The element mercury, also known as quicksilver (symbol Hg for hydrargyrum), and its

compounds have no known normal metabolic function. Their presence in the cells of living
organisms represents contamination from natural and anthropogenic sources; all such
contamination must be regarded as undesirable and potentially hazardous (U.S. National
Academy of Sciences [USNAS] 1978). Accumulation of mercury in tissues is reportedly
associated with an excess risk of myocardial infarction (Salonen et al., 1995; Gualler et al.,
2002), increased risk of death from coronary heart disease and cardiovascular disease (Salonen et
al., 1995), and accelerated progression of carotid atherosclerosis (Salonen et al., 2000). The most
important ore of mercury, cinnabar (mercuric sulfide), has been mined continuously since 415
BCE (Clarkson and Marsh, 1982). In the period before the industrial revolution, mercury was
used extensively in gold extraction and in the manufacture of felt hats and mirrors; in the 1800s,
it was used in the chloralkali industry, in the manufacture of electrical instruments, and as a
medical antiseptic; and since 1900, it has been used in pharmaceuticals, in agricultural
fungicides, in the pulp and paper industry as a slimicide, and in the production of plastics
(Clarkson and Marsh, 1982). World use of mercury is estimated at 10,000 to 15,000 metric tons
annually (Boudou and Ribeyre, 1983), of which the United States accounts for about 18.0%
(Clarkson and Marsh, 1982). Today, mercury is a leading public health concern, as judged by the
increases in regulations governing mercury emissions, in mercury fish advisories, in clinical
studies, and in media attention (Kales and Goldman, 2002; Hightower and Moore, 2003; Weil et
al., 2005). The first cases of fatal inorganic mercury poisoning in humans were reported for two
men in a European chemical laboratory in 1865, and the first documented human poisoning from
agricultural exposure to an organomercury compound was in 1940 (Das et al., 1982). Human
exposure to mercury compounds via dermal, dietary, and respiratory routes has severe
consequences. For example, 1600 infants in Argentina showed symptoms of mercury poisoning
after a laundry treated their diapers with a mercury disinfectant; numerous poisonings resulted
from ingestion of mercurycontaminated fish, pork, seafoods, and grains; and from occupational
exposure in Nicaraguan mercury fungicide applicators via respiration (Elhassani, 1983).
Sporadic incidences of human poisonings have occurred in the United States, the Soviet Union,
and Canada; while major epidemics have been reported in Japan, Pakistan, Guatemala, Ghana,
Yugoslavia, and Iraq (Bakir et al., 1973; Clarkson and Marsh, 1982; Das et al., 1982; Elhassani,
1983; Greener and Kochen, 1983). In Iraq, for example, a major mercury poisoning occurred in
the early 1970s, with 6530 hospital admissions and 459 hospital deaths (Bakir et al., 1973;
Amin-Zaki et al., 1974; Marsh et al., 1977, 1987; Das et al., 1982; Elhassani, 1983; Choi et al.,
1978; Inouye, 1989). In 1970, the Iraqi government decided to import seed grain from Mexico,
owing to a serious wheat shortage throughout Iraq. About 73,200 metric tons of seed wheat were
imported and distributed between September and November of 1971. The seed had been treated
with a methylmercury fungicide and colored with a red dye; it was delivered in 50-kg sacks with
a warning written in Spanish. A skull and crossbones was painted on the outside of each sack to
indicate that the seed had been treated with poison. However, both Spanish and the skull and
crossbones insignia were totally unfamiliar to the Iraqi farmers and the people decided to make
home-made bread instead of using the grain for seed; about half the wheat was consumed for this
purpose. The water-soluble red dye was washed off the wheat, with the assumption that the
mercury would be equally soluble (it was not). Before human consumption of the wheat, the
farmers fed the wheat for a few days to chickens and other livestock without apparent effect; it
was not realized that a lengthy latency period was involved. The wheat flour contained 4.8 to
14.6 mg methylmercury/kg, far in excess of the 0.5 mg Hg/kg regulatory limit. Consumption of
the bread lasted 1 to 2 months, and the first cases of poisoning appeared at the end of December
1971. In 1972, there were 6530 reported cases within 18 months, including 459 deaths, among
Iraqi farmers who ate bread made from seed wheat treated with a methylmercury fungicide.
Babies congenitally affected by methylmercury born in Iraq during this outbreak showed clinical
features of mental retardation, motor disorders resembling cerebral palsy, and other physical and
mental disturbances. Histopathological examination of the brain of victims in cases of death
showed degenerative neuronal damage and abnormal development of the cerebral cortex. There
was no effective antidote to counteract the effects of methylmercury on the central nervous
system. At Oak Ridge, Tennessee, liquid metallic mercury was used during the 1950s and 1960s
for uranium processing in a nuclear weapons plant (Silver et al., 1994). Accidental releases of
mercury of about 100 tons — equivalent to that released at Minamata Bay, Japan, in which
hundreds died resulted in heavy accumulations of mercury in the waste pipes and as a “lake of
Hgo” of about 7000 L under the plant sites. However, unlike Minamata, Japan (which is
discussed extensively in Chapter 10), there have been no documented human health problems at
the Oak Ridge site (Silver et al., 1994). The mercury at Oak Ridge is released into local waters at
about 75 kg annually, at which rate it will take more than 1000 years to disappear, although
microbial activities transform the mercury found in local waters within hours (Barkay et al.,
1991).
Mercury contamination is the most serious environmental threat to fishery and wildlife resources
in the southeastern United States, with fish consumption advisories issued in the ten states
comprising this region (Facemire et al., 1995). In March 1989, the Florida Department of Health
and Rehabilitative Services issued a health advisory prohibiting consumption of predatory fishes,
such as largemouth bass (Micropterus salmoides), bowfin (Amia calva), and gar (Lepisosteus
spp.) in southern Florida, and the entire Everglades watershed has been closed to hunting of
alligators (Alligator mississippiensis) due to excessive mercury in edible tissues of alligators
(Roelke et al., 1991; Sundolf et al., 1994; Kannan et al., 1998). Methylmercury concentrations of
2.0 to 3.0 mg/kg fresh weight (FW) muscle were documented in largemouth bass and other fish-
eating species (Fleming et al., 1995), or 4 to 10 times the allowable limit in foods for human
consumption (Eisler, 2000, 2004a). About 0.91 million ha of the South Florida Everglades
ecosystem are currently under fish consumption advisories because of mercury contamination
(Atkeson et al., 2003).
The number of mercury-contaminated fish and wildlife habitats has, in general, progressively
increased worldwide, almost all as a direct result of anthropogenic activities (Boudou and
Ribeyre, 1983). Long-range atmospheric transport of mercury since 1940 has resulted in elevated
mercury loadings in remote Canadian lakes up to 1400 km from the closest industrial centers
(Lucotte et al., 1995). Since 1985, annual mercury accumulation rates in flooded Florida
Everglades soils averaged 53.0 μg/m2, which is about 4.9 times greater than rates observed
around the turn of the century; the increase is attributed to increased global and regional
deposition and is similar to increases reported for lakes in Sweden and the northern United States
(Rood et al., 1995). In 1967, the Swedish medical board banned the sale of fish that contained
high concentrations of organomercury salts, originating from about 40 lakes and rivers (Das et
al., 1982). More than 10,000 Swedish lakes have been closed to fishing because of excessive
mercury loadings (Lindqvist et al., 1991). In 1970, after the discovery of high levels of mercury
in fish from Lake St. Clair, Canada, restrictions on
fishing and the sale of fish were imposed in many areas of the United States and Canada (Das
et al., 1982). Since 1970, a total of 26 of the 48 states in the conterminous United States have
reported mercury pollution in their waters as a direct result of human activities. These states have
banned sport or commercial fishing in mercury-contaminated waters, or have issued health
warnings
about the consequences of eating mercury-contaminated fish or seafood from selected water
courses,
or have placed restrictions on fish consumption from certain streams, lakes, or rivers polluted
with
mercury (USNAS, 1978; Becker and Bigham, 1995). At present, more than 40 states have issued
health advisories restricting fish consumption based on unacceptable mercury contents; similar
advisories have been issued in North America, Europe, and Asia (Atkeson et al., 2003). Fish
consumption advisories on mercury issued by the U.S. Food and Drug Administration (FDA) are
effective in reducing fish consumption; in Massachusetts; for example, there was an average
monthly
decline in fish consumption of 1.4 servings among pregnant women following an FDA advisory
on the health risks of mercury (Oken et al., 2003).
Poisoning of game birds and other wildlife in Sweden, apparently by seeds treated with
organomercurials, was first noted in 1960 (Das et al., 1982). Massive kills of the grey heron
(Ardea
cinerea) in the Netherlands during 1976 were attributed to a combination of low temperatures,
undernourishment, and high body burdens of mercury (Van der Molen et al., 1982). Mercury
contamination has resulted in the closure of pheasant and partridge hunting areas in Alberta,
Canada
(Mullins et al., 1977). Declining numbers of wading birds in southern Florida are attributed to
mercury contamination of their food supply (Sundolf et al., 1994).
Most authorities on mercury hazards to living organisms now agree on six points. First, mercury
and its compounds have no known biological function, and its presence in living organisms is
undesirable and potentially hazardous. Second, forms of mercury with relatively low toxicity can
be transformed into forms with very high toxicity through biological and other processes. Third,
methylmercury can be bioconcentrated in organisms and biomagnified through food chains,
returning mercury directly to human and other upper trophic level consumers in concentrated
form. Fourth, mercury is a mutagen, teratogen, and carcinogen, and causes embryocidal,
cytochemical, and histopathological effects. Fifth, high body burdens of mercury normally
encountered in some species of fish and wildlife from remote locations emphasize the
complexity of natural mercury cycles and human impacts on these cycles. And finally, the
anthropogenic use of mercury should be curtailed because the difference between tolerable
natural background levels of mercury and harmful effects in the environment is exceptionally
small. These, and other aspects of mercury and its compounds in the environment as a result of
anthropogenic or natural processes, are the subject of many reviews.*The current book builds
extensively on these reviews, emphasizing recent and credible information on mercury uses and
sources to the environment; biological, physical, and chemical properties of mercury and its
compounds; documentation and significance of mercury concentrations in abiotic materials,
plants, invertebrates, amphibians, reptiles, elasmobranchs, fishes, birds, and humans, and other
mammals; lethal and sublethal effects of inorganic and organic mercury compounds to plants,
animals, and humans; biological, chemical, and physical variables known to