have caused a veteran’s cancer in two situations. The first is illustrated by the example discussed above. In that example, if plutonium is an important contributor to dose and a cancer occurs more than 60 years after exposure, the 50-year committed dose would underestimate the relevant dose. That situation could occur in the future as the population of surviving atomic veterans ages.
The second situation involves cancers for which VA may have assumed that there is no appreciable increase in risk beyond some time after a radiation exposure. For example, studies of the Japanese atomic-bomb survivors indicate that there is little risk of a radiation-induced leukemia beyond about 25 years after exposure (see Section III.E), and a similar assumption may be made for a few other cancers, including lymphoma and multiple myeloma. However, there is an important difference between exposures of the Japanese atomic-bomb survivors and exposures of some atomic veterans that should be taken into account in applying assumptions about decreases in cancer risk at times long after exposure of the veterans. Essentially all of the dose to the atomic-bomb survivors was received at the time of the bombings or shortly thereafter, and there was little exposure due to inhalation of long-lived fission products and plutonium. In contrast, an atomic veteran who inhaled substantial amounts of plutonium and other long-lived radionuclides that are tenaciously retained in the body continued to receive a dose to bone marrow and lymphatic tissues long after the time of intake. Therefore, the practice in the NTPR program of assigning the entire 50-year committed dose from inhalation of plutonium and other long-lived radionuclides to the year of intake, which ignores that the dose is protracted over many decades after an intake, would greatly underestimate the dose that could have caused a veteran’s cancer if the risk of that cancer is assumed to be negligible beyond some time after exposure and the veteran’s cancer occurred at such a time.
 Dose coefficients for the lung used in the NTPR program could overestimate doses to particular tissues in the respiratory tract where lung cancers occur.
In the respiratory-tract model used by the NTPR program (ICRP, 1979a), dose coefficients for the lung represent the average dose to the tracheobronchial tree, pulmonary region, and pulmonary lymphatic tissues. That is, dose to the lung is calculated as the total energy absorbed in the three regions divided by an assumed total mass of tissue of 1,000 g.
Most lung cancers occur in the bronchial region, which also is the region where most excess lung cancers in the Japanese atomic-bomb survivors have occurred (ICRP, 1994b). In the respiratory-tract model used in dose reconstructions (ICRP, 1979a), calculated doses to the lung overestimate doses to the tracheobronchial tree in cases of inhalation of insoluble (Class Y) longer-lived radionuclides in respirable form (AMAD, 1 μm) by about a factor of 3 because of the influence of the relatively high dose to lymphatic tissues on the average dose in all tissues considered (see Table V.C.2). The difference is smaller when shorter-