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Leukemia risks among atomic-bomb survivors |
Excess leukemia was the earliest delayed effect of radiation exposure seen
in A-bomb survivors. Japanese physician Takuso Yamawaki in Hiroshima first
noted an increase of leukemia cases in his clinical practice in the late
1940s. This led to the establishment of a registry of leukemia and related
disorders and to the initial reports on elevated leukemia risks published
in the early 1950s.
Risks for radiation-induced leukemia differ in two major respects from
those for most solid cancers. First, radiation causes a larger percent
increase in leukemia rates (but a smaller number of cases since leukemia
is relatively rare, even in heavily exposed survivors), and second, the
increase appears sooner after exposure, especially in children. The excess
leukemias began appearing about two years after radiation exposure, and
the excess peaked at about 6-8 years after exposure. Today, little if any
excess of leukemia is occurring.
Because the Life Span Study (LSS) cohort was based on the 1950 national census, quantitative descriptions
of leukemia risks in A-bomb survivors have been based on cases diagnosed
from that year on. As of the year 2000, there were 204 leukemia deaths
among 49,204 LSS survivors with a bone marrow dose of at least 0.005 Gy,
an excess of 94 cases (46%) attributable to A-bomb radiation (Table). In
contrast to dose-response patterns for other cancers, that for leukemia
appears to be nonlinear; low doses may be less effective than would be
predicted by a simple linear dose response. Even for doses in the 0.2 to
0.5 Gy range, however, risk is elevated (Figure 1).
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Table. Observed and estimated excess number of leukemia deaths
in LSS population, 1950-2000
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Weighted marrow dose
(Gy)
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Subjects
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Deaths
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Attributable risk |
| Observed
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Estimated excess
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0.005 - 0.1
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30,387
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69
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4 |
6% |
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0.1 - 0.2
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5,841
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14
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5
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36% |
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0.2 - 0.5
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6,304
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27
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10
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37% |
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0.5 - 1.0
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3,963
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30
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19
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63% |
| 1.0 - 2.0 |
1,972 |
39 |
28 |
72% |
| >2.0 |
737 |
25 |
28 |
100% |
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Total
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49,204
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204
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94
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46% |
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*PY = person-years, in this case the number of excess leukemias per 10,000 persons per year
Figure 1. DS02 and DS86 non-parametric dose response of leukemia, 1950-2000.
Shown is the sex-averaged risk in 1970 for exposure age 20-39.
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Leukemia risk among LSS survivors has been increased only for acute and
chronic myelocytic leukemias and for acute lymphocytic leukemia. No evidence
of increased risk is seen for adult T-cell leukemia (endemic in Nagasaki
but virtually non-existent in Hiroshima) or for chronic lymphocytic leukemia,
which, in marked contrast to western countries, is extremely rare in Japan.
As in solid cancer risks, the leukemia risk also largely depends on the
age at exposure (Figure 2). The different age effect involves different
types of leukemias; acute lymphoblastic leukemia is more common among young
people whereas chronic myelogenous leukemia and acute myelogenous leukemia
are more common among elderly people.
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Figure 2. Effects of age at exposure and attained age on the excess deaths from
all types of leukemia (1-Gy exposure)
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| Because leukemia is a rare disease, the absolute number of leukemia cases
among A-bomb survivors is relatively small even though the relative risk
is high. Leukemia accounts for only about 3% of all cancer deaths and fewer
than 1% of all deaths, although it presently constitutes about 16% of all
excess LSS cancer deaths from radiation exposure. In an unexposed Japanese
population, the lifetime risk of leukemia is about seven cases per 1,000
people. For typical survivors in the LSS, who received 0.005 Gy or greater
(a mean dose of about 0.2 Gy), the lifetime leukemia risk increases to
about 10 cases per 1,000 (or the relative risk is nearly 1.5). |
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References about this subject
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Preston DL, Pierce DA, et al.: Effect of recent changes in atomic bomb survivor dosimetry on cancer mortality risk estimates. Radiation Research 2004; 162:377-89 |
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Preston DL, Kusumi S, et al.: Cancer incidence in atomic-bomb survivors. Part III: Leukemia, lymphoma, and multiple myeloma, 1950-1987. Radiation Research 1994; 137:S68-97 |
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