1. General description
Physicochemical properties
Property Value
Physical state
Dense, silver-white metal; liquid at normal temperatures
and pressures
Vapour pressure 0.16 Pa at 20 °C
Stability Carbon–mercury bond in organic mercury
compounds is chemically stable
Major uses
Mercury is used for the cathode in the electrolytic
production of chlorine and caustic soda, in electrical
appliances (lamps, arc rectifiers, mercury cells), in
industrial and control instruments (switches,
thermometers, barometers), in laboratory apparatus, in
dental amalgams, and as a raw material for various
mercury compounds. The latter are used as fungicides,
antiseptics, preservatives, pharmaceuticals, electrodes,
and reagents.
Environmental fate
The solubility of mercury compounds in water varies:
elemental mercury vapour is insoluble, mercury(II)
chloride is readily soluble, mercury(I) chloride much
less soluble, and mercury sulfide has a very low
solubility.
Methylation of inorganic mercury has been shown to
occur in columns of fresh water and in seawater (1), and
bacteria (Pseudomonas spp.) isolated from mucous
material on the surface of fish and soil were able to
methylate mercury under aerobic conditions. Some
anaerobic bacteria that possess methane synthetase are
also capable of mercury methylation (2). Once
methylmercury [the generic term "methylmercury"
is used throughout this text to refer to
monomethylmercury compounds] is released from microbes,
it enters the food chain as a consequence of rapid
diffusion and tight binding to proteins in aquatic
biota. The enzymology of CH3Hg+ hydrolysis and
mercury(II) ion reduction is now understood in some
detail. Environmental levels of methylmercury depend on
the balance between bacterial methylation and
demethylation (3).
2. Analytical methods
Inorganic mercury is determined by flameless atomic
absorption spectrometry (4). Cold vapour atomic
absorption spectrometry and atomic fluorescence
spectrometry have detection limits of 50 and 1 ng/litre,
respectively.
Gas chromatography is commonly used for the
determination of alkylmercury compounds. The neutron
activation procedure is regarded as the most accurate
and is generally used as the reference method (3).
3. Environmental levels and human exposure
Air
Mercury levels in air are in the range 2–10 ng/m3.
Water
Inorganic mercury
Levels of mercury in rainwater are in the range
5–100 ng/litre, but mean levels as low as 1 ng/litre
have been reported (3). Naturally occurring levels of
mercury in groundwater and surface water are less than
0.5 µg/litre, although local mineral deposits may
produce higher levels in groundwater. In 16 groundwaters
and 16 shallow wells surveyed in the USA, mercury levels
exceeded the maximum contaminant level of 2 µg/litre
set by the US Environmental Protection Agency for
drinking-water (5). An increase in the mercury
concentration up to 5.5 µg/litre was reported for wells
in Izu Oshima Island (Japan), where volcanic activity is
frequent (6). The concentration range for mercury in
drinking-water is the same as in rain, with an average
of about 25 ng/litre (3).
Organic mercury
In a contaminated lake system in Canada,
methylmercury was found to constitute a varying
proportion of total mercury, depending on the lake (3).
There have been no reports of methylmercury in
drinking-water.
Food
Food is the main source of mercury in
non-occupationally exposed populations. Fish and fish
products account for most of the organic mercury in
food. The average daily intake of mercury from food is
in the range 2–20 µg/day, but may be much higher in
regions where ambient waters have become contaminated
with mercury and where fish constitute a high proportion
of the diet (7).
Estimated total exposure and relative contribution of
drinking-water
On the assumption of an ambient air level of 10 ng/m3,
the average daily intake of inorganic mercury by
inhalation would amount to about 0.2 µg. If a level in
drinking-water of 0.5 µg/litre is assumed, the average
daily intake of inorganic mercury from this source would
amount to about 1 µg. The average daily intake of
mercury from food is in the range 2–20 µg/day.
4. Kinetics and metabolism in laboratory animals and
humans
Inorganic mercury
About 7–8% of ingested mercury in food is absorbed;
absorption from water may be 15% or less, depending on
the compound. About 80% of inhaled metallic mercury
vapour is retained by the body, whereas liquid metallic
mercury is poorly absorbed via the gastrointestinal
tract. Inhaled aerosols of inorganic mercury are
deposited in the respiratory tract and absorbed to an
extent depending on particle size (8).
Inorganic mercury compounds are rapidly accumulated
in the kidney, the main target organ for these
compounds. The biological half-time is very long,
probably years, in both animals and humans. Mercury
salts are excreted via the kidney, liver, intestinal
mucosa, sweat glands, salivary glands, and milk; the
most important routes are via the urine and faeces (8).
Organic mercury
Dimethylmercury is almost completely absorbed through
the gastrointestinal tract; after absorption it rapidly
appears in the blood, where, in humans, 80–90% is
bound to red cells. Demethylation of methylmercury to
inorganic mercury occurs at a slow but significant rate.
The greater intrinsic toxicity of methylmercury as
compared with inorganic mercury is due to its lipid
solubility, which enables it to cross biological
membranes more easily, and especially to enter the
brain, spinal cord, and peripheral nerves, and to cross
the placenta (3).
Most methylmercury is excreted in the inorganic form.
The site and mechanism of demethylation are still not
well understood (3).
5. Effects on laboratory animals and in vitro test
systems
Inorganic mercury
Short-term exposure
The toxic effects of inorganic mercury compounds are
mainly in the kidney.
Lesions in the proximal tubular cells were detected
after a single intraperitoneal injection of 1 µmol of
mercury(II) chloride per kg of body weight (0.2 mg/kg of
body weight as mercury) in male rats. Accumulation of
mercury in the kidneys, however, indicated that the
absorption efficiency was much greater than that
expected from the gastrointestinal tract (9).
When rats were given mercury(II) chloride (3 mg/kg of
body weight) by gavage twice a week for 60 days,
examination by immunofluorescence showed that deposits
for IgG were present in the renal glomeruli.
Morphological lesions of the ileum and colon were also
observed, with abnormal deposits of IgA in the basement
membranes of the intestinal glands and of IgG in the
basement membranes of the lamina propria (10).
When rats were exposed to mercury(II) chloride (1
mg/kg of body weight per day) by incubation or
subcutaneous injection for up to 11 weeks, the rate of
body weight gain decreased after 20 days, and actual
weight loss occurred after 65–70 days. There were also
neuropathological effects, first detected after 2 weeks,
namely peripheral vacuolization of cells in the dorsal
root ganglia, followed by the development of multiple
small lesions in the ganglia (11).
A single dose of 1 mg/kg of body weight of mercury(II)
chloride or methylmercury(II) chloride, either orally or
by subcutaneous injection, resulted in leakage of dye
into the nervous parenchyma within 12 h, indicating that
these compounds can increase the permeability of the
blood–brain barrier (11).
Long-term exposure
Rats injected subcutaneously 3 times weekly for up to
8 months with doses of inorganic mercury ranging from
0.05 to 2.5 mg/kg of body weight per injection
(0.02–1.07 mg/kg of body weight per day) developed
renal damage. This was characterized by an initial
production of antiglomerular basement membrane
antibodies, followed by the appearance of immune complex
deposits in the glomerular tufts and small renal
arteries accompanied by proteinuria and hypoalbuminaemia
(12).
Reproductive toxicity, embryotoxicity, and
teratogenicity
Controlled mating tests in which male mice were
injected with single doses of mercury(II) chloride (1 mg
of mercury per kg of body weight) showed a significant
decrease in fertility as compared with controls (13).
Normal fertility was restored after about 2 months.
Gradual changes in testicular tissues were noted in
rats treated with mercury(II) chloride at doses of 0.05
or 0.1 mg/kg of body weight intraperitoneally over 90
days (14). There was a decrease in seminiferous tubule
diameter, spermatogenic cell counts, and Leydig's cell
nuclear diameter as compared with controls.
Of female hamsters given a total of 3–4 mg of
mercuric chloride during the first estrous cycle, 60%
did not ovulate by day 1 of the third cycle (15).
Ovulation was inhibited in female hamsters injected with
mercury(II) chloride at high doses (6.4 or 12.8 mg of
mercury per kg of body weight) during day 1 of the
estrous cycle (16). Female hamsters injected with 1 mg
of mercury(II) chloride per day during one estrous cycle
exhibited significantly higher levels of
follicle-stimulating hormone in their pituitaries as
compared with controls (17).
Pregnant Wistar rats were exposed intravenously to
mercury(II) chloride on
different days of gestation. At mid-gestation, the
minimum effective teratogenic dose of mercury (0.79
mg/kg of body weight) was high in relation to the
maternal LD50, and the incidence of fetal malformations,
mainly brain defects, was 23% in all live fetuses. In
rats of different gestational ages, uptake of Hg2+ by
the fetuses at this dose level decreased sharply between
days 12 and 13 (18).
Organic mercury
Short-term exposure
In rats fed methylmercury dicyandiamide 5 days per
week for 59 days, extensive damage to the renal cortex
occurred with extensive inflammatory reaction
surrounding the tubules and some early fibrosis even at
the lowest dose of 0.6 mg/kg of body weight per day
(19). Tubular degeneration of the kidney was also
evident after subcutaneous injection of 10 mg/kg of body
weight per day into rats for 7 consecutive days (20). In
contrast to the effects of high doses of methylmercury
on rats, kidney damage was not reported in cats exposed
to 0.45 mg/kg of body weight (21) or in monkeys exposed
to either 0.05 mg/kg of body weight per day (22) or to
doses resulting in blood levels of up to 4 µg of
mercury per ml of blood (23).
In cats, convulsions occurred after 60–83 days of
exposure to 0.45 mg of methylmercury per kg of body
weight per day; they were preceded 4–11 days earlier
by progressive behavioural changes. Kittens were fed
commercially available tuna contaminated with 0.3–0.5
mg of methylmercury(II) chloride per kg for 11 months.
The total mercury intake over the period averaged 6.3 mg
per cat or about 19 µg/day. Neurological disturbances
were observed in three kittens after 7–11 months (24).
Squirrel monkeys were exposed for periods of up to 35
days to repeated oral doses of methylmercury(II) nitrate
mixed in the food or by stomach tube. The threshold for
both behavioural and central nervous system pathology
occurred at blood mercury concentrations in the range
0.75–1.2 mg/litre (25).
Long-term exposure
In a study in which cats were fed methylmercury(II)
chloride in a fish diet at doses of 0.003, 0.008, 0.020,
0.046, 0.074, or 0.176 mg/kg of body weight per day, 7
days a week for 2 years, detectable neurological
impairment occurred in the group given 0.046 mg/kg of
body weight per day after 60 weeks; this concentration
was the lowest at which such impairment occurred.
Pathological changes in the nervous system were
restricted to the brain and dorsal root ganglia and were
not seen at doses below 0.074 mg/kg of body weight per
day (26).
Stumptail, pigtail, and squirrel monkeys were given
methylmercury(II) chloride in food for periods in excess
of 1000 days. This dosage regime was designed to
maintain the blood mercury level at 1–4 mg/litre of
blood. The critical effects seen were reduced
sensitivity to visual stimuli at low luminescence and
tremor on reaching for a small object. All monkeys with
a blood concentration above 2 mg/litre developed
symptoms with latent periods ranging from less than 20
to 200 days (23).
Cynomolgus monkeys were fed methylmercury from birth
at doses of 0.05 mg/kg of body weight per day for 3–4
years. Blood concentrations of mercury peaked at
1.2–1.4 mg/litre, then declined after weaning to a
steady level of 0.6–0.9 mg/litre. No overt signs of
toxicity were noted but, when tested after 3–4 years,
the monkeys exhibited impaired spatial vision under
conditions of both high and low luminescence (22).
Reproductive toxicity, embryotoxicity, and
teratogenicity
Mice were given single doses of 3.6, 5.3, 8, 12, 18,
or 27 mg of methylmercury(II) chloride per kg of body
weight at 9.5, 12.5, or 15.5 days post-fertilization
(27). The trend among F1 females towards an adverse
effect of dose on litter size, although not
statistically significant, was in the direction to be
expected if methylmercury(II) chloride can affect
oogenesis in females exposed during fetal life.
A single dose of 2, 3, or 4 mg of mercury(II)
ethanoate (about 1.3–2.5 mg of
mercury) was injected intravenously in three groups of
female hamsters on day 8 of gestation (28). The exposed
groups showed resorption frequencies of 12, 34, and 52%,
respectively, as compared with 4% in the controls.
High doses of methylmercury given to pregnant rodents
produced cleft palate (29,30). Prenatal exposure of rats
can produce renal functional abnormalities detectable in
offspring at 42 days of age (31).
Female rats were injected with 0, 6, or 10 mg of
methylmercury(II) chloride per kg of body weight on
gestational days 6–9 (32). Dams given 10 mg/kg of body
weight either failed to give birth or the young were
stillborn. External morphology was normal for rats given
either of the two lower doses. Methylmercury produced
hydrocephalus, decreased thickness of the cerebral
cortex in the parietal section, and increased thickness
of the hippocampus in the occipital section; with these
exceptions, the brains of mercury-treated rats showed
normal development.
Hamsters were given either 10 mg of methylmercury per
kg of body weight on gestational day 10 or 2 mg/kg on
gestational days 10–15 (33,34). In the neonatal
cerebellar cortex, degenerative changes such as
accumulation of lysosomes and areas of floccular
cytoplasmic degradation were frequently observed in the
neuroblast granular layer as well as in more
differentiated neural elements in the molecular and
internal granular layers. Pyknotic nuclei were seen
singly and in groups throughout the external granular
layer of treated animals. In the adult cerebellum, focal
areas of astrogliosis were observed in the molecular
layer of treated animals.
Mutagenicity and related end-points
Animal and cell culture studies confirm that
methylmercury damages chromosomes if given orally at a
dose of 5 mg/kg of body weight to pregnant mice (16,35),
intraperitoneally at 2 mg/kg of body weight daily for 3
weeks to adult hamsters (36), and intraperitoneally at
10 mg/kg of body weight to ovulating Syrian hamsters
(37). Methylmercury at low concentrations (0.05–0.1 µmol/litre)
has been reported to interfere with gene expression in
in vitro cultures of glioma cells (38). Non-disjunction
and sex-linked recessive lethal mutations were induced
in Drosophila melanogaster by treatment with
methylmercury (39).
Carcinogenicity
Groups of mice were fed 15 or 30 mg of methylmercury
per kg of diet for up to 78 weeks. The majority of the
30 mg/kg group died from neurotoxicity by week 26.
Histopathological examination of kidney tissue from all
animals surviving after 53 weeks revealed renal tumours
in 13 of 16 males in the 15 mg/kg group. Of these, 11
were classified as adenocarcinomas and two as adenomas
(40).
6. Effects on humans
Inorganic mercury
Acute exposure
Mercury will cause severe disruption of any tissue
with which it comes into contact in sufficient
concentration, but the two main effects of mercury
poisoning are neurological and renal disturbances. The
former is characteristic of poisoning by methyl- and
ethylmercury(II) salts, in which liver and renal damage
are of relatively little significance, the latter of
poisoning by inorganic mercury.
In general, however, the ingestion of acute lethal
toxic doses of any form of
mercury will result in the same terminal signs and
symptoms, namely shock, cardiovascular collapse, acute
renal failure, and severe gastrointestinal damage. Acute
oral poisoning results primarily in haemorrhagic
gastritis and colitis; the ultimate damage is to the
kidney. Clinical symptoms of acute intoxication include
pharyngitis, dysphagia, abdominal pain, nausea and
vomiting, bloody diarrhoea, and shock. Later, swelling
of the salivary glands, stomatitis, loosening of the
teeth, nephritis, anuria, and hepatitis occur (41).
Ingestion of 500 mg of mercury(II) chloride causes
severe poisoning and
sometimes death in humans (42). Acute effects result
from the inhalation of air containing mercury vapour at
concentrations in the range of 0.05–0.35 mg/m3
(43,44). Exposure for a few hours to 1–3 mg/m3 may
give rise to pulmonary irritation and destruction of
lung tissue and occasionally to central nervous system
disorders (45).
Dermal exposure to alkyl mercurials may give rise to
acute toxic dermatitis and eczematous changes.
Long-term exposure
Many studies involving the observation of more than
1000 individuals indicate that the classical signs and
symptoms of elemental mercury vapour poisoning
(objective tremors, mental disturbances, and gingivitis)
may be expected to appear after chronic exposure to air
mercury concentrations above 0.1 mg/m3 (8). Nonspecific
neurological and physiological symptoms were also
associated with lower exposure levels.
Considerable mercury exposure of children of workers
at a thermometer plant has been reported (46). The
median urine mercury level of 23 such children was 25 µg/litre
as compared with 5 µg/litre in 39 controls. No signs of
mercury intoxication were seen on clinical examination
or reported by parents (3).
Organic mercury
The adverse health effects of occupational exposure
to alkylmercury compounds constitute what is known as
the Hunter-Russel syndrome (concentric constriction of
the visual field, ataxia, dysarthria, etc.); this was
seen in four workers exposed to methylmercury fungicide
(47).
Methyl- and ethylmercury compounds have been the
cause of the largest number of cases of mercury
poisoning and of fatalities in the general population as
a result of the consumption of contaminated fish or of
bread prepared from cereals treated with alkylmercury
fungicides. The earliest effects are nonspecific, e.g.
paraesthesia, malaise, and blurred vision. These are
followed by concentric constriction of the visual field,
deafness, dysarthria, and ataxia. In the worst cases,
the patient may go into coma and ultimately die. At high
doses, methylmercury affects the peripheral nervous
system in human subjects (48).
The two major epidemics of methylmercury poisoning in
Japan, in Minamata Bay and in Niigata, both known as
Minamata disease, were caused by the industrial release
of methylmercury and other mercury compounds into
Minamata Bay and into the Agano River, followed by
accumulation of the mercury in edible fish. The maximum
blood level of methylmercury without adverse health
effects was estimated to be 0.33 µg/ml based on the
epidemiological study of the Minamata disease endemic
area (49). By 1971, a total of 269 cases of Minamata
disease had been reported in Minamata and Niigata, of
which 55 proved fatal. By March 1989, 2217 cases of
Minamata disease had been officially recognized in
Minamata and 911 cases in Niigata (50).
The largest recorded epidemic caused by the ingestion
of contaminated bread prepared from wheat and other
cereals treated with alkyl (methyl- or ethyl-) mercury
fungicides took place in the winter of 1971–72 in
Iraq, and resulted in the admission of over 6000
patients to hospital and over 500 deaths (51). Previous
epidemics have occurred in Guatemala, Iraq, and
Pakistan, and on a limited scale in other countries
(3,8,52).
The Cree Indians of northern Quebec were also known
to be exposed to methylmercury through the consumption
of contaminated local fish. The relationship between
measures of exposure and neurological abnormalities was
studied in two communities. A positive association was
found between neurological abnormalities and
methylmercury exposure in both communities, but the
relationship was statistically significant only in one
of them (53,54).
The first indication of possible congenital Minamata
disease was the unusual occurrence of cerebral
palsy-like conditions in nine infants in the endemic
areas (population about 1700) during 21 months. These
infants had severe cerebral involvement (palsy and
mental retardation); mild or no symptoms of poisoning
were seen in their mothers, although there is a
possibility that slight symptoms might have been
overlooked (3).
According to an epidemiological study of an outbreak
in Iraq, the clinical picture was dose-dependent. In
those who were exposed to high maternal blood levels of
methylmercury, the picture was one of cerebral palsy
indistinguishable from that resulting from other causes
(microcephaly, hyper-reflexia, and gross motor and
mental impairment, associated with blindness or
deafness). Milder forms were not easy to diagnose during
the first few months of life, but became clearer with
time. The cases showed mainly psychomotor impairment and
persistence of pathological reflexes (53,55–57). The
relationship between prenatal exposure to methylmercury
and neurological and developmental abnormalities was
also studied. Abnormality of the tendon reflex was
positively associated with methylmercury exposure only
in boys, without a dose–response relationship (58).
Findings in the milder cases were quite similar to those
associated with the minimal brain syndrome (3).
Marsh et al. (59) demonstrated a dose–response
relationship between the deteriorated neurological score
in children and the maximum mercury concentration during
gestation in a single strand of maternal head hair.
7. Guideline value
Almost all mercury in uncontaminated drinking-water
is thought to be in the form of Hg2+. Thus,
it is unlikely that there is any direct risk of the
intake of organic mercury compounds, and especially of
alkymercurials, as a result of the ingestion of
drinking-water. However, there is a real possibility
that methylmercury will be converted into inorganic
mercury.
In 1972, JECFA established a provisional tolerable
weekly intake (PTWI) of 5 µg/kg of body weight of total
mercury, of which no more than 3.3 µg/kg of body weight
should be present as methylmercury (60). This PTWI was
reaffirmed in 1978 (61). In 1988, JECFA reassessed
methylmercury, as new data had become available; it
confirmed the previously recommended PTWI for the
general population, but noted that pregnant women and
nursing mothers were likely to be at greater risk from
the adverse effects of methylmercury. The available data
were considered insufficient, however, to allow a
specific methylmercury intake to be recommended for this
population group (62,63).
To be on the conservative side, the PTWI for
methylmercury was used to derive a guideline value for
inorganic mercury in drinking-water. As the main
exposure is from food, 10% of the PTWI was allocated to
drinking-water. The guideline value for total mercury is
0.001 mg/litre (rounded figure).
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