameters does not arise from a belief that this term is the most sensitive to changes. In fact, it is likely that the induction term contributes to the overall uncertainty in the model to a similar degree. Comparable data relating the induction parameters to different kinds of studies (i.e. human epidemiology versus cell studies) simply are not available at present ‘The third property of radiobiological interactions also is related to the ability of radiation to kill cells. Here, however, the focus is not on the killing of wo 151W. HOFMANN, D. J. CRAWFORD-BROWN and T. B. MARTONEN transformed cells, but rather the killing of cells in the immediate vicinity of the transformed cells. As demonstrated in other studies, cell killing following irradiation produces an increase in the mitotic index of surviving cells. In addition, it is assumed here that a necessary condition for a transformed cell to develop into a tumour is subsequent cell division", stimulus for cell division can be achieved by Killing cells in the vicinity of transformed cells, thereby allowing radiation to act as a promotion factor by inducing hyperplasia. If the probability of division is owch Jess than the probability of repair for cellular damage, then the promotion probability can be expressed by Pron: = K (hi + da 1 — expl-(yD + 3D?) 2) where k is an arbitrary scating constant, set equal to 1 in this text, Ay = LT, is the production rate by normal mitosis, hy = 1/7; is the production rate by stimulated cell division, and {1 — exp[-(yD + D?)}) is the fraction of killed cells at dose D. For the lung as a slowly dividing epithelial tissue, we may let T; = 100d as an average lifetime” 2, and T; = 1d as a typical cell cycle time under conditions of cellular replacement. The lung cancer probability P. is the product of Pra X pom integrated over all cells N(D) receiving dose D: Puc = [7 N(D) ((@D + BD*) exp[-(yD + 6D")|} x Oy +e {1 — exp[-(yD + oD) dD) For a uniform nuclide distribution in the lung, producing an average dose J in each cell, the lung cancer probability Pic may be written as Py (uniform) = n- m, { (al + BD*) exp[-(yD + 5D*)]} X Gr + by {1 — exp[-(7B + 5D4))}) 4) where m, is the mass of the lung (m, = 1 kg), and nis the number of cells per unit mass. [t is important to note the Equations 3 and 4 yield the classical ‘bell- shaped” dose-response curve when the dose is uniformly distributed. In the case of a hot particle, with the dose distribution D(r) expressed as a function of the radial distance, r, from the particle itis necessary to integrate over all distances r: Prec (hot particle) = n= py £ dmrde ((eD(r) + BDO) expl-G@D(r) + 6DG))T} x Oy + he {1 — expl-(D@) + SD(1)]}) 6) where p, = 0.26 g.cm™ is the average density of the lung, including the air volume. Assuming uniform cellular density throughout the lung, n may be set equal to I in both equations. ‘The dose for a given cumulative activity, integrated over a period of 1 year, as a function of the radial distance r has been calculated by using Loevinger’s empirical formula for a beta point source in a homogeneous, infinite absorbing medium”, By taking a cumulative activity, we neglect differences in dose rate because of radioactive decay during the course of the year. In other words, only an average dose rate is assumed, rather than formally including the effects of the changing dose rate over the year. MODEL PREDICTIONS Figure 1 presents the dose, the cellular transformation probability, Pian» aNd Pyage mulkiplied by the promotion probability, Pau, a8 4 function of the distance r for a 300 Bq "iu hot article using set (i) of the cell killing parameters. All three quantities are expressed in arbitrary units regarding their absolute values as well as relative to each other. The figure illustrates that doses in the immediate vicinity of the hot particle are extremely high, so that all cells in this neighbourhood will be Killed, and, subsequently, no tumour can arise. It is interesting to note that the intemal conversion electron from ™Rh™ does not contribute to the overall cancer risk, since the energy of this oes Pergne” Perane = pram (oeBeaniee) ot 0.6 08 LO 12 La Radial dioteace (mm) Figure 1. Dose, transformation probability (Pyaads and Joint probability for transformation and promotion (Pe % Ppaom)s a6 a function of the radial distance, r, from the centie of a 300 By ""Ru hot particle in tung tissue Radiosensitivity parameters for cell killing are: y = 3 = 10" Gy" and 8 = 1 x 10! Gy”, 16 Le 152BETA HOt PARTICLE DOSIMETRY clectron is delivered entirely within the region of complete cel killing. Between 0.7 and 0.8 mm from the “hot particle, the probability for cellular transformation and the joint probability for transformation and promotion exhibit a distinct maximum. The location of this maximum depends on the activity of the hot particle (i.e. the higher the activity the greater the distance), and on the assumed cell killing parameters. For example, for set (ii) this maximum lies between 0.6 and 0.7 mm, for 2 300 Bq particle. At greater distances, Paes decreases in a neatly parallel manners to dose, while the term Pyag X Pyron falls off more sharply because of the less effective promotion mechanism which saturates at high doses. ‘The probabilities for lung cancer, Py, integrated over all distances r, are given in Table | for the three selected hot particle activities, and are compared with the corresponding uniform dose distribaition, Several approaches were taken to modelling the movement of each particle in the lung. In order to investigate a potential hot particle effect, cancer risk in Table 1 is based only on the dose delivered by betas and conversion electrons, thereby neglecting the uniform gamma contribution. While the conversion electron contributes to the overall risk under uniform irradiation conditions, all its energy is wasted by cell killing in the hot particle case. First, risk was calculated for a stationary hot particle, i.e. a particle which remains at a given site for one year (denoted at 1 x 30 Bq, or 1 x 300 Bq, or 1 x 3000 Bq), When it is assumed that there is no radiological promotion mechanism (or, Pie = (Praca), then the 30 Bg hot particle has the highest ‘Table 1, Cancer risk probsbilities for stationary and moving risk, being typically greater than the corresponding uniform distribution. Conversely, the hot particle risk for a 3000 Bq particle is always smatler than that for its uniform distribution, If we include our promotion factor, Puc = | Pram Pyrams il! the analyses, then the 30 Bq particle has again the highest risk relative to the corresponding uniform distribution. However, now all particles have a higher lung cancer ‘risk than their uniform distributions, ranging up to two orders of magnitude, with the 3000 Bq particle having the highest risk. The maximum promotion factor, and thus risk enhancement factor, in our calculation is 100 (it should be recalled ‘that this calculation assumes T/T: = 100). Particles in vivo, however, do not remain tocalised for such long periods of time, but instead are continuously moving throughout the pulmonary tegion. For example, movement of a single 300 Bq particle may be simulated by the action of 10 smaller 30 Bq particles (denoted as 10 x 30 Bq), which is equivalent to one 300 Bq particle staying at 10 different non-overlapping sites for each 1/10 th of a year. For all modelling assumptions and sensitivity Parameters, particle movement increases lung cancer risk by up to two orders of magnitude, ‘Though the risks relative to the uniform distribution are the same for all multiples of 30 Bq, the tisk is highest for a very mobile 3000 Bq particle (100 x 30 Ba). ‘Vrresponding calculations for a unit density tissue show a similar pattern of response, reducing, however, the maximum relative risk to about one order of magnitude (Table 2). Thus, if a hot particle "Ra hot particles in lung tissue compared with a uniform radlonuctide distribution. Cancer risk Ra beta activity (Bq) (p = 0.26 gem") Pre "3000 300 30 (arbitrary units) 100% 30 10 x 300 1 = 3000 10% 30 1x 300 130 Unitorm distribution Zax 23%10° 23x18 3x0 23K 23% 10! Hotpantclet Pre = | Pras 21x10 60x10 13x10 21x mF 60x10! 24 x 10! Hot particle? Pic= | Pram z Poe 18 x10 25x10 56x10 75x10 25x10" 73x10" Hotpartictet Pac | Prease 5.4 10° 2110 5.310% 54x10 2.1 x 10? 54x 10! Hot Put Prom 16x18 Bax tot 2.3.x tot 16x10 84x 108 1.6% 108 * Additional gamma component risk: 8.8 (30'Bq), 8.8 x 10° ( + Refers to set (1) of ing parameters. $ Refers to set (i) of cell killing parameters, 153, 300 bg), and 8.8 x 10" (3000 Bq)W. HOFMANN, D. J. CRAWFORD-BROWN and T. B. MARTONEN is cleared from the lung and then trapped in an organ with unit density for a longer period of time, the hot particle effect is smaller than in the lung itself. ‘The simultaneously emitted gamma radiation produces a rather uniform distribution of risk, even in the case of a hot particle. If the gamma component is factored into our risk analyses, then an additional cancer risk (in arbitrary units) of 8.8 (30 Bq), 8.8% 10" (300 Bq), and 8.8 x 10° (3000 Bq), Tespectively, has to. be added to the risk of the beta component given in Tables 1 and 2. This additional risk contributes to the overall risk only in those cases where the hot particle risk is smaller than that from the corresponding uniform distribution. For most cases discussed here, however, it does not affect our hot particle estimates, and thus not the conclusions drawn from this analysis. DISCUSSION ‘The data presented in Tables 1 and 2 indicate that the carcinogenic response to hot particle irradiation relative to a uniform distribution of the same total activity can be smaller by one order of magnitude Pam)» OF higher by two orders of magnitude J Peo * Pprom), depending on modelling assumptions and sensitivity parameters. The highest risk values will be obtained for moving particles. The influence of two choices for cell killing parameters, as described earlier, may be seen in Tables 1 and 2. These tables do not, however, reflect differences which might arise from a choice of values for Ay and dy in Equation 5. Reference to Equation 5 indicates that the maximum contribution of the promotional term increases approximately linearly with increases in the ratio M/A), An assumed ratio of 100 (as used in our calculations), therefore, gives a higher promotional enhancement factor than would be the case for ratios of 50 or 10 (10 being a reasonable lower bound). The result of this consideration is that the risk values in Tables 1 and 2 for uniform irradiation would not change when the ratio AM changes, singe the mean lung doses are too low to cause significant cell killing. The risk from the various hot particles, however, will decrease approximately linearly as 2_/h, is lowered from 100 to 10. In addition, various assumptions might be employed for the ratio o/f in Equation 5. To test the influence of this ratio on the conclusions of the study, we varied o/8 from 0(pure quadratic) to 1 Gy (as used in our calculations) to 10 Gy. The value of 0 was suggested by the study of Chen ef afi) concerning mutagenicity in cultured human fibroblasts exposed to X rays, while the value of 10 Gy was taken from the study of Thacker et af concerning mutagenicity of cultured hamster cells following X ray exposure. Using these various values for a 300 Bg particle (as an example), the ratio of theOrisk from a hot particle (with promotion) to uniform irradiation is approximately 11 when adB is | Gy (see Table 1, set (i) of cell killing parameters). This ratio falls only to approximately 4 when aiB is set equal to 10 Gy. The risk ratio rises dramatically, however, to 2 value of about 4 x 10° when alf is set that the effectiveness of the uniform ‘Table 2. Cancer risk probabilities for stationary and moving "Ru bot particles in unit density tissue compared with » uniform radionwclide distribution. Cancer risk” Wu beta activity (Bq) (p = 1 gem ¥) Pie 000 300 0 (arbitrary units) 100% 30 10 x 300 1 3000 10x20 1x 300 130 Uniform distribution Dax AK ASK BK SKI 23 x10 12x 24x 10! 43 12x10! 2 12 52x 10° 14x 10° 2.0 x 10 52x 10° 14x 1 52x10! 45 x 107 11x10 1.9 x 10! 45x 10" 11 x 10" 45 Hot particle Pic = | Pram Prom 18x10 44x10 8.9% 10? 18x10 d4xto® 18K 10 * Additional gamma component risk: 8.8 (30 Bq), 8.8 x 10" (300 Bq), and 8.8 x 107 (3000 Bq). + Refers to set (i) of cell kiling parameters. + Refers to set (i) of cell 154BETA HOT PARTICLE DOSIMETRY irradiation is strongly dependant upon for a pure quad tion function, A similar pattern as shown in Tables 1 and 2 has been noted in the case of cells irradiated in vitro by alpha particles) and rats irradiated in vivo by p@) “in the former experiment, the mutation frequency for cells irtadiafed by a moving source ‘was higher than that from a stationary source at a given activity. Also, the mutation frequency of the agitated microspheres of low specific activity was found to be smaller than that of high specific activity, for the same total activity, but no difference could be observed for the stationary microspheres. In the lattes experiment, the cancer incidence for a 20 wCi (7.4 10? kBq) pellet was found to be 56%, while the incidence from a single 2 wi (7.410! kBq) pellet was 33%. From these results, it may be hypothesised that if 10 of the 2 wCi (7.4%10" kBq) pellets were assumed to be planted into each animal, the resulting risk would be approximately 98%. This calculation suggests that the incidence per unit dose is higher when a source is divided into several fractions, which is analogous to a moving source, Equations 3 and 4 also have been used to analyse the data by Coggle et af‘. At the outset, it should be mentioned that their data were obtained at average tung doses in the range of 0.2 ta 7.5 Gy which were approximately four orders of magnitude above those produced by the “Ru hot particle examined here. They report a lung cancer incidence which shows a slight increase at 2 to 5 Gy, while Equations 3 and 4 predict a maximum lying between 2and 6 Gy, dependent on the choice of cell killing parameters. Furthermore, both the experimental data and the model predictions indicate negligible risk at minimum (0.2 Gy) and maximum (7.5 Gy) doses investigated. In addition, our model predicts that the microbeam irradiation should be slightly less effective than the uniform irradiation, a prediction which is born out by their data, Finally, it is interesting to note that the present model suggests that the lung cancers in the microbeam experiment should not be induced in the 20% of the lung irradiated by the primary beam, but rather in the 30% ted by the scattered component of the REFERENCES beam. This situation would arise duc to the killing of cells within the primary beam, with the lower doses from the scattered component contributing most to the observed lung cancer risk. It may be concluded, therefore, that the present model provides a clear explanation of this experimental data Now we shall compare the doses and associated risks of these particles to: (i) other radionuclides in the Chernobyl fall-out, and (ii) the natural radiation burden Whole body doses from 41 incorporation and, especially, from "Cs ingestion in the most heavily exposed ateas in Central and Western Europe are in ‘the range of 0.4 to 1.5 mSv.y"™). Because of the rather uniform distribution of "Cs in the human body, we may consider these values to be valid for the lung too. Inhalation of a 3000 Bq particle, without any risk enhancement factors, produces an average dose of 0.16 mSv.y* in pulmonary tissue, a value lower than the dose equivalent from ‘Cs uptake. If we incorporate a maximum risk enhancement factor of 100, then the corresponding dose equivalent would be 16 mSv.y'. Under these assumptions, the risk from inhalation of a “Ru hot particle with an activity of some kBq might exceed that from all the other exposure pathways by up to an order of magnitude. ‘The most significant contribution of the natural radiation environment is the inhalation of radon ‘progeny causing the highest doses in the bronchial region of the lung”. Inhalation of a typical radon concentration within dwellings of 37 Bg.m™? (1 iI), with aa cquilibrium factor of 0.6 for the short-lived radon progeny, gives a basal cell dose in segmental and subsegmental bronchi of about 3.5 mGy.y"™, Assuming a quality factor for alpha particles of 20 indicates a dose equivalent of 70 mSv.y"!. Even under the assumption of a maximum risk enhancement factor, therefore, the hot particle dose equivalent is smaller than that for naturally ‘occurring radon progeny exposure. Heaceforth, we conclude that the potential lung cancer risk caused by the inhalation of “Ru hot particles lies within the fluctuations of the estimated radon induced cancer risk, and is thus unlikely to be detected from the spontaneous, natural tung cancer incidence. 1. Devell, L., Tovedat, H., Bosgstrm, U., Appelaren, A., Chyssler. J. and Anderson, L. Jnitial Observations of Fallout from the Reactor Accident at Chernobyl, Nature 321, 192-193 (1986). 2. Balashazy, f., Szabadine-Szende, G., Lérinc, M. and Zombori, P. Gamma-spectromtric Examination of Hot Particles Emined during the Chernobyl Accident. KFKI Report 1987-24/K (Central Research Institute for Physics, Budapest, Hungary) (1987), 3. Committee for the Peaceful Use of Nuclear Energy of the People’s Republic of Bulgaria, Results of Studies on the Radiation Exposure in Bulgaria aftr te Chernobyl Accident. (Sofia, Bulgaria) (1986). 155W. HOFMANN, D. J. CRAWFORD-BROWN and T. B. MARTONEN 4 Nuclear Data Group. Nuclear Level Schemes A-=45 through A=157 rom Nuclear Date Sheets (New Yor: Academic 5. Shieien, B. and Terpilak. M.S. The Health Physics and Radiological Health Handbook (Olney, MD: Nucleon Lectern Associates) (1984) 6. Burkart, W. ‘Hot particles’ im Tschernobyl-Ausfall: Abschatzung der Dosimetrie und Diskussion der biologischen Effekte. IN Radioahtivitdismessunginder Schweiz nach Tschemobylund ihre wissenschaftliche Interpretation, pp. 660- ‘670 (Bundesamt fr die Gesundheit: Bern, Switzerland (1986). 7, Hofmann, W. Dose Calculations forthe Respiratory Tractfrom Inhated Natural Radioactive Nuclidesasa Functionof Age -H. Basal Cell Dose Distributions and Associated Lung Cancer Risk. Health Phys. 43, 31-44 (1982), 8. Stahthofen, W. Human Dara on Deposition. IN Lung Modelling for Inhalation of Radioactive Material (Brussels: Commission of the European Communities) Report EUR 9384 EN, pp. 39-59 (1984) 9, International Commission on Radiological Protection, Limits for Intakes of Radionuclides by Workers. ICRP Publication 30, Part2, Ann. ICRP (3/4) (Oxford: Permamon Press) (1980), 10. ICRP Task Groupon Lung Dynamics. Depositionand Retention Models for Internal Dosimetry ofthe Human Respiratory Tract. Health Phys. 12, 173-207 (1966) 11. Bailey. M. Rand Fry, F. A. Pulmonary Retention of insoluble Particlesin Man. 1NCurrent Conceptsin Lung Dosimetry, ‘ed. D. R, Fisher. pp. 104-115 (Technical Information Center, U.S. Department of Energy) (1983). 12. International Commission on Radiological Protection. Limits for Intakes of Radionuclides by Workers. CRP Publication 30, Supplement to Part2, Ann. ICRP § (1-6) (Oxford: Pergamon Press) (1981). 13. Hohenemser, C., Deicher, M., Hofsiss. H., Lindner, G. Recknagel. E. and Budnick, J. 1. Agricultural Impact of Chernobyl: A Warning, Nature 321.817 (1986). 14, Tamplin, A. R. and Cochran, T. B. Radiation Standards for Hot Particles. Natural Sciences Defence Council, ‘Washington, DC. (1984), 15. National Council on Radiation Protection and Measurements. Alpha-Emitting Particles in Lungs, Report No. 46 (Washington DC: NCRP Publication) (1975). 16, International Commission on Radiological Protection. Biological Effects of Inhaled Radionuclides. ICRP Publication 3, Ann. SCRP 4 (1/2) (Oxford: Pergamon Press) (1980). 17. Coggle. J. E., Peel, D. M. and Tarling, J. D. Lung Tumor Induction in Mice after Uniform and Non-uniform External Thoracic X-irradiation. In. J. Radiat. Biol. 48, 95-106 (1985). 18, Hofmann, W. and Marionen. T. B. The Significance of Enhanced Radionuclide Deposition at Bronchial Bifurcation. ‘Ann. Occup. Hyg. (in press). 19. Mayneord, W. V. and Clarke, R. H. Carcinogenesis and Radiation Risk: A Biomathematical Reconnaissunce. Br. 1. Radiol. Supp!. 12(1975). 20. Mayneord, W. V. and Clarke, R. H. Quantitative Assessment of Carcinogenic Risks Associated with ‘Hot Particles. Nature 259, 535-539 (1976) 21. National Academy of Sciences, Committee on Biological Effects of lonizing Radiation. The Effects on Populations of Exposureto Low Levels of lonizing Radiation: 1980 (BEIR-Il1) (National Academy Press: Washington, DC} (1980). 2, Upton. C. Raiobictgial Efe of Low Dose: lmpition for Reco! Proton. Rat. Re. 7.514 23. Hall, E. J. Biological Problems in the Measurement of Survival et Low Doses. IN Cell Surv Radiation, ed. T. Alper, pp. 13-24 (London: Instituie of Physies and John Wiley) (1975) 24, Gross, N. J., Narine, K. R. and Colletti-Squinto, L. Replicative Activity of Lung Type 2 Cells Following Lung X Irradiation, Radiat. Res. 111, 143-150(1987).. 25. Kakunaga, T. Requirement for Cell Replication in the Fixation and Expression of the Transformed State in Mouse Cells Treated with 4-Nieroquinoline-t-Oxide. ln. J. Cancer 14, 736-72 (1974). 26, Hall,E.1.andHei, TK. Oncogenic Transformation with Radiationand Chemicals. It. J. Radiat. Biol. 48, 1-18(1985). 27, Brown, J. M. and Berry, R. J. Effects of X-irradiation on the Cell Population Kinetics ina Model Temour and Normal Tissue System: Implications forthe Treatment of Human Malignancies, Br. J. Radiol. 42,372-377 (1969). 28. Frankfurt, 0... Mitotic Cycle and Cell Differentiation in Squameous Cell Carcinomas. Int. J. Cancer 2, 304-310 (1967), 29, Hall,E.1. Radiobiology for the Radiotogist, p.257(New York: Harper & Row) (1978). 30, International Commission on Radiological Protection Reference Man: Anatomical, Physiological and Metabolic Characterisscs. ICRP Publication 23 (Oxford: Pergamon Press) (1975). 31. Fitzgerald, J.J.. Brownell, G. L. and Mahoney. F. J. Mathematical Theory of Radiation Dosimetry (New York: Gordon and Breach) (1967). 32, Chen, D. J., umiste, G, F, and Tokita, N. The Genoworicity of Alpha Particles in Human Embryonic Skin Fibroblasts. Radiat. Res. 100, 321-327 (1984), 33. Thacker, J.,Streteh, A. and Godhead, D. T. The Mutagenicity of « Particles from Plutonium-238. Radiat, Res.92,343- 3521982), I after Low Doses of 1564 38. 36, 3. BETA HOT PARTICLE DOSIMETRY Fisher. D. R. . Frazier, M. E. and Andrews Ir, T. K. Energy Distribution and the Relative Biological Effects of internal Alpha Eminers, Radiat, Prot, Dosim. 13, 223-227 (1985). Laskin, $.. Kuschner, B.. Altshuler. B. and Nelson. N. Tissue Reactions and Dose Relationships in Rats Following Intrapulmanary Beta Radiation. Health Phys. 10, 1229-1233 (1964). Steinhausler, F., Daschil. F., Hofmann. W. and Reubel, B. Chernobyl and its Radiological and Socio-Economic Consequences for the Province of Salzburg, Austria, Environ. Int. (inptess) Pohl, E..Steinhdusler, F., Hofmann, W. and Pohi-Raling, J. Methodology of Measurement ad Statistical Evaluation of Radietion Burden to Various Population Groups from ail Internal and External Natural Saurces. TN Biological and Environmental Effects of Low-Level Radiation, STUPUBI409. pp. 305-315 (Vienna: International Atomic Energy ‘Ageney) (1976). Hofmann, W.Cettular Lung Dosimetr; for Inhaled Radon Decay Products a Base for Radiation-Induced Lung Cancer Risk Assessment, Calculation of Mean Cellular Doses. Radiat. Environ. Biophys. 20,95-112(1982). 157