Chemistry Reference
In-Depth Information
of pregnant rats to radiolabeled mercury vapor during
late gestation, mercury accumulated in the placenta
and the fetus in about equal ratios (Clarkson
et al
.,
1972). There was substantial deposition of mercury in
fetal tissues after exposure to mercury vapor in mice
(Khayat and Dencker, 1982), guinea pigs (Yoshida
et al
.,
1986), and squirrel monkeys (Warfvinge
et al
., 1994).
High levels of mercury were found in fetal rat brain
after prenatal exposure, but no adverse effects were
noted except in the presence of maternal toxicity (Mor-
gan
et al
., 2002). When pregnant rats were given dental
amalgam restorations, mercury accumulated in fetal
tissues, but was lower than in maternal tissues (Taka-
hashi
et al.,
2003). Combined mercury vapor and etha-
nol exposure increased mercury levels in fetal tissues
(Dencker
et al
., 1983; Yoshida
et al
., 1997). In guinea
pigs, mercury vapor was oxidized in the fetal liver and
bound to metallothionein (Yoshida
et al
., 1987). Recent
studies have identifi ed a protective role for metal-
lothionein in preventing transplacental transfer after
mercury vapor exposure (Yoshida
et al
., 2002).
Some studies have demonstrated behavioral effects
of prenatal exposure to mercury vapor (Danielsson
et al
., 1993; Fredriksson
et al
., 1992), whereas others in
nonhuman primates showed no difference in various
behavioral measures after prenatal exposure to fairly
high levels of mercury vapor (Newland
et al.,
1996).
Earlier studies using several species of animals showed
little transport of inorganic mercury to the fetus (Berlin and
Ullberg, 1963a-c; Clarkson
et al
., 1972; Suzuki
et al
., 1967).
However, a more recent study using rats exposed to mer-
curic chloride during pregnancy and until weaning (post-
natal day 20) reported measurable levels of mercury in
fetal tissues, with the highest mercury levels in the kidney;
levels of mercury were higher in fetal brains than mater-
nal samples (Feng
et al
., 2004). Studies in BALB/c mice
have also shown that prenatal exposure to mercuric chlo-
ride resulted in persistent alterations in immune function.
Effects included inhibitory effects in females on cytokine
projection by thymocytes, lymph node cells, and spleno-
cytes; in contrast, stimulatory effects were observed in
males (Silva
et al
., 2005). Distribution of mercury after
administration of phenyl mercury exposure was similar
to that of mercuric mercury (Berlin and Ullberg, 1963b;
Garrett
et al
., 1972; Suzuki
et al
., 1967).
ers, have reduced weight at birth. It is diffi cult, however,
to attribute the decreased birth weight exclusively to cad-
mium. Among nonsmoking women, cadmium levels in
urine were higher in those with infants of below-normal
birth weight. Data were not confi rmed after adjusting
urine cadmium levels by creatinine (Cresta
et al
., 1989).
However, Nishijo
et al
. (2002) found an inverse correla-
tion between maternal urinary cadmium excretion and
gestational age after adjustment for maternal age.
Several studies in rats and mice indicate that cad-
mium may be fetotoxic from oral exposures before and
during gestation. This fetotoxicity is most often mani-
fested as reduced fetal weight and neurobehavioral
toxicity (Baranski, 1987; Gupta
et al
.; 1993, Kostial
et al
.,
1993; Sorell and Graziano, 1990; Whelton
et al
., 1988).
Nagymajtenyi
et al
. (1997) reported behavioral and
neurotoxicological changes in rats treated with cad-
mium chloride during pregnancy, lactation, and 8 weeks
after weaning (at doses ranging from 3, 5, to 14 mg/kg).
Open-fi eld behavior and spontaneous and evoked cor-
tical activity were investigated at the age of 12 weeks.
Vertical exploration and open-fi eld center exploration
were increased; spontaneous and evoked electrophysi-
ological variables showed dose-dependent and genera-
tion-dependent changes, thus indicating that low-level
exposure of rats to inorganic cadmium can affect some
nervous system functions. Changes in some electrophysi-
ological parameters and higher order nervous functions
were confi rmed by Desi
et al
. (1998) in rats at low-level
prenatal and postnatal inorganic cadmium exposure dur-
ing pregnancy.
4.4 Chromium
Little is known about the developmental effects of
chromium in humans or animals. A descriptive geo-
graphical study on congenital malformations in com-
munities around a site heavily polluted by chromium
waste was carried out by Eizaguiree
et al
. (2000). A
10-km circle centered on the polluted site was sub-
divided into one circle of 2-km radius and eight
1-km wide rings. The relative risk of congenital mal-
formations for the closest circle seemed to be markedly
lower than that for the rest; the relative risk peaked in
the rings 2-4 km away from the polluted site. The authors
excluded a possible teratogenic effect of the chromium
coming from waste with different distribution of the two
forms of chromium. Chromium (VI), which accumulates
in erythrocytes, was transferred readily to the fetal mouse
on day 13 of gestation, whereas there was little transfer
of chromium (III), which is bound mainly to plasma pro-
teins. Later in gestation, both chromium (VI) and chro-
mium (III) accumulated in calcifi ed areas of fetal skeleton
(Danielsson
et al
., 1982).
4.3 Cadmium
Data on the concentrations of cadmium in maternal
blood and placental and fetal blood indicate that cad-
mium accumulates in the placenta, reaching the human
fetus in detectable amounts (Lauwerys
et al
., 1978; Roels
et al
., 1978; Scanlon, 1972). Babies from smoking mothers,
whose cadmium body burden is higher than in nonsmok-
