Mercury - Toxicology of Metals - page 666

between acidifi cation of lakes and mercury content
in fi sh has been observed (Lindqvist et al ., 1984). For
a detailed discussion of the mechanism behind this
association, see Lindqvist et al . (1984). After agricul-
tural use of alkylmercury, levels of methylmercury in
game birds may reach toxic levels (Swedish Expert
Group, 1971). Methylmercury, but not ethylmercury,
has been recently reported in rice samples from 15
provinces of China (Shi et al ., 2005). Methylmer-
cury concentrations in the rice samples ranged from
1.9-10.5 ng MeHg/g and accounted for 7-44% of the
total mercury measured.
A large part of the mercury in food—at least in
animal products—is likely to be in the form of meth-
ylmercury. The major proportion of the mercury in
fi sh is methylmercury. The mercury concentration
in food products, excluding fi sh, varies from a few
micrograms to 50

Mercury from dental amalgam fi llings is the domi-
nant source of mercury exposure in terms of uptake
and retention in the organism for the general popula-
tion of industrialized countries (WHO, 1991). It is also
the overwhelmingly dominant source of mercury in
the central nervous system of the general population.
Dental amalgam primarily contributes to the daily
absorption of mercury in two ways. Mercury is released
in vapor form, inhaled, and reabsorbed to 80% in the
airways. Abraded amalgam particles are swallowed
and to a smaller extent oxidized in the intestinal tract.
Less than 10% of such ingested mercury is reabsorbed
as Hg +2 . Mercury can also be taken up in the nerve
endings and transported in a retrograde direction to
ganglia and central nerve cells (Arvidson, 1990; 1994).
The average daily retention in the population from
amalgam is estimated at 3-17 g with the note that

substantial individual variations exist (WHO, 1991).
This dose interval has since been confi rmed in several
studies (Halbach, 1995; Sandborgh-Englund, 1998;
Weiner and Nylander, 1995). The size of the variation
is illustrated by Barregård et al . (1995), who described
three patients experiencing symptoms of mercury tox-
icity who all eliminated large quantities of mercury
in their urine (54, 53, and 25

µ

g/kg (Bouquiaux, 1974). Thus,
the daily intake of methylmercury mainly depends
on fi sh consumption and the concentrations of MeHg
in consumed fi sh. Fish consumption varies among
countries, with some individuals and ethnic groups
having virtually no consumption to others having 500 g
or more per day. The average daily intake of fi sh
fl esh for the Swedish population was estimated at
30 g/day (Swedish Expert Group, 1971). This level
will result in a daily intake of MeHg of between 1 and
20

µ

g/g creatinine, respec-
tively) and had no source of exposure other than their
amalgam fi llings; all of them used nicotine chewing
gum. When the amalgam fi llings were removed in the
fi rst two cases with the highest elimination levels, the
mercury elimination fell to expected values and the
symptoms disappeared. In the third case, the patient
refused to have the amalgam removed, but the elimi-
nation seemed to decrease with reduced chewing
gum consumption. A similar case was published by
Langworth and Strömberg (1996). These cases dem-
onstrate a mercury uptake of approximately 100

µ

g/day with consumption of uncontaminated fi sh.
In epidemiological studies of the consumption of tuna
fi sh in the American Samoan population, blood levels
have been found indicating a daily intake of between
200 and 300

µ

g/day of MeHg (Clarkson et al ., 1975).
Should the water be polluted, the daily intake from
fi sh consumption can rise to toxic levels, as occurred
in Minamata and Niigata in Japan in the period 1953-
1966 (Swedish Expert Group, 1971). Concentrations
of methylmercury in fi sh of 1-20 mg/kg have been
reported to result in a maximum daily intake in per-
sons with high fi sh consumption (200-500 g/day) of
approximately 5 mg/day (Swedish Expert Group,
1971). More recently the USEPA and NAS/NRC
(EPA, 1997; NAS, 2001) have revised the acceptable
daily intake of fi sh species containing methylmercury
to lower consumption rates for pregnant or nursing
women. The current reference dose (RfD) for methyl-
mercury is now 0.1

µ

g/
day, approximately 10 times higher than the average
uptake from amalgam according to WHO (1991).
Mercury uptake from amalgam increases tissue
concentrations in the brain, plasma, and kidneys in
proportion to the number of amalgam fi llings. Mercury
concentration in plasma and urine in amalgam-free
subjects amounts to 0.2

µ

g/L, respectively
(Sandborgh-Englund et al ., 1998). Mercury content in
the brains (occipital cortex) of nonamalgam bearers
was found in autopsies to be approximately 7 ng/g
(mean, 6.7; range, 1.9-22.1). The brains of amalgam
bearers contained approximately 15 ng/g (mean,
15.2; range, 3.8-121.4) (WHO 1991). In the fetus, an
increase also occurs in the brain and kidneys, with an
average of twice the mercury concentration in those
with mothers who have amalgams compared with
those whose mothers do not (Drasch et al ., 1994; Lutz
et al ., 1996).

µ g/L and 2 µ

g/kg/day.
It should be noted that, in the absence of occupa-
tional exposure, the daily intake of inorganic mercury
would probably not exceed 10

µ

g/day from mercury
inhalation, drinking water, and food. However, a
major contribution may result from the release of mer-
cury vapor from dental amalgam fi llings, if present
(Aronsson et al , 1989; ATSDR, 1999; Brune and Evje,
1985; USEPA, 1998).

µ