Chemistry Reference
In-Depth Information
6.1.3 Indicators of Exposure and Concentration
in the Critical Organ
For ongoing exposure, the mercury concentrations
in blood plasma and urine are the optimal indices.
The mercury concentration in urine per gram creati-
nine is strongly correlated to the mercury concentration
in blood (Smith et al ., 1970). Thus, the mercury concen-
tration in urine per gram creatinine can be used as an
index of recent exposure in workers (Aito et al ., 1983;
Langworth, 1992; Lindstedt et al ., 1979; Piotrowski et al .,
1975; Smith et al ., 1970; Yoshida, 1985). Piotrowski et al .
(1975) observed a 24-hour variation in mercury excre-
tion that was confi rmed by Aito et al . (1983). The latter
authors, as well as Suzuki et al . (1968), found a strong
correlation between mercury excretion and creatinine
excretion in urine. All these authors reported consider-
able individual variations in mercury excretion.
It has been shown in animal studies that during
continuous exposure, the mercury concentrations in
blood and urine are not correlated to concentrations
of mercury in brain or kidney (Berlin et al ., 1969a).
Recent exposure is the dominant factor determining
mercury concentration in blood and urine (Berlin and
Gibson, 1963). Clinical and animal studies have shown
that there is a fairly good correlation between ongo-
ing exposure and mercury concentration in urine and
blood and that the kidneys contain a large part of the
body burden of mercury. It has been shown that renal
tubular cells take up mercury from blood, release
mercury into the blood, and that mercury is secreted
into the proximal tubular lumen and reabsorbed at
the distal part of the nephron (see Section 8.2.1) These
observations are consistent with the hypothesis that
the kidney under physiological conditions maintains
a constant relative mercury concentration gradient
between blood and distal tubular urine. This also
explains why there is a good correlation between
blood and urine mercury correlation irrespective of
renal load of mercury. The hypothesis is supported
by the observation by Cherian et al . (1978) that after
exposure to radioactive mercury vapor, the specifi c
activity of mercury in urine was lower than that in
blood, indicating a dilution with inactive mercury in
the renal storage compartment. To what extent renal
mercury load contributes to blood mercury concen-
tration and whether the contribution occurs through
tubular reabsorption or by direct release into the
blood from the storage compartment are so far not
studied.
At present, there is no suitable biological index of
the mercury concentration in critical organs such as
brain and kidney. Studies concerning the relationship
between mercury concentration in blood and mercury
concentration in brain and/or kidney under conditions
of no known exposure are not yet available.
6.1.4 Dose-Response Relationships
Dose-response relationships have been studied
in which the dose was determined by the degree of
exposure or by the mercury concentration in either
blood or urine (absorbed dose). Results from all three
approaches are summarized in the following. How-
ever, it is uncertain to what extent levels of mercury in
air refl ect actual exposure. Factors such as the release
of mercury vapor from mercury-contaminated clothes,
temporary, and spot-wise exposure to high levels in con-
nection with special work operations, and variations in
physical load that change the rate of lung ventilation
and limit the value of mercury concentrations in the air
as measurements of exposure. Mercury concentrations
in blood and urine are infl uenced by recent exposure
and the body burden of mercury from earlier exposure.
The relative contribution of these two parameters for
determining levels of mercury in blood and urine is still
poorly understood. The level of mercury in urine is also
affected by the physiological variation in metabolism.
6.1.4.1 Relationship Between Mercury in Air and Effects
Garnier et al . (1981) reviewed approximately 20
cases of acute exposure to mercury vapor, and Milne
et al . (1970) described four cases of pneumonitis
after exposure to mercury vapor. The mercury levels
exceeded 1-3 mg/m 3 for a few hours. Available epi-
demiological investigations (Friberg and Nordberg,
1972) indicate that at long-term exposure to mercury
concentrations in air of 0.1 mg/m 3 or higher, the prob-
ability of persons manifesting typical mercurialism
with tremor and behavioral changes will increase.
At concentrations of 0.1 mg/m 3 or lower, the prob-
ability of encountering cases of micromercurialism or
the asthenic syndrome decreases. There has as yet not
been substantial accumulation of evidence or any one
conclusive report concerning incidence of poisoning
at exposure concentrations <0.01 mg/m 3 mercury in
air. Smith et al . (1970) reported the prevalence of cer-
tain medical fi ndings in relation to mercury exposure
as shown in Figure 2.
Gambini (1978) reported on a study on two groups
of 145 and 129 workers at chloralkali factories. An in-
creased prevalence of tremor and micromercurialism at
urine mercury concentrations exceeding 50
g/L was
found. The author also found that this urine-mercury
concentration corresponded to a mercury concentra-
tion in air of 0.05 mg/m 3 . These fi gures are consistent
with the results reported by Lindstedt et al . (1979) and
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