choice than 10. The higher value corresponds more closely to the radiation weighting factor recommended by the ICRP (1991) for fission neutrons. However, with the higher value it becomes critical that the weighting factor stands for the neutron low-dose RBE (i.e., the ratio of the linear coefficients in the dose relations for neutrons and for γ-rays). The weighted dose, d, is then relevant only to the linear term in the dose-effect relation, while the dose-square term, which corresponds to a DDREF, has to contain the γ-ray absorbed dose alone. This change in the analysis might, in the case DDREF = 1, reduce the estimated ERR/Sv by roughly another 15% (Kellerer and others 2001).
A decline in the solid cancer ERR with increasing exposure age has been demonstrated in several epidemiologic studies (UNSCEAR 2000b), and most models for estimating risks of solid cancers in the last decade have included a term that allowed for such a decline. Analyses of A-bomb survivor incidence and mortality data from the recent past (Thompson and others 1994; Pierce and others 1996) emphasized models of the form
where D is dose in sieverts, βM and βF are sex-specific estimates of the ERR/Sv for exposure at age 30, and e is age at exposure in years. This model is often parameterized so that the βs are the risks at an exposure age of 30, that is, by replacing e by (e − 30).
Although allowing for dependence of the ERR on exposure age seems appropriate, quantifying this dependence is subject to considerable uncertainty, especially for cancers of specific sites. Most medically exposed cohorts involve limited ranges of exposure age, and there is no medically exposed cohort that covers the full range of exposure ages from early childhood to old age. Thus, statistical power for evaluating the effects of exposure age within any single cohort is usually low.
The LSS cohort of Japanese A-bomb survivors is unique in providing data on persons exposed at all ages and, for this reason, has been used in many past risk assessments to quantify the effects of age at exposure (BEIR V, UNSCEAR). Reasonably precise estimates can be obtained when all solid cancers are analyzed as a single outcome. However, sample sizes for individual cancer sites are usually too small to quantify the effects of exposure age precisely. Estimates of the parameter γ vary widely among sites, but it is not possible to determine the extent to which this variation reflects real differences and the extent to which it reflects statistical variation.
An additional problem in quantifying the effect of age at exposure is that since all A-bomb survivors were exposed at the same time, the effects of exposure age are confounded with birth cohort effects. Japanese baseline rates for cancers of many specific sites show strong secular trends, which probably result at least in part from changes in life-style that have come about with the Westernization of Japan. For example, baseline rates for cancers of the colon, lung, and female breast have increased over the past 50 years so that early birth cohorts have lower baseline risks than later birth cohorts. This means that the appropriate way to estimate the effects of exposure age depends on how the factors responsible for secular trends affect radiation risks. If these factors increase or decrease radiation risks to the same extent that they increase or decrease baseline risks (a multiplicative relationship), then estimation of the effect of age at exposure should be based on modeling the ERR. However, if the factors responsible for secular trends in baseline risks have no effect on radiation risks (an additive relationship), then estimation of the effects of age at exposure should be based on modeling the EAR. If the chosen model is not correct, then estimated exposure age effects may be influenced by secular trends in Japanese baseline rates and may not be applicable to populations other than the LSS cohort. Further discussion of secular trends and their influence on estimating the effects of age at exposure can be found in Preston and colleagues (2003).
With the Equation (12B-1) model, the ERR is assumed to be constant over the follow-up period for fixed exposure age. (This is likely to be an oversimplification since Little and others 1991, Thompson and others 1994, and Pierce and others 1996 have all demonstrated that the ERR declines with increasing attained age, or time since exposure, at least for those exposed early in life [under age 20]). In addition, it is now recognized that some and perhaps all of the decline in the ERR with exposure age can also be described as a decline in the ERR with attained age (Kellerer and Barclay 1992; Preston and others 2002a). Pierce (2002) describes the age-time patterns in A-bomb survivor cancer incidence data and discusses difficulties in interpreting them. He also discusses a possible biological rationale for a model in which the ERR decreases with attained age.
As noted in Annex 12A, UNSCEAR (2000b) provided two solid cancer models—one based on age at exposure (as shown by Equation (12B-1)) and one based on attained age. The UNSCEAR attained-age model is of the form
where D is dose in sieverts, βM and βF are sex-specific estimates of the ERR/Sv, and a is attained age in years. This model is often parameterized so that βs represents the ERR/Sv at attained age 60, that is, by replacing a by (a / 60).
Even when the exposure-age and attained-age models provide comparable fits to the data, estimated lifetime risks based on the two models are not the same, especially for specific age-at-exposure groups such as persons exposed