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William Emanuel

THE ENVIRONMENTAL IMPACT OF MERCURY 301-791-5776

wemanuel@peopleofcolor1.com

Morgan State University

Full Paper

Science and Technology

Environmental Engineering

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THE ENVIRONMENTAL IMPACT OF MERCURY For Academic Conference:

Atlanta - GA, USA October 14 - 16, 2010Submission Deadline: September 26, 2010

Prepared by

William Emanuel

Morgan State University

Key Words: Bioaccumulation, methyl-mercury, neosynephrine, toxicokinetics, neurotoxic, immunopathology, neurodevelopmental diseases

ABSTRACT

In light of understanding the Green House Effect, PCBs, Acid Rain, CFCs

and the hole over the Ozone in the Antarctic. One can realize that these

problems and issues are far beyond what we think. All these issues are a

direct correlation with the introduction of the industrial revolution and

the technologies implemented. This paper will look at some of the

consequences for not implementing a sustainable system that is in harmony

with our eco-system. This lays the foundation for engineers and

scientists to see the need to develop sustainable systems that take into

account the life cycle of their products and processes.

MERCURY’S CHEMICAL NATURE Mercury is a heavy metal of which some forms are known to be highly

toxic. Though mercury occurs naturally in the environment it is now mainly

released by human activities. Mercury is sometimes known as quicksilver that

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occurs naturally in the environment in different chemical forms. The pure

form, elemental mercury, is liquid at room temperature and slowly forms a

vapor in the air. Forms more commonly found in nature are inorganic mercury

and organic mercury (UEP, 2002).

As with other potentially-toxic trace elements, the environmental

impact of mercury depends in part on the availability of the element, and

its chemical form, in addition to its concentration in the environment.

Unlike most other heavy metals, mercury exhibits a substantial vapor

pressure and can develop significant gaseous concentrations. In addition,

mercury can be subject to processing by microorganisms, and its methylation

to organic forms is particularly important with respect to its environmental

toxicity. The cycling of mercury through the various environmental

compartments is particularly active and complicates the understanding of

source, transport, fate, and environmental impact of this heavy metal

(Lechler, 2003)

In the environment, mercury can migrate between various media, such as

air, soil and water.

Conceptually, movements

of mercury between these

different environmental

"compartments" are

commonly known as

"fluxes", and the

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quantities of mercury in the various compartments are often referred to as

"pools". These fluxes and pools are studied in order to help assess the

global mercury budget. Quantifying human versus natural mercury fluxes can

be challenging because mercury deposited from anthropogenic releases can be

re-emitted from land and water, undergo long-range transport in the

atmosphere, be re-deposited elsewhere, and so on. This process of emission

and re-emission is the reason why animals and peoples in remote areas with

no local mercury releases, such as in the Arctic, may have elevated mercury

levels. Mercury exists as a gas and in a range of organic and inorganic

forms that vary in toxicity and persistence in living organisms. In the

environment, mercury is transformed through complex biogeochemical

interactions that affect environmental and biological forms and

concentrations. Some mercury compounds are more easily absorbed by living

organisms than elemental mercury itself. When atmospheric mercury falls to

earth, it may be altered by bacterial or chemical action into an organic

form known as methyl-mercury. Methyl-mercury is much more toxic than the

original metal molecules that drifted in the air, and has the ability to

migrate through cell membranes and "bio-accumulate" in living tissue.

Bioaccumulation is the process by which a substance builds up in a living

organism from the surrounding air or water, or through the consumption of

contaminated food. Bioaccumulation will vary for different species and will

depend on emission sources as well as local factors like water chemistry and

temperature. In the following figure, the concept of accumulated methyl-

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mercury is illustrated by the dots, however the dots are not to scale. (If

the concentration of methyl-mercury in lake water is considered to have an

absolute value of 1, then approximate bioaccumulation factors for

microorganisms like phytoplankton are 105; for macro-organisms like

zooplankton and planktivores are 106 ; and for piscivores like fish, birds

and humans are 107.

The bioaccumulation of methyl-mercury in natural ecosystems is of

environmental concern because it inflicts increasing levels of harm on

species higher up in the food chain. This occurs through a process known as

"bio-magnification", whereby persistent substances like methyl-mercury will

increase in concentration from microorganisms, to fish, to fish eating

predators like otters and loons, and to humans. Elevated methyl-mercury

levels may lead to the decline of affected wildlife populations and may

affect human health when people consume significant quantities of fish or

other contaminated foods. The most infamous case of this impact occurred in

Minimata, Japan, where local residents consumed fish with toxic levels of

methyl-mercury originating from an industrial sewer discharge, leading to

the deaths of more than 1000 people. This type of exposure has now come to

be known as Minamata disease (EC, 2009).

MERCURY SOURCES FOUND IN NATURE

Mercury deposits are globally distributed in 26 mercury mineral belts.

Three types of mercury deposits occur in these belts: silica-carbonate, hot-

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spring, and Alma den. Mercury is also produced as a by-product from several

types of gold-silver and massive sulfide deposits, which account for 5% of

the world's production. Other types of mineral deposits can be enriched in

mercury and mercury phases present are dependent on deposit type. During

processing of mercury ores, secondary mercury phases form and accumulate in

mine wastes. These phases are more soluble than cinnabar, the primary ore

mineral, and cause mercury deposits to impact the environment more so than

other types of ore deposits enriched in mercury. Release and transport of

mercury from mine wastes occur primarily as mercury-enriched particles and

colloids. Production from mercury deposits has decreased because of

environmental concerns, but by-product production from other mercury-

enriched mineral deposits remains important (Rytuba, 2000)

Mercury is released into the environment through both natural

processes (e.g. volcanic activity, weathering of rocks) and human activities

(e.g. mining, fuel use, products and processes). Once released, mercury

enters air, water and soil, and moves from one to another until it comes to

rest in sediments or landfills. Mercury deposited from the atmosphere at any

particular place comes from both local and global sources. Human activity is

now the main source of mercury being released into the environment. Much is

released unintentionally from processes where mercury is an unwanted

impurity. Emissions into the air, mainly from fossil fuel power plants and

waste incinerators, are expected to increase unless other energy sources are

used or emissions are better controlled. However, mercury mining is

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decreasing and therefore releases from mining and mercury use may be in

decline (UEP, 2002).

Weathering and evaporation from mercury-rich rocks and soils lead to

natural mercury release, as do forest fires and volcanic activity. Although

natural emissions are difficult to determine, current estimates suggest that

less than 50% of total mercury releases come from natural sources (UEP,

2002).

Since industrialization, the amount of mercury found in the

environment has increased by a factor of 2 to 4, largely because of human

activities. Mercury has always been emitted from natural sources such as

volcanic eruptions, the weathering of soils and rocks and vaporization from

the oceans; however, scientists believe that more than half of the mercury

in the environment today is from anthropogenic sources. Canadian

anthropogenic emissions of mercury to the atmosphere in 2000 are estimated

to have been approximately 8 tonnes, while the U.S.A. and global emissions

were approximately 120 and 2200 tonnes respectively during 1995. In addition

to industrial releases, mercury can be found in thermometers, dental

fillings, fluorescent light bulbs, and other consumer products (EC, 2009).

HOW DID MERCURY GET INTO THE ENVIRONMENT?

Mercury sold on the world market comes mainly from cinnabar mines in

Spain, China, Kyrgyzstan and Algeria. It can also be recycled from

industrial processes (UEP, 2002).

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Mercury in the air may settle into water bodies and affect water

quality. This airborne mercury can fall to the ground in raindrops, in dust,

or simply due to gravity (known as “air deposition”). After the mercury

falls, it can end up in streams, lakes, or estuaries, where it can be

converted to methyl-mercury through microbial activity (EPA, 2010).

Mine drainage from mercury mines in the California Coast Range mercury

mineral belt is an environmental concern because of its acidity and high

sulfate, mercury, and methyl-mercury concentrations. Two types of mercury

deposits are present in the mineral belt, silica-carbonate and hot-spring

type. Mine drainage is associated with both deposit types but more commonly

with the silica-carbonate type because of the extensive underground workings

present at these mines. Mercury ores consisting primarily of cinnabar were

processed in rotary furnaces and retorts and elemental mercury recovered

from condensing systems. During the roasting process mercury become more

soluble than cinnabar are formed and concentrated in the mine tailings,

commonly termed calcines. Differences in mineralogy and trace metal

geochemistry between the two deposit types are reflected in mine drainage

composition. Silica-carbonate type deposits have higher iron sulfide content

than hot-spring type deposits and mine drainage from these deposits may have

extreme acidity and very high concentrations of iron and sulfate. Mercury

and methyl-mercury concentrations in mine drainage are relatively low at the

point of discharge from mine workings. The concentration of both mercury

species increases significantly in mine drainage that flows through and

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reacts with calcines. The soluble mercury phases in the calcines are

dissolved and sulfate is added such that methylation of mercury by sulfate

reducing bacteria is enhanced in calcines that are saturated with mine

drainage. Where mercury mine drainage enters and first mixes with stream

water, the addition of high concentrations of mercury and sulfate generates

a favorable environment for methylation of mercury. Mixing of oxygenated

stream water with mine drainage causes oxidation of dissolved iron(II) and

precipitation of iron oxyhydroxide that accumulates in the streambed. Both

mercury and methyl-mercury are strongly adsorbed onto iron oxyhydroxide over

the pH range of 3.2–7.1 in streams impacted by mine drainage. The dissolved

fraction of both mercury species is depleted and concentrated in iron

oxyhydroxide such that the amount of iron oxyhydroxide in the water column

reflects the concentration of mercury species. In streams impacted by mine

drainage, mercury and methyl-mercury are transported and adsorbed onto

particulate phases. During periods of low stream flow, fine-grained iron

hydroxide sediment accumulates in the bed load of the stream and adsorbs

mercury and methyl-mercury such that both forms of mercury become highly

enriched in the iron oxyhydroxide sediment. During high-flow events,

mercury- and methyl-mercury-enriched iron hydroxide sediment is transported

into larger aquatic systems producing a high flux of bio-available mercury

(Rytuba, 2002).

The environmental impact of heavy metals. One significant source of

emissions of heavy metals to air is waste incineration. Consumer batteries

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contributes significantly to this problem, as well as to heavy metal leakage

to groundwater from landfill deposits. The situation in Sweden is used as an

example to describe how the deposition from the atmosphere still is

increasing the load of heavy metals, like mercury, cadmium and lead, in top

soils and aquatic sediments. Critical factors effect levels for Hg, Cd, Pb,

Cu, Zn and As. (Lindqvist, 2002).

North American pollutant release and transfer registries have been

continuously developing with an eye to understanding source/receptor

relationships and ensuring that the polluter-paid principle is applied to

the appropriate parties. The potential contribution of mercury to the Great

Lakes Basin arising from the re-release of historic mercury pollution from

contaminated aquatic and terrestrial media is poorly understood and the

subject of concern. Although a considerable amount of data may be available

on the atmospheric component of mercury releases to the Basin, further

inventory work is needed to quantify the re-release of the historic mercury.

Much of the related existing inventory information is either not derived

from direct measurement or not bounded by a mass-balance accounting.

Critical to this determination is an increased confidence in the inventories

of mercury from past and current practices. This may be enhanced through

comprehensive and thorough surveys of contributions from specific products

and their life-cycle assessments. An even greater challenge is to determine

the bioavailability of the mercury emanating from land-based sources and

from aquatic media. The interplay among the sources and receptors of mercury

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provides a quantitative assessment of current Canadian contributions of

mercury as a contaminant to the Great Lakes (Trip, Luke, Bender, Tonya &

Niemi, David, 2003).

HEALTH EFFECTS OF MERCURY

Mercury (Hg) contamination from a variety of point and non-point

sources, including atmospheric inputs, is currently considered to be the

most serious environmental threat to the well being of fish and wildlife

resources in the southeastern United States. Fish consumption advisories

have been issued in all ten states comprising the U.S. Fish and Wildlife

Service's Southeast Region. Both freshwater and marine species have been

affected with levels ranging as high as 7.0 ppm in some individuals. Many

other species, including various species of reptiles, birds and mammals

(including humans) are also contaminated. Impacts noted range from

reproductive impairment to mortality (Netherlands, 1995).

The primary pathway of mercury from the environment to humans is

through the consumption of fish. The mercury in fish is thought to be >95%

organic mercury which is essentially 100% absorbed by humans during

consumption. Little mercury is currently being released to the environment

in its organic form, but certain environmental conditions promote the

conversion of inorganic forms to the more toxic organo-mercurials. In fact,

modern studies show that there is little relationship between total mercury

in the environment and its accumulation in fish and subsequently in humans.

More important is the biogeochemical cycling that results in availability of

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organic mercury. Conversely, natural and human-induced environmental

conditions or modifications can suppress the solubility, availability, and

chemical form of mercury. An understanding of these factors is critical to

assessing the environmental danger of mercury in discrete areas and in

guiding environmental manipulations that can suppress its environmental

impacts (Lechler, 2003).

Methyl-mercury accumulates in fish at levels that may harm the fish

and the other animals that eat them. Mercury deposition in a given area

depends on mercury emitted from local, regional, national, and international

sources. The amount of methyl-mercury in fish in different water-bodies is a

function of a number of factors, including the amount of mercury deposited

from the atmosphere, local non-air releases of mercury, naturally occurring

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mercury in soils, the physical, biological, and chemical properties of

different water-bodies and the age, size and types of food the fish eats.

This explains why fish from lakes with similar local sources of methyl-

mercury can have significantly different methyl-mercury concentrations (EPA,

2010).

Birds and mammals that eat fish are more exposed to methyl-mercury

than any other animals in water ecosystems. Similarly, predators that eat

fish-eating animals are at risk. Methyl-mercury has been found in eagles,

otters, and endangered Florida panthers. Analyses conducted for the Mercury

Study Report to Congress suggest that some highly-exposed wildlife species

are being harmed by methyl-mercury. Effects of methyl-mercury exposure on

wildlife can include mortality (death), reduced fertility, slower growth and

development and abnormal behavior that affect survival, depending on the

level of exposure. In addition, research indicates that the endocrine system

of fish, which plays an important role in fish development and reproduction,

may be altered by the levels of methyl-mercury found in the environment

(EPA, 2010).

In this issue of Alternative Therapies in Health and Medicine,

McGinnis, puts forth a theory of autism based on oxidative stress. In the

conference it was proposed that mercury might be a key part to understanding

autism and the toxin induced. The presentations ranged from an analysis of

the global cycle of mercury to the methylation cycles impaired by mercury

(Hyman, 2009).

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Clewell reviewed the epidemiologic studies from the Seychelles and

Faroe islands. He presented a continuum of risk model for mercury exposures.

Nearly all human exposures to methyl mercury derive from fish. In the

Seychelles Islands, there seemed be little effect from mercury on the

population; however, the islander’s fish consumption was predominately from

low-risk, small reef fish. Maternal-fetal transmission was analyzed in the

Faroe Islands. Elevated levels of mercury in umbilical cord blood correlated

with decrements in neurologic studies in 5/17 tests in 917 mother-infant

pairs. The mean umbilical cord blood level contained 22.9 micrograms per

liter. A major source of their fish consumption was whale blubber, which

contains over 3 parts per million of mercury. The health effects from

methyl-mercury upon infants and children depend on the dose, with severe

symptoms presenting with exposure to doses of 100 mcg/kg/day, mild symptoms

with greater than 10 mcg/kg/day, and sub-clinical symptoms with less than 1

mcg/kg/day. Symptoms include late development in walking and talking, and

decreased performance on neurological tests. Clewell reviewed the

limitations of various forms of testing for mercury. Methyl-mercury is found

predominately in red blood cells. Inorganic mercury from amalgams is found

in plasma but is rapidly cleared. Methyl-mercury is converted to inorganic

mercury in the body and is the main form of mercury in the brain (Hyman,

2009).

Ratard, reviewed the health effects of mercury upon infants and

newborns. Sources of exposure are widespread and include mercury vapors in

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ambient air, ingestion via drinking water, fish, vaccines, occupational

exposures, home exposures including fluorescent light bulbs, thermostats,

batteries, red tattoo dye, skin lightening creams, and over-the-counter

products such as contact lens fluid and neosynephrine, dental amalgams, and

more. Amalgam exposure is estimated to be from 3 to 17 micrograms per day

from slow corrosion, chewing, brushing and grinding. The toxicokinetics of

mercury were reviewed. Absorption is about 80% for mercury vapor and nearly

100% for oral absorption. It is primarily distributed in the kidneys and

brain and readily transferred to the fetus via the placenta. It is

eliminated via the urine, feces, expired air, and breast milk. Ratard

reported that the major toxicity is from mercury’s ability to covalently

bind to sulfhydryl groups of enzymes in microsomes and mitochondria and

other enzyme binding sites including carboxyl, amide, amine, and phosphoryl

groups. Clinical manifestations were reviewed, including the historical

context of mercury poisoning epidemics such as the Minamata Bay exposures in

Japan, acrodynia or pink disease in children from calomel (Hg Cl) used in

teething powder, mad hatter syndrome or erethism, and methyl-mercury

fungicide grain seed exposures in Iraq and Pakistan. The clinical

manifestations are varied and mimic many other conditions. Central Nervous

System (CNS) toxicity includes erythrism with symptoms of shyness, emotional

ability, nervousness, insomnia, memory impairment, and inability to

concentrate. Other CNS symptoms may include encephalopathy, peripheral

neuropathy, Parkinsonian symptoms, tremor, ataxia, impaired hearing, tunnel

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vision, dysarthria, headache, fatigue, impaired sexual function, and

depression. Renal toxicity includes proteinuria, renal syndrome, and acute

renal failure. Gastrointestinal symptoms include nausea, vomiting, diarrhea,

and colitis. Dermal toxicity includes allergic dermatitis, chelitis,

gingivitis, stomatitis, and excessive salivation (Hyman, 2009).

El Dahr, reported on the increase in autism in the last decade, its

correlation with the change in the vaccine schedule and explored in detail

the autism-mercury hypothesis. She discussed the immunological parallels

with autism and reviewed the epidemiological and toxicological research on

thimerosa. In California, rigorous standards for reporting of autism were in

place because social benefits were tied to the accurate diagnosis, so the

increases are very likely to be real. During the first 25 years, 6,527 cases

of autism were reported; but it took only three years during the 1990s to

add 6,596 additional cases. From 1987 to 1998 there was a 273% increase in

autism cases in California. The Centers for Disease Control and Prevention

(CDC) and American Academy of Autism released an “Autism Alarm” stating that

one in 166 children in the U.S. have autistic spectrum disorder (ASD).

Currently, one-sixth of all children under the age of 18 have a

developmental disability. That is nearly 20% of the population who may not

be able to be productive members of society. Much of the data she presented

is available on www.safeminds.org. The mercury-autism hypothesis was

proposed in part due to the analysis of the actual doses of thimerosal

received by children after the change in the vaccination schedule. In

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individuals with a genetic susceptibility, such as a defect in the enzymes

responsible for detoxifying heavy metals, prenatal and early postnatal

exposure to mercury leads to neurologic damage resulting in autistic

symptoms. Acrodynia or pink baby syndrome from exposure to calomel or

mercury in teething powder presented similarly to autism. Other potential

sources of early exposure in the fetus or infant include maternal amalgams,

fish consumption, eardrops, and nasal drops. Vaccines present a significant

source of exposure in RhoGam, influenza vaccines during pregnancy, and

childhood immunizations. The maximum exposure in the first six months of

life is 187.5 micrograms of mercury, far exceeding limits set by the World

Health Organization (WHO) and the Environmental Protection Agency (EPA).

These limits are set for methyl-mercury primarily from fish, not for ethyl-

mercury from vaccines (Hyman, 2009).

Questions remain about the relative toxicity of each. According to the

EPA, the “safe” daily level of mercury exposure for a 5 kg, 2-month-old

infant is 0.5 micrograms or 0.1 micrograms per kg. The typical 2-month

vaccination schedule includes diphtheria and tetanus (DtaP), Haemophilus

influenza type B (Hib), and hepatitis B vaccines. Combined, these vaccines

contain 62.5 micrograms of mercury or 125 times the EPA limits for a single-

day exposure. It should be remembered that, like lead, there may be no safe

level and children are more susceptible to toxic effects than adults. Dahr

advises us that there may be large variations in genetic susceptibility to

exposures. She also argues that there is a strong biologic plausibility to

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the mercury-autism hypothesis. Symptoms of mercury toxicity parallel autism.

Beside the neurotoxic effects, there appears to be correlation between the

immunopathology of both autism and mercury toxicity. She defines

immunopathology to include immune deficiency and dysfunction with defective

or ineffective responses, hypersensitivity with an overactive response out

of proportion to potential damage and autoimmunity or inappropriate reaction

to self. These specific immune abnormalities have been found in 30%-70% of

autistic children. She also reviewed the problematic Institute of Medicine

recommendations and analysis of the thimerosal issue (Hyman, 2009).

Cave has treated over 2,300 children with autistic spectrum disorder.

In her recent book, What Your Doctor May Not Tell You About Children’s

Vaccinations, outlines the data and debate in this highly charged field.

Cave also reported on the increased incidence of autism in the last 30 years

from 1/10,000 children to 1/150 children and 1/30 males in the United States

(Hyman, 2009).

Nash reviewed mercury-associated diseases, mechanisms, controversies,

and therapeutic options. Major sources of mercury exposure include dental

amalgams (vapor), fish (methyl-mercury), and vaccines (ethylmercury). Toxic

effects, he suggests, spread across a broad spectrum of diseases including

autism, Alzheimer’s disease, ALS, multiple sclerosis, Parkinson’s disease,

neurodevelopmental diseases, nephrotoxicity, and cancer. Reporting on the

review in the New England Journal of Medicine, he reports that the fetal

brain is more susceptible than the adult brain to mercury-induced damage

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including the division and migration of neuronal cells and disruption of the

cytoarchitecture of the developing brain. The mechanism of mercury toxicity

in the adult brain may be related to proteins involved in mercury excretion

including glutathione, glutathione transferase, metallothionine, and Apo E.

Glutathione carries Hg through biliary transport for excretion. Hg2+ rapidly

oxidizes glutathione. Glutathione transferase is an enzyme that may be

implicated in Alzheimer’s disease (Hyman, 2009).

However, most interesting were recent findings that Apo E 4 may

increase risk for Alzheimer’s disease because it has an impaired ability to

bind mercury and transport it from the brain. Apo E 4 has no binding sites

for mercury because it contains arginine at both positions 112 and 158 of

the lipoprotein. Apo E 2 has cysteine at both those sites enabling it to

bind and transport mercury from the brain. Nash suggests that most if not

all aberrant biochemistry in the Alzheimer’s brain can be mimicked by

mercury. The diagnostic hallmarks of the Alzheimer’s brain can be produced

by Hg concentrations lower than reported in human brain tissues. He further

concludes that the biological plausibility of Hg as a causal factor in

Alzheimer’s disease is more complete than thimerosal causation of autism

(Hyman, 2009).

Regarding amalgam fillings, Dr. Nash concludes that due to the

enhancement of mercury toxicity and retention by factors found in the diet,

antibiotics, other toxicants such as cadmium and lead, and genetic

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susceptibilities, no level of mercury exposure from amalgams can be

considered without risk.15”

“He also reviewed the literature linking mercury and cardiovascular disease.

Two studies have reported increased risk of myocardial infarction while

another has showed no risk. However, the data presented on idiopathic

cardiomyopathy was among the most compelling. Biopsy samples found 12,000

times the level of antimony and 22,000 times the level of mercury in

idiopathic cardiomyopathy compared to controls with viral, ischemic or

hypertensive cardiomyopathy. Mechanisms of toxicity include damage to DNA,

RNA, mitochondria, enzymes, immunopathology and autoimmunity, and generation

of oxidative stress. Mercury can act as a metabolic uncoupler, hapten or

immune sensitizing small molecule, enzyme inhibitor. It also depletes

glutathione and ascorbate, and inhibits thiamine (B1) and pyridoxine (B6).

Mercury can also affect the CNS by concentrating in the CSF and the kidney

by reducing concentrating capacity. It can also inhibit GTP binding

affecting brain tubulin microtubules reducing nerve function and

communication, which can lead to the development of neurofibrillary tangles.

Mercury also inhibits nerve growth, and passes easily through the placental

barrier. Dopamineric activity in the brain is reduced with mercury. Dr. Nash

concluded on an optimistic note. First he suggests that there appears to be

a subset of the population that cannot effectively excrete mercury and is at

greater risk than the general population, and that this susceptibility is

likely due to genetic differences, diet, exposure to other toxicants,

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antibiotics, etc. Given that susceptibility, he argues that mercury is a

risk factor in many diseases, but can be safely measured, and the body

detoxified, mitigating some of its toxic effects. He calls for more research

and improved detoxification agents (Hyman, 2009).

METHODS OF REMEDIATION FROM THE ENVIRONMENT

The challenge for governments is to ensure that the levels of mercury

in the environment do not exceed the concentrations which we would expect

from natural processes. As the dangers of mercury and its compounds become

more apparent, governments are working with concerned citizens, industries

and environmental organizations to examine a range of mercury management

tools. In Canada, mercury is managed by federal legislation and guidelines,

various programs and research groups, and through participation in

international initiatives. Provincial and territorial governments have also

established tools for reducing the impact of mercury pollution. Several

Canada-wide standards have been endorsed by Environment Ministers from

provinces, territories, and the federal government to ensure that efforts

are consistent across the country. Educational programs are being created to

answer the question, "what can I do?" in order to inform people of

appropriate reduction measures that can be used in the home, cars, schools

and the workplace.

In addition to providing information on the topics outlined above, this

website provides a selection of resources for visitors, including an

extensive list of links, fish consumption advisories, steps for cleaning up

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small mercury spills, information about mercury disposal, and a glossary of

terms related to mercury (UEP, 2002).

The reduction of mercury (Hg) releases to the environment,

particularly airborne mercury emissions, is currently a major focus of both

US state and federal regulatory agencies. While mercury emissions from

hazardous waste incinerators and fossil-fuel power plants have been and

continue to be regulated under the Resource Conservation and Recovery Act

(RCRA) and the Clean Air Act (CAA), non-hazardous waste cement kilns are

currently excluded from regularly controls. However, the US Environmental

Protection Agency (EPA) continues to assess the need for possible mercury

emission controls nationwide, under the CAA, and for specific facilities,

through the Total Maximum Daily Load (TMDL) Program of the Clean Water Act.

The EPA's major concern appears to be the potential impacts the

bioaccumulation of mercury in fish and other aquatic organisms may have on

humans and wildlife that consume them. This paper uses fate and transport

modeling to evaluate whether mercury emissions from cement kilns could pose

unacceptable risks to fish-consuming populations in the area of a source

because of high levels of methyl mercury that could accumulate in fish.

Emphasis is placed on assessing the effects that parameter variability and

the lack of the parameter specificity for environmental conditions have on

risk assessment results. The key parameters that are evaluated include

emission rates, mercury speciation, methylation rates, and watershed and

water body configurations. The results of this assessment indicate that

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mercury emissions from cement kilns pose much less of a risk to fish

consumers than mercury emissions from other types of combustion sources;

however, there is substantial uncertainty in the risk estimates. These

uncertainties in the EPA model for mercury emissions indicate that this

model is only refined enough currently to screen risks from combustion

facilities (to identify facilities that pose no significant risk of mercury

exposure), but is insufficient to characterize risks for populations at any

specific site. Finally, prior to any attempt at regulating Portland cement

kiln mercury emissions, the EPA should refine and validate its models based

on mercury emission and fish concentration data for actual sites (Richter &

Sheehan, 2005).

CONCLUSION

In light of understanding the health effects caused by Mercury on humans,

animals, fish and the eco-system; one can easily realize that the effects

of mercury are far beyond what most people think. All or most of these

issues can be minimized and avoided if engineers and scientists could

implement a sustainable system that is in harmony with our eco-system.

REFERENCES

EC (2009). Environment Canada. Mercury and the Environment. Retrieved September 2, 2009: http://www.ec.gc.ca/mercury/en/bf.cfm

(EPA, 2010). Fate and Transport and Ecological Effects of Mercury. Retrieved September 22, 2009. http://www.epa.gov/mercury/eco.htm

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Hyman, Mark H, MD, (2009). Retrieved September 22, 2009. http://www.drhyman.com/pdf/hyman_at.pdf

Lechler, Paul J., (2003). Retrieved September 2, 2009 CRUCIAL FACTORS IN THE ENVIRONMENTAL IMPACTS OF MERCURY. http://gsa.confex.com/gsa/2003NC/finalprogram/abstract_48965.htm

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