Environmental Engineering Reference
In-Depth Information
The main exposure/cancer risk is associated with inhalation of short-
lived RDPs and, secondarily, radon itself. Since radon is inert, only a very
small fraction of inhaled radon enters the bloodstream before it is exhaled,
and only a very small fraction decays while in the body. Radon decay
product exposures occur as a result of the inhalation of particle-attached
and unattached RDPs. Deposition of attached RDPs depends on particle
size. Large particles are deposited in the nose or pharynx; smaller particles
enter the lung and are typically deposited at the bifurcations of the upper
respiratory airways. Unattached RDPs usually settle on the surface of res-
piratory airways. Both attached and unattached RDPs can be absorbed into
fluids in the respiratory airways or removed by respiratory defense mech-
anisms such as cilia and mucus (and subsequently swallowed, entering the
gastrointestinal tract).
Radon-associated cancers in miners are bronchogenic (i.e., occur in the
bronchi), indicating that the primary effective site of RDP deposition is the
upper airways.
Though radon exposure and lung cancer have been strongly linked in
epidemiological studies of miners, a similar link has yet to be established
between RDP exposure in buildings (particularly dwellings) and lung cancer.
The difficulty in establishing a quantitative relationship between building
RDP exposures and lung cancer is due, in part, to the fact that lung cancer
rates associated with all causes are high and vary among different popula-
tions and in different environments. Since building RDP exposure on a
population basis is relatively low, an increase in lung cancer rates attributable
to RDP exposure is likely to be low as well. Study populations must be large
and exposures high in order to observe statistically significant differences in
lung cancer rates.
A limited number of epidemiological studies have been conducted to
determine whether exposure to indoor radon may be associated with
increased lung cancer rates. Most have defined RDP exposure groups by
geography and geology (i.e., ecologic studies). Of 15 such studies, seven
showed positive statistical associations; six, no association; and two, negative
associations. The power of these studies was limited because they did not
control for confounding factors such as smoking or resident mobility; they
were largely uninformative.
Studies based on the case-control approach can provide quantitative
assessments of residential radon exposures and lung cancer rates with a
much higher degree of statistical confidence than ecologic studies. With a
case-control design, radon exposures of those with lung cancer are compared
with appropriate controls who do not have lung cancer. To date, such studies
have been based on very small population sizes and, not unexpectedly, report
mixed results. In one of the largest case-control studies conducted to date
(Sweden), lung cancer risk was found to increase with increasing cumulative
exposure risk; the dose-response relationship was comparable to that
observed in miners. The combined effect of RDP exposure and smoking was
observed to be more than additive.
