Lead - Toxicology of Metals - page 601

exposure. It also refl ects the total body burden,
because the dominating fraction of the body burden
of lead is in the skeleton. Lead determination has
been carried out in different bones, mainly fi nger
bone (Nilsson and Skerfving, 1993; Skerfving and
Nilsson, 1992; Schütz et al ., 2005), patella (Hu et al .,
1998; Watanabe et al ., 1994), tibia, and calcaneus
(Erkkilä et al ., 1992; Todd and Chettle, 1994). The
trabecular bones, such as calcaneus and patella, have
a faster turnover than the cortical ones, such as the
tibia. Therefore, the trabecular bones refl ect a shorter
time span than the cortical ones (Hu et al ., 1998).
There is a reasonably good correlation between the
lead concentrations in the different bones (Erkkilä
et al ., 1992). Occasionally, determinations have been
reported also for the ulna and sternum, but the meas-
urements were less precise (Erkkilä et al ., 1992).
The lead concentrations in bone are much higher in
lead workers than in the general population. Usually,
the highest concentrations have been recorded in retired
workers, where levels on the order of 100

There is a clear association between the lead con-
centrations in urine and blood (Bergdahl et al ., 1997c;
Fukui et al ., 1999; Gulson et al ., 1998a), but the varia-
tion is too large to allow a prediction of an individual
blood-lead concentration from a urinary lead con-
centration. Partly, this is caused by the diffi culties in
handling the necessary adjustment for variations in
dilution of spot samples (Sata and Araki, 1996). For
example, the creatinine excretion, which is often used,
depends on muscle mass and meat intake (Suwazono
et al ., 2005). This makes comparisons between subjects
of different gender and age doubtful. Also, there is
some diurnal variation in the excretion, with the low-
est concentrations in the night (Yokoyama et al ., 2000).
Moreover, the association between urinary and blood-
lead concentrations has a curved shape because of the
saturation of lead-binding sites in the erythrocytes
(Section 2.5.2.1). In contrast, plasma-lead concentra-
tion seems to be rectilinearly related to urinary lead
(Bergdahl et al ., 1997c), as well as to the urinary excre-
tion of lead after chelation (Gerhardsson et al ., 1999).
In line with this, urinary lead has been suggested as a
possible surrogate for plasma lead (Fukui et al ., 1999;
Tsaih et al ., 1999), but data indicate that, just as in the
case of whole blood, the variation is too large to allow
a prediction of an individual plasma-lead concentra-
tion based on an analysis of urine (Bergdahl et al .,
1997c). Nevertheless, it may still be that urinary lead
can work as a surrogate for the fi lterable fraction of
lead in plasma.
Urinary excretion of lead after administration of a
chelating agent has often been used as an index of risk
and total body burden. After administration of calcium
disodium ethylenediamine tetraacetic acid (EDTA), the
concentration of lead increases in plasma because of
the presence of a Pb-EDTA complex, which is fi ltrated
into urine (Sakai et al ., 1998). An alternative to EDTA is
dimercaptosuccinic acid (DMSA); there are differences
between these two chelators in how they affect lead
excretion (Lee et al ., 1995).
Chelatable lead has been used as an index of the
total body burden, but it has been shown not to be a
good measure. It mainly refl ects lead concentrations
in blood and soft tissues (Gerhardsson et al ., 1998; Tell
et al ., 1992), and possibly trabecular bone (Tell et al .,
1992; Section 2.5.5), whereas it is not a good index of
total body burden, and thus not of long-term accumu-
lation, which mainly occurs in cortical bone. In accord
with this, chelation did not cause any decrease of either
tibia or calcaneus lead (Tell et al ., 1992).

g/g bone
mineral may be found (Gerhardsson et al ., 1993), the rea-
sons being the long exposure duration and high expo-
sure intensity in the past, in combination with the slow
elimination of lead from bone. In an old lead worker, the
skeleton may contain 1 g of lead. This causes an endog-
enous exposure, which may make up half of the B-Pb.
Several studies have been carried out on bone lead in
the general population. Determinations are possible for
tibia, calcaneus, and patella, at least in populations with
a relatively high exposure. However, for fi nger bone, the
sensitivity has not been suffi cient. Because bone lead
refl ects long-term exposure to lead, it is attractive in
epidemiological studies where retrospective exposure
assessment is required, such as in studies of the long-
term effects on the developing brain (Hu et al ., 1998).
Indeed, stronger associations to neurological outcome
have been shown for bone lead compared with B-Pb in
a study in Kosovo (Wasserman et al ., 2003).
Bone-lead concentrations are associated with the
lead concentration in both whole blood and plasma.
The associations are particularly close in retired work-
ers, but less in active ones, in whom the current expo-
sure is superimposed on the endogenous one from
bone (Börjesson et al ., 1997b; Christoffersson et al .,
1984; Erkkilä et al ., 1992). There is an increase in bone
lead with age (Lin et al ., 2004).

µ

2.6.1.3 Urinary Lead and Chelatable Lead
Urinary lead has been used in biological monitor-
ing of lead, but only to a limited extent. Urinary lead
excretion after administration of chelating agents (che-
latable lead) has, however, been fairly widely used as
an index of risk and the body burden of lead.

2.6.1.4 Other Indices
Lead is excreted in the saliva, which is probably the
explanation of the black gingival lead seam sometimes