of radon has received considerably less attention from radiation protection agencies who are primarily concerned with occupational exposures, in part because ingestion intakes are readily avoided in the workplace. Thus, recommendations of the International Commission on Radiological Protection (ICRP) and the National Council on Radiation Protection and Measurements (NCRP) have not included guidance for the control of ingested radon. In the absence of such guidance a number of investigators have undertaken dosimetric and risk assessments of ingested radon.
The fate of radon in the body has been the subject of several investigations. In 1951, Harley and others (1994; 1958) examined the elimination of radon from the body in a series of measurements of radon in exhaled air after chronic inhalation. Hursh and others (1965) investigated the fate of ingested radon and proposed a concentration limit on radon dissolved in water. Von Doebeln and Lindell (1964) investigated the retention of ingested radon in the body. Brown and Hess (1992) investigated the transfer and kinetics of ingested radon. The retention in the body of the noble gases argon, krypton, and xenon were studied by Tobias and others (1949), Ellis and others (1977), Susskind and others (1977; 1976), and Bell and Leach (1982). The results of those investigations support a number of general observations:
The absorption and retention of inert gases in human body tissues have been extensively studied by several authors, including: Smith and Morales (1944), Morales and Smith (1944), Kety (1951), Bernard and Snyder (1975), Bell and Leach (1982), Palazzi and others (1983), Peterman and Perkins (1988), Harley and Robbins (1994), Sharma and others (1996). In vitro studies have provided data on the solubilities and partition coefficients of the noble gases and other chemically inert substances in human blood, adipose tissue, and individual tissues; the data have been summarized by Steward and others (1973).
Hursh and others (1965) derived a value for the maximum permissible concentration of 222Rn in water on the basis of limiting the dose to the stomach. They assumed that radon diffuses through the stomach wall and enters the splanchnic blood flowing to the liver. The concentration of radon in the stomach wall was taken, conservatively, to be equivalent to that in the stomach contents. Von Doebeln and Lindell (1964) used the data of Hursh and others to estimate the dose to the stomach. More recently, Crawford-Brown (1991; 1989) estimated the dose to the stomach using a linear radon concentration profile in the wall. The dose to other organs was based on kinetics inferred from measurements of retention of ingested 133Xe (Correia and others 1987). Harley and Robbins (1994) used