Journal of Environment and Health Science Mercury and its Associated Impacts on Environment and Human Health: A Review Citation: Saturday, A. Mercury and its Associated Impacts on Environment and Human Health: A Review

Abstract

Mercury exists naturally and as a man-made contaminant. The release of processed mercury can lead to a progressive increase in the amount of atmospheric mercury, which enters the atmospheric-soil-water distribution cycles where it can remain in circulation for years. Mercury poisoning is the result of exposure to mercury or its compounds resulting in various toxic effects depending on its chemical form and route of exposure. The major route of human exposure to methylmercury (MeHg) is largely through eating contaminated fish, seafood, and wildlife which have been exposed to mercury through ingestion of contaminated lower organisms. MeHg toxicity is associated with nervous system damage in adults and impaired neurological development in infants and children. Ingested mercury may undergo bioaccumulation leading to progressive increases in body burdens. Mercury has profound neurological, endocrine, reproductive, and fetotoxicity effects. Although most countries recognize the need to combat mercury pollution, controls are either nonexistence or inadequate. Based on articles reviewed, we recommend community education on need for a reduction in use of products that contain mercury. Dentists should reduce or eliminate the use of mercury amalgam and use pre-encapsulated amalgam instead of mixing their own if they are to continue using amalgam. Environment management agencies should expand existing national research on environmental and health effects of mercury.

Full text

Journal of Environment
and Health Science ISSN: 2378-6841
OPEN ACCESS
Mercury and its Associated Impacts on Environment
and Human Health: A Review
Alex Saturday
Department of Environment and Natural Resources, Kabale University
*Corresponding author: Alex Saturday, Department of Environment and Natural Resources, Kabale University; E-mail: Saturday.alex@
yahoo.com
Citation: Saturday, A. Mercury and its Associated Impacts on
Environment and Human Health: A Review. (2018) J Environ
Health Sci 4(2): 37- 43.
Received date: May 31, 2018
Accepted date: July 24, 2018
Published date: July 30, 2018
Introduction
Mercury is one of the most toxic elements and a threat to wildlife
because it accumulates and magnies to unsafe levels in aquatic
food chains (Munthe et al., 2007). It is rapidly transformed by
microorganisms into organic compounds that tend to bioaccu-
mulate and biomagnify in animals (Ronchetti et al., 2006). All
mercury species are toxic, with organic mercury compounds
generally being more toxic than inorganic species. Because of
its high bioaccumulation, mercury concentrations escalate up
the food chain and for example, predatory sh can have up to
106 times higher mercury concentrations than the ambient wa-
ter (Joint FAO/WHO, 2006). The organic form of mercury is
most toxic as it passes the blood-brain barrier owing to its lipid
solubility. So the primary route of exposure to methylmercury
(MeHg) for humans is consumption of sh (Habiba et al., 2017).
Since the beginning of the industry, anthropogenic ac-
tivities like increased mining, high rate of fossil-fuel burning,
wide spread use of raw materials containing mercury are some
important contributors of mercury to the environment. The al-
lowable mercury level set by World Health Organization (WHO)
for drinking water is 1 μgL-1 (Azimi & Moghaddam, 2013).
Mercury is also considered by the U.S. Environmental Protec-
tion Agency (EPA) as a highly dangerous element because of its
Review Article DOI: 10.15436/2378-6841.18.1906
Vol 4:2 pp 37/43
Copyright: © 2018 Saturday, A. This is an Open access article
distributed under the terms of Creative Commons Attribution 4.0
International License.
accumulative and persistent character in the environment. The
damage has vast implications with human beings at the top of
food chain getting the worst of the deal owing to biomagnica-
tions (Azimi & Moghaddam, 2013). The amount of Hg mobi-
lized and released into the environment has increased since the
beginning of the industrial age. Hg pollution is primarily due to
human activities.
Mercury and its compounds are currently used in a
number of countries, especially in industrial countries such as
Iran. Mercury is applied in several dierent aspects including
Batteries (Bernardes, Espinosa, & Tenório, 2003), measuring
and control equipment: medical and other thermometers, blood
Abstract
Mercury exists naturally and as a man-made contaminant. The release of processed mercury can lead to a progressive
increase in the amount of atmospheric mercury, which enters the atmospheric-soil-water distribution cycles where it
can remain in circulation for years. Mercury poisoning is the result of exposure to mercury or its compounds resulting
in various toxic eects depending on its chemical form and route of exposure. The major route of human exposure to
methylmercury (MeHg) is largely through eating contaminated sh, seafood, and wildlife which have been exposed to
mercury through ingestion of contaminated lower organisms. MeHg toxicity is associated with nervous system damage
in adults and impaired neurological development in infants and children. Ingested mercury may undergo bioaccumula-
tion leading to progressive increases in body burdens. Mercury has profound neurological, endocrine, reproductive, and
fetotoxicity eects. Although most countries recognize the need to combat mercury pollution, controls are either nonex-
istence or inadequate. Based on articles reviewed, we recommend community education on need for a reduction in use
of products that contain mercury. Dentists should reduce or eliminate the use of mercury amalgam and use pre-encapsu-
lated amalgam instead of mixing their own if they are to continue using amalgam. Environment management agencies
should expand existing national research on environmental and health eects of mercury.
Keywords: Mercury; Toxicity; Environment

Citation: Saturday, A. Mercury and its Associated Impacts on Environment and Human Health: A Review. (2018) J Environ Health Sci 4(2): 37- 43.
www.ommegaonline.org Vol 4:2 pp 38/43
pressure gauges, manometers, pressure valves, gyroscopes,
Discharge lamps like uorescent lamps, laboratory chemicals,
electrodes and apparatus for analysis, color photograph paper,
slimicides for paper production, explosives, reworks, color
photograph paper, pharmaceuticals: preservatives in vaccines
and eye drops, disinfectants; skin lightening creams and soaps;
herbal medicine, cosmetics: biocides in eye cosmetics, arm and
leg bands, pesticides, especially for seed dressing.
Chemical Forms and Properties of Mercury
Mercury is classied as a heavy metal (atomic weight 200.59)
and is well known as being among the most toxic of metals
(World Health Organization, 2007). Mercury is a non-transition
metal and is an extremely rare element in the earth’s crust, hav-
ing an average mass abundance of only 0.08 ppm (Sinicropi et
al., 2010). Hg has three valence states (0, I and II), and exists in
three main forms, each of which have dierent toxicities, im-
plications for health and measures to prevent exposure (IPCS
2000). These three forms of mercury are elemental mercury or
Quick silver (Hg0, metallic mercury, and mercury vapor), in-
organic mercury (Hg+ and Hg2+), and organic mercury such as
methylmercury (CH3Hg, MeHg) and ethylmercury (C2H5Hg,
EtHg).
Elemental mercury
Elemental mercury (Hg) has a peculiar behavior, in that, it is
monoatomic in the vapor phase, and has a relatively high vapor
pressure at 20 °C (1.3 10−3 mm). It uniquely exists in liquid form
at room temperature and quickly turns to vapor when heated
above room temperature. The high volatility of Hg0 prolongs the
eects of anthropogenic releases through repeated atmospheric
recycling to and from the land and the sea (Mason et ., 1994).
Hg0 can remain suspended in the atmosphere for up to 1 year,
where it can be transported and deposited globally.
Elemental mercury is volatile at room temperature and
the vapors may represent a hazard to humans. Such exposure
may occur in laboratories, work places as well as in homes. In
private homes, the broken thermometers containing mercury
could become a source of exposure, as it can be very dicult to
collect the spilled mercury. In many countries, the use of mer-
cury in thermometers has now been banned as a policy to re-
duce the risk to consumer and the release of mercury into nature.
Work place exposure may occur in many types of industries,
where major uses of elemental mercury include chlorine-alkali
manufacture, dental amalgams, electronic switches and uores-
cent lamps.
Toxicokinetics: Elemental mercury exposure from the air is
readily taken up through the lungs and about 74% is retained in
the human body (Hursh et al., 1976). From blood, the elemen-
tal mercury distributes throughout the body, as it easily passes
through most cell membranes including the blood-brain barrier
and the placenta. In blood, the elemental mercury is oxidized to
mercuric mercury partly under the inuence of catalase (Carocci
et al., 2014) and this inuences brain uptake of mercury (Carocci
et al., 2014). It has been shown that uptake of elemental mercury
in the brain will decrease if the amount of catalase activity in
the brain is inhibited (Eide & Syversen, 1982). The uptake of
elemental mercury in brain tissue is also markedly dependent
on brain glutathione levels, as a 20% reduction in brain GSH
content will result in a 66% increase in brain mercury content
(Eide & Syversen, 1982).
Toxic eects: Acute inhalation exposure, at high concentrations,
may induce respiratory distress including dyspnea. Chronic ex-
posure may induce symptoms from the central nervous system
(CNS) including tremors, delusions, memory loss, and neuro-
cognitive disorders. Many of the signs and symptoms associ-
ated with slight poisonings will eventually disappear after the
exposure ends. However, severe exposure may result in a lasting
eect on brain function. Additionally, long-term exposure may
also cause eects in the kidney (Lohren et al., 2015).
Inorganic mercury compounds
Hg0 is oxidized in air to its inorganic forms (Hg+ and Hg2+) and is
released during rain events to be deposited in soil, or into the wa-
ters of rivers, lakes, and oceans. Inorganic mercury, derived from
industrial release and from contaminated water, is biomethylated
(in the aqueous environment and by phytoplankton in the ocean)
to methylmercury (MeHg), primarily by sulfate-reducing bacte-
ria (Morel et al. 1998). MeHg is accumulated to high concentra-
tions in shellsh, predatory sh (i.e., swordsh, shark and king
mackerel) and sea mammals. It is bioaccumulated especially by
the liver, brain, kidney, and muscle (Compeau and Bartha 1985).
Inorganic mercury compounds have been used in a very
extensive range of medical and cosmetic products; antiseptics,
teething powders, skin-lightening creams. Accidental or inten-
tional poisonings of mercuric chloride have not been uncom-
mon. Inorganic mercury compounds can be either mercury in
monovalent (mercurous – Hg2+) or divalent (mercuric – Hg2+)
form. Mercurous chloride has very low solubility in water and is
therefore regarded as non-hazardous. However, the use of teeth-
ing powder containing mercurous mercury by infants led to a
marked increase in their urinary mercury level (Warkany, 1966).
Toxicokinetics: Inorganic mercury accumulates primarily in
the kidney, followed by its accumulation in the liver. The ki-
netics of mercuric mercury in humans (Lohren, Blagojevic, et
al., 2015) demonstrate that about 1–16% of the initial dose is
absorbed with a body half-time of about 41 days. No signicant
deposition of mercury was found in the head region for the rst
58 days. Animal studies by Friberg et al. (1961) have shown that
8% of mercuric chloride applied to the skin can be absorbed in
5 h. In an experimental study on rats, it was shown that there is
an uneven distribution of mercury in the nervous system. More
mercury was found in the neurons compared to the glial cells,
and the mercury had accumulated in lysosomes. The motor neu-
rons contained more mercury than the sensory neurons and it
was noted that mercury was present in the cerebellum, but not in
the Purkinje cells.
Toxic eects: The organs primarily aected after acute poison-
ing of mercuric mercury are the intestine and kidneys. In the in-
testine, the corrosive eects will dominate while in the kidneys,
renal failure may occur within 24 h due to necrosis of the tubular
epithelium. As little as 1g can prove fatal to an adult human. The
most prominent eect of mercuric mercury is tubular necrosis
in the kidney and after prolonged exposure glomerulonephritis

Environment and Human Health
Saturday, A. Vol 4:2 pp 39/43
can also be seen. Mercuric mercury may also cause autoimmune
diseases (Stejskal, 2015).
Organic mercury
The rapid inter conversion of the inorganic forms into the or-
ganic ones, including the possibility of disproportionation reac-
tions, means that the environmental behavior of Hg is complex
(Rasmussen, 1994). Mercury has no known physiological role in
humans and is among the most harmful heavy metals to which
humans and wildlife can be exposed. Furthermore, the human
body lacks eective mechanisms to excrete it. The organometal-
lic compounds of mercury have a higher solubility in lipids than
its inorganic species.
The organic mercury compounds include alkyl and
phenyl groups as their organic molecular part. The phenylmer-
cury compounds are mainly used as preservatives in medicine.
Among the alkyl compounds, both the methyl and ethyl mercu-
ry compounds can be present in the environment. These com-
pounds may exist as monoalkyl or dialkyl compounds (Carocci
et al., 2014). The dialkyl compounds are very volatile and dif-
cult to handle for any practical purpose including toxicology
studies (Carocci et al., 2014). Further, these compounds are
readily absorbed both through the airways and intact skin and
are highly toxic even at very low exposure.
Human exposure to Mercury
Hg is released to the environment from both anthropogenic and
natural sources. Natural sources include weathering of rocks
and from geological movements. For instance annually, volca-
nic and geothermal activities release an estimated 1,500 tons of
mercury to the environment (Maria et al., 2017; Sundseth et al.,
2017). Anthropogenic release occurs from manifold industrial
point sources and is estimated to constitute 2,320 tons of mer-
cury emitted annually into the atmosphere (Nicola Pirrone et al.,
2010).
Sources of Hg exposure resulting from human enter-
prise include industrial consumption of fossil fuels, cement pro-
duction and incineration of solid wastes, contact with topical
medicines, thermometers, barometers, and batteries, in addition
to medical waste incineration, Hg-based substances used in rit-
ualistic practices and dental amalgams (Maria et al., 2017; N.
Pirrone et al., 2001). Autopsy studies have shown that dental
amalgams are the main source of mercury in human tissues.
Amalgam bearers have about 2–12 fold more mercury in their
tissues, including the brain, than individuals without amalgams
(Joachim Mutter, 2011).
In some countries, consumption of inorganic mercury
preparations is a signicant source of human intoxication. The
reason for this is that such preparations have long been used
as medications, germicidal soaps and skin creams (Guzzi and
La Porta 2008). Some skin creams contain as much as 6–10 %
mercurial chloride or calomel (Hg2Cl2). For many years, calo-
mel was used in infant teething powders, worm drugs, and as an
analgesic.
MeHg is an organomercurial compound primarily
found as a pollutant in the aquatic environment. When MeHg
is present in nature, its source is usually from biomethylation
of inorganic mercury that is carried out by aquatic anaerobic
sulfate-reducing bacteria (Morel et al., 1998). MeHg ultimate-
ly derives from anthropogenic sources, and when formed will
be released into rivers, lakes, and oceans. Consequently, people,
whose diet consists mainly of sh and shellsh, may be exposed
to high levels of MeHg.
Absorption, Distribution, and Toxicity of Mercury
The toxicity of metals and metal compounds largely depends
on the degree to which they are bioavailable, i.e. the degree to
which they are absorbed through cell membranes, are distributed
within the cell and bind to cellular macromolecules. When Hg0
from dental amalgams is inhaled as a vapor into the lungs, about
80% is absorbed (Joachim Mutter et al., 2010).
Due to its uncharged monoatomic form, Hg0 is highly
diusible and lipid soluble, and easily crosses the blood-brain
barrier and lipid bilayers of cells and cell organelles, such as
mitochondria. Mercury vapor also penetrates the mucosa and
connective tissue of the oral and nasal cavities and may be trans-
ported into nerve cells (Joachim Mutter et al., 2010).
Exposure to toxic Hg0 vapors may be either acute or
chronic. Both acute and chronic Hg0 exposures may result in hu-
man poisoning. In particular, such exposures can cause cough-
ing, dyspnea, fever, tremors, malaise, axonal sensor motor poly-
neuropathy, gingivitis, hallucinations and mercurial erythrism,
a syndrome that includes excitability, loss of memory, insom-
nia and neurocognitive disorders (Guzzi and La Porta 2008).
Case-control studies have demonstrated an association between
exposure to Hg0 and the potential to develop amyotrophic lateral
sclerosis (ALS).
In the inorganic form, mercury is absorbed from the
gastrointestinal tract and acts to produce inammatory reactions
in the kidneys and gastrointestinal apparatus. Intracellularly,
Hg++ is produced from metabolic oxidation of Hg0. Research
suggests that mercury induces autoimmune processes (Schiraldi
& Monestier, 2009), and may be mutagenic at low concentra-
tions (Schurz et al. 2000). Immunotoxic eects could potentially
enhance susceptibility to infections, to malaria (Silbergeld et al.,
1998) or immunologically-mediated diseases (McCabe & Law-
rence, 1994).
Inorganic mercury accumulates in the human breast
and is secreted in breast milk, which can damage the develop-
ing infant’s central nervous system, pulmonary and nephrotic
systems. Inorganic mercury exposure can also induce Kawasaki
disease (Mutter & Yeter, 2008), which results from impairment
of the immune system. The symptoms of children aected by
Kawasaki disease include fever, photophobia, pharyngitis, oral
lesions, skin rashes, and tachycardia, among others (Goyer &
Clarkson, 1996).
Among the most dangerous mercury compound is di-
methylmercury (CH3)2Hg) which is toxic enough to cause death
if only a few microliters is spilled on the skin, or even latex
gloves (Joshi et al., 2012). Mercury poisoning can result in
death, mental retardation, dysarthria, blindness, and neurolog-
ical decits, loss of hearing, developmental defects, and abnor-
mal muscle tone (Guzzi & La Porta, 2008).
Impacts of Mercury on Environment and Human Health
Environmental impacts of mercury: The majority of mercury
emissions to air are in the form of gaseous elemental mercury,
which can be transported globally to regions far from the emis-

Citation: Saturday, A. Mercury and its Associated Impacts on Environment and Human Health: A Review. (2018) J Environ Health Sci 4(2): 37- 43.
www.ommegaonline.org Vol 4:2 pp 40/43
sions source. The remaining emissions are in the form of gas-
eous inorganic ionic mercury forms (such as mercuric chloride)
or bound to emitted particles. These forms have a shorter atmo-
spheric lifetime and will deposit to land or water bodies within
roughly 100 to 1,000 kilometers of their source. The ocean cur-
rents are also media for long range mercury transport.
Air Pollution: Metallic, or elemental mercury, is a liquid at
room temperature and like any other liquid, it evaporates into
the air, where it can be inhaled. Very small amounts of metallic
mercury, released into an enclosed space, can raise air concen-
trations of mercury to levels that may be harmful to health. The
longer people breathe the contaminated air, the greater the risk
to their health. In addition, metallic mercury and its vapors are
extremely dicult to remove from clothes, furniture, carpet, and
other porous items (Muhlendahl, 2015).
Some mercury sources in air are household products,
including thermostats, glass thermometers, barometers, and
switches in large appliances. Barometers have small openings
in order to measure air pressure. Mercury vapors may be slowly
released from them without breakage. Fluorescent bulbs contain
a small amount of mercury vapor and a larger amount of mercu-
ry in a powder or dust form, whether accidental or intentional,
spills of metallic mercury in a home or apartment (Muhlendahl,
2015).
Water Pollution: Water pollution refers to the additional to the
water of an excess of material that is harmful to humans, ani-
mals and shes (Aboud, 2010). The materials found in water
and considered toxic to sh and other sea animals in one way or
another can be recognized in oxygen debilitating materials, toxic
gases, toxic organic compounds and pesticides, etc. The concen-
tration of freshwater with a wide range of pollutants has become
a matter of concern over the last few decades. The natural aquat-
ic systems may be extensively contaminated with heavy metals
released from domestic, industrial, mining and other man-made
activities (Domagalski et al., 2004).
Health Impacts of Exposure to Mercury: Mercury is in wide-
spread use in healthcare facilities. Thermometers and sphygmo-
manometers contain mercury and so do many medical batteries,
uorescent lamps, and electrical switches. Mercury compounds
are also in preservatives, xatives, and reagents used extensively
in hospital laboratories. The impacts of mercury exposure are
discussed in the subsequent sub-sections.
Nervous System: The nervous system is very sensitive to all
forms of mercury. Methylmercury and metallic mercury vapors
are more harmful than other forms because more mercury in
these forms reaches the brain. Exposure to high levels of me-
tallic, inorganic, or organic mercury can permanently damage
the brain, kidneys, and developing fetus. Eects on brain func-
tioning may result in irritability, shyness, tremors, changes in
vision or hearing, and memory problems (Azimi & Moghadd-
am, 2013). Damage to the nerves of the arms and legs has been
reported in employees with high exposures. Reduced sensation
and strength in the arms and legs, muscle cramps and decreased
nerve conduction have been observed.
Digestive and Renal Systems: Mercury is absorbed through the
epithelial cells when ingested. This absorbed mercury can cause
various digestive disturbances as it can inhibit the production of
the digestive trypsin, chymotrypsin, and pepsin along with the
function of xanthine oxidase and dipeptidyl peptidase IV (Voj-
dani et al ., 2003). The eects of mercury on the gastrointestinal
system typically present as abdominal pain, indigestion, inam-
matory bowel disease, ulcers and bloody diarrhea. Mercury in-
gestion has also been associated with the destruction of intestinal
ora which can increase the amount of undigested food products
in the bloodstream causing immune-mediated reactions and re-
duced resistance to pathogenic infection (Summers et al., 1993).
Various reports have shown mercury exposure can lead
to various kidney injuries including subacute-onset nephrotic
syndrome, tubular dysfunction, secondary focal segmental glo-
merulosclerosis, nephritic syndrome, nephrotic-range protein-
uria, glomerular disease, and membranous glomerulonephritis
(Oliveira et al., 1987).
Endocrine System: Low exposure levels of mercury may af-
fect the endocrine system in animals and people by disruption
of the pituitary, thyroid, adrenal glands and pancreas (Rice et
al ., 2014). It is thought that mercury might impair endocrine
function through its ability to reduce hormone-receptor binding
(Iavicoli et al ., 2009). Hormones that appear to be the most af-
fected by mercury are insulin, estrogen, testosterone, and adren-
aline.
In addition, autopsy studies in 1975 revealed that the
thyroid and pituitary retain more inorganic mercury than the kid-
neys. Mercury levels in the pituitary gland ranged from 6.3 to 77
ppb in one study, while another found the mean levels to be 28
ppb, levels found to be neurotoxic and cytotoxic (Nylander &
Weiner, 1991). Low levels of pituitary function are associated
with depression and suicidal thoughts and appear to be a major
factor in suicide of teenagers and other vulnerable groups. Be-
cause of its eect on the pituitary, mercury is known to cause
frequent urination as well as high blood pressure (McGregor &
Mason, 1991).
Reproductive System: Mercury can precipitate pathophysio-
logical changes along the hypothalamus-pituitary-adrenal and
gonadal axis that may aect reproductive function by altering
the circulating levels of follicle-stimulating hormone (FSH), lu-
teinizing hormone (LH), inhibin, estrogen, progesterone, and the
androgens (Davis et al., 2001). Reduced fertility among dental
assistants with occupational exposure to mercury has been noted
(Nagpal et al ., 2017). Studies in Hong Kong demonstrated that
increased mercury levels were associated with infertility in both
men and women (Dickman, Leung, & Leong, 1998). In males,
mercury can have adverse eects on spermatogenesis (Martinez
et al., 2017), epididymal sperm count, and testicular weight.
Evidence also exists linking mercury with erectile dysfunction
(Schrag & Dixon, 1985). In females, mercury has been shown
to inhibit the release of FSH and LH from the anterior pituitary
which in turn can aect estrogen and progesterone levels leading
to ovarian dysfunction, painful or irregular menstruation, prema-
ture menopause, and tipped uterus (Chen et al., 2006). There is
good evidence linking mercury with menstrual disorders includ-
ing abnormal bleeding, short, long, irregular cycles, and painful

Environment and Human Health
Saturday, A. Vol 4:2 pp 41/43
periods (Davis et al., 2001).
Fetotoxicity: In addition to reproductive issues, mercury is also
associated with the fetotoxicity which can present as miscar-
riage, spontaneous abortions, stillbirth, and low birth weights
(Aaseth, Hilt, & Bjørklund, 2018; Yoshida, 2002). In the ne-
onate, mercury exposure during pregnancy has been linked to
neural tube defects, craniofacial malformations, and delayed
growth (Yoshida, 2002). Mercury is known to cross the placenta
where it can inhibit fetal brain development resulting in cerebral
palsy and psychomotor retardation in the latter stages of devel-
opment (Castoldi et al., 2001).
In primates, maternal MeHg blood levels were moder-
ately related to increased abortion rates and decreased pregnan-
cy rates (Burbacher et al., 1984). MeHg easily enters through the
placenta and damages the brain of the fetus. Babies may be born
with a variety of birth defects (Finkelman & Tian, 2018). A study
of 64 children exposed in utero to mercury and showed mer-
cury associated damage including mental retardation (100%),
primitive reexes (100%), strabismus (77%), cerebellar ataxia
(100%), dysarthria (100%), chorea and athetosis (95%), de-
formed limbs (100%), hypersalivation (95%), epileptic attacks
(82%), and growth disorders (100%) (Harada et al., 1999).
Historical Cases Studies Depicting Health Impacts of Mer-
cury
There are two epidemics that have occurred from MeHg poison-
ing events that are worthy of mention: The rst case occurred in
the Japanese villages of Minamata Bay (1953) and the second
occurred in rural Iraq in 1971–1972 (Bakir et al., 1973).
Minamata disease is the term used to describe the poi-
soning that occurred among Japanese residents of Minamata
Bay from ingesting methylmercury-containing sh and shellsh.
Over a period of 36 years (1932–1968), the Chisso Corporation’s
chemical factory dumped about 27 tons of methylmercury-as-
sociated waste into Minamata Bay. MeHg is bioaccumulated
within the food chain from plankton, microorganisms up to sh
and shellsh. More than 10,000 Japanese living in the bay, who
ate sh and shellsh contaminated with methylmercury, were
aicted by Minamata disease (Tsubaki & Irukayama, 1977). In
the early 1950s, the people of Minamata Bay began to exhibit
symptoms of neurological illness, i.e., uncontrollable trembling,
loss of motor control, and partial paralysis. Newborn babies also
exhibited symptoms of Minamata disease (Tsubaki & Irukaya-
ma, 1977).
The second epidemic of severe methylmercury intoxi-
cation resulted in the hospitalization of about 7,000 people and
the death of 460 individuals in rural Iraq in 1971–1972 (Bakir
et al., 1973). This incident occurred as a result of bread being
prepared and eaten from wheat seed that had been treated with
a mercury-based fungicide. The wheat seed was supposed to be
planted, but labeling problems and other errors resulted in the
treated wheat seed being used to bake bread. Both the Japanese
and Iraq methylmercury poisoning incidents produced not only
deaths, but multiple and long-lasting intoxication symptoms that
included blindness, deafness, mental retardation, cerebral palsy,
and dysarthria, especially in children exposed in utero (Guzzi &
La Porta, 2008).
Conclusion
A number of body organ systems are aected by mercury in var-
ious forms. Evaluation of the consequences of mercury toxicity
over the years has added greatly to the understanding of mercury
toxicity and its human impact. History has left us with a wide
array of information regarding the eects of mercury toxicity:
the 1950s industrial spill in Minamata and Niigat Japan where it
was dened as “Minamata disease”, the rural poisoning in Iraq
in 1971 to 1972 from MeHg-based fungicide and many among
others not mentioned in this review. All of these events have
left us with an indelible account of the detrimental eects of
mercury on human health. In light of these historic events and
the toxicological evidence presented in this review regarding the
systemic eects of mercury include neurological, endocrine, re-
productive, and embryonic development, and eorts should be
made to insure adequate steps are taken to reduce the occurrence
of mercury exposure and raise public awareness.
Recommendations
Based on the views from dierent scholars who have done re-
search on mercury and its health and environment impacts, the
following recommendations are important:
i. There is need for community education on need for a reduction
in use of products that contain mercury. For instance, thermom-
eters and thermostats are the two most obvious consumer prod-
ucts for which mercury-free alternatives exist.
ii. There is need to encourage dentists to reduce or eliminate the
use of mercury amalgam and use pre-encapsulated amalgam in-
stead of mixing their own if they are to continue using amalgam.
Pre-encapsulated amalgam eliminates the need for elemental
mercury in the dentist’s oce and the spills and dangers associ-
ated with elemental mercury.
iii. Whereas many studies have been conducted to assess health
and environmental impacts of mercury, none has made an eort
to establish mercury concentration in gray water (water from
washing machines, showers, and sinks). There is need to ascer-
tain mercury concentration in these waters to encourage actions
that prevent the mercury-containing gray water from entering
the sewer system.
iv. Combustion of fossil fuels, where Hg is emitted because of
its presence in coal, oil, and gas, is an example of how mercury
gets into the environment. This can be reduced using ue gas
cleaning. All new generation sources using fossil fuels and waste
incinerators should be equipped with ecient ue gas cleaning
systems at the time of construction.
v. There is need for Environment management agencies, for in-
stance, NEMA (for Uganda) to expand existing national research
on environmental and health eects of mercury.
References
• Aaseth, J., Hilt, B., Bjørklund, G. Mercury exposure and health
impacts in dental personnel. (2018) Environ Res 164: 65–69.
PubMed│Crossref│Others
• Aboud, O. Impact of pollution with lead, mercury, and cadmium
on the immune response of Oreochromis niloticus. (2010) NY Sci
J 3(9): 9–16.
PubMed│Crossref│Others

Citation: Saturday, A. Mercury and its Associated Impacts on Environment and Human Health: A Review. (2018) J Environ Health Sci 4(2): 37- 43.
www.ommegaonline.org Vol 4:2 pp 42/43
• Azimi, S., Moghaddam, M.S. Eect of mercury pollution on the
urban environment and human health. (2013) Environ Ecol Res
1(1): 12–20.
PubMed│Crossref│Others
• Bakir, F., Damluji, S.F., Amin-Zaki, L., et al. Methylmercury poi-
soning in Iraq. (1973) Science 181(4096): 230–241.
PubMed│Crossref│Others
• Bernardes, A.M., Espinosa, D.C.R., Tenório, J.A.S. Collection and
recycling of portable batteries: a worldwide overview compared to
the Brazilian situation. (2003) J Power Sources 124(2): 586–592.
PubMed│Crossref│Others
• Burbacher, T.M., Monnett, C., Grant, K.S., et al. Methylmercury
exposure and reproductive dysfunction in the nonhuman primate.
(1984) Toxicol Appl Pharmacol 75(1): 18–24.
PubMed│Crossref│Others
• Carocci, A., Rovito, N., Sinicropi, M.S., et al. Mercury toxicity
and neurodegenerative eects. (2014a) Rev Environ Contam Tox-
icol 229: 1–18.
PubMed│Crossref│Others
• Carocci, A., Rovito, N., Sinicropi, M.S., et al. Mercury toxicity
and neurodegenerative eects. (2014b) Rev Environ Contam Tox-
icol (pp. 1–18). Springer.
PubMed│Crossref│Others
• Castoldi, A.F., Coccini, T., Ceccatelli, S., et al. Neurotoxicity and
molecular eects of methylmercury. (2001) Brain Res Bull 55(2):
197–203.
PubMed│Crossref│Others
• Chen, Y.W., Huang, C.F., Tsai, K.S., et al. Methylmercury induc-
es pancreatic β-cell apoptosis and dysfunction. (2006) Chem Res
Toxicol 19(8): 1080–1085.
PubMed│Crossref│Others
• Davis, B.J., Price, H.C., O’connor, R.W., et al. Mercury vapor and
female reproductive toxicity. (2001) Toxicol Sci 59(2): 291–296.
PubMed│Crossref│Others
• Dickman, M.D., Leung, C.K., Leong, M.K. Hong Kong male sub-
fertility links to mercury in human hair and sh. (1998) Sci Total
Environ 214(1–3): 165–174.
PubMed│Crossref│Others
• Domagalski, J.L., Alpers, C.N., Slotton, D.G., et al. Mercury and
methylmercury concentrations and loads in the Cache Creek wa-
tershed, California. (2004) Sci Total Environ 327(1–3): 215–237.
PubMed│Crossref│Others
• Eide, I., Syversen, T.L. Uptake of Elemental Mercury and Activity
of Catalase in Rat, Hamster, Guinea-pig, Normal and Acatalasemic
Mice. (1982) Acta Pharmacol Toxicol (Copenh) 51(4): 371–376.
PubMed│Crossref│Others
• Finkelman, R.B., Tian, L. The health impacts of coal use in China.
(2018) Int Geol Rev 60(5–6): 579–589.
PubMed│Crossref│Others
• Friberg, L., Skog, E., Wahlberg, J.E. Resorption of mercuric chlo-
ride and methylmercury dicyandiamide in guinea-pigs through
normal skin and through skin pretreated with acetone, alkyl
aryl-sulphonate, and soap. (1961) Acta Derm Venereol 41: 40–52.
PubMed│Crossref│Others
• Goyer, R.A., Clarkson, T.W. Toxic eects of metals. Casarett &
Doull’s Toxicology. The Basic Science of Poisons, Fifth Edition,
Klaassen, CD [Ed]. (1996) McGraw-Hill Health Professions Divi-
sion, ISBN, 71054766.
PubMed│Crossref│Others
• Guzzi, G., La Porta, C.A. Molecular mechanisms triggered by
mercury. (2008) Toxicol 244(1): 1–12.
PubMed│Crossref│Others
• Habiba, G., Abebe, G., Bravo, A.G., et al. Mercury human expo-
sure in populations living around Lake Tana (Ethiopia). (2017)
Biol Trace Elem Res 175(2): 237–243.
PubMed│Crossref│Others
• Harada, M., Nakachi, S., Cheu, T., et al. Monitoring of mercu-
ry pollution in Tanzania: relation between head hair mercury and
health. (1999) Sci Total Environ 227(2–3): 249–256.
PubMed│Crossref│Others
• Harvie, J. Eliminating mercury use in hospital laboratories: a step
toward zero discharge. (1999) Public Health Rep 114(4): 353.
PubMed│Crossref│Others
• Hursh, J.B., Clarkson, T.W., Cherian, M.G., et al. Clearance of
mercury (Hg-197, Hg-203) vapor inhaled by human subjects.
(1976) Arch Environ Health 31(6): 302–309.
PubMed│Crossref│Others
• Iavicoli, I., Fontana, L., Bergamaschi, A. The eects of metals as
endocrine disruptors. (2009) J Toxicol Environ Health B Crit Rev
12(3): 206–223.
PubMed│Crossref│Others
• Joint FAO/WHO Expert Committee on Food Additives, M., &
World Health Organization. (2006). Safety evaluation of certain
food additives. World Health Organization.
PubMed│Crossref│Others
• Joshi, D., Mittal, D.K., Shukla, S., et al. Therapeutic potential of
N-acetyl cysteine with antioxidants (Zn and Se) supplementation
against dimethylmercury toxicity in male albino rats. (2012) Exp
Toxicol Pathol 64(1–2): 103–108.
PubMed│Crossref│Others
• Lohren, H., Blagojevic, L., Fitkau, R., et al. Toxicity of organic
and inorganic mercury species in dierentiated human neurons
and human astrocytes. (2015) J Trace Elem Med Biol 32: 200–208.
PubMed│Crossref│Others
• Lohren, H., Bornhorst, J., Galla, H.-J., et al. The blood-cerebro-
spinal uid barrier–rst evidence for an active transport of organic
mercury compounds out of the brain. (2015) Metallomics 7(10):
1420–1430.
PubMed│Crossref│Others
• Maria, A., Jose, M., Jose, S., et al. National inventory of mercury
release into dierent environmental sectors estimated by united
nations environment programme (UNEP) toolkit in Costa Rica.
(2017) Open J Air Poll 6(2): 76.
PubMed│Crossref│Others
• Martinez, C.S., Peçanha, F.M., Brum, D.S., et al. Reproductive
dysfunction after mercury exposure at low levels: evidence for
a role of glutathione peroxidase (GPx) 1 and GPx4 in male rats.
(2017) Reprod Fertil Dev 29(9): 1803–1812.
PubMed│Crossref│Others
• Mason, R.P., Fitzgerald, W.F., Morel, F.M. The biogeochemical
cycling of elemental mercury: anthropogenic inuences. (1994)
Geochimica et Cosmochimica Acta 58(15): 3191–3198.
PubMed│Crossref│Others
• McCabe, M.J., Lawrence, D.A. The eects of metals of the devel-
opment of the immune system. (1994) Xenobiotics and Inamma-
tion. Academic Press, New York, 193–216.
PubMed│Crossref│Others
• McGregor, A.J., Mason, H.J. Occupational mercury vapor ex-

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posure and testicular, pituitary and thyroid endocrine function.
(1991) Human Exp Toxicol 10(3): 199–203.
PubMed│Crossref│Others
• Morel, F.M., Kraepiel, A.M., Amyot, M. The chemical cycle and
bioaccumulation of mercury. (1998) Annual Rev Ecol Sys 29(1):
543–566.
PubMed│Crossref│Others
• Muhlendahl, K. Intoxication from mercury spilled on carpets.
(2015) Lancet 336(8730–8731): 1578.
PubMed│Crossref│Others
• Munthe, J., Bodaly, R.A., Branreun, B.A., et al. Recovery of mer-
cury-contaminated sheries. (2007) AMBIO 36(1): 33–44.
PubMed│Crossref│Others
• Mutter, J., Yeter, D. Kawasaki’s disease, acrodynia, and mercury.
(2008) Curr Med Chem 15(28): 3000–3010.
PubMed│Crossref│Others
• Joachim, M. Is dental amalgam safe for humans? The opinion of
the scientic committee of the European Commission. (2011) J
Occup Med Toxicol 6(1): 2.
PubMed│Crossref│Others
• Joachim, M., Curth, A., Naumann, J., et al. Does inorganic mercu-
ry play a role in Alzheimer’s disease? A systematic review and an
integrated molecular mechanism. (2010) J Alzheimer’s Dis 22(2):
357–374.
PubMed│Crossref│Others
• Nagpal, N., Bettiol, S.S., Isham, A., et al. A review of mercury
exposure and health of dental personnel. (2017) Saf Health Work
8(1): 1–10.
PubMed│Crossref│Others
• Nylander, M., Weiner, J. Mercury and selenium concentrations and
their interrelations in organs from dental sta and the general pop-
ulation. (1991) Br J Ind Med 48(11): 729–734.
PubMed│Crossref│Others
• Oliveira, D.B., Foster, G., Savill, J., et al. Membranous nephrop-
athy caused by mercury-containing skin lightening cream. (1987)
Postgrad Med J 63(738): 303–304.
PubMed│Crossref│Others
• Pirrone, N., Costa, P., Pacyna, J.M., et al. Mercury emissions to the
atmosphere from natural and anthropogenic sources in the Medi-
terranean region. (2001) Atmos Environ 35(17): 2997–3006.
PubMed│Crossref│Others
• Nicola, P., Cinnirella, S., Feng, X., et al. Global mercury emissions
to the atmosphere from anthropogenic and natural sources. (2010)
Atmos Chem Phys 10(13): 5951–5964.
PubMed│Crossref│Others
• Rasmussen, P.E. Current methods of estimating atmospheric mer-
cury uxes in remote areas. (1994) Environ Sci Technol 28(13):
2233–2241.
PubMed│Crossref│Others
• Rice, K.M., Walker Jr, E.M., Wu, M., et al. Environmental mercu-
ry and its toxic eects. (2014) J Prev Med Public Health 47(2): 74.
PubMed│Crossref│Others
• Ronchetti, R., Zuurbier, M., Jesenak, M., et al. Children’s health
and mercury exposure. (2006) Acta Paediatrica 95(s453): 36–44.
PubMed│Crossref│Others
• Schiraldi, M., Monestier, M. How can a chemical element elicit
complex immunopathology? Lessons from mercury-induced auto-
immunity. (2009) Trends Immunol 30(10): 502–509.
PubMed│Crossref│Others
• Schrag, S.D., Dixon, R.L. Occupational exposures associated with
male reproductive dysfunction. (1985) Annual Rev Pharmacol
Toxicol 25(1): 567–592.
PubMed│Crossref│Others
• Silbergeld, E.K., Woodru, S., Gutirrez, P., et al. Eects of mer-
cury (HG) on immune function in male and female mice.(Abstr.
1012). (1998) Toxicol Sci
PubMed│Crossref│Others
• Sinicropi, M.S., Amantea, D., Caruso, A., et al. Chemical and bi-
ological properties of toxic metals and use of chelating agents for
the pharmacological treatment of metal poisoning. (2010) Arch
Toxicol 84(7): 501–520.
PubMed│Crossref│Others
• Stejskal, V. 5 Allergy and Autoimmunity Caused by Metals: A
Unifying. (2015) Vaccines and Autoimmunity 57.
PubMed│Crossref│Others
• Summers, A.O., Wireman, J., Vimy, M.J., et al. Mercury released
from dental” silver” llings provokes an increase in mercury and
antibiotic-resistant bacteria in oral and intestinal oras of primates.
(1993) Antimicrob Agents and Chemother 37(4): 825–834.
PubMed│Crossref│Others
• Sundseth, K., Pacyna, J.M., Pacyna, E.G., et al. Global sources and
pathways of mercury in the context of human health. (2017) Int J
Environ Res Public Health 14(1): 105.
PubMed│Crossref│Others
• Tsubaki, T., Irukayama, K. Minamata disease. Methylmercury
poisoning in Minamata and Niigata, Japan. (1977) North-Holland
Publishing Company, PO Box 211, Amsterdam, The Netherlands.
PubMed│Crossref│Others
• Vojdani, A., Pangborn, J.B., Vojdani, E., et al. Infections, toxic
chemicals and dietary peptides binding to lymphocyte receptors
and tissue enzymes are major instigators of autoimmunity in au-
tism. (2003) Int J Immunopathol Pharmacol 16(3): 189–199.
PubMed│Crossref│Others
• Warkany, J. Acrodynia—postmortem of a disease. (1966) Am J
Dis Child 112(2): 146–156.
PubMed│Crossref│Others
• World Health Organization. Prevention of cardiovascular disease.
(2007) World Health Organization.
PubMed│Crossref│Others
• Yoshida, M. Placental to fetal transfer of mercury and fetotoxicity.
(2002) Tohoku J Exp Med 196(2): 79–88.
PubMed│Crossref│Others