Mercury - Toxicology of Metals - page 671

In the cerebellum, the cerebellar nuclei contained
the highest amount of mercury, seen in both neuron
and glia cells. A high amount was also seen in the
Purkinje cell layer in Purkinje cells and Bergmann
glia cells. Mercury was also visualized in medul-
lary layer astrocytes, in the molecular layer, and the
granule cell layer. Three years after the cessation of
exposure, mercury could still be visualized in the
cerebellum. No difference between adult and off-
spring brains in mercury distribution was observed
(Warfvinge, 2000).
A part of the brain of the squirrel monkey show-
ing a conspicuous accumulation of mercury is the
retina (Khayat and Dencker, 1983; 1984). Warfvinge
and Bruun (2000) studied the microdistribution in the
retina. They visualized mercury mainly in the optic
disc, retinal pigment epithelium, capillary walls,
and ganglion cells and found retention of mercury
in these structures up to 5 years after exposure. Off-
spring exposed in utero had similar retinal distribu-
tion but seemed to eliminate mercury faster than seen
in the adult.
The evidence from animal experiments also indi-
cates that the distribution in the kidney and other
organs accumulating mercury after exposure to mer-
cury vapor is similar to that seen after exposure to
mercuric salts.

6.1.2 Symptoms and Signs in Poisoning
Caused by Exposure to Mercury Vapor

As noted previously, mercury is a potent cell toxin
that affects basic functions of the cell by modifying the
tertiary and quaternary structure of proteins by bond-
ing strongly with sulfhydryl and selenohydryl groups.
This metal may interact with receptor, ion channel,
and intracellular signal link functions. As the struc-
ture of protein molecules is genetically determined,
this leaves ample scope for genetic polymorphism
to manifest itself in varying sensitivity and types of
reaction to mercury exposure. There are also several
target functions for mercury toxicity. In most cases the
central nervous system seems to be the most sensi-
tive organ. Peripheral nerve function, renal function,
the immune system, endocrine system, and muscle
function are also affected. A review (Berlin, 2003) of
published cases of accidental mercury poisoning dur-
ing the 5-year period of 1998-2002 revealed an aston-
ishing variation in symptoms and signs. Several case
descriptions were found. These have most likely been
published because the symptoms are unexpected.
Mercury concentrations were documented with urine
and blood values, and the symptoms subsided when
the exposure ceased. Accordingly, there is no doubt
that mercury caused the symptoms. The symptoms
observed included a range of dermal syndromes, such
as systemic contact dermatitis (baboon syndrome)
(Alegre et al ., 2000; Bartolome et al ., 2000). Three cases
of nummular dermatitis, which were cured by amal-
gam removal, are described by Adachi et al . (2000) and
Pigatto et al . (2002). In a review article, Britschgi and
Pichler (2000) state that mercury can induce acute gen-
eralized exanthematous pustulosis. In another review
article, Boyd et al . (2000) summarize skin diseases
caused by mercury.
One article describes a 5-year-old boy who, after
massive mercury exposure, developed tics, extensive
blinking, head-twisting, and shoulder-jerking as his sole
symptoms (Li et al ., 2000). There have also been descrip-
tions of several cases in children with hypertension and
elevated catecholamine secretion induced by mercury
exposure, the symptomatology has resembled phaeo-
chromocytoma (Kosan et al ., 2001; Laurans et al ., 2001;
Torres et al ., 2000; Wössmann et al ., 1999). A 48-year-
old man developed aspects of severe, acute polyarthri-
tis (Karatas et al ., 2002) as a result of massive mercury
exposure. Dalén (2000) describes a historical case with
symptoms suggesting gastroenteric infl uence.
This variability in symptoms and signs at the upper
end of the dose scale is likely to refl ect genetic poly-
morphism, which most likely will also manifest itself at
the lower end. The existence of cases with genetically

6.1.1.4.1 Elimination and Excretion The elimination
of mercury after exposure to mercury vapor occurs
mainly by excretion of mercuric mercury. However,
exhalation of small quantities of mercury vapor has
been demonstrated in animals (Clarkson and Rothstein,
1964) and man (Hursh et al ., 1976). A fraction of the
mercury vapor exhaled is the result of reduction of
divalent mercuric mercury stored in the tissues (Dunn,
1978).

6.1.1.4.2 Excretion The rate of excretion is dose-
dependent, and considerable species differences
have been observed. The best mathematical model
seems to be a multicompartment model with at
least two or more excretion rates and with one small
compartment, including the brain, with a very long
biological half-time. The limited data from human
studies indicate that the bulk of mercury accumulated
in the body (80%) is excreted with biological half-
time of approximately 60 days (Hursh et al ., 1976;
Rahola et al ., 1971). Part of the mercury accumulated
in the brain is slowly eliminated with a biological
half-time that may exceed several years (Kosta
et al ., 1975; Rossi et al ., 1976). For renal, hepatic,
and intestinal excretion of divalent mercury, see the
following.