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Dosimetry of Radon

The health effects of exposure to low and moderate levels of radiation are the appearance, at long times after exposure, of a small excess of cancers in any irradiated population and, one or more generations later, of a small excess of genetic disorders. The more important for setting radiation protection standards is the risk of radiation induced cancer. It is not possible, at present, to distinguish a radiation-induced cancer from one arising naturally, so that any estimate of the risk has to be made from a statistical analysis of the long-term health of irradiated populations. Although there are several population groups who were exposed in the past to high doses of radiation and from which estimates of cancer risk can be made, the single most important source of information is from the follow-up of the survivors of the Hiroshima and Nagasaki atomic bombings.

There is still considerable uncertainty concerning the long-term carcinogenic effects of low doses of radiation in man. The value of the cancer risk coefficient at low doses or dose-rates has markedly increased during the past decade. In 1977, its value was estimated by the ICRP (1977) to be 1.2x1 0-2 Sv-1. One year later United Nations Scientific Committee on the Effects of Atomic radiation (UNSCEAR) estimated it at 2.5x10-2 Sv-1 but since it estimated the dose reduction factor (DRF) as 2.5, for low doses the risk remained unchanged. UNSCEAR (1988) estimated its value at between 5 and 6x10-2 Sv-1 for adults. Finally, the 1990 ICRP Recommendations (ICRP, 1991) estimated the cancer risk coefficient to be 8x10-2 Sv-1 with a dose, dose-rate reduction factor equal to 2, hence at low doses its value was estimated at 4x10-2 Sv-1. The main cause of this three-fold increase was the introduction of risk projection models and a much smaller extent the new assessment in 1986 of the doses received by the A-bomb survivors.

This brief historical review shows that the evaluation of the risks with low dose irradiation's is a two-step process. The first is the assessment of the carcinogenic effects at doses higher than SOOmSv (range 0.5-1.0 Sv) where data are available. The second is the extrapolation from these doses to low doses (below 200 mSv). Exposure to ionising radiation occurs from radionuclides deposited within the body as well from sources outside the body. Differences in the characteristics of these two types of exposure must be considered when interpreting the possible health effects of radon radionuclides and its daughters.

With an internally deposited radionuclide, the radionuclide enters the body at the time of exposure but the doses it delivers to various organs and tissues of the body continue to accumulate until the radionuclide is removed by physical or biological processes. Thus, the radiation is delivered to various organs gradually, at changing dose rates, over what may be an extended range of ages. An internally deposited radionuclide also frequently produces nonuniform irradiation to the organs and tissues in which or near which it is corporated, depending on its radioactive emissions and metabolic characteristics.


Both Rn222 and Rn220 have relatively short radioactive half-lives and decay to isotopes of solid elements known as radon (or thorn) progeny. When the atoms are first produced they are chemically and physically very reactive and will attach themselves firstly to water or other molecules in the atmosphere and, if the opportunity offers, to particles of natural aerosols (including dusts) in the air. Radon progeny are said to be `unattached' if they are associated only with a few small molecules or `attached' if they are no large aerosol particles (where dimension might typically be up to one micrometre). If they are breathed in, a large number of both the attached and unattached radon progeny will be trapped in the lungs where they will often be retained for long periods, thus giving considerable opportunities for lung tissue to be irradiated by later decays. Conversely, if radon gas is inhaled it is largely breathed out again and it is unlikely that radioactive decay will take place in the lung. It is thus the radioactive progeny rather than the radon itself that presents the greatest health hazard. However, it is the movement of radon gas that determines the potential for exposure and it is often convenient to use `radon' in a generic sense to include both the parent gas and the radioactive progeny.

Deposition and residence time depend on whether the radioactivity is attached to air borne dust particles, or is unattached (following inhalation unattached daughters are able to deposit deeper in the lung than dust particle-attached radon daughters). Respiratory factors (breathing rate and depth, mucociliary clearance, and site of impaction in the bronchial tree) influence depth of penetration into the lung with deeper particles having a longer residence time.
Although radon-related lung cancers are mainly seen in the upper airways, radon increases the incidence of all histological types of lung cancer, including small cell carcinoma, adenocarcinoma, and squamous cell carcinoma. Lung cancer due to inhalation of radon decay products constitutes the only known risk associated with radon. In studies done on miners, variables such as age, duration of exposure, time since initiation of exposure and especially the use of tobacco have been found to influence individual risk.

Results from the largest domestic case-control study to date were published by researchers in Sweden (Pershagen et al., 1994). This study was based on 1360 lung cancer cases and roughly twice as many controls, and involved radon measurements in nearly 9000 dwellings occupied by the study subjects over a period of more than 30 years. The lung cancer risk was shown to increase to a statistically significant degree with increasing radon exposure. In particular, the relative risk was 1.3 (95% confidence interval 1.1-1.6) for an average radon concentration in the range 140-400 Bq m-3 and 1.8 (95% confidence interval 1.1-2.9) for concentrations in excess of 400 Bq m -3 These risk estimates are consistent with those from the miner studies. Moreover, there was statistically significant evidence that the joint effect of radon and smoking exceeded additivity, and the data were consistent with a multiplicative effect.

There is thus clear epidemiological and biological evidence for the role of radon in inducing lung cancer. Although there are some uncertainties in quantifying the risk, particularly at low radon exposures, the information available has allowed ICRP, NRPB and other authoritative bodies to adopt risk factors that can be used as the basis of programmes to prevent excessive human exposure by adopting remedial and preventative measures.

Within the Northern Ireland context the risk coefficient that emerges is 0.3% per 20 Bq-3 lifelong gas concentration. For the estimated exposure to radon in dwellings throughout Northern Ireland. the implied annual mortality is about 60 people, which is around 7% of the 800 or so deaths from lung cancer that occur annually, and about 2% of the 3500 or so deaths annually from all malignancies. At the action level of 200 Bq m-3, the lifetime risk of premature death from lung cancer is about 3%. This compares with an observed risk of lung cancer from all causes of 5% in the whole population of Northern Ireland.

   
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