Chemistry Reference
In-Depth Information
4.1 Lead
Developmental effects of lead have been predomi-
nantly associated with postnatal exposure; however,
evidence is emerging that both prenatal and postna-
tal exposures are important, and occur, for example,
in areas where drinking water is contaminated by the
metal.
Several studies have documented placental trans-
fer of lead and lead levels in maternal blood, placenta,
and cord blood. Environmental exposure in areas with
water concentrations of lead >50
signifi cant, should be interpreted with caution. These
results combined with those from studies carried out
in seven different countries provide little evidence
that low or moderate lead exposure is associated with
an increased risk of major malformations. Effects of
higher exposures are more equivocal. Needleman et al .
(1984) examined 5183 consecutive deliveries of at least
20 weeks' gestation, correlating the congenital anom-
alies and lead concentration in umbilical cord blood.
Lead was associated, in a dose-related fashion, with an
increased risk of minor anomalies but not with the risk
of malformations. However, an increased risk of neu-
ral tube defects was observed in an English study of
mothers exposed to lead from the general environment
(Bound et al., 1997).
An effect on growth (stature about 2 cm shorter at 15
months of age) was noted for children whose mothers
had a PbB concentration exceeding 77
g/L was associ-
ated with increased lead concentrations in cord blood
and placenta, as well as in maternal blood. Lead lev-
els in maternal blood were generally higher than in
cord or neonatal blood, despite the higher affi nity
of fetal hemoglobin for lead (Alexander and Delves,
1981; Hubermont et al ., 1978; Miller and Shaikh 1983;
Ong and Lee, 1980; Roels et al., 1978). Wibberley et
al . (1977) studied placental lead levels in a series of
Birmingham births classifi ed as stillbirth, neonatal
death, or survival beyond 1 week. Despite a wide
range of lead levels even in normal births (15-356
µ
µ
g/L, and the
infant PbB increased to 100
g/L during the fi rst 3-15
months of life (Shukla et al ., 1989). Bellinger et al . (1991)
evaluated the relationship between prenatal low-level
lead exposure and fetal growth in a sample of 4354
pregnancies. The authors concluded that the risk of
adverse fetal growth is not increased at cord blood lead
levels <150
µ
g/
L) the results showed a pronounced excess of lead in
those who failed to survive both birth and the neonatal
period. There was no association of placental lead with
impaired birth weight among survivors but, in agree-
ment with other authors, seasonal variation was noted:
with higher levels during the summer months. A study
in Cassandra, Zambia, near a lead mine and smelting
factory found mean blood lead (PbB) levels of 412
µ
g/L but that modest increases in risk may
be associated with levels
µ
g/L. Factor-Litvak et al .
(1991) tested the hypothesis that exposure to lead dur-
ing pregnancy from residence in a lead smelter town
is associated with reduced intrauterine growth and an
increase in preterm delivery. Mean PbB at midpreg-
nancy was around 192
150
µ
µ
g/L
and 370
g/L for mothers and infants, respectively, with
a signifi cant correlation ( r = 0.77; P < 0.001) (Clark, 1977).
The increased lead transfer, however, did not seem to
have an adverse effect on the newborn's birth weight or
red cell values.
The main current human data indicate that a direct
association between moderate low-level lead exposure
and malformations has not yet been proven, and there
is a predominance of negative results. In particular,
no evidence of association of low lead exposure with
major congenital malformations has been reported.
However, Nordstrom et al . (1979a,b) investigated
the frequencies of congenital malformations in the off-
spring of female employees at a smelter in northern
Sweden and in the population living nearby. The fre-
quency of single and multiple malformations was sig-
nifi cantly higher (approximately twofold and fourfold,
respectively) in the offspring of the women who had
worked at the smelter during pregnancy. A signifi cantly
increased risk was found only in pregnancies where
the mother had worked at the smelter. The numbers
of malformations in the offspring of female employees
were low; therefore, the results, although statistically
µ
µ
g/L in the exposed women
and 60
g/L in the control group. After adjustment
for the effects of potential confounders, no signifi cant
relationships were found between maternal PbB meas-
ured at midpregnancy, at delivery, or in the umbilical
cord and birth weight or length of gestation or preterm
delivery.
Dietrich et al . (1986; 1987) correlated prenatal, cord,
and 10-day neonatal PbB levels and performance tests
at 3 and 6 months. PbB levels during prenatal peri-
ods were inversely related to a series of sensorimotor
developmental indices at 6 and 12 months of age, as
well as lower birth weight. Further analyses by struc-
tural equation modeling showed that the effect of
prenatal lead exposure, all less than 300
µ
g/L, was in
part mediated through its effects on birth weight and
gestational age.
Bellinger and coworkers (1994) investigated the
association between prenatal and postnatal lead expo-
sure and behavioral problems in 8-year-old Boston
children. Prenatal and postnatal lead exposure was
assessed by umbilical cord PbB (mean, 68
µ
g/L) and
dentin lead of a shed deciduous tooth (mean, 3.4
µ
µ
g/g).
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