Health Risks of Ionizing Radiation: - Clark University
Health Risks of Ionizing Radiation: - Clark University
Health Risks of Ionizing Radiation: - Clark University
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50 Atomic Bomb Survivors<br />
(ALL), acute myeloid (AML), chronic myeloid<br />
(CML) and adult T-cell leukemia (ATL). A fourth<br />
subtype, chronic lymphocytic leukemia (CLL), is<br />
typically not associated with radiation. The study<br />
found strong evidence for radiation induced risks <strong>of</strong><br />
all leukemia subtypes except ATL, some evidence<br />
for a lymphoma risk, and no significant evidence for<br />
a multiple myeloma risk.<br />
The shapes <strong>of</strong> the dose-response curves and the<br />
effects <strong>of</strong> age and gender appeared to be distinctly<br />
different among these diseases. The pattern <strong>of</strong> ALL<br />
risk was consistent with a linear dose-response<br />
model having a high risk coefficient (ERR 10.3/<br />
Sv, 4.3-25). Risk appeared higher for childhood<br />
exposures and declined over time. CML risk was<br />
also consistent with a linear dose-response model<br />
and a decline in risk over time. Age at exposure was<br />
not found to have a significant effect on risk; the<br />
average ERR estimate for this subtype was 6.2/Sv.<br />
The dose-response pattern for AML was nonlinear,<br />
concave-up, and less dependent on age at exposure<br />
or time since exposure. The estimated ERR at 1 Sv<br />
was 3.3 (Preston et al. 1994).<br />
It is important to point out that the LSS followup<br />
began in 1950, five years after the bombings.<br />
Leukemia has a latent period <strong>of</strong> as few as 2 years,<br />
so a significant number <strong>of</strong> early cases were probably<br />
missed. Preston et al. (1994), after considering some<br />
information about these early cases, estimated that<br />
leukemia risk estimates might have been 10-15%<br />
higher if these early cases had been included.<br />
Results for the other diseases studied by<br />
these authors were inconclusive. ATL is endemic<br />
to Nagasaki and rare in Hiroshima and has been<br />
associated with the HTLV-1 virus. Of the 25 ATL cases<br />
in the cohort, 24 were from Nagasaki, suggesting<br />
that the virus may have independently caused the<br />
leukemia cases. Furthermore, when analysis was<br />
limited to Nagasaki there was no evidence <strong>of</strong> a doseresponse<br />
pattern. There was some evidence <strong>of</strong> an<br />
increased risk <strong>of</strong> non-Hodgkin’s lymphoma among<br />
males but there was not a significant relationship<br />
between dose and ERR. Multiple myeloma was not<br />
significantly related to dose in the main analysis,<br />
although previous analyses had shown an association<br />
with incidence and mortality. Some cases were<br />
excluded from the main analysis because they had<br />
high doses (>4 Gy) or because their first primary<br />
cancer diagnosis was not multiple myeloma. If these<br />
cases were included then a significant dose-response<br />
relationship was observed (ERR 0.9/Sv, p = 0.02).<br />
Little et al. (1999) pooled the leukemia data from<br />
the atomic bomb survivors, cervical cancer patients<br />
treated with radiation, and ankylosing spondylitis<br />
patients also treated with radiation. These medically<br />
exposed cohorts received much higher doses than the<br />
atomic bomb survivors and therefore contribute more<br />
information about high-dose dynamics and little or<br />
no information about low-dose effects. These authors<br />
used a model that included an exponential decline in<br />
risk as doses increase; this accounts for the killing <strong>of</strong><br />
precancerous cells and has been used to model the<br />
risks <strong>of</strong> the medical exposure in other contexts (see<br />
sections 3.3 and 3.4). This analysis demonstrated<br />
the differences among leukemia subtypes. When<br />
all leukemias were modeled together the cohorts<br />
were not showing compatible risk estimates; when<br />
leukemia subtypes were modeled independently the<br />
cohorts were consistent with each other.<br />
4.5 Incidence <strong>of</strong> noncancer disease<br />
Wong et al. (1993) examined noncancer disease<br />
incidence through 1986. This study found significant<br />
linear dose-response patterns for thyroid disease<br />
(ERR 0.3/Gy, 0.16-0.47), chronic liver disease and<br />
cirrhosis (ERR 0.14/Gy, 0.04-0.27), and uterine<br />
myoma 10 (ERR 0.46/Gy, 0.27-0.70). Results for<br />
Parkinson’s disease were based on 50 cases and were<br />
suggestive although not significantly positive (ERR<br />
0.44/Gy, -0.06-1.57). When analysis was restricted<br />
to the 1968-1986 time period there was an apparent<br />
risk <strong>of</strong> heart attack among those who were younger<br />
than 40 at the time <strong>of</strong> the bombings (ERR 0.57/Gy,<br />
0.26-1.76). Hayashi et al. (2003) reported a dosedependent<br />
increase <strong>of</strong> certain proteins in the blood<br />
(interleukin 6, C-reactive protein) that indicate<br />
an inflammatory response. These measurements<br />
were made in 1995-1997, so they indicate a longterm<br />
change in the status <strong>of</strong> the blood, and this<br />
10 A uterine myoma is a common benign tumor <strong>of</strong> the uterine muscle, present in about 40% <strong>of</strong> adult women and usually<br />
asymptomatic.