Appendix E

Exposure to Radon (222Rn) and Its Decay Products

Lung cancer is well documented in underground mines, where miners are exposed to the short-lived decay products of 222Rn gas. The decay products are solids (218Po, 214Pb, and 214Bi), and although they are formed as atoms, the majority rapidly attach to the ambient aerosol particles (0.1 to 0.2 µm diameter). These particles are inhaled, and a fraction deposit on the bronchial airway epithelium, a thin layer where the target cells for carcinogenesis are located. The decay products have a very short half-life, ranging from 3.05 to 26.8 minutes, and therefore the decay products have the opportunity to emit alpha particles before bronchial clearance removes them.

The most complete analysis of the health detriment to underground miners is published in the document "Radon and Lung Cancer Risk: A Joint Analysis of 11 Underground Miners Studies" (NIH, 1994). This work brought together the investigators from each of the 11 mining groups, and their data were analyzed jointly to provide the best information for estimating the lung cancer risk from exposure to 222Rn and decay products. There were 2,701 lung cancer deaths among 68,000 miners accumulating about 1.2 million person-years of exposure.

In all of the 11 cohorts, the excess relative risk (ERR) of lung cancer (the fractional increase in lung cancer) was linearly related to the cumulative exposure estimated in working level months (WLM). Thus, although other carcinogens may be present in mine atmospheres, a clear relationship was associated with exposure to 222Rn decay products.

One important aspect of the data is that the ERR at very high exposures tends to flatten out. This observation is erroneously called the inverse exposure effect. It is usually stated that the lung cancer risk per unit exposure increases for low exposures compared with high exposures. The flattening of the response curve is likely the result of cell killing due to multiple traversals of cell nuclei. Therefore, the effect is a reduced response at high exposure, not an increased response at low exposure.

This terminology has caused considerable confusion with the implication that domestic exposure can somehow be "more dangerous" than mine exposure. This is not true, and it has been demonstrated that no additional risk above the linearity showed in all cohorts is present in domestic exposures. In fact, no domestic study has yet shown a statistically significant excess of lung cancer.

The main features of the lung cancer risk model derived from the jointly analyzed data are as follows:

  1. There is a reduction in risk subsequent to cessation of mining. This is called the time since exposure (TSE factor) effect.

  2. There appears to be no clear age at start of exposure effect (i.e., the age at start of mining is not an obvious factor). However, the age attained after start of mining is a factor and there is decreased risk with older age (AGE factor).

  3. Longer duration (DUR factor) or lower 222Rn concentration (WL factor) gives rise to larger risk. As this is the way the model parameters are derived, it is the reason for the so called "inverse exposure effect."

The two models derived from the joint analysis are considered equally likely as a fit to the observations. A striking feature of the data is the time since exposure effect, with three time windows modeled for the joint analysis versus two time windows modeled in the BEIR IV report when four cohorts were available for analysis.

The nature of the short-lived decay products of 222Rn provides an efficient means to irradiate target cells for cancer in the bronchial epithelium. They attach to very small ambient aerosol particles (about 0.1 to 0.2 µm diameter) and a few percent of these deposit on the airway surface on inhalation. The majority of the decay products actually deposit in the pulmonary region (about 25 percent), but the large area of the gas exchange region in the pulmonary compartment yields few alpha particle decays per unit area, yielding less dose. Thus the majority of lung cancer associated with 222Rn decay products is bronchogenic, similar to that for tobacco-related lung cancer (Saccomanno, et al., 1996).

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