oa ere ee
two fatalities that might be causally linked to
discussed previously (Adamsetal.. 1986). and it
was noted that the prevalence of hepatitis B
hepatitis B virus. infection with this organism
must be considered a public health problem of
“reat concern. The Marshall Islands Medical
surface antigenemia was 3.3". in the Rongelap
group. 18.8". in the Utirik group. and 10.5". in the
Comparison group.Thereis evidence suggesting
an association between radiation dose and prevalence of cirrhosis, but not hepatoma.in survivors of the atomic bombings in Japan ( Asano et
al.. 1982). Assuming that two of the three deaths
from hepatoma and cirrhosis in Marshallese
resulted from chronic hepatitis B infection, the
Program annually tests ail persons previously
shown to be hepatitis B surface antigen-positive
for the presence of alpha-fetoprotein. a tumor
marker tor hepatoma. Shouid an elevatedlevel
be detected the affected subject would be
promptiv referred for evaiuation in the hope
that early detection might permit curative
resection of a localized lesion ( Heywardetal.
1984).
The question arises as to whether the exposed
Marshallese are at increased risk for the late
complications of hepatitis B. This problem was
frequency of hepatitis B-related deaths. as per-
cent of hepatitis B surface antigen-positive persons is: exposed Rongelap - 0% (0:2); exposed
Utirik - 9.5% (2/21); Comparison group - 0%
(0°10).
ADENOMATOUS NODULES
AS FUNCTION OF RADIATION DOSE AND TIME
T
REM ( thousands }
5
ke
|
= se
a
|
T
|
T
]
T
a
—
a
2
a
a
—
Bs
=
oe
—
a
te
a
0 Ys
0
s
{|
10
|
14
{
6s
a
{| om
18
|
.
OCG
m6
|
ce
|
a
a
|
a
26
*
—
l
a
|
30
a
|
34
YEARS POST-EXPOSURE
Fig. 4: The time required to develop adenomatousnodulesfollowing radiation exposure appears.in this graph, to
be dose-related. However. the thyroid-absorbed radiation dose was highly dependent on the age at exposure.
J O04 ll2