44
and to determine whether the accumulation of lead in aduits
simplyreflects a long biological half-life or is caused by changing levels of intake of lead.
and Japanese populations. However,there is sti
question about the total mass of soft tissue a
sampling of the wet bone in the Japanese study.
This increase of skeletal lead content with a
INTRODUCTION
Lead, because of its wide commercial application,
ubiquity in the environment, and high toxicity, has
probably been the subject of more toxicological studies
than any other single substance. Consequently, the
toxicity is well known for high levels of acute and
chronic exposure to Jead. Patterson’ and Hardy‘*? are
very concerned about a possible health hazard to per-
sons not. occupationally exposed to lead, since in urban
areas, the average lead concentration in blood is as high
as one-third to one-half that at which symptoms of
toxicity may be clinically apparent following an acute
exposure. ‘3)
Despite extensive toxicological, metabolic, and en-
vironmental studies,"*) muchstill remains to be learned
about the metabolic parameters of this element andits
distribution in man and the environment. Thereis also
disagreement about the variation of lead in man as a
function of age, residence history, and occupation in
other than industrial exposure to this element.‘*?
Part of the controversy on the toxicity of lead concerns the ability of the body to compensate for in-
creased intake levels, that is, the tendency for excre-
tion rates of lead to approach asymptotically those of
intake,“ *) The change in lead content of the human
bodyas a function of age may, therefore, be a sensitive
method of assessing the degree of this compensation.
In recent work by Nusbaum etal. the lead concen-
tration in calvarium and rib bone from subjects in the
Los Angeles area wasslightly higher for subjects over
20 years of age than below. Above 30 years of age the
concentration did not appear to change. The lead concentration in lung, bone, kidney, pancreas, liver, and
aorta was shown by Schroeder and Balassa’s analyses
of Tipton’s data‘® to increase up to ages of at least
30-40 years. More recently Schroeder and Tipton"™
reported that the concentrations of lead and calcium in
aortas increased with age, and that the lead concentration increased faster than calcium. Horiuchiet al." in
Japan found a similar increase in rib, vertebra, and
femur up to age 40, and the concentrations of lead and
calcium in the various bones were correlated at the
0.05 level of significance. They estimated that the
total body lead content increased from about 78 mg in
adolescence to about 131 mg at age 50. The similarity
between these estimates and the 111-mg total body
content") estimated from the data of Tipton et al.0%
and more recent estimates of 131mg by Tipton and
Schroeder’ indicates a similarity between the U. 8.
plies, as stated by Schroeder and Tipton,‘ th
bodyis not in a steady state with respect to lea
is, the human bodyretains a portion of all le
gested. Thus, the increase in lead content of
50 mg in 30 years (Horiuchi) represents a rete
about 4yg/day, or about 1% of the 400 ug in
daily.11) This low level of retention is well
the experimental error of most metabolic balanc¢
ies. Accumulation could be due to the long bio
half-life of lead in the skeleton or to changes in «i
and smoking habits on reaching adulthood. Sm
as shown by Nusbaum et al.,{) may increasesl
lead by as much as 30%.
Corroboration of increases in skeletal lead wi
is shown in previously reported data of 7!°Pb, a
rally-occurring radioactive nuclide with a 22-yeai
life, which is also ubiquitous in humans and the
vironment. ‘!*)
The purpose of this study is to determine th.
concentration in bone from a large numberof p:
for whom age, sex and residential histories were
able. Occupational histories were also availab
85 of the 105 subjects.
EXPERIMENTAL METHOD
The bone samples were obtained during norma
gical or autopsy procedures. No two samples were
the same subject, and the cause of death or bas
surgery was known. None are believed to have
exposed to lead occupationally.
Lead concentration was also determined in
from 29 other subjects from Chicago and neighh
regions of Iliois. These teeth were pooled in ‘
groups of 2 to 4 teeth each.
The concentration of lead was determined bi
spectrophotometric method of Ileewicz et al.‘
this method the bone is ashed 8 hr at 600° C and
solved in 9. HCl at a concentration of up to
ash/ml. After extraction with triisooctylamine t:
move interfering elements, mainly iron, the lead 1
termined from the absorbance at a wave lengt
271 mu. Comparison of dry-ashed with identical’
ashed specimens showed no loss of lead due to he:
or to the solvent extraction procedure. Because 01
variability of bone weights, as discussed elsewhere.
the high likelihood of lead being associated with
mineral fraction of bone, the concentrations are ¢
as a function of the ash weight of bone.“*) The ov
analytical errors are estimatedto be less than 5%.