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Abstract
We postulated that patients with hereditary hemochromatosis (HH) absorb increased
quantities of lead, as do iron-deficient subjects. To test this hypothesis, whole
blood lead concentration ([blood Pb]) was quantified by atomic absorption spectrometry
in HH homozygotes (n = 44), obligate heterozygotes (n = 19), normal control subjects
(n = 33), and abnormal controls with transfusion-induced iron overload (n = 8). HH
homozygotes had higher [blood Pb] than did normal control subjects (5.6 ± 0.6μg/dl
vs 3.6 ± 0.5 μg/dl; p < 0.005); significantly increased mean [blood Pb] was observed in both male and female
homozygotes. In heterozygotes, the mean [blood Pb](4.1 ± 0.5 μ-g/dl) was intermediate
between that of homozygotes and normal control subjects. The mean [blood Pb] of subjects
with transfusion-induced iron overload (2.2 ± 0.6 μg/dl) did not differ significantly
from that of normal controls. The findings in homozygotes could not be related to
age, serum ferritin concentration, presence or absence of iron loading, or the extent
of therapeutic phlebotomy. Lead exposure in all of our subjects was due primarily
to ambient sources. Analysis of our data, when using a mathematical biokinetic model
of human lead metabolism, suggests that the most likely explanation for our findings
is that homozygotes (and, to a lesser extent, heterozygotes) absorb increased quantities
of lead, a conclusion that corresponds to the increased absorption of iron and cobalt
previously documented in homozygotes.
Abbreviations:
[blood Pb] (blood lead concentration), HH (hereditary hemochromatosis)To read this article in full you will need to make a payment
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Article info
Publication history
Accepted:
February 18,
1994
Received in revised form:
February 17,
1994
Received:
December 21,
1993
Footnotes
☆Supported by: Veterans Administration Medical Research Funds; grants AM-20630 and RR-00064 from the National Institutes of Health; the Office of Radiation Programs, U.S. Environmental Protection Agency, under Interagency Agreement DOE No. 1824-C148-A1 under contract DE-AC05-84OR21400 with Martin Marietta Energy Systems, Inc.; and Iron Overload Diseases Association, Inc.
☆☆An editorial relevant to this article appears on p. 152 of this issue of the Journal.
Identification
Copyright
© 1994 Published by Elsevier Inc.
