Host: The Japan Radiation Research Society
The term “radon dose”is used most often to indicate the doses of inhaled radon decay products. Gaseous Rn-222 itself makes a contribution less than one percent to the total “radon dose”. The removal of inhaled airborne particles from the tidal airflow through the respiratory airways is governed by the state of local airflow condition and the physical properties of the aerosol particles. The former is related to the airway morphometry and respiratory physiology of the subject and the latter includes the size and density of the particles. The particles deposited in the respiratory tract are cleared mainly by absorption into the blood and by mucociliary movement to the pharynx. The location at which the radionuclide decays depends on the rates of these clearance mechanisms as well as its initial deposition site. Basal cells in bronchial epithelium are long considered to be cells at risk. In addition, secretory cell layers are also assigned to risk-relevant target tissues in the ICRP human respiratory tract model. The depth of them in bronchial and bronchiolar epithelium is important for calculation of dose to man. A method to derive dose coefficient by modeling the processes from particle deposition to energy absorption by target tissues is often called “The Dosimetric Approach”. On the other hand, ICRP has derived a value of dose conversion convention by another method often called “The Epidemiological Approach”, in which the detriment per unit radon exposure was assessed from the data on lung cancer induction in miners and was directly compared with the detriment associated with a unit effective dose, which was based mainly on the epidemiological studies on atomic bomb survivors. This paper will provide outlines of both approaches with emphasis on factors influencing dose and risk estimation.
