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ATSDR Draft Toxicological Profile for Radon_September 2008.pdf

ATSDR Draft Toxicological Profile for Radon_September 2008.pdf

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RADON 483. HEALTH EFFECTSthe gastrointestinal and respiratory tracts are likely to be similar. In<strong>for</strong>mation on elimination of inhaledradon progeny is discussed in Section 3.4.4.1.3.4.4.3 Dermal ExposureIn<strong>for</strong>mation on the excretion of radon and its progeny following dermal exposure is very limited. Within24 hours, 4.5% of the radon, which was applied as a salve to intact human skin, was eliminated byexhalation, while 10% was exhaled after application of the radon to an open wound (Lange and Evans1947). Bathers breathing compressed air while immersed in radon-containing water had exhaledapproximately one-third of radon measured in blood immediately after bathing (Pohl 1965). By 6–8 minutes after bathing, these persons were exhaling one-half of the amounts exhaled immediately afterbathing. The author stated that the remaining radon which distributed to fatty tissue was excreted moreslowly.3.4.4.4 Other Routes of ExposureExperiments in animals have reported the retention of radon after exposure by the intraperitoneal andintravenous routes. Following intravenous administration, 1.6–5.0% of the administered activity wasretained in the animals after 120 minutes (Hollcroft and Lorenz 1949). Retention was greatest at120 minutes following intraperitoneal administration, but by 240 minutes, it was nearly the same <strong>for</strong> bothroutes of administration. These authors also reported that the amount of radon retained in tissues wasgreater in obese mice than in normal mice, especially after intraperitoneal administration (Hollcroft andLorenz 1949). <strong>Radon</strong> retention has also been studied in dogs following intravenous administration of226 Ra. The amount of radon in bone was found to increase with increasing time after injection (Mays etal. 1975).3.4.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) ModelsPhysiologically based pharmacokinetic (PBPK) models use mathematical descriptions of the uptake anddisposition of chemical substances to quantitatively describe the relationships among critical biologicalprocesses (Krishnan et al. 1994). PBPK models are also called biologically based tissue dosimetrymodels. PBPK models are increasingly used in risk assessments, primarily to predict the concentration ofpotentially toxic moieties of a chemical that will be delivered to any given target tissue following variouscombinations of route, dose level, and test species (Clewell and Andersen 1985). Physiologically based***DRAFT FOR PUBLIC COMMENT***

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