Mercury - Toxicology of Metals - page 698

Some reports seem to indicate that regeneration and
compensatory adaptation during this period are bet-
ter than during adulthood. When neurological signs
because of MeHg poisoning appear, the duration of
exposure is of importance for recovery and rehabili-
tation. The outlook for recovery and for rehabilita-
tion seems to be better in the case of acute exposure
compared with prolonged exposure (Amin-Zaki
et al ., 1978).
In the rat, MeHg has been observed to inhibit sper-
matogenesis (Katsuragi, 1978; Lee and Dixon, 1975;
Sakai, 1972). Studies of spermatogenesis of MeHg-
exposed men have, however, not been reported. MeHg
in moderate toxic doses has an inhibiting effect on
both primary and secondary immune response with a
decreased resistance against viral infections in rodents
as a result (Koller, 1980). Human data are not available
regarding effects of MeHg on spermatogenesis.

is the most reliable index of MeHg body burden and
brain concentration. However, there are large species
differences in the rate of MeHg binding to hemoglobin
because of varying numbers of cysteinyl groups (Doi,
1991), resulting in varying blood-brain ratios in
MeHg content. This is also true for primates. Thus,
the blood/brain ratio in Squirrel monkeys is about
twice that of Macaca fascicularis (Evans et al . 1977;
Stinson et al . 1989) and the human ratio is about twice
that of Squirrel monkeys (see previously), although
the MeHg concentration in brain tissue is the same at
equivalent toxic effect.
MeHg is deposited in the hair during the forma-
tion of the pile. The deposition of the MeHg in the
pile is proportional to the mercury concentration in
blood at the time of pile formation. Thus, the mercury
concentration in the hair pile constitutes a calendar of
mercury concentrations in blood that occurred dur-
ing the formation of the pile. The MeHg concentra-
tion in the hair can be used as an indicator of mercury
concentration in blood, and in the critical organ, or
body burden of mercury, provided that allowance is
made for the growth rate of the hair pile—approxi-
mately 1 cm a month, depending on age (Pelfi ni et al .,
1969) and for the time lag between hair formation
and extrusion. As mentioned previously, the quotient
between MeHg concentration in human blood and
hair is 1:250. Under occupational conditions, the pos-
sibility of external contamination of hair should be
kept in mind.
Because urinary excretion of MeHg is very small,
MeHg concentration in urine is easily masked by the
presence of inorganic mercury. Thus, urine concentra-
tion of Hg is not a good index of MeHg body burden or
of MeHg concentration in the critical organ.

7.1.3.3 Genetic Effects
Because MeHg reacts with DNA and RNA, it can
be expected that genetic effects can arise from MeHg
exposure. MeHg has been proved to be mutagenic
under experimental conditions (Ramel, 1972). Little
evidence of such an effect is available from clinical
experience. However, Skerfving et al . (1974) reported
chromosome aberration in lymphocytes of consum-
ers of MeHg-contaminated fi sh, and Verschaeve et al .
(1976) reported aberration and aneuploidy in ethyl-
mercury-exposed workers. C. T. Miller et al . (1979)
reported decreased DNA-repair activity in the leu-
kocytes from cats exposed to MeHg at dose levels
that were not neurotoxic. They also observed chro-
mosome aberrations in leukocytes and bone-marrow
cells. Mitsumori et al . (1981) reported that ICR mice
given MeHg chloride in drinking water at toxic doses
developed renal cancer (adenocarcinoma), which is a
rare tumor in this animal. However, a large number
of chronic toxicity studies have been made on labo-
ratory animals like rats, cats, and monkeys, as well
as epidemiological studies on MeHg-exposed human
populations, and yet no evidence of tumor induction
or promotion has appeared.

7.1.5 Dose-Response Relationships

Most of our knowledge about dose-response rela-
tionships in MeHg is derived from studies of the epi-
demics of MeHg poisoning in Iraq (Bakir et al ., 1973)
and Japan (Swedish Expert Group, 1971) and from
studies of populations eating mercury-contaminated
fi sh (Clarkson et al ., 1975; Skerfving, 1974b). When
considering the dose-response relationships in MeHg
poisoning, three main effects can be discussed: the
neurotoxic effect, the embryo toxic effect, and the
genetic effect as shown in chromosomal aberrations of
the lymphocytes. The dose-response relationship for
each of these effects is discussed separately in the fol-
lowing.
The dose of MeHg can be expressed in terms of level
of intake, amount absorbed as refl ected by concentra-
tion of MeHg in blood or hair, and fi nally in terms of

7.1.4 Indicators of Exposure and
Concentration in the Critical Organ

Experimental studies in man and primates have
shown that mercury concentration in blood is, under
steady-state conditions, linearly correlated to intake
of MeHg and to the concentration of MeHg in the
critical organ (the brain), at nontoxic body burdens.
Because >90% of MeHg in blood is to be found in the
erythrocytes, the mercury concentration in red cells