RSH Data & Documents

"Low Level
Radiation Health
Effects: Compiling
the Data"

Revision 2
March 30, 1999
by Radiation, Science, and
Health, Inc.,
Edited by J. Muckerheide

1.2.6.3
Natural Activity and Radiation - Radon

"..the research suggests a linear extrapolation may overestimate hazard. First, it has been determined that there are multiple steps in the carcinogenesis process and that cells undergo many changes in transformation from a normal cell to a cancer cell (Cohen and Ellwein 1991). Large doses of radiation are capable of inducing all the changes needed to produce cancer. However, low radiation doses may cause only a few of the changes that are necessary for carcinogenesis. This would result in a sublinear dose-response relationship (less than a proportional response to dose) for the induction of lung cancer. This scenario has been reported in animal studies for lung cancer following plutonium exposure (Sanders et al 1993) or radon exposures delivered at low exposure rates (Morlier et al 1993).

"Empirical modeling supported by molecular and cellular research has helped explain these observations by indicating that tumor formation involves multiple events including cell proliferation, mutation events, and chromosomal changes. Research has shown that some of these cellular processes have a threshold below which significant alterations in normal tissues are not produced."

"Second, it has been determined that there is substantial repair (rejoining of alpha-particle-induced chromosome breaks), in contrast to what was previously postulated from cell survival studies in vitro..."

"Evidence exists for two types of repair of alpha-induced damage. The first repair type occurs at the cellular level and has been demonstrated by observing the frequency of chromosome damage induced by alpha particles by means of the 'premature chromosome condensation' technique (Cornforth and Goodwin 1991). In this method, irradiated cells are evaluated and the frequency of chromosome aberrations is recorded at short times after radiation exposure. Studies show that the frequency of broken chromosomes decreases as a function of time after exposure, indicating that damage induced by high-LET radiation is repaired."

"Repair also has been demonstrated for metaphase chromosome aberrations following radon exposure (Wolff et al 1991). When a small dose of X rays is given before radon exposure, there is a decrease in the amount of damage induced following exposure to radon only. This indicates that small doses of X rays can induce changes in the cells that either block radon-induced damage or increase its repair.

"The second repair type for radon-induced damage occurs at the tissue level. This repair relates to cell death that occurs when damaged cells attempt to divide. After radon exposure, tissue repair is expressed as a slow loss of damaged cells that contained chromosome aberrations and micronuclei (Khan et al submitted 1993). This repair was noted in both epithelial cells and fibroblasts from the respiratory tract.

"There are also indications that radon inhalation causes an increase in cell proliferation in the respiratory epithelium--a process that is a form of tissue repair. If repair is present at low dose rates or total radon doses, there may be a practical threshold below which there will be no increase in biological damage. If this situation is true for humans, average residential radon levels may not cause cancer."

"In contrast to the information that suggests a decrease in frequency of cancer at low total doses and dose rates, some data suggest that the effectiveness of alpha particles increases at low total doses and dose rates. This is called the inverse dose-rate effect, defined as an increase in the amount of damage per unit of exposure for high-LET radiation as the dose-rate decreases.

"Such an effect has been observed in experimental cell systems in vitro (Han and Elkind 1980) and in vivo studies of both underground miners and experimental animals (Cross et al 1984)."

"At the dose rates and total doses observed in homes, there is almost no chance for a cell to receive more than a single alpha particle during its lifetime and the probability that a cell will receive a second alpha particle during the time that it is in the sensitive stage of the cell cycle is extremely low. There is virtually no chance for the multiple interactions needed to cause the inverse dose-rate effect at these low levels of exposure."

"Of particular relevance to this issue are the results of the recent French study (Morlier et al 1993) examining the effects of low-level protracted radon exposures. In this study, two groups of 500 rats received 25 WLM of radon in either short or protracted exposures. The group exposed for 4 months had a lung cancer incidence 3.7 times higher than the controls. However, the lung cancer incidence in the group exposed for 18 months was the same as that of the controls."

"…These results, taken together with recently published cell biology studies and microdosimetry-based models, indicate that a nonlinear threshold risk model for radon-induced lung cancer cannot be ruled out."