Health physicists define the biologic radiation dose as the amount of energy actually deposited in your body. The more energy absorbed by cells, the greater the biological damage. The absorbed dose, the amount of energy absorbed per gram of body tissue, is usually measured in units called rads. The relationship between exposure to radon and the dose of radiation from decay products that reaches target cells in the respiratory tract is complex.
A radioactive dose primarily depends on such factors as:
- The number and energy level of the radiation particles emitted by the source (the source's activity, measured in units called curies).
- The distance from the source (distance is especially important with alpha radiation; more than a few centimeters from the source, the amount of the dose approaches zero).
- The amount of exposure time.
- The degree to which radiation dissipates in the air or in other substances between the source and the recipient.
Extensive research has developed a one-to-one, or linear relationship hypothesis between the radon dose and its effect. This technique, known as the linear no-threshold hypothesis, uses mathematical models to estimate the risks of very low exposures based on the known risks of high-level exposures. A brief description of the hypothesis is supplied below:
Whereas an increase in alpha particle exposure causes an increase in the number of effected cells, an increase in exposure does not affect the amount of insult to any one particle interacted cell. That is, small doses have a small risk in direct proportion to the known effects of large doses. This relationship holds true for rising concentrations of radon exposure, until a point where cells interact with more than one particle in its lifetime.
Some scientists question the linear hypothesis because of the lack of evidence of health effects from extremely low radiation doses, as well as the fact that many other hazardous substances harmful at high doses have little or no effect at low doses. The U.S. Committee on the Biological Effects of Ionizing Radiation (BEIR), convened by the National Academy of Sciences (NAS), acknowledged in 1990, that there is no data showing that low doses of radiation cause cancer.
The BEIR Committee, however, recommended the use of the linear no-threshold hypothesis because it is consistent with other approaches to public health policy. The United States and other countries use linear estimates to set limits and standards on all potential exposures to radon and other types of radiation, both for the public and for workers in jobs that expose them to ionizing radiation.
The alpha-particle dose delivered to the target cells in the respiratory tract is necessarily modeled on the basis of physical and biologic factors.
Physical factors affecting the dose:
- Characteristics of inhaled air radon. Progeny that are attached to dust particles (the attached fraction) deposit much more efficiently than free or unattached progeny; of the attached progeny, only those adhering to the smallest particles are likely to reach the alveoli.
- Amount of air inhaled. The amount and deposition of inhaled radon decay products vary with the flow rate in each airway segment.
- Radon concentration in air and duration of exposure.
- Equilibrium between Radon gas and solid progeny.
- Airborne particulate levels.
- Aerosol size distribution.
Biological factors affecting the dose:
- Breathing pattern. The proportion of oral to nasal breathing will affect the number of particles reaching the airways. Oral breathing deposits more of the larger particles in the nasopharyngeal region. Regardless of the breathing pattern, the smaller the particle, the deeper it penetrates into the lung and the more likely it is to deposit there.
- Architecture of the lungs. Sizes and branching pattern of the airways affect deposition; these patterns may differ between children and adults and between males and females. Preferential deposition of larger particles occurs at all branch points because of inertial impaction.
- Biologic characteristics of the lungs. The radiation dose occurs in those areas where mucociliary action is either absent or ineffective in removing the particles. Particles moving with the mucous flow cause essentially no radiation dose to tissue because of the short range of alpha particles in fluids.
- Bronchial morphology.
- Lung tidal volume. Deposition increases with increased tidal volume.
- Oral vs. nasal inhalation route.
- Clearance rate from the lungs.
It is possible, therefore, that two environments with the same radon measurement (e.g., a dusty mine and a home environment) might cause different deposition patterns and, therefore, deliver different doses of alpha radiation to a person's lungs. Likewise, two persons in the same environment might receive differing doses of alpha radiation to the target cells in the upper portion of their lungs because of differing breathing patterns and pulmonary architecture.
Long lived radon progeny (lead-210, bismuth-210, and polonium-210) contribute little to the dose because they are eventually removed by the mucous and cilia in GI tract before they can decay.
Factors that affect the ingestion dose:
- Stomach contents
- Food vehicle/fat content
- Emptying of stomach contents into small intestine
The stomach and small intestines, the portals of entry of ingested radon into the body, receive a negligible radiation dose. The range of alpha particles emitted by radon and its short-lived decay products is such that alpha particles emitted within the stomach are unable to reach the cells at risk in the stomach and large intestine walls. Thus, the dose to the walls depends heavily on the extent to which radon diffuses from the contents into the wall.
Radon is an inert noble gas that does not readily interact chemically with cellular macromolecules. Radon does not undergo metabolism in biological systems.