to be poor for this category and likely to include many misclassified leukemias and malignant lymphoma deaths. Among 128 deaths for which additional diagnostic information was available, there were 57 nonneoplastic disease deaths. When these deaths were analyzed separately, the resulting ERR/Sv was 2.0 (90% CI 0.6, 4.4), nearly identical to that based on the full 191 deaths. Analyses suggested that the effect was limited to nonaplastic anemias (29 cases), since the estimate for aplastic anemias (31 cases) was essentially zero. There was also a suggestion of a strong dose-response based on 13 deaths from myelodysplastic syndrome, a neoplastic disease thought to be a precursor of acute myelogenous leukemia.
Although the data evaluated by Shimizu and colleagues (1999) included 379 deaths attributed to benign neoplasms or neoplasms of unspecified nature, only 31 deaths were specifically indicated on the death certificate as being due to benign neoplasms. There was no convincing evidence of a dose-response for these 31 deaths.
With regard to deaths from external causes, suicide rates showed a statistically significant decline with increasing dose, whereas no evidence of a dose-response relationship was found for deaths from other external causes.
Wong and colleagues (1993) evaluated the relationship between exposure to radiation and the incidence of 19 nonmalignant disorders using data from the AHS cohort for 1958–1986. They found statistically significant positive dose-response relationships (p < .05) for thyroid disease (p < .001), chronic liver disease and cirrhosis (p = .007), and uterine myoma (p < .001). In addition, myocardial infarction showed a significant dose-response for 1968–1986 among those who were under 40 years of age at exposure (p = .03). Statistically significant relationships were not detected for hypertension, hypertensive heart disease, ischemic heart disease, occlusion and stenosis of precerebral and cerebral arteries, aortic aneurysm, stroke, cataract, gastric ulcer, duodenal ulcer, viral hepatitis, calculus of kidney and ureter, cervical polyp, hyperplasia of prostate, dementia, and Parkinson’s disease. Modification of the ERR/Sv by sex, city, age at exposure, and time since exposure was also investigated for those end points that showed overall associations. Age at exposure was found to be a significant modifier of risk for thyroid disease (decreasing ERR/Sv with increasing age); modifying effects for uterine myoma are discussed above (“Benign Neoplasms”).
Kodama and colleagues (1996) reviewed results of studies addressing noncancer diseases and their relationship to radiation exposure in A-bomb survivors. They also update some of the analyses by Wong and colleagues (1993) to include data through 1990, but do not present nearly as much detail as the latter. They found a statistically significant association for myocardial infarction based on all of the data (p = .02), with an estimated ERR/Sv of 0.17 (95% CI 0.01, 0.36). The association remained significant when analyses were adjusted for various risk factors including blood pressure and cholesterol. Positive dose-response relationships were also found for several other end points of atherosclerosis, which the authors interpreted as supporting a real association between radiation exposure and atherosclerosis. Kodama and colleagues (1996) confirmed previously identified radiation associations for uterine myoma, hyperparathyroidism, and chronic liver disease with an ERR/Gy of 0.46 (0.27, 0.70), 3.1 (0.7, 13), and 0.14 (0.04, 0.27) for the three respective end points.
Wong and colleagues (1999) used AHS data to examine long-term trends in total serum cholesterol levels over the 28 years from 1958 to 1986. Dose-response relationships for the increase in cholesterol levels over time were demonstrated for women in general but only in the youngest birth cohort (1935–1945) for men. Age, body mass index, city, and birth year were considered in the analyses, and some analyses were adjusted for cigarette smoking. These results may partially explain the dose-response relationship for coronary heart disease that has been observed in other studies of atomic bomb survivors.
Cologne and Preston (2000) investigated life shortening in the LSS cohort using mortality data through 1995. Although dose-related increases in both cancer and noncancer mortality imply that longevity is also related to dose, earlier papers addressing these effects (Pierce and others 1996; Shimizu and others 1999) did not specifically attempt to quantify the degree of radiation-induced life shortening, an end point that reflects the effects of both cancer and noncancer mortality. The investigation of longevity was undertaken in part because of earlier reports in both the scientific literature and the press that certain atomic bomb survivors had greater-than-average life expectancy.
A clear decrease in median life expectancy with increasing radiation dose was found. Among cohort members with estimated doses between 0.005 and 1.0 Gy, the median loss of life was estimated to be about 2 months, while among cohort members with estimated doses of 1 Gy or more, the median loss of life was estimated to be about 2.6 years. The median loss of life among all cohort members with doses estimated to be greater than zero was about 4 months.
Cologne and Preston (2000) present estimates of life expectancy for groups defined by dose. For those with zero dose, separate estimates are presented for groups defined by distance from the hypocenter, including estimates for those who were not in the city (>10 km from the hypocenter). Although the relative mortality for all nonzero-dose groups compared to the combined in-city, zero-dose group was 1.0 or greater, results for those in the lowest-dose category