Chemistry Reference
In-Depth Information
observed. Fukuda (1971) exposed rabbits to mercury
vapor and found the highest mercury concentrations
in the cerebellum, tegmentum, and thalamus. In rab-
bits with a pronounced tremor, the concentration in
brain was 4
the experiments on monkeys (
n
= 14) was 100% in the
studied dose range (0.6, 0.2, 0.1, and 0.06 mg Hg/
m
3
of air during 24 hours) (Berlin
et al
., 1992; New-
land
et al
., 1996; Warfvinge
et al
., 1994). With the
two higher exposure levels, 50% of the pregnancies
ended with abortion or neonatal death, whereas with
the two lower exposure levels, 10% ended in neona-
tal death. Only normal pregnancy outcomes were
observed for the lowest exposure level. All surviv-
ing offspring showed behavioral changes compared
with unexposed controls. It is of the utmost impor-
tance to establish a LOAEL for the human fetal brain.
Presently available information is not suffi cient to
allow risk evaluation. It is a factor of 10 between
brain mercury concentration at the lowest exposure
dose (50-100 ng/g) and the mercury levels reported
for human fetal brains (2-9 ng/g). It is questionable
whether this is enough to move from 100% response
rate to less than 1%. There is no reason to assume
that the human fetal brain would be less sensitive
to mercury than other primate brains. Two cases of
mercury vapor exposure during pregnancy and with
normal pregnancy outcome are reported. In one case,
the mother was occupationally exposed and had
a urine mercury excretion of 875
g/g. No morphological changes could be
observed at this concentration. Kishi
et al
. (1978) tried
to titrate the mercury concentration in the brain asso-
ciated with behavioral changes in the rat using stud-
ies of conditioned avoidance refl exes. They observed
clear effects at concentrations of 20
µ
g Hg/g brain tissue.
These effects disappeared at approximately 10
µ
µ
g/g.
In squirrel monkeys, levels up to 8
g/kg in the occip-
ital cortex were observed (Berlin, 1976) in the absence
of any defi nite morphological changes in the brain.
However, the possibility of behavioral disturbances
at these levels could not be precluded.
Sällsten
et al
. (1994) analyzed the mercury content
in cerebrospinal fl uid from 10 chloralkali workers
and 16 nonexposed workers. The ongoing exposure
was between 20 and 50
µ
µ
g/m
3
and average urine
excretion was 29
g/g creatinine for the exposed
workers. The concentration in CSF averaged 0.07
ng/mL (range, 0.018-0.17) for the referents and 0.13
ng/mL (range, 0.022-0.30) for the exposed. They
found a signifi cant correlation between plasma and
CSF levels of mercury and observed a decrease in CSF
mercury in two workers 6 months and 19 months,
respectively, after the end of exposure.
µ
g/L at the 15th
gestational week (Melkonian and Baker, 1988). The
other case involved a woman exposed in her home
to mercury vapor during the fi rst 17 weeks of gesta-
tion. The child seemed to have developed normally
as an infant (Thorp
et al
., 1992). It can be concluded
from the animal experience and human reports that
if there is an effect on human fetal brain development
from maternal dental amalgams, the effect is likely
to be limited to behavioral changes within the nor-
mal variation as seen in low-dose lead, alcohol, or
PCB exposure. Such effects can only be detected on a
group basis with epidemiological methods.
µ
6.1.4.4 Fetal Brain
Fetal nerve tissue contains the type of cell that
shows the most sensitivity to the mercury ion Hg
2+
.
Clear effects arise at the concentration level of 5-50
nmol/L or 1-10 ng/g tissue (Abdulla
et al
., 1995,
Monnet-Tschudi, 1998; Monnet-Tschudi
et al
., 1996;
Söderström and Ebendal, 1995), which is the con-
centration level found in neonatal infants of amal-
gam-bearing mothers (Drasch
et al
., 1994; Lutz
et al
.,
1996). Experimental studies on rats and primates
have shown that exposure to mercury vapor gives
rise to developmental disorders in the brain resem-
bling those seen after exposure to methylmercury.
This means migration disturbances and permanent
behavioral changes with reduced abilities/capac-
ity to learn and adapt (Berlin
et al
., 1992; Daniels-
son
et al
., 1993; Newland
et al
., 1996; Warfvinge
et al
.,
1994). The effects are seen over a mercury concentra-
tion range in a monkey fetal brain of 50-300 ng/g
brain tissue, which is 10 times lower than the con-
centration required with exposure to methylmercury.
In rats, it has been shown that methylmercury expo-
sure and exposure to mercury vapor has an additive
effect on fetal brain development (Fredriksson
et al
.,
1996). The prevalence of disturbed development in
6.2 Mercuric Mercury
6.2.1 Metabolism
6.2.1.1 Absorption, Inhalation
No data are available.
6.2.1.2 Ingestion
Acute poisoning caused by accidental or inten-
tional intake of mercuric chloride was not uncom-
mon at the beginning of this century. Data from
reports of such cases (Sollmann and Schreiber, 1936)
and experimental studies (Clarkson and Shapiro,
1971; Miettinen, 1973; Rahola
et al
., 1973) indicate
that approximately 2% of ingested mercuric chlo-
ride is absorbed. On high intake, the corrosive
