Air Quality Criteria for Lead Volume II of II - (NEPIS)(EPA) - US ...

AX5-55
Citation
Burright et al.
(1989)
Coffigny et al.
(1994) †
Corpas et al.
(2002a)
Cory-Slechta
et al. (2004) †
Dearth et al.
(2002) †
Dearth et al.
(2004)
Table AX5-4.3. Effect of Lead on Reproduction and Development in Mammals Effects on Females
Species/
Strain/Age
Mouse/HET,
neonates
Rat/Sprague-
Dawley, adult
Rat/Wistar,
adult
Rat/Long-Evans,
adult
Rat/Fisher 344,
150–175 g
Rat/Sprague-
Dawley and
Fisher-344,
adult
Dose/Route/
Form/Duration Endpoint
0.5% Pb acetate solution via
milk, or drinking water
chronic beginning PND 1
Inhalation exposure to
5 mg/m 3 Pb oxide daily for
13 days during gestation
(GD 2, 3, 6–10, 13–17, 20)
300 mg/L acetate Pb in
drinking water from mating
until PND 12 or PND 21
Pb acetate in drinking water
beginning 2 mo before
breeding through weaning
12 mg/mL Pb acetate gavage
from 30 days prior breeding
until pups were weaned
21 days after birth; 10–
32 litters per group, control
group, gestation and lactation
exposure, gestation only
exposure, lactation only
exposure
12 mg/mL Pb acetate by
gavage 30 days prior to
breeding through PND 21
(gestation and lactation
exposure)
Plasma prolactin levels implied that Pb exposure alone decreased circulating prolactin
in primiparous; low prolactin levels in non-behaviorally tested females suggests that
dietary Pb alone may alter plasma-hormone in these lactating HET dams; pattern of
plasma prolactin appear to be inconsistent with the observation that Pb exposure
decreases dopamine; prolactin levels of Pb exposed dams were very low.
No effects on the incidence of pregnancy, prenatal death, or malformations when male
and female rats from mothers who had been exposed.
Neither abnormalities in the liver structure nor depositions of Pb, toxicant produced
biochemical alterations; pups exhibited decrease in hemoglobin, iron and alkaline, and
acid phosphatase levels and an increase in Pb content; protein, DNA, and lipid total
amounts were reduced, and hepatic glycogen content was diminished at 12 and 21 PN,
with a higher dose of glucose in blood; decrease in alkaline phosphatase in liver of pups
at day 21 PN, but acid phosphatase was unaltered.
Observed potential effects of Pb and stress in female; Pb alone (in male) and Pb plus
stress (in females) permanently elevated corticosterene levels in offspring.
Delay in onset of puberty (p < 0.05); reduced serum levels of IGF1 (p < 0.001), LH
(p < 0.001), and E2 (p < 0.001).
Pb delayed the timing of puberty in PbB 37.3 µg/dL Pb group and suppressed serum
levels of LH and E2, these effects did not occur in PbB 29.9 µg/dL Pb group, when
doubling dose to 29.9 µg/dL group the PbB levels rose to 62.6 µg/dL, yet no effect was
noted; results indicate that offspring are more sensitive to maternal Pb exposure with
regard to puberty related insults than are 29.9 µg/dL rats.
Blood Lead Concentration
(PbB)
PbB ~100 µg/dL
PbB 71.1 µg/dL (dam)
PbB 83.2 µg/dL (fetal)
PbB 22 µg/dL
PbB 30–40 µg/dL
Maternal PbB: ~40 µg/dL
Pups PbB as follows:
Gest+lact: ~38 µg/dL PND 10
Gest+lact: ~15 µg/dL PND 21
Gest+lact: ~3 µg/dL PND 30
Gest: ~14 µg/dL PND 10
Gest: ~3 µg/dL PND 21
Gest: ~1 µg/dL PND 30
Lact: ~28 µg/dL PND 10
Lact: ~15 µg/dL PND 21
Lact: ~3 µg/dL PND 30
PbB 29.9 µg/dL (Sprague-
Dawley)
PbB 37.3 µg/dL (Fisher)