Mercury exposure and poisoning – Better Health Channel

Mercury is a natural substance present in the earth, but it is also produced in various industrial and medical uses. In our environment, the three forms of mercury present are:

• elemental metal – such as in mercury thermometers and dental fillings
• organic compound – mercury is converted by bacteria in the water into methylmercury and this enters the fish food chain
• inorganic compound – naturally present in coal, mercury is released into the air when coal is burned to generate power. mercury is also produced as a waste product in various industrial processes.

The majority of exposure to humans is through organic methylmercury that has entered the food chain and accumulates at higher levels in larger species of fish. The major threat to human health from mercury poisoning is from inhaling mercury as a vapour.

Preventing or minimising exposure to mercury in your environment is the best way to reduce your risk of mercury poisoning.

Mercury in the environment

There are a number of common sources of mercury in our environment including:

• larger fish species – if eaten in large quantities, these can increase the amount of mercury in your body
• fluorescent and low-energy light bulbs – if broken, there is some risk from inhaling mercury vapour and skin contact with mercury
• mercury thermometers – the pure mercury (or ‘quicksilver’) from broken thermometers could pose some risk to people if they inhale mercury vapour or have skin contact with mercury
• dental fillings – modern amalgam fillings have a low level of mercury, which is considered safe for most people
• batteries – some batteries contain mercury that can enter the environment if they end up in landfill.

Reducing exposure to mercury

There are a number of precautions that you can take to minimise your exposure to mercury while also reducing the amount of mercury in our environment.

Reducing exposure to mercury from fish

Educate yourself about the types of fish that are more likely to contain higher levels of mercury. These include:

• shark (flake)
• orange roughy
• swordfish
• marlin
• southern bluefin tuna
• gemfish
• ling.

Some freshwater species of fish in Victoria can have high levels of mercury. This is because of Victoria’s goldmining history. Goldmining has increased the level of mercury in the sediment of riverbeds, and this means that large brown trout and redfin in the Upper Goulburn and Lake Eildon (and surrounding rivers) may have high levels of mercury.

Most people can still eat fish with higher levels of mercury, but Food Standards Australia New Zealand recommend that they should be eaten less often than fish species with lower levels of mercury. People in high-risk groups (such as pregnant women, children and people with kidney disease) should check the recommendations before eating these fish.

The recommendations for the quantities of fish that can be eaten are different for pregnant women and children compared with the rest of the adult population. Pregnant women, nursing mothers, women planning pregnancy and children up to six years old should avoid fish high in mercury.

Many people take supplements of fish oil to increase their intake of omega-3 fats. While it is better to get your omega-3 fats from fish rather than supplements, if you do use fish oil capsules, check to see if the product has been tested for mercury levels.

Reducing exposure to mercury from fluorescent bulbs and lamps

In 2010, new standards were introduced for low-energy bulbs in Australia. This means that the number of low-energy bulbs has greatly increased and these bulbs contain small levels of mercury. The mercury-containing bulbs include fluorescent tube lamps and the compact low-energy bulbs mostly used in homes.

The amount of mercury in a single bulb or lamp is very small and unlikely to harm people. Commercial and public lighting uses many more lamps and FluoroCycle is a voluntary national scheme to recycle mercury-containing lamps for industrial and public lighting.

For information on lamps used at home, you can contact your local council to find out how best to dispose of light bulbs and lamps.

Broken tubes, bulbs or lamps can be cleaned up as follows:

• Air (ventilate) the room.
• Wear gloves and scoop up all the glass fragments and powder.
• Put all the broken globe or tube into a rigid, sealed container.
• Use sticky tape to pick up any remaining small glass fragments and powder.
• Wipe the area clean with damp paper towels or disposable wet wipes and place them in a glass jar or plastic bag.
• Continue to air the room for 12 to 24 hours.
• Dispose of the mercury and any contaminated items in the rubbish, not in the recycling bin.

Reducing exposure to mercury from thermometers and other devices

Spirit-containing thermometers are now widely available, but some people still use thermometers containing silver mercury. Intact, these are not dangerous, but when broken there is the possibility of inhaling mercury vapour and of skin contact. These spills should be cleaned up carefully.

The procedure includes the following steps:

• Clear the room of people and pets.
• Air (ventilate) the room for 15 minutes (turn off ducted heating or cooling) before cleaning up.
• Do not use a vacuum cleaner or broom.
• Remove jewellery, wear gloves and wear old clothing that you can throw away.
• Clean up using an eyedropper or syringe to pick up droplets of mercury or use a pen or card to guide the droplets onto a piece of card.
• Use sticky tape to pick up small droplets.
• Place mercury droplets into a strong plastic container with a lid.
• Keep the room ventilated for 24 hours.
• Place any item (including clothes) that came into contact with the mercury into a sealed plastic bag and place in the rubbish.
• Contaminated carpet and other absorbent items will need to be cut out or removed and disposed of carefully.
• More detailed information is available for cleaning procedures.

Other devices around the home can contain more than two tablespoons of mercury. These include thermostats and some medical equipment (such as a sphygmomanometer – to measure blood pressure). Large mercury spills need to be professionally cleaned up. The following steps should be taken:

• Evacuate the area.
• Air (ventilate) the area.
• Contain the spill – call triple zero (000) and ask for fire services.
• Clean up the spill – this should be performed by experienced professionals who specialise in hazardous chemicals.

Reducing exposure to mercury from dental fillings

Dental fillings are used to treat damaged or worn teeth and can be made of amalgam that contains mercury, silver and tin. This substance is used because of its strength, especially in the back teeth that are under a lot of pressure during chewing. Modern amalgam has low levels of mercury and is considered safe for most people.

Alternate materials for fillings that are similar in colour to teeth do not contain mercury but these are not as strong as amalgam. You can replace your amalgam fillings with this material, but it might not last as long, especially in your back teeth. Replacing fillings can also be expensive. Speak with your dentist about your options.

Some people are advised to avoid getting new amalgam fillings and to avoid having existing amalgam removed or replaced if possible including:

• pregnant women – mercury may cross the placenta and enter the bloodstream of the unborn baby
• women who are breastfeeding – mercury may be passed to the baby through breastmilk
• children – growing and developing teeth are more sensitive to the effects of any chemical substances in the environment, including mercury
• people with kidney disease – high levels of mercury exposure can affect the kidneys, so exposure to mercury should be minimised.

While there is currently no scientific evidence directly linking amalgam with either ill health or birth defects, these recommendations have been made for precautionary reasons.

Reducing exposure to mercury from batteries

Not all batteries contain mercury, but those that do can damage the environment if they end up in landfill. Your local council can give you advice about safe disposal of batteries.

People at risk of exposure to mercury

The effect of mercury exposure depends on the type of mercury. In general, mercury tends to affect the nervous system. This means that unborn babies and children are at more risk because their nervous systems are developing.

People at higher risk from mercury exposure include:

• unborn babies
• infants
• children up to six years of age
• workers in industrial settings where mercury is used or produced
• people with kidney disease
• people born before the 1950s who were exposed to mercury in baby products and contracted pink disease.

Pregnant women should avoid mercury so that it is not transmitted to their unborn baby via the bloodstream. Levels of mercury in breastmilk are normally not high enough to be a risk for babies.

Pink disease

In the first half of the twentieth century, teething powders and other products for babies contained mercury and some babies contracted pink disease. In this condition, the feet, hands and the tip of the nose are bright pink. Other skin problems, diarrhoea and lethargy were also symptoms. Pink disease is now rare, but adults who had pink disease are more sensitive to mercury and may have a number of other health complaints.

Symptoms of mercury poisoning

Symptoms of mercury poisoning depend on the form of the mercury that was the source of the exposure. Early symptoms of mercury poisoning can include a metallic taste in the mouth and numbness and tingling in the hands, feet and face.

Symptoms of methylmercury poisoning from fish

Most people have some methylmercury in their tissues, but these are at a level that not does cause damage. Excess methylmercury particularly affects the nervous symptom. For unborn babies, infants and children this is especially damaging as their brains and nervous systems are developing.

Methylmercury poisoning can cause disturbances in:

• peripheral vision
• sensation, especially on the hands, feet and mouth
• coordination and walking
• speech and hearing
• muscle strength.

Symptoms of poisoning from elemental mercury

This type of poisoning is most likely to occur if there is a spill of mercury from a thermometer or other mercury-containing device. Poisoning is often caused by inhaled mercury vapour, especially in places where there is poor ventilation. Symptoms include:

• tremors
• headaches
• difficulty sleeping
• impaired sensations
• muscle weakness and twitching
• emotional changes (mood swings, irritability, nervousness)
• kidney damage
• breathing difficulties
• death.

Symptoms of poisoning from inorganic mercury

This type of poisoning is more likely to be related to industrial exposure. Symptoms of inorganic mercury poisoning include:

• skin conditions (rashes and dermatitis)
• breathing problems
• mood changes
• problems with memory
• mental health issues
• reduction in muscle strength.

Diagnosis of mercury poisoning

Poisoning from methylmercury can take weeks or months to appear. A chemical spill with elemental mercury or inorganic mercury might give you symptoms more rapidly.

Mercury poisoning is diagnosed by testing your blood and urine for mercury levels. Urine might be collected over a 24-hour period. Your doctor will ask about the history of your possible exposure and may also monitor your temperature, pulse rate, blood pressure and breathing.

If mercury poisoning is suspected, treatment might begin before the diagnosis is confirmed. This is because the test results can take some time to come back to the doctor.

Treatment of mercury poisoning

If mercury poisoning is suspected in people who are critically ill, your doctor will most likely treat you with chelation therapy, no matter what form of mercury caused the poisoning. Chelation therapy is made up of compounds that enter your bloodstream and bind to the mercury so that it can be eliminated by your body.

Where to get help

• Victorian Poisons Information Centre Tel. 13 11 26 – for advice when poisoning or suspected poisoning occurs and poisoning prevention information (24 hours, 7 days)
• Your doctor
• Your dentist
• Detox your Home, Sustainability Victoria Tel. 1300 363 744 – for advice about energy, waste and recycling items such as fluorescent lamps

Things to remember

• There are a number of common sources of mercury in our environment.
• Certain species of fish, fluorescent and low-energy lamps, mercury-containing thermometers, some batteries and amalgam dental fillings contain some mercury.
• Preventing or minimising exposure to mercury in your environment is the best way to reduce the risk of mercury poisoning.
• Pregnant women, infants and children, and people with kidney disease should especially avoid exposure to excess mercury.

Health Risks of Mercury | SCDHEC

Mercury is a naturally occurring element that has several forms. Mercury is toxic. Exposure to mercury, even small amounts, may cause serious health problems. People can be exposed to mercury through skin contact, by eating contaminated fish or by breathing mercury vapors that are invisible and odorless.

Mercury is released into the environment from many sources. Mercury is found in air, water and soil. It becomes airborne when rocks erode, volcanoes erupt and soil decomposes. Mercury then circulates in the atmosphere and is redistributed throughout the environment.

Human activities, such as burning coal, oil and natural gas, burning household trash, and mining ore deposits, add mercury to the environment. Once in the air, mercury falls to the ground with rain, sleet and snow, landing on soil or water bodies and causing contamination. In addition, many common products that we use every day contain mercury and may contaminate the environment when disposed of in trash, burned or poured down a drain. Mercury also may enter water bodies through a direct discharge of industrial waste or municipal sewage. A less common exposure to mercury is when elemental mercury or products containing elemental mercury break and release mercury vapors into the air.

Mercury has been a very useful element throughout history. The most common way people in the United States are exposed to mercury is by eating fish containing methylmercury – a form of mercury. Other exposures may result from using or disposing of products containing mercury.

Whether exposure to mercury will harm a person’s health depends on several factors including:

• the type of mercury
• the dose (how much)
• the duration of exposure (how long)
• route of exposure (eating, breathing, injecting, touching)
• characteristics of the person (age and health)

All Mercury is Toxic

Although some forms of mercury are more dangerous than others, all are toxic. Depending on the type and amount, exposures to mercury can damage the nervous system, kidneys, liver and immune system.

Breathing mercury vapors can harm the nervous system, lungs and kidneys. Mercury vapors can pass easily from the lungs to the bloodstream. Elemental (also known as metallic) mercury, the shiny silver-white liquid found in some thermometers and switches, is most dangerous when inhaled and must be handled with care.

Mercury Is Especially Dangerous To Pregnant Women

Children of women who consumed large amounts of contaminated fish during pregnancy are at highest risk of mercury-related developmental problems. The Centers for Disease Control and Prevention estimates that about 6% of child-bearing aged women in the United States have a blood mercury level that is unsafe for a developing fetus. Mercury exposure in the womb – which can result from a mother’s consumption of fish and shellfish that contain methylmercury – can adversely affect a baby’s growing brain and nervous system.

The National Research Council estimates that each year about 60,000 children might be born in this country with permanent, irreversible neurological problems because of mercury exposure before birth. Fetuses, infants and young children are four to five times more sensitive to mercury exposure than adults. High levels of mercury can impair a child’s physical and mental development, including motor skills, learning capacity and memory.

A national advisory issued in March 2004 says that women who are pregnant, may become pregnant or are nursing, and children under 14 should only eat one meal of freshwater fish each week. The advisory also says that they should not eat king mackerel, shark, swordfish and tilefish. This advisory includes fresh, frozen and canned fish that you buy in a store or restaurant.

Children Under 14 Are Most Sensitive To Mercury

The developing brains and nervous systems of children are very sensitive to mercury and may be irreversibly damaged by it. Children can be exposed to methylmercury by eating certain types of fish or if their mothers ate mercury-contaminated fish before their birth.

Breaking mercury-containing products such as thermometers used in homes and schools can also result in exposure to mercury.

Families Can Reduce Their Risk

• Look for and follow state and national fish consumption advisories.
• Consider not buying products that contain mercury such as thermometers – buy a digital thermometer instead.
• Carefully handle, properly dispose of or recycle products that contain mercury.
• Do not use a vacuum to clean up a mercury spill (see the “Cleaning up mercury spills” fact sheet in this series).
• Properly dispose of older medicines that contain mercury.
• Keep all mercury away from children and pets.

Consult A Doctor

Anyone who has concerns about mercury exposure should consult a doctor. Doctors may be able to identify exposure and health risks.

A doctor may help decide if mercury testing is appropriate given the physical condition and symptoms. DHEC offers analytical services through a doctor’s office for mercury blood levels. DHEC charges a nominal fee for this service.

For more information on the health effects of mercury exposure, please visit www.epa.gov/mercury/effects.htm . You also can visit the Agency for Toxic Substances and Disease Registry at www.atsdr.cdc.gov/toxprofiles/tp46.html for a toxicological profile of mercury.

Symptoms of Mercury Poisoning

• Vision, speech, hearing and walking impairment
• Numbness in hands, feet and sometimes around the mouth
• Uncoordinated movement
• Muscle weakness
• Skin rashes
• Mood swings, memory loss and mental disturbances

2. What are the impacts of mercury on human health?

2. What are the impacts of mercury on human health?

• 2.1 What are the potential health effects of mercury?
• 2. 2 How are we exposed to mercury?
• 2.3 What levels of mercury might cause harm?
• 2.4 How great are the risks from mercury today?

2.1 What are the potential health effects of mercury?

The toxicity of mercury
depends on the form of mercury to which people are
exposed.

Although mercury and its compounds are
toxic substances, there is
ongoing debate about exactly how toxic they are. Toxic effects,
especially in the case of
methylmercury, may be
taking place at lower
concentrations than
previously thought, but this is proving difficult to establish
because the suspected toxic effects are subtle and their
mechanisms complex. Methylmercury is of particular concern
because it can accumulate
in the food chain to reach high concentrations
(biomagnification).
More…

2.1.1
Methylmercury is special
among
organic mercury compounds
because large numbers of people are
exposed to it and its
toxicity is better
understood. Methylmercury in food, such as fish, is a particular
health hazard because it is easily
taken up into the body
through the stomach and intestines.

It is a poison for the nervous system.
Exposure during pregnancy is
of most concern, because it may
harm the
development of the unborn
baby’s brain. Some studies suggest that small increases in
exposure may affect the
heart and circulatory system.

Moreover, there is some evidence at present that
methylmercury can cause
cancer in humans, but it is
far from conclusive: the International Agency for Research on
Cancer
(IARC)
has classified methylmercury as
“possibly carcinogenic to humans”
(Group 2B).

Methylmercury’s poisonous potential was highlighted by an
incident in Minamata (Japan), in the 1950s, where wastes from a
chemical factory using mercury were discharged into the local
bay.
More…

2.1.2
Elemental mercury is also
poisonous to the nervous system. Humans are mainly
exposed by
inhaling vapours. These are
absorbed into the body via
the lungs and move easily from the bloodstream into the brain.
However, when elemental mercury is
ingested, little is absorbed
into the body.

The inhalation of
elemental mercury vapours
can cause
neurological and behavioural
disorders, such as tremors,
emotional instability,
insomnia, memory loss,
neuromuscular changes and
headaches. They can also
harm the kidneys and
thyroid. High
exposures have also led to
deaths. However, there is no evidence at present that elemental
mercury causes cancer in
humans and it has been classified by
IARC
into Group 3
“unclassifiable as to carcinogenicity in humans”
More. ..

2.2 How are we exposed to mercury?

The main source of
elemental mercury vapour is
dental amalgam (a tooth
filling).

Diet, particularly fish, is generally the main source of both
inorganic and
organic mercury.
Methylmercury is by far the
most common organic form, and is especially found in fish and
other seafood.

For some people, the workplace may also be an important source
of exposure. Examples include
chlor-alkali plants,
mercury mines, thermometer factories, refineries and dental
clinics, as well as the mining and manufacturing of gold
extracted with mercury.

People can also receive extra
doses in specific
situations, such as when mercury compounds are used in
skin-lightening creams, soaps and traditional medicine.
Exposure may also arise from
localised pollution through air and water, and from mercury
spills at home or work (e.g. from certain old gas meters
containing mercury).
More…

2.3 What levels of mercury might cause harm?

For methylmercury, the US
Environmental Protection Agency
(US EPA)
has estimated a safe daily
intake level of 0.1
µg/kg body weight per day.
This was based on a study in the Faroe Islands, where fish
containing significant levels of mercury form a large part of
the diet. The study compared
development test scores for
children whose mothers had been
exposed during
pregnancy¹.
A European Union scientific review, in 2001, has supported this
safe daily intake level.

For elemental mercury
vapour, several studies show that long-term workplace exposures–
at around 20 µg/m³ of air or higher – have subtle
toxic effects on the central
nervous system.

Other adverse effects of various forms of mercury have been
seen in humans, but either the findings are less consistent or
the doses involved are much
higher.

The Working Group that prepared this assessment, in line with
its mandate, did not assess the potential effects of
exposures to
elemental mercury vapour
from dental amalgams or
reach any conclusions about whether or not dental amalgams cause
adverse effects. This remains a matter of scientific
debate².
More…

2.4 How great are the risks from mercury today?

2.4.1
Whilst the diet and
amalgam fillings in teeth
are respectively the main sources of
methylmercury and mercury
vapour exposure for most
people, sources such as local pollution, exposure at work,
cultural practices and traditional medicines are important in
some regions
(see 2.2).

Assessments of mercury
exposure have been made in
various parts of the world. For example, a recent study of 1700
women in the USA found that about 8% of them had mercury
concentrations in their
blood and hair exceeding the levels that correspond to the
US EPA’s
estimated safe dose.

Data indicate that
exposures in Greenland, Japan
and some other areas are generally higher than in the USA. On
the other hand, measures have been taken in recent decades to
reduce emissions of mercury in various countries
(see 6.3).
More…

2.4.2
Fish is the main food source in many parts of the world and
provides nutrients that are not easily replaced. Mercury
contamination adds health
risks to this important
food supply.

Many countries, international organizations and scientific
investigations have reported mercury
concentrations in fish
between about 0.05 and 1.4
mg/kg of fish
tissue, depending on the
water and the fish.

Predator fish and marine mammals that eat other fish tend to
have higher levels of mercury because mercury
bioaccumulates in fish and
is biomagnified up the food
chain
(see 3.1).
Mercury levels are thus higher in such fish as king mackerel,
pike, shark, swordfish, walleye, barracuda, large tuna (as
opposed to the small tuna usually used for canned tuna),
scabbard and marlin, as well as in seals and toothed
whales.

Moderate consumption of fish with low mercury levels is not
likely to result in worrying levels of
exposure for humans. However,
people who consume higher amounts of contaminated fish or marine
mammals may be highly exposed
to mercury and are, therefore, at
risk. Indeed, high
concentrations of mercury in
fish have led governments in a number of countries to give
warnings to consumers. These advise people, especially sensitive
groups (such as pregnant women and young children), to limit or
avoid consumption of certain types of fish from specific
areas.
More…

A Review of the Literature

J Environ Public Health. 2012; 2012: 460508.

Robin A. Bernhoft

¹Bernhoft Center for Advanced Medicine, Suite 208, 11677 San Vicente Boulevard, Los Angeles, CA 90049, USA

²Los Angeles Center for Advanced Medicine, Brentwood Gardens Suite 208, 11677 San Vicente Boulevard, Los Angeles, CA 90049, USA

¹Bernhoft Center for Advanced Medicine, Suite 208, 11677 San Vicente Boulevard, Los Angeles, CA 90049, USA

²Los Angeles Center for Advanced Medicine, Brentwood Gardens Suite 208, 11677 San Vicente Boulevard, Los Angeles, CA 90049, USA

Academic Editor: Margaret E. Sears

Received 2011 Jul 4; Accepted 2011 Nov 1.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

This article has been cited by other articles in PMC.

Abstract

Mercury is a toxic heavy metal which is widely dispersed in nature. Most human exposure results from fish consumption or dental amalgam. Mercury occurs in several chemical forms, with complex pharmacokinetics. Mercury is capable of inducing a wide range of clinical presentations. Diagnosis of mercury toxicity can be challenging but can be obtained with reasonable reliability. Effective therapies for clinical toxicity have been described.

1. Introduction

Mercury is a heavy metal of known toxicity, noted for inducing public health disasters in Minamata Bay, Japan [1] and in Iraq [2–4]. The clinical impact of smaller mercury exposures remains controversial. It exists in several forms: inorganic mercury, which includes metallic mercury and mercury vapor (Hg⁰) and mercurous (Hg₂ 
⁺⁺) or mercuric (Hg⁺⁺) salts; and organic mercury, which includes compounds in which mercury is bonded to a structure containing carbon atoms (methyl, ethyl, phenyl, or similar groups). The biological behavior, pharmacokinetics, and clinical significance of the various forms of mercury vary with chemical structure. There is some interconversion in vivo between the various forms of mercury. Inhaled elemental mercury vapor, for example, is easily absorbed through mucus membranes and the lung and rapidly oxidized to other forms (but not so quickly as to prevent considerable deposition of elemental mercury in the brain). Methyl mercury is easily absorbed through the gut and deposits in many tissues, but does not cross the blood-brain barrier as efficiently as elemental mercury; however, on entering the brain it is progressively demethylated to elemental mercury [5]. Mercury salts, in contrast, tend to be insoluble, relatively stable, and poorly absorbed.

Human toxicity varies with the form of mercury, the dose and the rate of exposure. The target organ for inhaled mercury vapor is primarily the brain [5]. Mercurous and mercuric salts chiefly damage the gut lining and kidney [5], while methyl mercury is widely distributed throughout the body [5]. Toxicity varies with dosage: large acute exposures to elemental mercury vapor induce severe pneumonitis, which in extreme cases can be fatal [5]. Low-grade chronic exposure to elemental or other forms of mercury induces subtler symptoms and clinical findings, as discussed hereinafter.

There is considerable controversy about the clinical significance of exposure to the various forms of mercury and some disagreement regarding techniques for clinical assessment of mercury burden. This paper is intended to review published data on these issues and to assess published clinical experience using DMPS to remove mercury from the human body. Most of the authors cited hereinafter consider DMPS to be a stronger chelator than DMSA, with one exception citing evidence that DMSA is more effective at removing organic mercury [6]. This is a complicated issue. The absorption of DMPS and DMSA by ingestion is highly variable from one patient to the next; DMPS can be given intravenously, while DMSA cannot. DMPS is considerably safer than penicillamine or British anti-Lewisite, as discussed hereinafter. It is available for compounding in the United States and is available over the counter in Germany.

2. Sources of Mercury Exposure

Most human exposure to mercury is caused by outgassing of mercury from dental amalgam, ingestion of contaminated fish, or occupational exposure, according to the World Health Organization [7, 8].

Mercury exists in nature primarily as elemental mercury or as a sulfide and is found in the earth’s crust at approximately 0.5 parts per million. Atmospheric exposures occur from outgassing from rock or through volcanic activity. Human sources of atmospheric mercury include coal burning [9] and mining (mercury and gold in particular). Atmospheric elemental mercury settles in water, where it is converted by microorganisms into organic (methyl or ethyl) mercury, which is ingested by smaller creatures which are eventually consumed by larger fish. Fish at the top of the food chain (e.g., tuna, swordfish, or shark) may concentrate considerable mercury in their tissues.

Human mercury exposures occur chiefly [7, 8] through inhalation of elemental mercury vapor via occupational or dental amalgam exposure or through ingestion of mercury bonded to organic moieties (methyl, dimethyl, or ethyl mercury), primarily from seafood. Most human metallic mercury exposure comes from mercury vapor outgassing from amalgam fillings, at a rate of 2 to 28 micrograms per facet surface per day, of which about 80% is absorbed, according to the World Health Organization [7, 8] and Berglund et al. [10]. A less common source of mercury vapor is spilled mercury [11], and there is a report in the literature of Idiopathic Thrombocytopenic Purpura [12] caused by vacuuming spilled mercury (thereby producing a major acute exposure to mercury vapor).

Methyl and dimethyl mercury (organic mercury) usually originate from biological sources, chiefly fresh or salt water fish. Over three thousand lakes in the United States have been closed to fishing due to mercury contamination [5] and many species of ocean fish are also tainted with considerable concentrations of mercury [13].

3. Pharmacokinetics of Mercury Exposure

3.1. Inorganic Mercury

3.1.1. Elemental or Metallic (Hg

⁰) Mercury

Approximately 80% of metallic mercury vapor outgassed from amalgams is absorbed through inhalation [10, 14, 15], compared with about 7 to 10% absorption of ingested metallic mercury [5], and about 1% absorption of metallic mercury through skin contact [5]. On entry to the body, mercury vapor has great affinity for sulfhydryl groups and bonds to sulfur-containing amino acids throughout the body. Mercury vapor is transported to the brain [16], either dissolved in serum or adherent to red cell membranes. Metallic mercury passes easily through the blood brain barrier [17] and through the placenta, where it lodges in the fetal brain [18]. Metallic mercury is, however, rapidly oxidized to mercuric mercury on entry to the blood stream [5], although not so quickly as to prevent considerable uptake by the central nervous system while still in the metallic form.

In addition to the brain [16, 19–26], metallic mercury is also deposited in the thyroid [5, 19, 21], breast [27], myocardium [28, 29], muscles [5, 21], adrenals [5], liver [5, 30–32], kidneys [5, 7, 8, 19, 20, 23, 30–32], skin [5, 7, 8], sweat glands [5], pancreas [5], enterocytes [5, 30], lungs [5, 23, 30], salivary glands [5], testes, and prostate [5] and may be associated with dysfunction of those organs. Mercury also has affinity for binding sites on the surface of T cells and for sulfhydryl groups influencing T cell function [33, 34]. Mercury deposits readily in placenta and fetal tissues and is found in breast milk. [5, 18, 31, 35]

Metallic mercury is largely excreted as mercuric mercury [5]. The excretory half lives of metallic and mercuric mercury vary widely, depending on the organ of deposition and redox state, with values ranging from a few days to several months [5], with some pools (e.g., CNS) having a half life exceeding several years [5]. Hair mercury does not correlate with brain content of metallic mercury [5]. These complexities make accurate assessment of body burden challenging (see Section 9 hereinafter).

3.1.2. Mercurous (Hg

₂ 
⁺⁺) Mercury

Mercurous mercury salt in the form of Hg₂Cl₂ (calomel) is poorly soluble in water and poorly absorbed by the intestine, although some portion is thought to undergo oxidation to more readily absorbable forms [36]. It is doubtful that mercurous mercury survives in the body, other than as a transitional form between metallic and mercuric mercury [5].

Some absorption evidently occurs, however, as calomel is occasionally associated with pink disease, or acrodynia.

3.1.3. Mercuric (Hg

⁺⁺) Mercury

Historically, mercuric chloride (HgCl₂) was used as a preservative and for development of photographic film and was ingested accidentally or as a suicide measure. It is a component of some skin-lightening creams. Only about 2% of ingested mercuric chloride is absorbed initially [37], although it is believed that its corrosive effect on the intestine may increase permeability and, hence, absorption, with prolonged exposure [38]. Available data on skin penetration of mercuric mercury are insufficient to make quantitative comparison with ingestion or with metallic mercury.

Like metallic mercury, mercuric mercury in the bloodstream adheres to sulfhydryl groups on erythrocytes, metallothionein, or glutathione or is suspended in plasma [26]. Mercuric mercury does not cross the blood-brain barrier efficiently, but it does accumulate in quantity in the placenta, fetal tissues, and amniotic fluid [35]. Evidence exists showing transport of mercuric mercury via one or more amino acid transporters [39], particularly that for cysteine, which may account for accumulation in the brain [5]. Much of the body burden of mercuric mercury resides in the proximal convoluted renal tubule [40] bonded to metallothionein [41]. Significant deposition also occurs periportally in the liver [42] and lesser amounts in epithelial tissues, choroidal plexus, and testes.

Excretion of mercuric mercury is largely through urine and stool, although significant amounts are shed through sweat, tears, breast milk, and saliva [5, 43]. Half lives appear to be multiphasic, as with metallic mercury, with human studies suggesting an effective half life of 42 days for 80% of an oral tracer dose; the other 20% did not appear to have a measureable rate of excretion [44]. This may reflect demethylation to metallic mercury in the brain and other organs or mechanisms yet to be determined.

3.2. Organic Mercury Compounds

Most available data on organic mercury compounds refer to methyl mercury, which is a major source of human mercury exposure, is found naturally in fish, and is relatively stable. Ethyl mercury behaves in a similar fashion to methyl mercury at the cellular level, but with an excretory half life about one third as long [5].

Methyl mercury vapor is absorbed with similar (80%) efficiency as metallic mercury vapor [5]. Intestinal absorption of methyl mercury from fish is also fairly efficient, as is absorption through the skin [5]. On entry to the bloodstream, methyl mercury adheres to sulfhydryl groups, particularly to those in cysteine. Methyl mercury is deposited throughout the body, with equilibrium between blood and body occurring approximately four days after exposure [45]. Distribution to peripheral tissues seems to occur through one or more transporters, especially the cysteine transporter, probably adherent to the sulfhydryl group in cysteine [5].

Concentration of methyl mercury occurs in the brain, liver, kidneys, placenta, and fetus, especially in the fetal brain, as well as in peripheral nerves and bone marrow [5]. Deposited methyl mercury slowly undergoes demethylation to inorganic mercury [46].

The excretory half life of methyl mercury in man is about 70 days, with approximately 90% being excreted in stool. Some degree of enterohepatic circulation apparently occurs. Perhaps 20% of methyl mercury is excreted in breast milk, with the actual amount varying with severity of exposure [5]. Hair mercury reflects blood methyl mercury at the time of incorporation, but not elemental mercury [47], and hence is not a good index of total body burden [5], given the short half life of methyl mercury in blood.

Dimethyl mercury is also efficiently absorbed through the skin, and there is a reported death of a scientist caused by minimal skin contact [48].

4. Toxicity

4.1. Inorganic Mercury

4.1.1. Metallic Mercury Vapor

Mercury in all forms poisons cellular function by altering the tertiary and quaternary structure of proteins and by binding with sulfhydryl and selenohydryl groups. Consequently, mercury can potentially impair function of any organ, or any subcellular structure. The chief target organ of mercury vapor is the brain, but peripheral nerve function, renal function, immune function, endocrine and muscle function, and several types of dermatitis have been described [49].

With massive acute exposure to mercury vapor, erosive bronchitis and bronchiolitis potentially leading to respiratory failure may be accompanied by CNS symptoms such as tremor or erethism [50].

Chronic exposure to clinically significant doses of mercury vapor usually produces neurological dysfunction. At low-level exposures, nonspecific symptoms like weakness, fatigue, anorexia, weight loss, and gastrointestinal disturbance have been described [51]. Higher exposure levels are associated with mercurial tremor: fine muscle fasciculations punctuated every few minutes by coarse shaking. Erethism may also be observed: severe behavior and personality changes, emotional excitability, loss of memory, insomnia, depression, fatigue, and in severe cases delirium and hallucination [10]. Gingivitis and copious salivation have been described [5].

These symptoms may regress with cessation of exposure, but in many cases do not. Persistent neurological symptoms are common [52].

4.1.2. Mercurous Mercury

Calomel (Hg₂Cl₂) is still used in some regions of the world as a laxative. Although poorly absorbed, some is converted to mercuric mercury, which is absorbed, and induces toxicity as expected with mercuric mercury.

4.1.3. Mercuric Mercury

Acute poisoning with mercuric salts (typically HgCl₂) generally targets the gastrointestinal tract and the kidneys. Extensive precipitation of enterocyte proteins occurs, with abdominal pain, vomiting, and bloody diarrhea with potential necrosis of the gut mucosa. This may produce death either from peritonitis or from septic or hypovolemic shock. Surviving patients commonly develop renal tubular necrosis with anuria [53].

Chronic poisoning with mercury salts is rare, usually also involving concomitant occupational exposure to mercury vapor. Kidney toxicity involves either renal tubular necrosis or autoimmune glomerulonephritis, or both [53]. Immune dysfunctions include hypersensitivity reactions to mercury exposure, including asthma and dermatitis, various types of autoimmunity [54], and suppression of natural killer cells [55] and disruption of various other lymphocyte subpopulations [5].

Brain dysfunction is less evident than with other forms of mercury. Thyroid dysfunction seems associated with inhibition of the 5′ deiodonases, with decreased free T3 and increased reverse T3 [56]. Accumulation in the testicles appears to inhibit spermatogenesis [57]. Atrophy and capillary damage have been described in thigh muscle [58].

4.2. Organic Mercury

Methyl mercury reacts with sulfhydryl groups throughout the body, therefore potentially interfering with the function of any cellular or subcellular structure. Mercury is believed to interfere with DNA transcription and protein synthesis [59], including protein synthesis in the developing brain, with destruction of endoplasmic reticulum and disappearance of ribosomes [60]. Evidence suggests disruption of numerous subcellular elements in the central nervous system and other organs and in mitochondria; adverse effects have also been described on heme synthesis [61], cell membrane integrity in many locations [5], free radical generation [27, 62, 63], neurotransmitter disruption, and stimulation of neural excitoxins [5], resulting in damage to many parts of the brain and peripheral nervous system [5].

Methyl mercury has been associated with reduction in Natural Killer cell activity [64–67], as well as an imbalance in Th3 : Th2 ratios favoring autoimmunity [34, 68, 69]. Mercury is also possibly associated with disruption of DNA repair [5, 27]. The affinity of mercury for sulfhydryl groups of the mitochondrial oxidative phosphorylation complex [70] associated with destruction of mitochondrial membranes may contribute to chronic fatigue syndrome.

5. Clinical Presentation

5.1. Inorganic

5.1.1. Elemental (Metallic) Mercury

Acute exposure to a large quantity of mercury vapor induces pneumonitis, as discussed previously. Symptoms of low-grade chronic exposure are more subtle and nonspecific: weakness, fatigue, anorexia, weight loss, and gastrointestinal distress [5], sometimes referred to as micromercurialism [71]. At higher exposures, the mercurial fine tremor punctuated by coarse shaking occurs; erethism, gingivitis, and excessive salivation have also been described [5], as has immune dysfunction [34].

Objective findings include altered evoked potentials and decreased peripheral nerve conduction velocity [72]. Objective measures of short-term memory may be inversely correlated with urinary mercury in chloralkali workers [73]. Reduced color vision and visual acuity have also been observed [74]. Changes in coordination, tremor, mental concentration capacity, facial expression, and emotional state are also described [75], as are polyarthritis, various forms of dermatitis, and a syndrome mimicking pheochromocytoma [76].

Subtler clinical findings among dentists have been documented, including delayed reaction time, poor fine motor control, and deficits in mental concentration, vocabulary, task switching, and the One Hole test, as well as mood lability, all correlating with urinary mercury excretion [75]. Evidence also links elemental mercury to depression, excessive anger, and anxiety [77], as well as acute myocardial infarction, lipid peroxidation, and carotid atherosclerosis, in Finland [78]; the Finnish experience may possibly be explained by dietary selenium deficiency, since selenium antagonizes mercury toxicity. Other investigators, however, have described associations between mercury and hypertension, lipid peroxidation, ischemic heart disease, and stroke [79].

5.1.2. Mercuric Salts

Ingestion of mercuric chloride produces extensive precipitation of intestinal mucosal proteins, mucosal necrosis, generalized abdominal pain, bloody diarrhea, and shock. If the patient survives, acute renal failure may follow [5].

5.2. Organic Mercury

Methyl mercury and ethyl mercury produce similar signs and symptoms. Most published data refer to methyl mercury. Symptoms relate more to magnitude of methyl mercury retention than to the rate of deposition. Acute exposures tend to have a latency period of one or more weeks; once acquired, toxic doses are cleared slowly, if at all [5].

Massive prenatal poisoning may induce a form of cerebral palsy [5]. Lesser prenatal doses have been associated with neurodevelopmental delays and cognitive deficits [80–82].

Postnatal exposures generate a range of symptoms ranging from paresthesias, with lesser exposures, to ataxia, visual, auditory, and extrapyramidal impairments with moderate exposures and clonic seizures in more severe exposures, as in Minamata [1] and Iraq [2–4].

Objective physical findings are similar to those seen with elemental mercury exposure.

6. Laboratory Assessment of Mercury Exposure

Given the wide range of excretory half lives of the various mercury pools, discussion of laboratory assessment will combine the various forms into one discussion. It is important to recall that blood, hair, and urine mercury levels reflect recent exposure and do not correlate with total body burden [83–86]. Blood and urine levels correlate fairly well to each other, but not to total body burden [87]. With half life of all mercury pools in the blood estimated to be in the range of three to five days [88], during which either excretion or deposition in solid organs occurs, more accurate means of estimating body burden have been required.

That being said, the US federal biological exposure index (BEI) is currently set at 50 mcg/L urine. Aside from the obvious problems associated with basing a monitoring index on a measurement which only reflects current or recent exposure, and not overall body burden, several clinical studies show objective symptoms well below 50 mcg/L, with many proband values extending down into the low end of the reference range for urinary mercury excretion [75, 89–94], effectively rendering the US federal BEI useless for clinical or investigational purposes. Similar criticisms have been made of the EPA Reference Dose for methylmercury [95]. As summarized by Kazantzis, “it has not been possible to set a level for mercury in blood or urine below which mercury related symptoms will not occur” [96].

Because of these difficulties, provocation with a chelator has been proposed as providing a more reliable estimate of body burden, and DMPS (2,3 Dimercapto-1-Propanesulfonate) has been found by a number of investigators to provide a reliable estimate of body burden, safer than British Anti-Lewisite and more potent than DMSA [75, 97–101].

7. DMPS: Safety

DMPS is an analog of British Anti-Lewisite (BAL) with high affinity for mercury. Due to its superior safety, it has been widely used in Germany for the past fifty years and is available over the counter in that country. Protocols determining the pharmacokinetics of DMPS and evaluating its use for diagnostic purposes have been published in Germany [101], Sweden [102, 103], New Zealand [100], and Mexico [104] and in the United States [105–109].

Maiorino et al. [106] gave his volunteers DMPS 300 mg orally; over 90% of the absorbed DMPS was converted rapidly to disulfide forms. Published absorption of ingested DMPS varies from 39% [107] to 60% [110]. The excretory half life of unaltered DMPS was 4.4 ± 1.1 hours. The excretory half life of the disulfide forms of DMPS was  9.9 ± 1.6  hours.

Hurlbut et al.’s [107] volunteers were given an unusually large dose of DMPS (3 mg/kg intravenously over 5 minutes). Two subjects had a transient 20 mmHg drop in systolic blood pressure during infusion, without other changes in vital signs. Excretory half life of unaltered DMPS ranged from 1.3 to 4.0 hours. Half life of the altered DMPS was from 19.8 to 37.5 hours.

In each of the cited studies, mercury output following provocation with DMPS correlated significantly with amalgam number and/or occupational or dietary exposure. There were no significant complications in any of the trials. Consequently, all the investigators but one [111] concluded that urine output provoked by DMPS represented a fair estimate of body burden.

8. DMPS: Efficacy

Each of the test trials cited in the previous section and others [112] showed statistically significant increases in urinary mercury output with administration of DMPS. With prolonged treatment, evidence of decreased body burden has been inferred [113].

Several controlled clinical trials support this conclusion. The largest was undertaken in the Phillippines in a gold mining area [114]. Workers in gold mining who sustained ongoing exposure to elemental mercury were compared to people living downstream who ate fish, which contained considerable methyl mercury, and to controls without significant known mercury exposure. Probands from the two exposed areas were chosen with elevated blood, urine and hair mercury levels, and appropriate symptoms (tremor, sleeplessness, memory loss, etc.)[115]; controls had normal levels and were asymptomatic.

One hundred six probands completed the fourteen-day trial with oral DMPS 400 mg per day. The only complication was an allergic rash in one patient, who was excluded from the trial. Blood mercury did not decrease during the trial, despite increases in urine mercury up to 85-fold.

Despite the short (fourteen-day) duration of the trial, significant improvements were observed in objective measures like hypomimia, Romberg test, tests for tremor and ataxia, pencil tapping, and Frostig visual perception. Most of the patients reported subjective improvement in memory, sleeplessness, metallic taste, fatigue, anxiety, and paresthesias. Treatment efficacy was similar in the metallic mercury group (miners) and in the methyl mercury group (downstream fish eaters). Similar results were presented in a parallel study by Drasch et al. [115].

A university case report from the United States of treatment of occupational exposures to mercury vapor [116] showed relief of muscle twitching, arthralgias, paresthesias, night sweats, weight loss, and excessive salivation following two weeks of oral DMPS 100 mg TID followed by DMPS 100 mg QID for an additional six weeks. Reduction of symptoms closely paralleled urine mercury output, which tapered over time.

9. Discussion

Mercury toxicity is not often included in the differential diagnosis of common subjective complaints such as fatigue, anxiety, depression, odd paresthesias, weight loss, memory loss, and difficulty concentrating, but these are the symptoms of low-grade chronic mercury exposure described by the investigators cited previously. Given the ability of the various forms of mercury to deposit in most parts of the human body, the range of symptoms potentially caused by mercury is quite large.

Animal studies linking mercury toxicity to neurodegenerative diseases [117, 118] raise clinical concern, as do a series of associations between mercury and neurodegenerative diseases in humans [119–123].

Mercury exposure is not insignificant according to WHO, as cited previously, and the NHANES reports suggest widespread exposure in the United States, especially among women [124, 125].

Diagnosis of mercury overload is difficult. The commonly used modalities (blood, urine, and/or hair levels) do not correlate with total body burden and offer little diagnostically useful information. Provocation with DMPS appears to offer a more accurate assessment of body burden.

Since provocation is safe and inexpensive, indications for provocation must rest on clinical grounds: does the patient have multiple, vague symptoms similar to those described in the mercury literature, without other plausible, and potentially reversible, explanation? Is there a significant history of mercury exposure: multiple amalgam fillings, high seafood intake, and history of multiple thimerosal-containing vaccinations or significant occupational exposures? Is there a family history of Alzheimer’s, Parkinson’s, or other diseases with postulated links to mercury exposure? Is there a history of known glutathione transferase (GST) polymorphisms, which decrease the body’s ability to clear heavy metals like mercury?

If so, then provocation with a chelator may be indicated. Published protocols [126–130] exist which call for provocation with DMPS with or without EDTA, in sequence. These are designed for safety, and for diagnostic breadth. DMPS has far better affinity for mercury than EDTA, but EDTA is more effective in removing lead, cadmium, nickel, and other toxic metals. Provocation with both gives a fuller picture of overall metal burden. Patients with GST enzyme abnormalities may also receive glutathione to expedite excretion of chelated metal. For unknown reasons, patients with GST polymorphisms tend to excrete mercury later in their course of treatment than other heavy metals [131]; this can sometimes produce early false negatives for mercury, due to preferential excretion of lead and other metals. All effective chelation protocols call for replacement of beneficial minerals, which are also removed by EDTA and DMPS.

There are currently no consensus criteria for the diagnosis of mercury overload, nor for overload of other toxic metals. Clinicians who specialize in this area generally consider a provoked urine metal output more than 2 standard deviations above the NHANES reference range a positive result.

Further research is required to clarify the relation between provoked urine results and clinical disease and to document clinical outcomes.

References

1. Environmental Health Department, Ministry of the Environment. Minimata Disease: The History and Measures. Tokyo, Japan: Ministry of the Environment, Government of Japan; 2002. [Google Scholar]2. Bakir F, Damluji SF, Amin Zaki I. Methylmercury poisoning in Iraq: an interuniversity report. Science. 1973;181(4096):230–241. [PubMed] [Google Scholar]3. Skerfving SB, Copplestone JF. Poisoning caused by the consumption of organomercury dressed seed in Iraq. Bulletin of the World Health Organization. 1976;54(1):101–112. [PMC free article] [PubMed] [Google Scholar]4. Clarkson TW, Magos L, Cox C. Tests of efficacy of antidotes for removal of methylmercury in human poisoning during the Iraq outbreak. Journal of Pharmacology and Experimental Therapeutics. 1981;218(1):74–83. [PubMed] [Google Scholar]5. Berlin M, Zalups RK, Fowler BA. Mercury. In: Nordberg GF, Fowler BA, Nordberg M, Friberg LT, editors. Handbook on the Toxicology of Metals. 3rd edition. chapter 33. New York, NY, USA: Elsevier; 2007. [Google Scholar]6. Aposhian HV. DMSA and DMPS—water soluble antidotes for heavy metal poisoning. Annual Review of Pharmacology and Toxicology. 1983;23:193–215. [PubMed] [Google Scholar]7. World Health Organization. International Programme on Chemical Safety. Geneva, Switzerland: World Health Organization; 1991. Inorganic mercury: environmental health criteria 118. [Google Scholar]8. Richardson M. The Safety of Dental Amalgam. Canada: Minister of Health; 1996. (ISBN 0-662-24873-2). [Google Scholar]9. Boylan HM, Cain RD, Kingston HM. A new method to assess mercury emissions: a study of three coal-fired electric-generating power station configurations. Journal of the Air and Waste Management Association. 2003;53(11):1318–1325. [PubMed] [Google Scholar]10. Berglund A, Pohl L, Olsson S, Bergman M. Determination of the rate of release of intra-oral mercury vapor from amalgam. Journal of Dental Research. 1988;67(9):1235–1242. [PubMed] [Google Scholar]11. Zeitz P, Orr MF, Kaye WE. Public health consequences to mercury spills: hazardous substances emergency events surveillance system, 1993–1998. Environmental Health Perspectives. 2002;110(2):129–132. [PMC free article] [PubMed] [Google Scholar]12. Schwartz JG, Snider TE, Montiel MM. Toxicity of a family from vacuumed mercury. American Journal of Emergency Medicine. 1992;10(3):258–261. [PubMed] [Google Scholar]13. Burger J, Jeitner C, Gochfeld M. Locational differences in mercury and selenium levels in 19 species of saltwater fish from New Jersey. Journal of Toxicology and Environmental Health. 2011;74(13):863–874. [PMC free article] [PubMed] [Google Scholar]14. Kudsk FN. The influence of ethyl alcohol on the absorption of mercury vapour from the lungs in man. Acta Pharmacologica et Toxicologica. 1965;23(2):263–274. [PubMed] [Google Scholar]15. Hursh JB, Clarkson TW, Cherian MG. Clearance of mercury (Hg-197, Hg-203) vapor inhaled by human subjects. Archives of Environmental Health. 1976;31(6):302–309. [PubMed] [Google Scholar]16. Eggleston DW, Nylander M. Correlation of dental amalgam with mercury in brain tissue. The Journal of Prosthetic Dentistry. 1987;58(6):704–707. [PubMed] [Google Scholar]17. Nordberg GF, Serenius F. Distribution of inorganic mercury in the guinea pig brain. Acta Pharmacologica et Toxicologica. 1969;27(4):269–283. [PubMed] [Google Scholar]18. Clarkson TW, Magos L, Greenwood MR. The transport of elemental mercury into fetal tissues. Biology of the Neonate. 1972;21(3):239–244. [PubMed] [Google Scholar]19. Guzzi G, Grandi M, Cattaneo C, et al. Dental amalgam and mercury levels in autopsy tissues: food for thought. American Journal of Forensic Medicine and Pathology. 2006;27(1):42–45. [PubMed] [Google Scholar]20. Reinhardt JW. Side-effects: mercury contribution to body burden from dental amalgam. Advances in Dental Research. 1992;6:110–113. [PubMed] [Google Scholar]21. Björkman L, Lundekvam BF, Lægreid T, et al. Mercury in human brain, blood, muscle and toenails in relation to exposure: an autopsy study. Environmental Health. 2007;6, article 30 [PMC free article] [PubMed] [Google Scholar]22. Wenstrup D, Ehmann WD, Markesbery WR. Trace element imbalances in isolated subcellular fractions of Alzheimer’s disease brains. Brain Research. 1990;533(1):125–131. [PubMed] [Google Scholar]23. Nylander M, Friberg L, Lind B. Mercury concentrations in the human brain and kidneys in relation to exposure from dental amalgam fillings. Swedish Dental Journal. 1987;11(5):179–187. [PubMed] [Google Scholar]24. Mutter J, Curth A, Naumann J, Deth R, Walach H. Does inorganic mercury play a role in Alzheimer’s disease? A systematic review and an integrated molecular mechanism. Journal of Alzheimer’s Disease. 2010;22(2):357–374. [PubMed] [Google Scholar]25. Siblerud RL. The relationship between mercury from dental amalgam and mental health. American Journal of Psychotherapy. 1989;43(4):575–587. [PubMed] [Google Scholar]26. Clarkson TW, Gatzy J, Dalton E. UR-582. Rochester, NY, USA: Division of Radiation Chemistry and Toxicology, University of Rochester Atomic Energy Project; 1961. [Google Scholar]27. Crespo-López ME, Macêdo GL, Pereira SID, et al. Mercury and human genotoxicity: critical considerations and possible molecular mechanisms. Pharmacological Research. 2009;60(4):212–220. [PubMed] [Google Scholar]28. Frustaci A, Magnavita N, Chimenti C, et al. Marked elevation of myocardial trace elements in idiopathic dilated cardiomyopathy compared with secondary cardiac dysfunction. Journal of the American College of Cardiology. 1999;33(6):1578–1583. [PubMed] [Google Scholar]29. Matsuo N, Suzuki T, Akagi H. Mercury concentration in organs of contemporary Japanese. Archives of Environmental Health. 1989;44(5):298–303. [PubMed] [Google Scholar]30. Hahn LJ, Kloiber R, Vimy MJ, Takahashi Y, Lorscheider FL. Dental ’silver’ tooth fillings: a source of mercury exposure revealed by whole-body image scan and tissue analysis. FASEB Journal. 1989;3(14):2641–2646. [PubMed] [Google Scholar]31. Vimy MJ, Takahashi Y, Lorscheider FL. Maternal-fetal distribution of mercury released from dental amalgam fillings. American Journal of Physiology. 1990;258(4):R939–R945. [PubMed] [Google Scholar]32. Danscher G, Horsted-Bindslev P, Rungby J. Traces of mercury in organs from primates with amalgam fillings. Experimental and Molecular Pathology. 1990;52(3):291–299. [PubMed] [Google Scholar]33. Hultman P. Immunotoxicology of metals. In: Nordberg GF, Fowler BA, Nordberg M, Friberg LT, editors. Handbook on the Toxicology of Metals. 3rd edition. Amsterdam, The Netherlands: Elsevier; 2007. pp. 205–206. [Google Scholar]34. Park SH, Araki S, Nakata A, et al. Effects of occupational metallic mercury vapour exposure on suppressor-inducer (CD4+CD45RA+) T lymphocytes and CD57+CD16+ natural killer cells. International Archives of Occupational and Environmental Health. 2000;73(8):537–542. [PubMed] [Google Scholar]35. Suzuki T, Takemoto TI, Shishido S, Kani K. Mercury in human amniotic fluid. Scandinavian Journal of Work, Environment and Health. 1977;3(1):32–35. [PubMed] [Google Scholar]36. Goodman. The Pharmacological Basis of Therapeutics. 8th edition 1990. [Google Scholar]37. Norseth T, Clarkson TW. Intestinal transport of ²⁰³Hg-labeled methyl mercury chloride. Role of biotransformation in rats. Archives of Environmental Health. 1971;22(5):568–577. [PubMed] [Google Scholar]39. Jansson T. Amino acid transporters in the human placenta. Pediatric Research. 2001;49(2):141–147. [PubMed] [Google Scholar]40. Taugner R, zum Winkel K, Iravani J. The localization of mercuric chloride concentration in the rat kidney. Virchows Archiv. 1966;340(4):369–383. [PubMed] [Google Scholar]41. Cherian MG, Clarkson TW. Radioactive mercury distribution in biological fluids and excretion in human subjects after inhalation of mercury vapor. Archives of Environmental Health. 1978;33(3):109–114. [PubMed] [Google Scholar]42. Berlin M, Ullberg S. Accumulation and retention of mercury in the mouse. I. An autoradiographic study after a single intravenous injection of mercuric chloride. Archives of Environmental Health. 1963;6:589–601. [PubMed] [Google Scholar]43. Björnberg KA, Vahter M, Berglund B, Niklasson B, Blennow M, Sandborgh-Englund G. Transport of methylmercury and inorganic mercury to the fetus and breast-fed infant. Environmental Health Perspectives. 2005;113(10):1381–1385. [PMC free article] [PubMed] [Google Scholar]44. Rahola T, Hattula T, Lorolainen A. The Elimination of ²⁰³Hg-methylmercury in man. Scandinavian Journal of Clinical and Laboratory Investigation. 1971;27(supplement 116):p. 77. [Google Scholar]45. Kershaw TG, Clarkson TW, Dhahir PH. The relationship between blood levels and dose of methylmercury in man. Archives of Environmental Health. 1980;35(1):28–36. [PubMed] [Google Scholar]46. Suda I, Takahashi H. Degradation of methyl and ethyl mercury into inorganic mercury by other reactive oxygen species besides hydroxyl radical. Archives of Toxicology. 1992;66(1):34–39. [PubMed] [Google Scholar]47. Berglund M, Lind B, Björnberg KA, Palm B, Einarsson O, Vahter M. Inter-individual variations of human mercury exposure biomarkers: a cross-sectional assessment. Environmental Health. 2005;4, article 20 [PMC free article] [PubMed] [Google Scholar]48. Nierenberg DW, Nordgren RE, Chang MB, et al. Delayed cerebellar disease and death after accidental exposure to dimethylmercury. New England Journal of Medicine. 1998;338(23):1672–1676. [PubMed] [Google Scholar]49. Berlin M. In: Dental Materials and Health. Lidmark A, editor. Stockholm: Statens Offentliga Utredningar; 2003. pp. 17–57. [Google Scholar]50. Garnier R, Fuster JM, Conso F. Acute mercury vapour poisoning. Toxicological European Research. 1981;3(2):77–86. [PubMed] [Google Scholar]51. Friberg L, Nordberg GF, editors. Mercury in the Environment. Boca Raton, Fla, USA: CRC Press; 1972. [Google Scholar]52. Baldi G, Vigliani EC, Zurlo N. Mercury poisoning in hat industry. La Medicina del Lavoro. 1953;44(4):160–199. [PubMed] [Google Scholar]53. Barnes JL, McDowell EM, McNeil JS. Studies on the pathophysiology of acute renal failure. V. Effect of chronic saline loading on the progression of proximal tubular injury and functional impairment following administration of mercuric chloride in the rat. Virchows Archiv Abteilung B Cell Pathology. 1980;32(3):233–260. [PubMed] [Google Scholar]54. de Vos G, Abotaga S, Liao Z, Jerschow E, Rosenstreich D. Selective effect of mercury on Th3-type cytokine production in humans. Immunopharmacology and Immunotoxicology. 2007;29(3-4):537–548. [PubMed] [Google Scholar]55. Ilback NG, Sundberg J, Oskarsson A. Methyl mercury exposure via placenta and milk impairs natural killer (NK) cell function in newborn rats. Toxicology Letters. 1991;58(2):149–158. [PubMed] [Google Scholar]56. Ellingsen DG, Efskind J, Haug E, Thomassen Y, Martinsen I, Gaarder PI. Effects of low mercury vapour exposure on the thyroid function in chloralkali workers. Journal of Applied Toxicology. 2000;20(6):483–489. [PubMed] [Google Scholar]57. Rao MV, Sharma PSN. Protective effect of vitamin E against mercuric chloride reproductive toxicity in male mice. Reproductive Toxicology. 2001;15(6):705–712. [PubMed] [Google Scholar]58. Nadorfy-Lopez E, Torres SH, Finol H, Mendez M, Bello B. Skeletal muscle abnormalities associated with occupational exposure to mercury vapours. Histology and Histopathology. 2000;15(3):673–682. [PubMed] [Google Scholar]59. Gruenwedel DW, Lu DS. Changes in the sedimentation characteristics of DNA due to methylmercuration. Biochemical and Biophysical Research Communications. 1970;40(3):542–548. [PubMed] [Google Scholar]60. Herman SP, Klein R, Talley FA, Krigman MR. An ultrastructural study of methylmercury-induced primary sensory neuropathy in the rat. Laboratory Investigation. 1973;28(1):104–118. [PubMed] [Google Scholar]61. Fowler BA, Woods JS. Ultrastructural and biochemical changes in renal mitochondria during chronic oral methyl mercury exposure. The relationship to renal function. Experimental and Molecular Pathology. 1977;27(3):403–412. [PubMed] [Google Scholar]62. Olivieri G, Brack C, Müller-Spahn F, et al. Mercury induces cell cytotoxicity and oxidative stress and increases β-amyloid secretion and tau phosphorylation in SHSY5Y neuroblastoma cells. Journal of Neurochemistry. 2000;74(1):231–236. [PubMed] [Google Scholar]63. Yee S, Choi BH. Oxidative stress in neurotoxic effects of methylmercury poisoning. NeuroToxicology. 1996;17(1):17–26. [PubMed] [Google Scholar]64. Ilback NG, Sundberg J, Oskarsson A. Methyl mercury exposure via placenta and milk impairs natural killer (NK) cell function in newborn rats. Toxicology Letters. 1991;58(2):149–158. [PubMed] [Google Scholar]65. Park SH, Araki S, Nakata A, et al. Effects of occupational metallic mercury vapour exposure on suppressor-inducer (CD4+CD45RA+) T lymphocytes and CD57+CD16+ natural killer cells. International Archives of Occupational and Environmental Health. 2000;73(8):537–542. [PubMed] [Google Scholar]66. Santarelli L, Bracci M, Mocchegiani E. In vitro and in vivo effects of mercuric chloride on thymic endocrine activity, NK and NKT cell cytotoxicity, cytokine profiles (IL-2, IFN-γ, IL-6): role of the nitric oxide-l-arginine pathway. International Immunopharmacology. 2006;6(3):376–389. [PubMed] [Google Scholar]67. Vimercati L, Santarelli L, Pesola G, et al. Monocyte-macrophage system and polymorphonuclear leukocytes in workers exposed to low levels of metallic mercury. Science of the Total Environment. 2001;270(1–3):157–163. [PubMed] [Google Scholar]68. de Vos G, Abotaga S, Liao Z, Jerschow E, Rosenstreich D. Selective effect of mercury on Th3-type cytokine production in humans. Immunopharmacology and Immunotoxicology. 2007;29(3-4):537–548. [PubMed] [Google Scholar]69. Tanigawa T, Takehashi H, Nakata A. Naïve (CD4+CD45RA+) T cell subpopulation is susceptible to various types of hazardous substances in the workplace. International journal of immunopathology and pharmacology. 2004;17(supplement 2):109–114. [PubMed] [Google Scholar]70. Gruenwedel DW, Cruickshank MK. Effect of methylmercury(II) on the synthesis of deoxyribonucleic acid, ribonucleic acid and protein in HeLa S3 cells. Biochemical Pharmacology. 1979;28(5):651–655. [PubMed] [Google Scholar]71. Friberg L, Nordberg GF, editors. Mercury in the Environment. Boca Raton, Fla, USA: CRC Press; 1972. [Google Scholar]72. Andersen A, Ellingsen DG, Morland T, Kjuus H. A neurological and neurophysiological study of chloralkali workers previously exposed to mercury vapour. Acta Neurologica Scandinavica. 1993;88(6):427–433. [PubMed] [Google Scholar]73. Smith PJ, Langolf GD, Goldberg J. Effects of occupational exposure to elemental mercury on short term memory. British Journal of Industrial Medicine. 1983;40(4):413–419. [PMC free article] [PubMed] [Google Scholar]74. Cavalleri A, Belotti L, Gobba F, Luzzana G, Rosa P, Seghizzi P. Colour vision loss in workers exposed to elemental mercury vapour. Toxicology Letters. 1995;77(1–3):351–356. [PubMed] [Google Scholar]75. Echeverria D, Heyer NJ, Martin MD, Naleway CA, Woods JS, Bittner Jr. AC. Behavioral effects of low-level exposure to Hg° among dentists. Neurotoxicology and Teratology. 1995;17(2):161–168. [PubMed] [Google Scholar]76. Kosan C, Topaloglu AK, Ozkan B. Chronic mercury intoxication simulating pheochromocytoma: effect of captopril on urinary mercury excretion. Pediatrics International. 2001;43(4):429–430. [PubMed] [Google Scholar]77. Siblerud RL, Motl J, Kienholz E. Psychometric evidence that mercury from silver dental fillings may be an etiological factor in depression, excessive anger, and anxiety. Psychological Reports. 1994;74(1):67–80. [PubMed] [Google Scholar]78. Salonen JT, Seppanen K, Nyyssonen K, et al. Intake of mercury from fish, lipid peroxidation, and the risk of myocardial infarction and coronary, cardiovascular, and any death in Eastern Finnish men. Circulation. 1995;91(3):645–655. [PubMed] [Google Scholar]79. Chan HM, Egeland GM. Fish consumption, mercury exposure, and heart diseases. Nutrition Reviews. 2004;62(2):68–72. [PubMed] [Google Scholar]80. Booth S, Zeller D. Mercury, food webs, and marine mammals: implications of diet and climate change for human health. Environmental Health Perspectives. 2005;113(5):521–526. [PMC free article] [PubMed] [Google Scholar]81. Grandjean P, Weihe P, White RF, et al. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury. Neurotoxicology and Teratology. 1997;19(6):417–428. [PubMed] [Google Scholar]82. Ramirez GB, Pagulayan O, Akagi H, et al. Tagum study II: follow-up study at two years of age after prenatal exposure to mercury. Pediatrics. 2003;111(3):289–295. [PubMed] [Google Scholar]83. Aitio A, Valkonen S, Kivisto H, Yrjanheikki E. Effect of occupational mercury exposure on plasma lysosomal hydrolases. International Archives of Occupational and Environmental Health. 1983;53(2):139–147. [PubMed] [Google Scholar]84. Berlin M, Fazackerley J, Nordberg G. The uptake of mercury in the brains of mammals exposed to mercury vapor and to mercuric salts. Archives of Environmental Health. 1969;18(5):719–729. [PubMed] [Google Scholar]85. Berlin M, Gibson S. Renal uptake, excretion, and retention of mercury. I. A study in the rabbit during infusion of mercuric chloride. Archives of Environmental Health. 1963;6:617–625. [PubMed] [Google Scholar]86. Drasch G, Wanghofer E, Roider G. Are blood, urine, hair, and muscle valid biomonitors for the internal burden of men with the heavy metals mercury, lead and cadmium? An investigation on 150 deceased. Trace Elements in Medicine. 1997;14(3):116–123. [Google Scholar]87. Smith RG, Vorwald AJ, Patil LS, Mooney TF. Effects of exposure to mercury in the manufacture of chlorine. American Industrial Hygiene Association journal. 1970;31(6):687–700. [PubMed] [Google Scholar]88. Centers for Disease Control and Prevention; 2005. 3rd National report on human exposure to environmental chemicals. Tech. Rep. [Google Scholar]89. Haut MW, Morrow LA, Pool D, Callahan TS, Haut JS, Franzen MD. Neurobehavioral effects of acute exposure to inorganic mercury vapor. Applied Neuropsychology. 1999;6(4):193–200. [PubMed] [Google Scholar]90. Chaffin DB, Dinman DB, Miller JM, et al. Tech. Rep. contract no HSM-099-71-62. Ann Arbor, Mich, USA: University of Michigan; 1973. Final report NIOSH. [Google Scholar]91. Meyer-Baron M, Schaeper M, Seeber A. A meta-analysis for neurobehavioural results due to occupational mercury exposure. Archives of Toxicology. 2002;76(3):127–136. [PubMed] [Google Scholar]92. Lucchini R, Cortesi I, Facco P, et al. Neurotoxic effect of exposure to low doses of mercury. Medicina del Lavoro. 2002;93(3):202–214. [PubMed] [Google Scholar]93. Echeverria D, Vasken Aposhian H, Woods JS, et al. Neurobehavioral effects from exposure to dental amalgam Hg⁰: new distinctions between recent exposure and Hg body burden. FASEB Journal. 1998;12(11):971–980. [PubMed] [Google Scholar]94. Roels HA, Hoet P, Lison D. Usefulness of biomarkers of exposure to inorganic mercury, lead, or cadmium in controlling occupational and environmental risks of nephrotoxicity. Renal Failure. 1999;21(3-4):251–262. [PubMed] [Google Scholar]95. Rice DC. The US EPA reference dose for methylmercury: sources of uncertainty. Environmental Research. 2004;95(3):406–413. [PubMed] [Google Scholar]96. Kazantzis G. Mercury exposure and early effects: an overview. Medicina del Lavoro. 2002;93(3):139–147. [PubMed] [Google Scholar]97. Aposhian HV, Arroyo A, Cebrian ME, et al. DMPS-arsenic challenge test. I: increased urinary excretion of monomethylarsonic acid in humans given dimercaptopropane sulfonate. Journal of Pharmacology and Experimental Therapeutics. 1997;282(1):192–200. [PubMed] [Google Scholar]98. Kazantzis G. Diagnosis and treatment of metal poisoning—general aspects. In: Nordberg GF, editor. Handbook on The Toxicology of Metals. 3rd edition. chapter 15. New York, NY, USA: Elsevier; 2007. pp. 313–314. [Google Scholar]99. Schiele VR, Schaller KH, Weltle D. Aus dem Institut fur Arbeits-und Sozialmedizin und der Poliklinik fur Berufskrankheiten de Universitat Erlangen-Nurnberg. 1989:249–251. [Google Scholar]100. Godfrey M, Campbell N. Confirmation of mercury retention and toxicity using 2,3 dimercapto-1-propane sulphonic acid sodium salt (DMPS) Journal of Advancement in Medicine. 1994;7(1):19–30. [Google Scholar]101. Daunderer M. Mobilization test for environmental metal poisonings. Forum des Praktischen und Allgemein-Arztes. 1989;28(3):88–94. [Google Scholar]102. Molin M, Schutz A, Skerfving S, Sallsten G. Mobilized mercury in subjects with varying exposure to elemental mercury vapour. International Archives of Occupational and Environmental Health. 1991;63(3):187–192. [PubMed] [Google Scholar]103. Aaseth J, Jacobsen D, Andersen O, Wickstrom E. Treatment of mercury and lead poisonings with dimercaptosuccinic acid and sodium dimercaptopropanesulfonate. A review. Analyst. 1995;120(3):853–854. [PubMed] [Google Scholar]104. Torres-Alanis O, Garza-Ocanas L, Pineyro-Lopez A. Evaluation of urinary mercury excretion after administration of 2,3-dimercaptol-propane sulfonic acid to occupationally exposed men. Journal of Toxicology—Clinical Toxicology. 1995;33(6):717–720. [PubMed] [Google Scholar]105. Aposhian HV, Maiorino RM, Rivera M, et al. Human studies with the chelating agents, DMPS and DMSA. Journal of Toxicology—Clinical Toxicology. 1992;30(4):505–528. [PubMed] [Google Scholar]106. Maiorino RM, Dart RC, Carter DE, Aposhian HV. Determination and metabolism of dithiol chelating agents. XII. Metabolism and pharmacokinetics of sodium 2,3-dimercaptopropane-1-sulfonate in humans. Journal of Pharmacology and Experimental Therapeutics. 1991;259(2):808–814. [PubMed] [Google Scholar]107. Hurlbut KM, Maiorino RM, Mayersohn M, Dart RC, Bruce DC, Aposhian HV. Determination and metabolism of dithiol chelating agents XVI: pharmacokinetics of 2,3-dimercapto-1-propanesulfonate after intravenous administration to human volunteers. Journal of Pharmacology and Experimental Therapeutics. 1994;268(2):662–668. [PubMed] [Google Scholar]108. Aposhian HV. Mobilization of mercury and arsenic in humans by sodium 2,3-dimercapto-1-propane sulfonate (DMPS) Environmental Health Perspectives. 1998;106(4):1017–1025. [PMC free article] [PubMed] [Google Scholar]109. Aposhian HV, Maiorino RM, Gonzalez-Ramirez D, et al. Mobilization of heavy metals by newer, therapeutically useful chelating agents. Toxicology. 1995;97(1–3):23–38. [PubMed] [Google Scholar]111. Sallsten G, Barregard L, Schutz A. Clearance half life of mercury in urine after the cessation of long term occupational exposure: influence of a chelating agent (DMPS) on excretion of mercury in urine. Occupational and Environmental Medicine. 1994;51(5):337–342. [PMC free article] [PubMed] [Google Scholar]112. Torres-Alanis O, Garza-Ocanas L, Pineyro-Lopez A. Evaluation of urinary mercury excretion after administration of 2,3-dimercaptol-propane sulfonic acid to occupationally exposed men. Journal of Toxicology—Clinical Toxicology. 1995;33(6):717–720. [PubMed] [Google Scholar]113. Gonzalez-Ramirez D, Zuniga-Charles M, Narro-Juarez A, et al. DMPS (2,3-dimercaptopropane-1-sulfonate, dimaval) decreases the body burden of mercury in humans exposed to mercurous chloride. Journal of Pharmacology and Experimental Therapeutics. 1998;287(1):8–12. [PubMed] [Google Scholar]114. Böse-O’Reilly S, Drasch G, Beinhoff C, et al. The Mt. Diwata study on the Philippines 2000—Treatment of mercury intoxicated inhabitants of a gold mining area with DMPS (2,3-Dimercapto-1-propane-sulfonic acid, Dimaval®) Science of the Total Environment. 2003;307(1–3):71–82. [PubMed] [Google Scholar]115. Drasch G, Böse-O’Reilly S, Beinhoff C, Roider G, Maydl S. The Mt. Diwata study on the Philippines 1999—Assessing mercury intoxication of the population by small scale gold mining. Science of the Total Environment. 2001;267(1–3):151–168. [PubMed] [Google Scholar]116. Campbell JR, Clarkson TW, Omar MD. The therapeutic use of 2,3-dimercaptopropane-1-sulfonate in two cases of inorganic mercury poisoning. Journal of the American Medical Association. 1986;256(22):3127–3130. [PubMed] [Google Scholar]117. Pendergrass JC, Haley BE, Vimy MJ, Winfield SA, Lorscheider FL. Mercury vapor inhalation inhibits binding of GTP to tubulin in rat brain: similarity to a molecular lesion in Alzheimer diseased brain. NeuroToxicology. 1997;18(2):315–324. [PubMed] [Google Scholar]118. Fujimura M, Usuki F, Sawada M, Takashima A. Methylmercury induces neuropathological changes with tau hyperphosphorylation mainly through the activation of the c-jun-N-terminal kinase pathway in the cerebral cortex, but not in the hippocampus of the mouse brain. NeuroToxicology. 2009;30(6):1000–1007. [PubMed] [Google Scholar]119. Monnet-Tschudi F, Zurich MG, Boschat C, Corbaz A, Honegger P. Involvement of environmental mercury and lead in the etiology of neurodegenerative diseases. Reviews on Environmental Health. 2006;21(2):105–117. [PubMed] [Google Scholar]120. Aschner M, Onishchenko N, Ceccatelli S. Toxicology of alkylmercury compounds. Metal Ions in Life Sciences. 2010;7:403–423. [PubMed] [Google Scholar]121. Mutter J, Curth A, Naumann J, Deth R, Walach H. Does inorganic mercury play a role in Alzheimer’s disease? A systematic review and an integrated molecular mechanism. Journal of Alzheimer’s Disease. 2010;22(2):357–374. [PubMed] [Google Scholar]122. Johnson FO, Atchison WD. The role of environmental mercury, lead and pesticide exposure in development of amyotrophic lateral sclerosis. NeuroToxicology. 2009;30(5):761–765. [PMC free article] [PubMed] [Google Scholar]123. Yang DJ, Shi S, Zheng LF, Yao TM, Ji LN. Mercury(II) promotes the in vitro aggregation of tau fragment corresponding to the second repeat of microtubule-binding domain: coordination and conformational transition. Biopolymers. 2010;93(12):1100–1107. [PubMed] [Google Scholar]124. Centers for Disease Control and Prevention; 2005. (NHANES III) 3rd National report on human exposure to environmental chemicals. Tech. Rep. [Google Scholar]125. Centers for Disease Control and Prevention; 2009. (NHANES IV) 4th National Report on Human Exposure to Environmental Chemicals. Tech. Rep. [Google Scholar]

127. Diagnostic and Treatment Protocols for safer, effective mercury human biohazard management. Consensus Development Working Group of the International College of Integrative Medicine. 2003

128. Chelation Module. Irvine, Calif, USA: American College for Advancement in Medicine; 2010. [Google Scholar]129. Advanced Medical Education and Services Physician Association. Introduction to Clinical Metal Toxicology. San Antonio, Tex, USA: Advanced Medical Education and Services Physician Association; 2007. [Google Scholar]130. Clinician Seminar Level 1. San Diego, Calif, USA: Autism Research Institute; 2010. [Google Scholar]131. Bernhoft RA, Buttar RA. Autism: a multi-system oxidative and inflammatory disorder. Townsend Letter. 2008:86–90. [Google Scholar]

Toxic Effects of Mercury on the Cardiovascular and Central Nervous Systems

J Biomed Biotechnol. 2012; 2012: 949048.

,
^1
,*,
¹
,
²
,
³
,
⁴
,
¹
,
¹
,
¹
,
⁵
,
⁶
,
¹
,
⁷
,
⁸
and
^1
,
9

Bruna Fernandes Azevedo

¹Programa de Pós-Graduação em Ciências Fisiológicas, Universidade Federal do Espírito Santo, 29042-755 Vitória, ES, Brazil

Lorena Barros Furieri

¹Programa de Pós-Graduação em Ciências Fisiológicas, Universidade Federal do Espírito Santo, 29042-755 Vitória, ES, Brazil

Franck Maciel Peçanha

²Curso de Fisioterapia, Universidade Federal do Pampa, 97050-460 Uruguaiana, RS, Brazil

Giulia Alessandra Wiggers

³Programa de Pós-Graduação em Bioquímica, Universidade Federal do Pampa, 97050-460 Uruguaiana, RS, Brazil

Paula Frizera Vassallo

⁴Hospital Universitário Cassiano Antônio de Morais, Universidade Federal do Espírito Santo, 29040-091 Vitória, ES, Brazil

Maylla Ronacher Simões

¹Programa de Pós-Graduação em Ciências Fisiológicas, Universidade Federal do Espírito Santo, 29042-755 Vitória, ES, Brazil

Jonaina Fiorim

¹Programa de Pós-Graduação em Ciências Fisiológicas, Universidade Federal do Espírito Santo, 29042-755 Vitória, ES, Brazil

Priscila Rossi de Batista

¹Programa de Pós-Graduação em Ciências Fisiológicas, Universidade Federal do Espírito Santo, 29042-755 Vitória, ES, Brazil

Mirian Fioresi

⁵Departamento de Enfermagem, Universidade Federal do Espírito Santo, 29040-090 Vitória, ES, Brazil

Luciana Rossoni

⁶Departamento de Fisiologia e Biofísica, Universidade de São Paulo, 05508-900 São Paulo, SP, Brazil

Ivanita Stefanon

¹Programa de Pós-Graduação em Ciências Fisiológicas, Universidade Federal do Espírito Santo, 29042-755 Vitória, ES, Brazil

María Jesus Alonso

⁷Departamento de Fisiologia, Universidad Rey Juan Carlos, 28922 Alcorcón, Spain

Mercedes Salaices

⁸Departamento de Farmacología, Universidad Autónoma de Madrid, 28029 Madrid, Spain

Dalton Valentim Vassallo

¹Programa de Pós-Graduação em Ciências Fisiológicas, Universidade Federal do Espírito Santo, 29042-755 Vitória, ES, Brazil

⁹Escola Superior de Ciências da Santa Casa de Misericórdia de Vitória, EMESCAM, 29045-402 Vitória, ES, Brazil

¹Programa de Pós-Graduação em Ciências Fisiológicas, Universidade Federal do Espírito Santo, 29042-755 Vitória, ES, Brazil

²Curso de Fisioterapia, Universidade Federal do Pampa, 97050-460 Uruguaiana, RS, Brazil

³Programa de Pós-Graduação em Bioquímica, Universidade Federal do Pampa, 97050-460 Uruguaiana, RS, Brazil

⁴Hospital Universitário Cassiano Antônio de Morais, Universidade Federal do Espírito Santo, 29040-091 Vitória, ES, Brazil

⁵Departamento de Enfermagem, Universidade Federal do Espírito Santo, 29040-090 Vitória, ES, Brazil

⁶Departamento de Fisiologia e Biofísica, Universidade de São Paulo, 05508-900 São Paulo, SP, Brazil

⁷Departamento de Fisiologia, Universidad Rey Juan Carlos, 28922 Alcorcón, Spain

⁸Departamento de Farmacología, Universidad Autónoma de Madrid, 28029 Madrid, Spain

⁹Escola Superior de Ciências da Santa Casa de Misericórdia de Vitória, EMESCAM, 29045-402 Vitória, ES, Brazil

Academic Editor: Marcelo Farina

Received 2012 Apr 3; Accepted 2012 May 15.

Copyright © 2012 Bruna Fernandes Azevedo et al.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

This article has been cited by other articles in PMC.

Abstract

Environmental contamination has exposed humans to various metal agents, including mercury. This exposure is more common than expected, and the health consequences of such exposure remain unclear. For many years, mercury was used in a wide variety of human activities, and now, exposure to this metal from both natural and artificial sources is significantly increasing. Many studies show that high exposure to mercury induces changes in the central nervous system, potentially resulting in irritability, fatigue, behavioral changes, tremors, headaches, hearing and cognitive loss, dysarthria, incoordination, hallucinations, and death. In the cardiovascular system, mercury induces hypertension in humans and animals that has wide-ranging consequences, including alterations in endothelial function. The results described in this paper indicate that mercury exposure, even at low doses, affects endothelial and cardiovascular function. As a result, the reference values defining the limits for the absence of danger should be reduced.

1. History

More than 2500 A.C., the prehistoric man used the cinabrio (mercury sulfide), due to its red-gold color, to draw on cave walls and perform face painting. Subsequently, mercury has been used in the amalgamation (direct burning of metallic mercury on the gravel, promoting the separation of gold), in photography and as an antiseptic in the treatment of syphilis [1, 2].

Exposure to mercury brought harmful effects to health of humans, but changes resulting from human exposure to mercury only called the attention of the scientific society after the accidents in Japan and Iraq [3]. In Japan, a serious accident occurred resulting from the deposition of industrial waste with large quantities of mercury in the Minamata Bay. Mercury was then ingested by human through fish intake, thus triggering signs and symptoms such as ataxia, speech impairment, visual field constriction, sensory disturbance, deafness, blindness, tremors, involuntary movements, mental retardation, coma, and death. Infants whose mothers were infected developed mental retardation, peripheral neuropathy, cerebral palsy, and blindness. These changes became known as Minamata disease or Russell-Hunter syndrome [4, 5]. In Iraq, mercury poisoning occurred in 1971 when wheat grains were treated with fungicides containing organic mercury. This poisoning killed over 500 people who ate bread made with contaminated wheat [6, 7].

2. Mercury Characteristics

Mercury is characterized as a highly malleable liquid at normal temperature and pressure [8]. Its name is derived from the Latin word hydrargyrum, meaning metal that resembles liquid silver [8]. Mercury is classified into three main groups: elemental mercury, inorganic mercury, and organic mercury. Mercury exists in several forms: inorganic mercury, among which There have been the metallic mercury and mercury vapor (Hg⁰) and mercurous mercury (Hg⁺) or mercuric mercury (Hg⁺⁺) salts; organic mercury, also called organometallic, which results from a covalent bond between mercury and a carbon atom of an organic functional group such as a methyl, ethyl, or phenyl group. The biological behavior, pharmacokinetics, and clinical significance of the various forms of mercury vary according to its chemical structure [3].

2.1. Inorganic Mercury Compounds

2.1.1. Elemental Mercury or Metalic Mercury Compounds

In its liquid form, the elemental mercury (Hg⁰) is poorly absorbed and presents little health risk. However, in the vapor form, metallic mercury is readily absorbed through the lungs and can produce body damage [9–11]. Because of its soluble characteristics, elemental mercury is highly diffusible and is able to pass through cell membranes as well as the blood-brain and placental barriers to reach target organs. Once in the bloodstream, mercury undergoes catalase and peroxidase-mediated oxidation in red blood cells and tissues and is transformed into inorganic mercuric mercury (Hg⁺⁺) and mercurous mercury (Hg⁺), a process that limits its absorption [9, 12]. Inorganic mercury has low lipophilicity and thus has a limited ability to cross cell membranes [9].

Elemental mercury is used in thermometers and sphygmomanometers because of its uniform volumetric expansion, high surface tension, and lack of vitreous adherence to surfaces. Low electrical resistance and high thermal conductivity allow metallic mercury to be used in electrical and electronic materials. Because of its high oxidation power, metallic mercury is used in electrochemical operations in the chlorine and soda industries. Metallic mercury is also used in metallurgy, mining, and dentistry because of the easy amalgam formation with other metals. In addition, gold extraction with archaic and dangerous methods predispose miners to mercury poisoning. The burning of metallic mercury on the gravel promotes the separation of gold, a process called amalgamation, which causes emission of large amounts of mercury vapor that is inhaled immediately by the miner, since they do not use appropriate personal protective equipment [13, 14].

Occupational exposure to mercury vapor and the release of mercury from or during removal of amalgam dental fillings increase its blood and plasma concentration [15, 16] After exposure, blood concentrations attain 18 nmol/L [15], and after exposure to dental and removal of amalgam fillings plasma concentrations attain 5 nmol/L [17]. Occupational exposure also affects central nervous system [15] and amalgam tooth fillings impair sheep kidney function [18]. However, toxicological consequences are still a matter of debate [3, 19–23].

2.1.2. Mercurous Mercury and Mercuric Mercury Compounds

The mercurous mercury in the form of mercurous chloride (Hg₂Cl₂) is little absorbed in the body. It is believed that in the body the form of metallic mercury is changed to elemental mercury and mercuric mercury [24].

Mercuric mercury compounds, such as mercury salts, result from the combination of mercury with chlorine, sulfur, or oxygen. Mercuric mercury can be found in different states when combined with other chemical elements, including mercuric chloride (HgCl₂), which is highly toxic and corrosive; mercury sulfide (HgS), which is often used as a pigment in paints due to its red color; mercury fulminate (Hg(CNO)₂), which is used as an explosive detonator [8, 25]. Among the mercuric mercury compounds, mercuric chloride (HgCl₂) calls the attention. It was used as a preservative for development of photographic film and has been ingested accidentally or as a suicide measure [26]. As elemental mercury, the mercuric mercury in the blood stream binds to sulfhydryl groups on erythrocytes, glutathione, or metallothionein or is transported suspended in plasma [27]. Mercuric mercury accumulates in placenta, fetal tissues, and amniotic fluid, but it does not cross the blood-brain barrier efficiently [28]. Evidence exists showing the transport of mercuric mercury via one or more amino acid transporters [29]. Evidence also shows that the accumulation in the brain occurs through its binding to cysteine [24].

In the cardiovascular system, acute inorganic mercury exposition in vivo promotes reduction of myocardial force development [30] and inhibited myosin ATPase activity [31]. Chronic exposure increases vascular resistance and induces hypertension [32–34]. Numerous studies have also revealed that mercury generates oxygen free radicals mainly by activation of NAPHoxidase [35, 36].

2.2. Organic Mercury

Organic mercury compounds, also called organometallic, result from a covalent bond between mercury and the carbon [8] atom of an organic functional group such as a methyl, ethyl, or phenyl group. Methylmercury (CH₃Hg⁺) is by far the most common form of organic Hg to which humans and animals are exposed. CH₃Hg⁺ in the environment is predominantly formed by methylation of inorganic mercuric ions by microorganisms present in soil and water [37–39]. The expression methylmercury monomethylmercurial is used to denote compounds that contain the cation methylmercury (CH₃Hg⁺). Some of these compounds were used as pesticides and had medical applications as antiseptics and diuretics. The organomercury antiseptics still used are Merthiolate, Bacteran, and Thimerosal [40].

Thimerosal is an organomercurial compound that since 1930 has been widely used as a preservative in biological material such as vaccines and serums used to prevent microbiological growth [41]. Thimerosal is metabolized in the human body and degraded into ethylmercury and thiosalicylate. The chemical difference between these compounds is an important determinant of their toxicity [42, 43].

3. Forms of Mercury Exposure

Mercury is now considered an environmental pollutant of high risk to public health because of its high toxicity and mobility in ecosystems [11, 44]. Exposure to mercury can occur from both natural and artificial sources. Human activities that can result in mercury exposure include the burning of fossil fuels, chlor-alkali industries, mining, the burning of waste, and the use of coal and petroleum [10, 40, 45].

More natural sources of mercury include volcanic activity, earthquakes, erosion, and the volatilization of mercury present in the marine environment and vegetation [10, 46–48]. Mercury emitted both naturally or as a result of human activity is primarily found as inorganic metal vapor (Hg⁰) [49]. Among the natural sources of mercury, the largest emissions are from the degassing of the earth’s crust. More than five tons of mercury is estimated to be released into the sea every year as a result of erosion and geochemical cycles [50].

Mercury contaminates the environment through a cycle involving the initial emission, the subsequent atmospheric circulation of the vapor form, and the eventual return of mercury to the land and water via precipitation () [46]. The emission of mercury is an important part of this cycle of contamination and can occur through natural processes or as a result of human activities, as mentioned above [48].

Cycle of mercury in the environment. Modified from Azevedo and Chasin 2003 [53]. Scheme demonstrating constant flow of mercury compounds in the hydrosphere, lithosphere, atmosphere, and biosphere.

Mercury present in seas and rivers after methylation can contaminate fish [51, 52]. The consumption of fish contaminated with mercury is a major source of mercury exposure in the Amazon basin. Studies show that the concentration of mercury in the muscles of fish that are widely consumed in the Amazon region are greater than the limit set by WHO (World Health Organization) as safe for human consumption (0.5 g/kg) [4, 10].

4. Transport and Elimination of Mercury

Inhaled elemental mercury vapor, for example, is readily absorbed through mucous membranes and the lung and is rapidly oxidized but not as quickly as to prevent the deposition of considerable amount in the brain [54]. Methylmercury is easily absorbed through the gut, and it is deposited in most tissue but does not cross the blood-brain barrier as efficiently as elemental mercury. However, to enter the brain, it is progressively demethylated to elemental mercury () [24]. Mercury salts, in contrast, tend to be insoluble, relatively stable, and hardly absorbed.

Scheme showing the entry of organic mercury in organisms and their distribution in different organs.

Then, toxicity for man varies depending on the form of mercury, dose, and rate of exposure. The target organ for inhalted mercury vapor is primarily the brain [24]. Mercurous and mercury salts especially damage the lining of the intestine and kidneys [5], and as methyl mercury, it is widely distributed throughout the body () [24]. Toxicity varies with dosage; a large acute exposure to elemental mercury vapor induces severe pneumonia, which in extreme cases can be fatal [24]. Low level of chronic exposure to elemental or other forms of mercury induces more subtle symptoms and clinical findings [3].

Scheme showing the entry of elemental mercury in organisms and their distribution in different organs.

Oxidized mercury binds strongly to SH groups; this reaction can inactivate enzymes, lead to tissue damage and interfere with various metabolic processes [55–57]. Ingested methylmercury is almost completely absorbed and transported into the bloodstream [10]. Methylmercury enters cells mainly by forming a complex with L-cysteine and homocysteine and is eliminated in conjunction with glutathione [58]. After absorption, it is distributed primarily to the central nervous system and kidneys. Methylmercury elimination usually occurs in the urine and feces [59].

5. Doses of Mercury and Safety Legislation

The chemical form of mercury in the air affects its time of permanence and its dispersion in the atmosphere. The elemental mercury form can persist for more than four years in the air, while its compounds are deposited in a short time at locations near their origin. In the northern hemisphere, their average concentration in the atmosphere is estimated at 2 ng/m³  and in the southern hemisphere is less than 1 ng/m³. In urban areas, there is a great variability of these concentrations being found up to 67 ng/m³  with a mean of 11 ng/m³  in Japan [53]. FUNASA (Fundação Nacional de Saúde) standards of mercury in the air consider a mean of 1 ng/m³  in the period of one year [60].

In 2004, the Joint FAO (Food and Agriculture Organization of the United National)/WHO Expert Committee on Food Additives (JECFA) established that the safe concentration of methylmercury intake, without the appearance of neurological disorders, is 1.6 mg/kg of body weight. However, in 2006, JECFA stated that this concentration is not safe for intrauterine exposure, because fetuses are more sensitive to the onset of neurological disorders after exposure to methylmercury [61].

Currently, the general population is exposed to mercury by the following main sources: the consumption of contaminated fish, the use and manipulation of dental amalgam, thimerosal contained in vaccines, workers in industries of chlorine, caustic soda, miners, and workers in industries of fluorescent lamps [62, 63]. Each of these sources of exposure contains specific toxicological characteristics [64].

In Brazil, the rules for vaccination of the Ministry of Health, published in June 2001, shows that thimerosal is used in many vaccines. These vaccines prevent flu (influenza vaccine), rabies (rabies vaccine), infection with meningococcus serogroup b, and hepatitis B [65].

The US Environmental Protection Agency’s recommended a reference blood concentration of mercury to be 5.8 ng/mL; concentrations below this level are considered to be safe [66, 67]. Some studies have reported that the blood mercury concentration in the control population is approximately 1 ng/mL. On the other hand, levels of 7–10 ng/mL have been reported in workers exposed to mercury or in residents of Guizhou (China), an area that is known to suffer mercury contamination [68, 69]. In a recent biomonitoring study in New York City, the blood mercury concentration was found to be 2.73 ng/mL, and levels reached 5.65 ng/mL in adults that consumed fish regularly [70].

WHO [10] states that an allowable concentration of mercury in human hair is less than 6 μg/g. In the Amazon basin, where fish is the main source of dietary protein, mercury concentrations in hair reached up to 150 μg/g. Furthermore, only two of 40 cities studied have average mercury concentrations below the recommended amount [10, 71]. In individuals who have amalgam, the daily release of mercury amalgam is approximately 4-5 μg/day, and a positive correlation exists between the blood concentration of mercury and the number of amalgams. It is estimated that each dental amalgam releases 3–17 μg mercury vapor per day and that the blood concentration of mercury after removal of the restoration can reach 5 nmol/L [72–74]. However, even at concentrations below recommended levels, there is strong evidence that exposure to ethyl mercury, the major component of thimerosal, is associated with the onset of neurological and heart disorders in children [75].

In the following sections, we will describe results obtained from animals with chronic and acute exposure to mercury. Some of these studies were performed with mercury exposure protocols that led to blood concentrations slightly above the reference values. Nevertheless, these concentrations could be easily found in exposed populations and may even be considered low when compared with concentrations in humans who consume large amounts of fish or who live in areas contaminated with mercury.

6. Effect of Mercury on the Central Nervous System (CNS)

Among the compounds of mercury, the methylmercury is primarily responsible for the neurological alterations present in humans and experimental animals. It is believed that the mechanisms are related to the toxic increase in reactive oxygen species (ROS). Oxidative stress is associated with the etiology of neurodegenerative diseases such as amyotrophic lateral sclerosis, Parkinson’s disease, and Alzheimer’s disease [54, 55], but these mechanisms have yet to be fully recognized.

Reinforcing the hypothesis that the majority of injuries caused by methylmercury (MeHg) in the central nervous system are related to its ability to increase reactive oxygen species, Zhang et al. (2009) [20] reported that after pretreatment of bovine cells with pyrroloquinoline quinone (PQQ), an antioxidant, the cytotoxicity induced by MeHg is significantly attenuated. PQQ reduces the percentage of apoptotic cells, decreased significantly ROS production, suppressed lipid peroxidation, and increased antioxidant enzyme activity in cells exposed to MeHg. Furthermore, the protective effects elicited by an antioxidant (ebselen) strengthen the idea that seleno-organic compounds represent promising approaches to neutralize MeHg-induced neurotoxicity [19].

Studies also demonstrate that mercury has the ability to reduce the number of neuron and cytoarchitecture in individuals with prenatal exposure to mercury [76, 77]. In animal models, some of these symptoms are reproduced. Low-dose prenatal exposure to methylmercury during 10 gestational days impairs motor and mnemonic function in adult mice [23]. This hypothesis is supported by studies that describe methylmercury inhibition of cell division and migration both “in vivo” and “in vitro” [76–78].

In addition, because of its high affinity for sulfhydryl groups in tubulin, methylmercury inhibits the organization of microtubules that are important in CNS development [79–81]. The binding to SH groups also interferes with the intracellular signaling of multiple receptors (e.g., muscarinic, nicotinic, and dopaminergic) and promotes the blockade of Ca⁺⁺ channels in neurons [82, 83]. In addition, inorganic mercury has the ability to increase the permeability of chloride channels of GABA A receptors in the dorsal root ganglion, which is associated with neuronal hyperpolarization [84].

Corroborating these findings, the study conducted by Maia et al., (2010) [21] demonstrates that the poisoning by methylmercury changes the nitrergic activities of adult mice, and the predominance of alterations may be related to different locations. Besides increasing the nitrergic activity methylmercury and mercuric chloride also have the ability to increase the release of neurotransmitters such as acetylcholine, dopamine, norepinephrine, and serotonin. Similar findings have also been reported to be a mechanism implicated in the effects of methylmercury and HgCl₂ on the central nervous system function [85–89].

Halbach et al. [90] studied a correlation in Iraqi children between the level of maternal exposure to methylmercury during pregnancy and psychomotor retardation. Sandborgh-Englund et al. [91] corroborated this finding in children from the Faroe Islands; they found that children exposed to mercury in the prenatal period had defects in attention, memory, language, and motor function. In addition, exposure to methylmercury in pregnant women or early childhood leads to changes in the CNS development of the fetus or child, respectively [50, 92, 93]. Thereupon, changes caused by mercury poisoning result in significant clinical deficit in motor skills, coordination, and general activity rate of cognitive and psychological disorders [23].

7. Effect of Mercury on the Cardiovascular

System

For decades, the toxic effects of mercury were associated mainly with the central nervous system; however, inorganic mercury also produces profound cardiotoxicity [94–99]. Halbach and collaborators [100] showed that mercury concentrations in hair reached up to 150 μg/g in populations living in the Amazon basin. Furthermore, nearly all of the inhabitants of 40 cities studied have blood concentrations above the reference values. In this population, it has been demonstrated that exposure to mercury by frequent consumption of fish has a strong positive correlation with increased arterial blood pressure [101]. Other studies also correlate mercury exposure with increased risk of hypertension, myocardial infarction, coronary dysfunction, and atherosclerosis [102–105]. Data presented by Yoshizawa et al. [106] showed that mercury exposure was associated with the progression of atherosclerosis and an increased risk of developing cardiovascular disease. Houston [107] followed patients for approximately 13.9 years and found an association between the concentration of mercury in the hair and the risk of developing cardiovascular events or dying from cardiovascular disease and other causes.

Mercury levels are predictors of the levels of oxidized low-density lipoprotein (LDL) [106]. Oxidized LDL particles are frequently found in atherosclerotic lesions and are associated with the development of atherosclerotic disease [107, 108] and acute coronary insufficiency [109]. Another mechanism by which mercury exerts toxic effects on the cardiovascular system is through the inactivation of the “paraoxonase” [110], an enzyme that slows the LDL oxidation process and that has an important antiatherosclerotic action [101].

The mechanism by which mercury produces toxic effects on the cardiovascular system is not fully elucidated, but this mechanism is believed to involve an increase in oxidative stress. Exposure to mercury increases the production of free radicals, potentially because of the role of mercury in the Fenton reaction [111–113] and a reduction in the activity of antioxidant enzymes, such as glutathione peroxidase. The MeHg reaction with the glutathione peroxidase occurs via thiol (–SH) and/or selenol (–SeH) groups from endogenous molecules [114]. Even though there are 4 of glutathione molecules containing selene in their active sites, only the cytoplasmic glutathione peroxidase 1 (GPx 1) changes hydrogen peroxide to water [115, 116].

The reduction in glutathione peroxidase with selenium-dependent activity is the result of the decreased bioavailability of selenium, a molecule that is required for enzymatic activity [117–119]. The high affinity of mercury to the thiol group can lead to decreased glutathione peroxidase selenium-dependent activity. Other antioxidant enzymes which participate against reactive oxygen species due to mercury intoxication are catalase and superoxide dismutase. The increment of ROS and reduction of the antioxidant activity increase the risk of developing cardiovascular disease [118, 120, 121].

Sherwani et al. (2011) [122] showed that MeHg has the capacity to induce phospholipase D (PLD) activation through oxidative stress and thiol-redox alterations. They investigated the mechanism of the MeHg-induced PLD activation through the upstream regulation by phospholipase A₂ (PLA₂) and lipid oxygenases such as cyclooxygenase (COX) and lipoxygenase (LOX) in the bovine pulmonary artery endothelial cells. Their results showed that MeHg significantly activates both PLA₂ and PLD. MeHg also induces the formation of COX- and LOX-catalyzed eicosanoids in endothelial cells.

Cardiovascular changes resulting from mercury poisoning are also described in animal models. However, the mechanism involved in the effects of mercury on the cardiovascular system is not fully understood but seems to be dependent on both the dose and time of exposure. Raymond and Ralston [123] studied the hemodynamic effects of an intravenous injection of HgCl₂ (5 mg/kg) in rats and observed that mercury produced cardiac diastolic failure and pulmonary hypertension. Moreover, Naganuma et al. [124] reported that acute exposure to HgCl₂ (680 ng/kg) increased blood pressure, heart rate, and vascular reactivity to phenylephrine in rats; this increased reactivity seems to depend on an increased generation of free radicals. Perfused hearts from animals exposed acutely to HgCl₂ showed a reduction in left ventricular systolic pressure, heart rate, and atrioventricular conduction delay [125, 126].

Our group has found that chronic exposure to low doses of mercury (1st dose 4.6 μg/kg followed by 0.07 μg/kg/day for 30 days, im) attained a blood mercury concentration of approximately 8 ng/mL, a concentration similar to the levels found in exposed humans. This exposure produced a negative inotropic effect in perfused hearts, although increasing myosin ATPase activity. In vivo, arterial or ventricular pressures did not change [127]. The reduction in contractility was explained by alterations in calcium-handling mechanisms; protein expression of SERCA, Na⁺ K⁺ ATPase (NKA), and sodium/calcium exchanger (NCX) was diminished; phospholamban (PLB) expression was increased; the response to β-adrenergic stimulation was reduced following mercury exposure [128, 129].

The chronic exposure to low concentrations of mercury was also able to induce endothelial dysfunction in resistance and conductance vessels, most likely because of the decreased nitric oxide (NO) bioavailability due to the increased superoxide anion (O₂^•−) production from NADPH oxidase [36, 130, 131]. This study was evidenced by the following effects of mercury treatment observed in aorta, coronary, and mesenteric arteries: (1) the endothelium-dependent vasodilator response induced by acetylcholine (ACh) was decreased [36, 130]; (2) vasoconstrictor responses to phenylephrine or serotonin were increased, and NO endothelial modulation of these responses was decreased [36, 130, 131]; (3) vascular superoxide anion production, the expression of SOD-2, NOX-1, and NOX-4 (two main isoforms of NADPH oxidase), plasmatic malondialdehyde levels, and plasmatic antioxidant status were all increased [36, 130]; (4) both the superoxide anion scavenger SOD and the NADPH oxidase inhibitor apocynin restored the NO endothelial modulation of vasoconstrictor responses and the impaired ACh-induced vasodilatation in vessels from the mercury-treated rats [36, 130]. We also observed that mercury treatment increased the participation of COX-2-derived vasoconstrictor prostanoids in vasoconstrictor responses [132]. Other researchers have also observed a selective loss of NO-mediated vasodilatation with no effect on the EDHF-mediated component of relaxation, implying that chronic mercury exposure selectively impairs the NO pathway as a consequence of oxidative stress, while EDHF is able to maintain endothelium-dependent relaxation at a reduced level [133]. On the other hand, using this low dose of mercury, Blanco-Rivero et al. [134] observed an increase in vasoconstriction responses to electrical field stimulation mediated by alterations of adrenergic and nitrergic function in rat mesenteric arteries. HgCl₂ reduced neuronal NO bioavailability, most likely as a result of reduced nNOS (neuronal nitric oxide synthase) activity and increased O₂⁻ production as well as increased noradrenaline release and vasoconstrictor response. It is important to emphasize, regarding chronic low-dose exposure to mercury for 30 days, that although rats grow normally and have no changes in arterial blood pressure, endothelial function is already blunted affecting vascular reactivity [36, 131].

Taken together, these data show that chronic low doses of mercury have an important and deleterious effect on vascular function by reducing NO bioavailability. The degree of severity of mercury exposure is comparable to traditional cardiovascular risk factors, such as hypertension diabetes or hypercholesterolemia. Therefore, mercury could be considered an important risk factor for cardiovascular disease that could play a role in the development of cardiovascular events. The association between mercury exposure and an increased risk of developing cardiovascular and neurological diseases is apparent. Thus, continuous exposure to mercury can be dangerous, and current reference values, once considered to be without risk, should be reevaluated and reduced.

Acknowledgments

These studies were supported by Grants from CAPES and CNPq/FAPES/FUNCITEC (39767531/07), Brazil and MCINN and MECD (SAF 2009-07201, RD06/0014/0011, and PHB2011-0001-PC) and Banco Santander, Spain. All participants of the group who performed experiments that were used in this paper are listed as authors. Dr. M. Salaices and Dr. M. J. Alonso advised several students of the group during their Doctoral Sandwich Program in the Universidade Autonóma de Madrid, Spain.

References

1. Hylander LD, Meili M. 500 Years of mercury production: global annual inventory by region until 2000 and associated emissions. Science of the Total Environment. 2003;304(1–3):13–27. [PubMed] [Google Scholar]2. Ekino S, Susa M, Ninomiya T, Imamura K, Kitamura T. Minamata disease revisited: an update on the acute and chronic manifestations of methyl mercury poisoning. Journal of the Neurological Sciences. 2007;262(1-2):131–144. [PubMed] [Google Scholar]3. Bernhoft RA. Mercury toxicity and treatment: a review of the literature. Journal of Environmental and Public Health. 2012;2012:10 pages.460508 [PMC free article] [PubMed] [Google Scholar]4. Gochfeld M. Cases of mercury exposure, bioavailability, and absorption. Ecotoxicology and Environmental Safety. 2003;56(1):174–179. [PubMed] [Google Scholar]5. Takeuchi T, Eto K, Kinjo Y, Tokunaga H. Human brain disturbance by methylmercury poisoning, focusing on the long- term effect on brain weight. NeuroToxicology. 1996;17(1):187–190. [PubMed] [Google Scholar]6. Bakir F, Damluji SF, Amin Zaki I. Methylmercury poisoning in Iraq: an interuniversity report. Science. 1973;181(4096):230–241. [PubMed] [Google Scholar]7. Clarkson TW. Molecular and ionic mimicry of toxic metals. Annual Review of Pharmacology and Toxicology. 1993;33:545–571. [PubMed] [Google Scholar]9. Houston MC. The role of mercury and cadmium heavy metals in vascular disease, hypertension, coronary heart disease, and myocardial infarction. Alternative Therapies in Health and Medicine. 2007;13(2):S128–S133. [PubMed] [Google Scholar]11. Mesquita RCDCM, Bueno MIMS, Jardim WDF, Jardim WDF. Compostos de mercúrio. Revisão de métodos de determinação, tratamento e descarte. Quimica Nova. 2000;23(4):487–495. [Google Scholar]12. Roulet M, Lucotte M, Canuel R, et al. Distribution and partition of total mercury in waters of the Tapajos River Basin, Brazilian Amazon. Science of the Total Environment. 1998;213(1–3):203–211. [Google Scholar]13. Nriagu JO, Pfeiffer WC, Malm O, Magalhaes De Souza CM, Mierle G. Mercury pollution in Brazil. Nature. 1992;356(6368, article 389) [PubMed] [Google Scholar]14. Pestana MHD, Formoso MLL. Mercury contamination in Lavras do Sul, south Brazil: a legacy from past and recent gold mining. Science of the Total Environment. 2003;307(1–3):125–140. [PubMed] [Google Scholar]15. Langworth S. Exposure to mercury vapor and impact on health in the dental profession in Sweden. Journal of Dental Research. 1997;76(7):1397–1404. [PubMed] [Google Scholar]16. Halbach S, Kremers L, Willruth H, et al. Systemic transfer of mercury from amalgam fillings before and after cessation of emission. Environmental Research. 1998;77(2):115–123. [PubMed] [Google Scholar]17. Björkman L, Sandborgh-Englund G, Ekstrand J. Mercury in saliva and feces after removal of amalgam fillings. Toxicology and Applied Pharmacology. 1997;144(1):156–162. [PubMed] [Google Scholar]18. Boyd ND, Benediktsson H, Vimy MJ, Hooper DE, Lorscheider FL. Mercury from dental “silver” tooth fillings impairs sheep kidney function. American Journal of Physiology. 1991;261(4):R1010–R1014. [PubMed] [Google Scholar]19. Yin Z, Lee E, Ni M, et al. Methylmercury-induced alterations in astrocyte functions are attenuated by ebselen. NeuroToxicology. 2011;32(3):291–299. [PMC free article] [PubMed] [Google Scholar]20. Zhang P, Xu Y, Sun J, Li X, Wang L, Jin L. Protection of pyrroloquinoline quinone againts methylmercury-induced neurotoxicity via reducing oxidative stress. Free Radical Research. 2009;43(3):224–233. [PubMed] [Google Scholar]21. Maia CDSF, Ferreira VMM, Kahwage RL, et al. Adult brain nitrergic activity after concomitant prenatal exposure to ethanol and methyl mercury. Acta Histochemica. 2010;112(6):583–591. [PubMed] [Google Scholar]22. Castoldi AF, Onishchenko N, Johansson C, et al. Neurodevelopmental toxicity of methylmercury: laboratory animal data and their contribution to human risk assessment. Regulatory Toxicology and Pharmacology. 2008;51(2):215–229. [PubMed] [Google Scholar]23. Montgomery KS, Mackey J, Thuett K, Ginestra S, Bizon JL, Abbott LC. Chronic, low-dose prenatal exposure to methylmercury impairs motor and mnemonic function in adult C57/B6 mice. Behavioural Brain Research. 2008;191(1):55–61. [PubMed] [Google Scholar]24. Clarkson TW, Vyas JB, Ballatori N. Mechanisms of mercury disposition in the body. American Journal of Industrial Medicine. 2007;50(10):757–764. [PubMed] [Google Scholar]25. Mesquita RCDCM, Bueno MIMS, Jardim WDF. Compostos de mercúrio. Revisão de métodos de determinação, tratamento e descarte. Quimica Nova. 2000;23(4):487–495. [Google Scholar]26. Geier DA, Geier MR. An assessment of the impact of thimerosal on childhood neurodevelopmental disorders. Pediatric Rehabilitation. 2003;6(2):97–102. [PubMed] [Google Scholar]27. Ballatori N, Clarkson TW. Biliary secretion of glutathione and of glutathione-metal complexes. Fundamental and Applied Toxicology. 1985;5(5):816–831. [PubMed] [Google Scholar]28. Halbach S, Vogt S, Köhler W, et al. Blood and urine mercury levels in adult amalgam patients of a randomized controlled trial: interaction of Hg species in erythrocytes. Environmental Research. 2008;107(1):69–78. [PubMed] [Google Scholar]29. Grandjean P, Weihe P, White RF, et al. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury. Neurotoxicology and Teratology. 1997;19(6):417–428. [PubMed] [Google Scholar]30. Vassallo DV, Moreira CM, Oliveira EM, Bertollo DM, Veloso TC. Effects of mercury on the isolated heart muscle are prevented by DTT and cysteine. Toxicology and Applied Pharmacology. 1999;156(2):113–118. [PubMed] [Google Scholar]31. Moreira CM, Oliveira EM, Bonan CD, Sarkis JJF, Vassallo DV. Effects of mercury on myosin ATPase in the ventricular myocardium of the rat. Comparative Biochemistry and Physiology C. 2003;135(3):269–275. [PubMed] [Google Scholar]32. Carmignani M, Boscolo P, Artese L, et al. Renal mechanisms in the cardiovascular effects of chronic exposure to inorganic mercury in rats. British Journal of Industrial Medicine. 1992;49(4):226–232. [PMC free article] [PubMed] [Google Scholar]33. Wakita Y. Hypertension induced by methyl mercury in rats. Toxicology and Applied Pharmacology. 1987;89(1):144–147. [PubMed] [Google Scholar]34. Houston MC. The role of mercury and cadmium heavy metals in vascular disease, hypertension, coronary heart disease, and myocardial infarction. Alternative Therapies in Health and Medicine. 2007;13(2):S128–S133. [PubMed] [Google Scholar]35. Massaroni L, Rossoni LV, Amaral SMC, Stefanon I, Oliveira EM, Vassallo DV. Haemodynamic and electrophysiological acute toxic effects of mercury in anaesthetized rats and in Langendorff perfused rat hearts. Pharmacological Research. 1995;32(1-2):27–36. [PubMed] [Google Scholar]36. Furieri LB, Fioresi M, Junior RFR, et al. Exposure to low mercury concentration in vivo impairs myocardial contractile function. Toxicology and Applied Pharmacology. 2011;255(2):193–199. [PubMed] [Google Scholar]37. Zalups RK. Molecular interactions with mercury in the kidney. Pharmacological Reviews. 2000;52(1):113–143. [PubMed] [Google Scholar]38. Clarkson TW, Magos L. The toxicology of mercury and its chemical compounds. Critical Reviews in Toxicology. 2006;36(8):609–662. [PubMed] [Google Scholar]39. Rooney JPK. The role of thiols, dithiols, nutritional factors and interacting ligands in the toxicology of mercury. Toxicology. 2007;234(3):145–156. [PubMed] [Google Scholar]40. World Health Organization. Methyl Mercury. Vol. 1. Geneva, Switzerland: International Progranme on Chemical Safety; 1990. [Google Scholar]42. Guzzi G, La Porta CAM. Molecular mechanisms triggered by mercury. Toxicology. 2008;244(1):1–12. [PubMed] [Google Scholar]44. Johnson CL. Mercury in the environment: sources, toxicities, and prevention of exposure. Pediatric Annals. 2004;33(7):437–442. [PubMed] [Google Scholar]45. Davis LE, Kornfeld M, Mooney HS, et al. Methylmercury poisoning: long-term clinical, radiological, toxicological, and pathological studies of an affected family. Annals of Neurology. 1994;35(6):680–688. [PubMed] [Google Scholar]46. Alexandre SC. Avaliação de área contaminada por mercúrio total em descoberto [Dissertação de Mestrado] Minas Gerais, Brazil: Programa de Pós-Graduação em Engenharia Civil. Universidade Federal de Viçosa; 2006. [Google Scholar]47. Davidson PW, Myers GJ, Weiss B, Shamlaye CF, Cox C. Prenatal methyl mercury exposure from fish consumption and child development: a review of evidence and perspectives from the Seychelles Child Development Study. NeuroToxicology. 2006;27(6):1106–1109. [PubMed] [Google Scholar]48. Lindberg S, Bullock R, Ebinghaus R, et al. A synthesis of progress and uncertainties in attributing the sources of mercury in deposition. Ambio. 2007;36(1):19–32. [PubMed] [Google Scholar]49. Boening DW. Ecological effects, transport, and fate of mercury: a general review. Chemosphere. 2000;40(12):1335–1351. [PubMed] [Google Scholar]50. Swain EB, Jakus PM, Rice G, et al. Socioeconomic consequences of mercury use and pollution. Ambio. 2007;36(1):45–61. [PubMed] [Google Scholar]51. Environmental Protection Agency. Mercury Study Report to Congress. Washington, DC, USA: U.S. Environmental Protection Agency; 1997. [Google Scholar]52. Hansen JC, Danscher G. Organic mercury: an environmental threat to the health of dietary-exposed societies? Reviews on Environmental Health. 1997;12(2):107–116. [PubMed] [Google Scholar]53. Azevedo FA, Chasin AM. As Bases Toxicológicas da Ecotoxicologia. São Paulo, Brazil: São Carlos: RiMa, Atheneu/InterTox; 2003. [Google Scholar]54. Bridges CC, Zalups RK. Transport of inorganic mercury and methylmercury in target tissues and organs. Journal of Toxicology and Environmental Health—Part B. 2010;13(5):385–410. [PMC free article] [PubMed] [Google Scholar]55. Roulet M, Lucotte M, Canuel R, et al. Distribution and partition of total mercury in waters of the Tapajos River Basin, Brazilian Amazon. Science of the Total Environment. 1998;213(1–3):203–211. [Google Scholar]56. Roulet M, Lucotte M, Guimarães JRD, Rheault I. Methylmercury in water, seston, and epiphyton of an Amazonian river and its floodplain, Tapajos River, Brazil. Science of the Total Environment. 2000;261(1–3):43–59. [PubMed] [Google Scholar]57. Dórea JG, Marques RC, Brandão KG. Neonate exposure to thimerosal mercury from hepatitis B vaccines. American Journal of Perinatology. 2009;26(7):523–527. [PubMed] [Google Scholar]58. Asano S, Eto K, Kurisaki E, et al. Acute inorganic mercury vapor inhalation poisoning. Pathology International. 2000;50(3):169–174. [PubMed] [Google Scholar]59. Zalups RK, Lash LH. Advances in understanding the renal transport and toxicity of mercury. Journal of Toxicology and Environmental Health. 1994;42(1):1–44. [PubMed] [Google Scholar]60. Azevedo FA, Chasin AAM. Bases Toxicológicas da Ecotoxicologia. São Paulo, Brazil: São Carlos: RiMa, Atheneu/InterTox; 2003. [Google Scholar]61. JECFA. Methylmercury. Summary and conclusions of the 67thThe Joint FAO/WHO Expert Committee on Food Additives. Geneva, World Health Organization, International Programme on Chemical Safety. WHO Technical Report Series. 2006;(940) http://www.who.int/foodsafety/chem/en/62. Mahaffey KR. Mercury exposure: medical and public health issues. Transactions of the American Clinical and Climatological Association. 2005;116:127–154. [PMC free article] [PubMed] [Google Scholar]63. Zavariz C, Glina DM. Clinico-neuro-psychological evaluation of workers exposed to metallic mercury in the electric lamp industry. Revista de Saude Publica. 1992;26(5):356–365. [PubMed] [Google Scholar]65. Peterson C. Medical slang in Rio de Janeiro, Brasil. Cadernos de saúde pública / Ministério da Saúde, Fundação Oswaldo Cruz, Escola Nacional de Saúde Pública. 1998;14(4):671–682. [PubMed] [Google Scholar]66. Choi BH, Cho KH, Lapham LW. Effects of methylmercury on human fetal neurons and astrocytes in vitro: a time-lapse cinematographic, phase and electron microscopic study. Environmental Research. 1981;24(1):61–74. [PubMed] [Google Scholar]67. Ballatori N, Clarkson TW. Biliary secretion of glutathione and of glutathione-metal complexes. Fundamental and Applied Toxicology. 1985;5(5):816–831. [PubMed] [Google Scholar]68. Brodkin E, Copes R, Mattman A, Kennedy J, Kling R, Yassi A. Lead and mercury exposures: interpretation and action. CMAJ. 2007;176(1):59–63. [PMC free article] [PubMed] [Google Scholar]69. National Academy of Sciences. Toxicological Effects of Methylmercury. Washington, DC, USA: National Research Council; 2000. [Google Scholar]70. Stern AH. A revised probabilistic estimate of the maternal methyl mercury intake dose corresponding to a measured cord blood mercury concentration. Environmental Health Perspectives. 2005;113(2):155–163. [PMC free article] [PubMed] [Google Scholar]71. Gupta M, Bansal JK, Khanna CM. Blood mercury in workers exposed to the preparation of mercury cadmium telluride layers on cadmium telluride base. Industrial Health. 1996;34(4):421–425. [PubMed] [Google Scholar]72. Chen C, Qu L, Li B, et al. Increased oxidative DNA damage, as assessed by urinary 8-hydroxy-2′- deoxyguanosine concentrations, and serum redox status in persons exposed to mercury. Clinical Chemistry. 2005;51(4):759–767. [PubMed] [Google Scholar]73. Bastos WR, Gomes JPO, Oliveira RC, et al. Mercury in the environment and riverside population in the Madeira River Basin, Amazon, Brazil. Science of the Total Environment. 2006;368(1):344–351. [PubMed] [Google Scholar]74. Halbach S. Combined estimation of mercury species released from amalgam. Journal of Dental Research. 1995;74(4):1103–1109. [PubMed] [Google Scholar]75. McKelvey W, Gwynn RC, Jeffery N, et al. A biomonitoring study of lead, cadmium, and mercury in the blood of New York City adults. Environmental Health Perspectives. 2007;115(10):1435–1441. [PMC free article] [PubMed] [Google Scholar]76. Grandjean P, Weihe P, White RF, et al. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury. Neurotoxicology and Teratology. 1997;19(6):417–428. [PubMed] [Google Scholar]77. Graeme KA, Pollack CV. Heavy metal toxicity, part I: arsenic and mercury. Journal of Emergency Medicine. 1998;16(1):45–56. [PubMed] [Google Scholar]78. Grandjean P, Budtz-Jørgensen E, White RF, et al. Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. American Journal of Epidemiology. 1999;150(3):301–305. [PubMed] [Google Scholar]79. Sager PR, Aschner M, Rodier PM. Persistent, differential alterations in developing cerebellar cortex of male and female mice after methylmercury exposure. Brain Research. 1984;314(1):1–11. [PubMed] [Google Scholar]80. Kishimoto T, Oguri T, Tada M. Effect of methylmercury (CH₃HgCl) injury on nitric oxide synthase (NOS) activity in cultured human umbilical vascular endothelial cells. Toxicology. 1995;103(1):1–7. [PubMed] [Google Scholar]81. Ponce RA, Kavanagh TJ, Mottet NK, Whittaker SG, Faustman EM. Effects of methyl mercury on the cell cycle of primary rat CNS cells in vitro. Toxicology and Applied Pharmacology. 1994;127(1):83–90. [PubMed] [Google Scholar]82. Choi BH, Cho KH, Lapham LW. Effects of methylmercury on human fetal neurons and astrocytes in vitro: a time-lapse cinematographic, phase and electron microscopic study. Environmental Research. 1981;24(1):61–74. [PubMed] [Google Scholar]83. Castoldi AF, Barni S, Turin I, Gandini C, Manzo L. Early acute necrosis, delayed apoptosis and cytoskeletal breakdown in cultured cerebellar granule neurons exposed to methylmercury. Journal of Neuroscience Research. 2000;59(6):775–787. [PubMed] [Google Scholar]84. Mottet NK, Vahter ME, Charleston JS, Friberg LT. Metabolism of methylmercury in the brain and its toxicological significance. Metal ions in Biological Systems. 1997;34:371–403. [PubMed] [Google Scholar]85. Yee S, Choi BH. Methylmercury poisoning induces oxidative stress in the mouse brain. Experimental and Molecular Pathology. 1994;60(3):188–196. [PubMed] [Google Scholar]86. Weinsberg F, Bickmeyer U, Wiegand H. Effects of inorganic mercury (Hg²⁺) on calcium channel currents and catecholamine release from bovine chromaffin cells. Archives of Toxicology. 1995;69(3):191–196. [PubMed] [Google Scholar]87. Huang CS, Narahashi T. Mercury chloride modulation of the GABA(A) receptor-channel complex in rat dorsal root ganglion neurons. Toxicology and Applied Pharmacology. 1996;140(2):508–520. [PubMed] [Google Scholar]88. Atchison WD, Narahashi T. Methylmercury-induced depression of neuromuscular transmission in the rat. NeuroToxicology. 1982;3(3):37–50. [PubMed] [Google Scholar]89. Atchison WD. Extracellular calcium-dependent and -independent effects of methylmercury on spontaneous and potassium-evoked release of acetylcholine at the neuromuscular junction. Journal of Pharmacology and Experimental Therapeutics. 1986;237(2):672–680. [PubMed] [Google Scholar]90. Halbach S, Vogt S, Köhler W, et al. Blood and urine mercury levels in adult amalgam patients of a randomized controlled trial: interaction of Hg species in erythrocytes. Environmental Research. 2008;107(1):69–78. [PubMed] [Google Scholar]91. Sandborgh-Englund G, Elinder CG, Langworth S, Schütz A, Ekstrand J. Mercury in biological fluids after amalgam removal. Journal of Dental Research. 1998;77(4):615–624. [PubMed] [Google Scholar]92. Geier DA, Geier MR. An assessment of the impact of thimerosal on childhood neurodevelopmental disorders. Pediatric Rehabilitation. 2003;6(2):97–102. [PubMed] [Google Scholar]93. Cox C, Clarkson TW, Marsh DO, Amin-Zaki L, Tikriti S, Myers GG. Dose-response analysis of infants prenatally exposed to methyl mercury: an application of a single compartment model to single-strand hair analysis. Environmental Research. 1989;49(2):318–332. [PubMed] [Google Scholar]94. Hussain S, Rodgers DA, Duhart HM, Ali SF. Mercuric chloride-induced reactive oxygen species and its effect on antioxidant enzymes in different regions of rat brain. Journal of Environmental Science and Health—Part B. 1997;32(3):395–409. [PubMed] [Google Scholar]95. Brawer JR, McCarthy GF, Gornitsky M, Frankel D, Mehindate K, Schipper HM. Mercuric chloride induces a stress response in cultured astrocytes characterized by mitochondrial uptake of iron. NeuroToxicology. 1998;19(6):767–776. [PubMed] [Google Scholar]96. Königsberg M, López-Díazguerrero NE, Bucio L, Gutiérrez-Ruiz MC. Uncoupling effect of mercuric chloride on mitochondria isolated from an hepatic cell line. Journal of Applied Toxicology. 2001;21(4):323–329. [PubMed] [Google Scholar]97. Massaroni L, Oliveira EM, Stefanon I, Vassallo DV. Effects of mercury on the mechanical and electrical activity of the Langendorff-perfused rat heart. Brazilian Journal of Medical and Biological Research. 1992;25(8):861–864. [PubMed] [Google Scholar]98. Oliveira EM, Vassallo DV, Sarkis JJF, Mill JG. Mercury effects on the contractile activity of isolated heart muscle. Toxicology and Applied Pharmacology. 1994;128(1):86–91. [PubMed] [Google Scholar]100. Halbach S, Schonsteiner G, Vierling W. The action of organic mercury compounds on the function of isolated mammalian heart muscle. European Journal of Pharmacology. 1989;167(2):255–264. [PubMed] [Google Scholar]101. Halbach S. Mercury compounds: lipophilicity and toxic effects on isolated myocardial tissue. Archives of Toxicology. 1990;64(4):315–319. [PubMed] [Google Scholar]102. Rhee HM, Choi BH. Hemodynamic and electrophysiological effects of mercury in intact anesthetized rabbits and in isolated perfused hearts. Experimental and Molecular Pathology. 1989;50(3):281–290. [PubMed] [Google Scholar]103. Bastos WR, Gomes JPO, Oliveira RC, et al. Mercury in the environment and riverside population in the Madeira River Basin, Amazon, Brazil. Science of the Total Environment. 2006;368(1):344–351. [PubMed] [Google Scholar]104. Fillion M, Mergler D, Sousa Passos CJ, Larribe F, Lemire M, Guimarães JRD. A preliminary study of mercury exposure and blood pressure in the Brazilian Amazon. Environmental Health. 2006;5, article 29 [PMC free article] [PubMed] [Google Scholar]105. Guallar E, Sanz-Gallardo MI, Van’T Veer P, et al. Mercury, fish oils, and the risk of myocardial infarction. The New England Journal of Medicine. 2002;347(22):1747–1754. [PubMed] [Google Scholar]106. Yoshizawa K, Rimm EB, Morris JS, et al. Mercury and the risk of coronary heart disease in men. The New England Journal of Medicine. 2002;347(22):1755–1760. [PubMed] [Google Scholar]107. Houston MC. The role of mercury and cadmium heavy metals in vascular disease, hypertension, coronary heart disease, and myocardial infarction. Alternative Therapies in Health and Medicine. 2007;13(2):S128–S133. [PubMed] [Google Scholar]108. Salonen JT, Seppanen K, Nyyssonen K, et al. Intake of mercury from fish, lipid peroxidation, and the risk of myocardial infarction and coronary, cardiovascular, and any death in Eastern Finnish men. Circulation. 1995;91(3):645–655. [PubMed] [Google Scholar]109. Virtanen JK, Voutilainen S, Rissanen TH, et al. Mercury, fish oils, and risk of acute coronary events and cardiovascular disease, coronary heart disease, and all-cause mortality in men in Eastern Finland. Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25(1):228–233. [PubMed] [Google Scholar]110. Hulthe J, Fagerberg B. Circulating oxidized LDL is associated with subclinical atherosclerosis development and inflammatory cytokines (AIR study) Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22(7):1162–1167. [PubMed] [Google Scholar]111. Ehara S, Ueda M, Naruko T, et al. Elevated levels of oxidized low density lipoprotein show a positive relationship with the severity of acute coronary syndromes. Circulation. 2001;103(15):1955–1960. [PubMed] [Google Scholar]112. Gonzalvo MC, Gil F, Hernández AF, Villanueva E, Pla A. Inhibition of paraoxonase activity in human liver microsomes by exposure to EDTA, metals and mercurials. Chemico-Biological Interactions. 1997;105(3):169–179. [PubMed] [Google Scholar]113. Mackness M, Mackness B. Paraoxonase 1 and atherosclerosis: is the gene or the protein more important? Free Radical Biology and Medicine. 2004;37(9):1317–1323. [PubMed] [Google Scholar]114. Farina M, Aschner M, Rocha JBT. Oxidative stress in MeHg-induced neurotoxicity. Toxicology and Applied Pharmacology. 2011;256(1):405–417. [PMC free article] [PubMed] [Google Scholar]115. Flohé L. Glutathione peroxidase. Basic Life Sciences. 1988;49:663–668. [PubMed] [Google Scholar]116. Arthur JR. The glutathione peroxidases. Cellular and Molecular Life Sciences. 2000;57(13-14):1825–1835. [PubMed] [Google Scholar]117. Brigelius-Flohé R. Glutathione peroxidases and redox-regulated transcription factors. Biological Chemistry. 2006;387(10-11):1329–1335. [PubMed] [Google Scholar]118. Magos L, Clarkson TW. Overview of the clinical toxicity of mercury. Annals of Clinical Biochemistry. 2006;43(4):257–268. [PubMed] [Google Scholar]119. Clarkson TW. The toxicology of mercury. Critical Reviews in Clinical Laboratory Sciences. 1997;34(4):369–403. [PubMed] [Google Scholar]120. Valko M, Rhodes CJ, Moncol J, Izakovic M, Mazur M. Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chemico-Biological Interactions. 2006;160(1):1–40. [PubMed] [Google Scholar]121. Ganther HE. Interactions of vitamin E and selenium with mercury and silver. Annals of the New York Academy of Sciences. 1980;355:212–226. [PubMed] [Google Scholar]122. Sherwani SI, Pabon S, Patel RB, et al. Eicosanoid signaling and vascular dysfunction: methylmercury-induced phospholipase D activation in vascular endothelial cells. Cell Biochemistry and Biophysics. In press. [PubMed] [Google Scholar]123. Raymond LJ, Ralston NVC. Mercury: selenuim interactions and health implications. Seychelles Medical and Dental Journal. 2004;7(1):72–77. [Google Scholar]124. Naganuma A, Koyama Y, Imura N. Behavior of methylmercury in mammalian erythrocytes. Toxicology and Applied Pharmacology. 1980;54(3):405–410. [PubMed] [Google Scholar]125. Rungby J, Ernst E. Experimentally induced lipid peroxidation after exposure to chromium, mercury or silver: interactions with carbon tetrachloride. Pharmacology and Toxicology. 1992;70(3):205–207. [PubMed] [Google Scholar]126. Rossoni LV, Amaral SMC, Vassallo PF, et al. Effects of mercury on the arterial blood pressure of anesthetized rats. Brazilian Journal of Medical and Biological Research. 1999;32(8):989–997. [PubMed] [Google Scholar]127. Machado AC, Padilha AS, Wiggers GA, Siman FDM, Stefanon I, Vassallo DV. Small doses of mercury increase arterial pressure reactivity to phenylephrine in rats. Environmental Toxicology and Pharmacology. 2007;24(2):92–97. [PubMed] [Google Scholar]128. Massaroni L, Oliveira EM, Stefanon I, Vassallo DV. Effects of mercury on the mechanical and electrical activity of the Langendorff-perfused rat heart. Brazilian Journal of Medical and Biological Research. 1992;25(8):861–864. [PubMed] [Google Scholar]129. Furieri LB, Fioresi M, Junior RFR, et al. Exposure to low mercury concentration in vivo impairs myocardial contractile function. Toxicology and Applied Pharmacology. 2011;255(2):193–199. [PubMed] [Google Scholar]130. Massaroni L, Rossoni LV, Amaral SMC, Stefanon I, Oliveira EM, Vassallo DV. Haemodynamic and electrophysiological acute toxic effects of mercury in anaesthetized rats and in Langendorff perfused rat hearts. Pharmacological Research. 1995;32(1-2):27–36. [PubMed] [Google Scholar]131. Furieri LB, Galán M, Avendaño MS, et al. Endothelial dysfunction of rat coronary arteries after exposure to low concentrations of mercury is dependent on reactive oxygen species. British Journal of Pharmacology. 2011;162(8):1819–1831. [PMC free article] [PubMed] [Google Scholar]132. Pecanha FM, Wiggers GA, Briones AM, et al. The role of cyclooxygenase (COX)-2 derived prostanoids on vasoconstrictor responses to phenylephrine is increased by exposure to low mercury concentration. Journal of Physiology and Pharmacology. 2010;61(1):29–36. [PubMed] [Google Scholar]133. Wiggers GA, Peçanha FM, Briones AM, et al. Low mercury concentrations cause oxidative stress and endothelial dysfunction in conductance and resistance arteries. American Journal of Physiology. 2008;295(3):h2033–h2043. [PubMed] [Google Scholar]134. Blanco-Rivero J, Furieri LB, Vassallo DV, Salaices M, Balfagón G. Chronic HgCl₂ treatment increases vasoconstriction induced by electrical field stimulation: role of adrenergic and nitrergic innervation. Clinical Science. 2011;121(8):331–341. [PubMed] [Google Scholar]

Mercury Factsheet | National Biomonitoring Program

Mercury is an element and a metal that is found in air, water, and soil. It exists in three forms that have different properties, usage, and toxicity. The three forms are called elemental (or metallic) mercury, inorganic mercury compounds, and organic mercury compounds.

Elemental mercury is liquid at room temperature. It is used in some thermometers, dental amalgams, fluorescent light bulbs, some electrical switches, mining, and some industrial processes. It is released into the air when coal and other fossil fuels are burned.

Inorganic mercury compounds are formed when mercury combines with other elements, such as sulfur or oxygen, to form compounds or salts. Inorganic mercury compounds can occur naturally in the environment. Inorganic mercury compounds are used in some industrial processes and in the making of other chemicals. Outside the United States, inorganic mercury salts have been used in cosmetic skin creams.

Organic mercury compounds are formed when mercury combines with carbon. Microscopic organisms in water and soil can convert elemental and inorganic mercury into an organic mercury compound, methylmercury, which accumulates in the food chain. Thimerosal and phenylmercuric acetate are other types of organic mercury compounds made in small amounts for use as preservatives.

How People Are Exposed to Mercury

Elemental mercury: People may be exposed when they breathe air containing elemental mercury vapors. Vapors may be present in such workplaces as dental offices, smelting operations, and locations where mercury has been spilled or released. In the body, elemental mercury can be converted to inorganic mercury.

Inorganic Mercury: People may be exposed if they work where inorganic mercury compounds are used.

Organic Mercury: People may be exposed when they eat fish or shellfish contaminated with methylmercury. Methylmercury can pass through the placenta, exposing the developing fetus.

How Mercury Affects People’s Health

Elemental mercury: The human health effects from exposure to low environmental levels of elemental mercury are unknown. Very high mercury vapor concentrations can quickly cause severe lung damage. At low vapor concentrations over a long time, neurological disturbances, memory problems, skin rash, and kidney abnormalities may occur.

Inorganic Mercury: When eaten in large amounts, some inorganic mercury compounds can be very irritating and corrosive to the digestive system. If repeatedly eaten or applied to the skin over long period of time, some inorganic mercury compounds can cause effects similar to what is seen with long term mercury vapor exposure, including neurological disturbances, memory problems, skin rash, and kidney abnormalities.

Organic Mercury: Large amounts of methylmercury eaten over weeks to months have caused damage to the nervous system. Infants born to women who were poisoned with methylmercury had developmental abnormalities and cerebral palsy.

Levels of Mercury in the U.S. Population

In the Fourth National Report on Human Exposure to Environmental Chemicals (Fourth Report), CDC scientists measured total mercury in the blood of 8,373 participants aged one year and older who took part in the National Health and Nutrition Examination Survey (NHANES) during 2003–2004. Total blood mercury is mainly a measure of methyl mercury exposure. In the same 2003–2004 NHANES, CDC scientists measured mercury in the urine of 2,538 participants aged six years and older. Mercury in the urine is a measure of inorganic mercury exposure. By measuring mercury in blood and in urine, scientists can estimate the amount of mercury that has entered people’s bodies.

• CDC scientists found measureable mercury in most of the participants. Both blood and urine mercury levels tend to increase with age.
• Defining safe levels of mercury in blood continues to be an active research area. In 2000, the National Research Council of the National Academy of Sciences determined that a level of 85 micrograms per liter (µg/L) in cord blood was associated with early neurodevelopmental effects. The lower 95% confidence limit of this estimate was 58 µg/L. All blood mercury levels for persons in the Fourth Report were less than 33 µg/L.
• Blood and urine mercury in the U.S. population were similar to levels seen in other developed countries.

Finding a measurable amount of mercury in blood or urine does not imply that levels of mercury cause an adverse health effect. Biomonitoring studies on levels of mercury provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of mercury than are found in the general population. Biomonitoring data can also help scientists plan and conduct research about exposure and health effects.

Additional Resources

Agency for Toxic Substances and Disease Registry

CDC Emergency Preparedness and Response

Environmental Protection Agency

Food and Drug Administration

Health Effects of Mercury

Author: Mike Everett

This case study is part of a collection of pages developed by students in the 2012 introductory-level Geology and Human Health course in the Department of Earth Sciences, Montana State University. Learn more about this project.

Mercury is a devastating neurotoxin that has signficant health consequences in the United States and across every other developed country. Where there is any type of industry there is usually a risk of higher mercury levels effecting every envirnoment. Learn more about how mercury gets into the environment, what the health impacts are, and how to protect yourself from mercury poisoning.

Introduction

Mercury exists in three different states and can form both organic and inorganic compounds. The central nervous system is the target organ for mercury poisoning, though mercury is also toxic to the kidneys. Chelation therapy with DMPS can increase the elimination of mercury and there are case reports showing that chelation therapy can reverse neurological damage due to mercury poisoning.

Mercury primarily effects the centreal nervous system. In clinical situations mercury poisoning presents itself in a variety of ways and is measured by the amount involved, the type of exposere, and whether that exposure was single or repeated.

Sources of Mercury

Elemental mercury vapor can be absorbed quickly if inhaled and can easily cross the blood-brain barrier (the blood-brain barrier is a barrier maintained to separate the blood in the brain from the blood in the rest of the body to prevent the blood in the brain from becoming contaminated by things we eat and breath in on a daily basis). The vapor form is the most important when looking at the poisoning from the toxicology view because mercury vapor accumulates in the brain. When mercury is ingested the toxic effects are not as wide spread because the body will not absorb metallic mercury as much as the vapor form. If mercury is ingested it will accumulate in the appendix which could potentially cause infection or appendicidis due to the bodies inability to completely eliminate toxins from the appendix. Elemental mercury can be injected intravascularly which may lead to embolism and a person would exhibit systemic features of mercury poisoning. If mercury deposits in the soft tissues of the body (muscles are a good example) the result would be a reaction that produced granular deposits of mercury. The body would react to the mercury as a foreign body.

Bioavailability:

Rainbow trout caught in the Lower Madison River. Photo by Mike Everett

The major and most commonly know way the mercury gets into the biosphere is through the intake of fish. Minning of heavy metals are also avenues for mercury to get exposed to humans.

REAL WORLD PROBLEMS

Near Bozeman Montana, the Madison River has higher than normal levels of mercury, according to Montana Fish Wildlife and Parks. Montana FWP warns that pregnant women and young children do not consume fish caught in the Lower Madison River on a regular basis. With this being said, it would be wise for all people to not consume fish caught in this portion of the river on a regular basis. Enjoying a rainbow or two caught on this part of the river every once in a while for the average joe shouldn’t have any health effects but it is still better to understand the problems that can happen if mercury is consumed in larger amounts.

Impacts on Human Health

Inhaling mercury vapors causes headaches, coughing, nausea, vomiting, a metallic taste, chest pain, an inflammation of the tissues of the eye, and a shortness of breath. Pneumonia may develop and in some severe cases kidney and liver failure may occur. If repeated exposure to mercury continues (even at low levels) tremors, memory loss, changes in an individuals personality, lethargy, insomnia, and an effect of motor movements. Other health problems that may develop are and inflammation the the gums, an overproduction of saliva, and damage to the tubules of the kidneys that are responsible to reabsorbing nutrients and secreting toxins and body wastes. Periperal neuropathy between motor and sensory commands may develop.

Symptoms include the impairment of vision, hearing and sight as well as impairing sensation and a lack of coordination. Symptoms of mercury poisoning and the type and extent that a patient would exhibit depend upon the individual toxin, the amount they were exposed to, and how the exposure occured and how long it lasted.

Prevention or Mitigation

To prevent mercury poisoning people should be aware of the levels of mercury of the environment where they are getting their food (especially where fish is concerned). To diagnose mercury poisoning in a clinical setting doctors can look at the fingernails. With mercury poisoning a line will form parallel to the cuticle of the nail. Blood and urine samples can also be taken and analyzed to determine the amount of mercury and form there the doctor will formulate a plan to remove the mercury. Neurological symptoms also play a role in diagnosis. If long term exposure of mercury is suspected a urine sample is taken as it is the most appropriate measurment but it a one time esxposure to mercury is suspected a blood test is run because mercury would not have made it into the excratory system in a short period of time. Chelation therapy is used to increase urinary elimination of mercury and will reduce the amount of mercury in the blood. If long term mercury exposure is diagnosed filtration of the blood is a common.

Recommended Readings

To find out more about mercury and all of its side effects read: Mercury as a Global Pollutant (D.B. Porcella, J.W. Huckabee, and B. Wheatley, editors), Water, Air and Soil Pollution, 80 (1-4), 1995. / Human disease and conditions, 2nd edition, 2010, volume 3. pp.1098-1103 / Mercury poisoning, Epstein, P.R. Lancet, ISSN 0140-6736, 06/1991, Volume 337, Issue 8753, p. 1344.

Related Links

To find out more about mercury and all of its side effects visit the web sites:

• http://www.usgs.gov/themes/factsheet/146-00/
• http://www.fda.gov/ForConsumers/ConsumerUpdates/ucm294849.htm
• http://www.michigan.gov/dnr/0,4570,7-153-10370_12150_12220-26953–,00.html

Deadly metal: how dangerous is mercury and how to avoid poisoning | Healthy life | Health

Why is mercury dangerous?

According to the hazard class, mercury belongs to the first class, that is, it is considered an extremely hazardous chemical substance. The penetration of mercury into the body often occurs by inhalation of its odorless vapors.

Exposure to even small amounts of mercury can cause health problems and severe poisoning. Mercury has toxic effects on the nervous, digestive and immune systems, lungs, kidneys, skin and eyes.

Mercury poisoning is divided into light (food poisoning), acute (after accidents at enterprises, due to safety violations) and chronic.

Chronic poisoning increases the risk of tuberculosis, atherosclerosis, hypertension. In this case, the consequences of mercury poisoning can appear several years after the termination of contact with it.

Acute mercury poisoning can lead to death. Also, if no treatment is carried out in case of poisoning, then the functions of the central nervous system may be impaired, mental activity is reduced, convulsions, exhaustion appear.Acute stages of mercury poisoning cause loss of vision, complete paralysis, baldness.

Especially mercury and its compounds are dangerous for pregnant women, as they pose a threat to the development of the child.

Until the 1970s, mercury compounds were actively used in medicine, but due to its high toxicity, this metal was almost no longer used for the manufacture of medicines.

Today mercury compounds (merthiolate) are used

– as a preservative for vaccines;

– for medical thermometers – one medical thermometer contains up to 2 g of mercury;

– energy-saving gas-discharge fluorescent lamps contain up to tens of milligrams of mercury.

Mercury is also found in fish and shellfish, so it is recommended to avoid seafood during pregnancy.

Note that heat treatment of food does not destroy the mercury it contains.

Mercury poisoning

Chronic forms of mercury poisoning are called mercurialism, which occurs due to prolonged exposure to small doses of mercury vapor on a person. Mercurialism can cause not only physical, but also mental deviations.

Symptoms of poisoning .Acute mercury poisoning manifests itself a couple of hours after the onset of poisoning. Symptoms of acute poisoning: weakness, headache, sore throat, metallic taste in the mouth, salivation, swelling and bleeding of the gums, nausea and vomiting. Often there are severe abdominal pains, diarrhea, chest pains, coughing, severe chills, and the body temperature rises to 38–40 ° C.

Chronic mercury poisoning is indicated by fatigue, drowsiness, general weakness, headache, dizziness, apathy, irritability.

What to do? At the first sign of mercury poisoning, it is important to call a doctor as soon as possible. Before the ambulance arrives, the victim needs to drink milk and then induce vomiting to remove the fluid.

Prevention

In everyday life, mercury thermometers are the main source of possible poisoning. To keep yourself and your children safe, it is worth purchasing thermometers that do not contain mercury.

How to get rid of mercury in a room

Special services are involved in the disposal of mercury, including those that are part of the Russian Emergencies Ministry. On a household call, if you break the thermometer, they usually do not leave. You can get rid of a small amount of mercury yourself.

First, you need to take the children and pets out of the room and open the window to provide fresh air.

Before removing mercury, you should protect yourself as much as possible – wear a respirator or gauze bandage, rubber gloves.

Fragments of the thermometer can be placed in a tight plastic bag and tied tightly. Mercury itself is best placed in an airtight container, for example, in a jar of cold water. During collection, you can use a paper envelope or paper towel. Before you start collecting mercury, illuminate the space with a lamp – under the rays of light, the balls of mercury will be noticeable, as they begin to shine.

You can collect mercury using:

– brushes made of amalgamating metals;

– pieces of wire, they will help to collect mercury in the cracks;

– adhesive tape – suitable for collecting small balls;

– pipettes with a fine tip.

Place the collected mercury and used items in a previously prepared sealed container.

The room needs to be treated with chemicals. The simplest composition for treating a room is an alcohol solution of 5% iodine. You can also fill the place where the mercury was, with a solution of “potassium permanganate”. The floor must be thoroughly washed the next day.

Do not dispose of mercury in a garbage chute or sewer.After collecting the mercury, call the local emergency department, they are obliged to take it for disposal.

Strongly prohibited:

Sweep mercury with a broom. The rods break the ball of mercury into smaller ones, making them harder to assemble.

Collect mercury with a vacuum cleaner, as it heats up during operation and the evaporation of mercury increases. In addition, the mercury will settle inside the vacuum cleaner and have to be thrown away.

Wash clothes in which you removed mercury, as this can lead to contamination of the washing machine with harmful metal.All things that have come into contact with mercury must be thrown away.

See also:

90,000 Mercury poisoning: signs, symptoms, effects

Glossy silvery balls, behaving so surprisingly on the surface, rolling, overflowing into each other, breaking into small droplets and re-assembling into large ones – mercury. Inhaling its vapors, you can get severe chemical poisoning. To do this, simply break a thermometer or, for example, an energy-saving light bulb.The amount of mercury they contain is more than enough for poisoning.

The most dangerous of poisoning

The most dangerous poisoning is mercury! This fact defies refutation for a number of reasons:

• metal is considered one of the most dangerous air pollutants in the home;

• this substance is highly hazardous due to the formation of toxic fumes;

• has a large area of ​​distribution in everyday life, that is, the likelihood of respiratory poisoning in each of us is quite real.

Symptoms and Manifestations

An attentive attitude to one’s own and the health of one’s loved ones will help to avoid harmful consequences for the body. In most situations, we know for sure that the children have broken the thermometer, or the energy-saving lamp has burst, so it is advisable to monitor the health of the household for 8 hours after the incident. As a rule, it is the culprit of the “catastrophe” that is in greater danger, that is, the one who broke the device and the one who eliminated the consequences.

The main symptoms of chemical poisoning are:

• Strong headache;

• urge to vomit;

• nausea;

• signs of onset diarrhea;

• fast fatiguability.

It is advisable to immediately seek help from a doctor. The listed symptoms are very similar to those of other diseases, so you may not even realize that you have poisoned yourself with mercury.

Minor and severe poisoning

This situation can arise with those who entered a room where mercury has already been spilled. If a person’s immunity is normal and he does not complain about his health, then he is unlikely to notice any changes in his condition.Otherwise, migraine, drowsiness, apathy may appear. As a rule, they pass during the day.

Industrial poisoning can be classified as severe. It is no less dangerous if the mercury is spilled in the house, and it has not been collected or collected, but not all. In case of severe mercury poisoning, the following manifestations from the body can be observed:

• hand tremor;

• violation of the sense of smell;

• numbness in the fingers;

• a sharp drop in blood pressure;

• drowsiness occurs more and more often, and it is very difficult to overcome it;

• for the body of women is characterized by a violation of the menstrual cycle.

What are the consequences?

For mercury poisoning, accompanied by vomiting without diarrhea, upset stools, headache, drowsiness, or other manifestations, seek immediate medical attention. Otherwise, the victim’s condition can worsen significantly and develop into more serious health problems:

• liver disease;

• malfunctioning of the gallbladder;

• blood pressure surges

• the formation of atherosclerotic plaques;

• in especially severe cases – to tuberculosis.

In a very severe stage of poisoning, the patient may fall into a coma.

Drug in contact with mercury

At the first symptoms of metal poisoning, you should immediately call an ambulance. Before the arrival of the carriage, it is recommended to stop the toxic effects of the poison on the internal organs. To do this, take a sorbent. One of the most famous and effective today is Polysorb.The drug is indicated for acute poisoning with poisonous substances. The drug has a high sorption capacity – up to 300 mg / g and acts as early as 2-4 minutes after administration.

You should start taking Polisorb as quickly as possible, that is, immediately after poisoning with mercury vapor. The sooner the drug enters the intestinal lumen, the higher the likelihood that the poisoning will not cause serious damage to the body.

Polysorb is a white powder that is tasteless and odorless.It is absolutely harmless to the body, it is mixed in water at room temperature. Once in the body, it is able to identify “aggressors”, envelop them, depriving them of the opportunity to poison the tissues, binds them together and quickly displays them in a natural way. The active substance does not penetrate into the bloodstream, does not have a negative effect on the body.

The standard single dosage of the substance is 1 heaping tablespoon of powder mixed in half a glass of water. As a rule, in case of poisoning, you need to drink a dose of medicine every hour for 5 hours.The next day and all subsequent (up to 7 days) 4 times a day are enough.

Reception of the sorbent does not cancel the consultation with a specialist! Treatment of poisoning in a hospital is much faster and more effective than recovery at home. Without designating themselves with any manifestations, poisons can infect various internal organs, and the consequences can be the most unpredictable.

Measures for the prevention of mercury poisoning from a thermometer

In this case, children are at risk.It is very important to explain to the baby that the thermometer is broken – for the parents it will not become a reason for clarifying the relationship and punishment. However, it can become a source of severe illness for any of the household. It is advisable for the child to immediately report the trouble to adults.

If the thermometer still crashed, do not panic, follow a simple algorithm of actions:

• Get all people and animals out of the room;
• call the rescue service;
• If necessary, act on your own: put on rubber gloves, shoe covers and a mask, carefully collect all the mercury, taking precautions;
• use a thin sheet of paper or tape for work;
• Place the collected metal in a glass jar;
• If mercury gets on a carpet or other fabric, the rescuers should be told about it;
• when collecting mercury from a thermometer, it must be sprinkled with potassium permanganate, and then, using a syringe without a needle, collect drops of mercury;
• after removing mercury, carry out a wet cleaning of the room;
• invite employees of the Ministry of Emergencies with a request to check the level of air toxicity in your house using a special device;
• in any of the listed cases, you should be calm, detect the problem in a timely manner and involve specialists to solve it.

Why is Polysorb right for you?

• Recommended for use by people of all ages.

• Begins to act in 1-4 minutes after ingestion.

• Contains no preservatives, colors or sweeteners. Taste neutral.

• Gently removes harmful and normalizes the intestinal microflora.

The dosage of the drug is calculated individually depending on its weight in accordance with instructions .

If you have any difficulties in calculating the individual dose of Polysorb, you can get a free consultation by phone: 8-800-100-19-89 or in section of consultation .

Learn more

90,000 Mercury poisoning symptoms, first aid

Mercury is an extremely toxic substance, the handling of which requires a person to have certain knowledge.That is why it is worth paying special attention to such an object in the house as a mercury thermometer.

We all know perfectly well that fragile things in the house sometimes break and break. A mercury thermometer is a rather fragile device; it is quite easy to break it. In this case, it is also necessary to correctly collect the poisonous metal.

But a person may not even notice that the thermometer is broken, and the insidious mercury at this time already begins to evaporate its poisonous vapors. Therefore, everyone should know the main symptoms of poisoning with this harmful substance. Knowledge of the symptoms will help to identify poisoning in time and remove the toxins that have entered the body as soon as possible.

Main symptoms of mercury poisoning

Contents: Show

The physical properties of mercury are such that its vapors penetrate into your body imperceptibly. Signs of poisoning will be the same in children and adults. Look for the following symptoms:

Weakness throughout the body, no desire to eat, sore throat when swallowed, pain in the head, metal taste in the mouth, salivation and swelling.All these signs can be observed shortly after the release of mercury vapor.

As a result of mercury poisoning, pain in the abdomen can be observed, it can also be diarrhea along with mucus and blood, increased bleeding of the gums and vomiting.

From the respiratory tract in case of mercury poisoning, you can observe such disorders as cough, shortness of breath, chills, pain in the chest when a person breathes.

In case of poisoning with mercury vapors in humans, the body temperature can rise sharply to critical levels of .

All the main signs of mercury poisoning can be divided into several types:

Chronic symptoms

Such signs can develop due to prolonged exposure to an environment that contains mercury, such as a laboratory. The human nervous system is primarily affected by such prolonged contacts.

Poisoning manifests itself in the form of severe fatigue, weakness, drowsiness. A person may feel frequent headaches, apathy and instability of the emotional background.

People with chronic mercury vapor poisoning may experience increased nervousness, intellectual abilities of a person decrease, concentration of attention disappears.

And after a long time, the person begins to show tremors throughout the body.

You need to know that the consequences can be felt, many years later, after contact with this metal.

Acute symptoms

These symptoms mainly include the appearance of headaches, difficulty breathing, pain when swallowing, abdominal pain, diarrhea with blood, an increase in body temperature.

Such acute symptoms are very difficult for women and children, and they can occur due to overheating of the harmful substance, and the hood will be turned off or absent altogether.

Mercury vapors can also enter the body when devices containing mercury break.

This type of symptoms of mercury poisoning begins to appear within an hour or two after it enters the human body.

Of course, do not panic if an energy-saving fluorescent light bulb breaks, the main thing is to properly assemble and dispose of it.

First aid for mercury vapor poisoning

Mercury vapor poisoning is very dangerous. And if you do not provide proper help in time and do not pay attention to the symptoms, then irreparable damage can happen. So, what to do with victims of mercury vapor:

• First of all, you need to pay attention to the signs and call the rescue service.
• Collect the mercury immediately and open the windows.
• Remove the victim from the room.
• Without waiting for the arrival of doctors, flush the victim’s stomach and give him activated charcoal to drink in the amount required for his weight.
• Give the victim as much liquid as possible. It can be ordinary water, tea, milk. Fluid will lead to faster removal of toxins from the body. It is advisable to induce vomiting.
• Give the victim to drink water mixed with sulfur compounds, add egg white and activated charcoal there.
• Be sure to lay the victim so that his head is turned on the side, otherwise he may drown.
• If the victim is unconscious, make sure that his tongue is not swallowed, and be sure to provide him with access to fresh air before the arrival of doctors.
• If your home medicine cabinet contains calcium chloride or glucose solution, you can give the victim an injection before the ambulance arrives.
• Any laxative can be used to thoroughly flush the stomach.

When providing first aid to victims of mercury vapor, it is important to remember that the lives of victims may depend on you. That is why you should not panic in such cases. Do everything thoughtfully and calmly, not forgetting that you need to clean the room of mercury.

90,000 LRT FACTS. Aluminum in vaccines: pseudoscience and what you need to know

Vaccines contain heavy metals, aluminum, mercury, formaldehyde – these are popular statements from the Internet, where they write about the dangers and dangers of vaccination.

Thus, at first glance, scientific articles are written and published about aluminum in vaccines, informational television commercials are created, discussions are held on Internet forums how to “cleanse” the body of the metal obtained as a result of vaccination.LRT FACTS find out how a vaccine actually works and what to fear and what not.

Affect the brain

Aluminum hydroxide is indeed used in some vaccines, vaccine opponents first of all point to its negative effects on the nervous system.

“Vaccine distributors have no evidence that aluminum compounds are safe when it comes to neurological disorders (eg, mental illness, autism, schizophrenia, panic attacks, depression),” states the article “Aluminum, which is included in the vaccine goes to the brain ”on the Lithuanian website healwithlifestyle.com dedicated to health topics.

The article reports that the brain is especially sensitive to even a minimal amount of aluminum, and the effect of the metal that has entered the human body is compared to the “Trojan horse”.

There is no consensus on the effects of aluminum, but vaccines contain a small dose of it

According to Professor Aurelia Zvirblene from the Center for Life Sciences of Vilnius University, there really is no consensus about the effect of aluminum on the nervous system, however, in vaccines, contrary to what is often written, such an amount that is safe for human health is used. into our bodies with food and is removed from it.

“If the body constantly receives large doses of aluminum, it can accumulate in various cells, and also enter the nervous system. This has been linked to neurotoxicity, some neuroinflammatory processes, such as Alzheimer’s disease or the development of dementia, although scientific evidence is conflicting.

Some scientific studies show some relationship between the increase in the amount of aluminum and neurological diseases, others argue that this relationship is not traced.For example, a number of scientific studies show that in those places where there is an increased amount of aluminum in drinking water, residents have a slightly increased risk of developing Alzheimer’s disease, ”says the professor.

According to the recommendations of the European Food Safety Agency (EFSA), the amount of aluminum received by the body should not exceed 1 milligram per 1 kg of body weight per week.

According to A. Zhvirblene, one dose of the vaccine contains up to 0.5 milligrams of aluminum.For comparison: we get 12 milligrams of metal by eating a kilogram of bread or other baked goods, there is a lot of it in soy products, not to mention such things that are often used in the household as foil and antiperspirants.

“From a biochemical point of view, there is not much difference in what way aluminum enters the body (with food, through the skin or muscles), it in any case enters the circulatory system and with its help is carried to all organs” – this is how the professor debunks Another popular myth is that the metal that got as a result of vaccination is especially dangerous and accumulates in the body.

Why do we feel bad after vaccination?

It is aluminum that is responsible for the fact that after vaccination we feel a negative reaction of the body: the injection site swells, turns red, the temperature rises. Professor Aurelia virblene explains that this is a manifestation of the activation of the immune system.

“Aluminum compounds are adjuvants in the vaccine and must induce an immune response – that is, attract the cells of the immune system to the injection site and activate them.Otherwise, the vaccine will not be effective. The activated cells begin to produce various molecules that cause inflammation, and this encourages the formation of immunity. Therefore, the injection site turns red, it can be painful to the touch, and sometimes there is a systemic inflammatory reaction – the body temperature rises, a headache, chills, etc., ”she explains.

According to the professor, similar symptoms occur in infectious patients, and reactions to a vaccine, as well as to a disease, depend on the characteristics of a particular organism.

The professor also emphasized that strong post-vaccination reactions should be registered at the Center for Infectious Diseases and AIDS, as well as reported to the family doctor.

Calls to “cleanse” the body are unfounded

Parents raising children can find discussions on various forums on how to protect the body from the negative effects of metal. One of the popular theories is that the body must be “cleansed”.For this purpose, we also offer remedies – from food additives with zinc to specific cereals, oils, beets.

Professor Aurelia virblene says that such proposals are not scientifically substantiated.

“After vaccination, an inflammatory reaction can occur, with the formation of certain active molecules. But the body itself clears itself of them, since these are mostly molecules of protein origin that live shortly, they disintegrate by themselves. Aluminum is also excreted from the body – insoluble salts are converted into soluble compounds that enter the bloodstream, later excreted in urine, sweat and other secretions.Half of the ingested aluminum is removed from it within 24 hours, more than 75 percent – within 2 weeks, ”says the scientist.

Pseudoscientific articles provoke fear

Despite the available information, some people are not convinced by the arguments about the harmlessness of aluminum in vaccines. Polls show that in Lithuania a growing number of those who refuse to vaccinate children, most explain this by fears of complications.

On the Internet, one can find allegedly serious scientific articles and films translated into Lithuanian. Professor Aurelia Zhvirblene, whom we asked to view the publication mentioned at the beginning of the article, says that this is a pseudoscientific publication, describing the pathway of aluminum to the brain in it is impossible for a healthy person.

“This is a pseudoscientific article, really masterfully cobbled together, it contains a lot of scientific terms and a lot of experiments described.<...> It is very difficult to refute such articles, because it is impossible to describe very complex immunological and molecular processes in simple language, “says the professor. She noted that there used to be a lot of talk about mercury in vaccines, now there are similar claims about aluminum.

According to her, the vaccine production technology is unlikely to change in the near future and there will be no aluminum compounds in them.

“Aluminum compounds have been used as adjuvants in vaccines for many decades and there is no scientific conclusion about their harm.<...> Aluminum adjuvants are the most effective, tested for many years, so there is no reason to refuse them in vaccines yet. Without adjuvants, vaccines would not be effective enough, would not induce the desired immune response, ”explains the professor.

VERDICT

Pseudoscience

Aluminum compounds are an inevitable component of many vaccines, they determine their effectiveness, although they can cause discomfort after vaccination.Aluminum has become an anti-vaccine argument, which is presented with ostensibly scientific justification, but authoritative scientific research shows and proves the opposite and does not provide evidence of the harm of aluminum in vaccines.

90,000 Infertility, mercury and infection through an injection. COVID-19 Vaccine Myths | Hromadske TV

Vaccination today is the only way to fight the COVID-19 pandemic. Scientists have not yet created a specific treatment, and the rate of spread of the virus is terrifying throughout the world.And despite the millions of cases, astounding death rates and the emergence of new strains of coronavirus, many prefer to believe in the numerous myths about vaccination and refuse to be vaccinated.

Our partners from Euroradio decided to debunk the most widespread and ridiculous myths about vaccines against coronavirus with links to scientific sources.

“Vaccines change DNA and have long-term effects”

DNA is not something that can be changed with a single shot. Even if it’s a shot with the coronavirus vaccine.

The most common concern that the vaccine will change the DNA is due to the fact that some drugs work with matrix ribonucleic acid (mRNA).

To put it simply, a vaccine delivers “instructions” to the cells of the body to create a defense against the coronavirus. But the material from the vaccine cannot get into the cell nucleus, where the DNA is stored. And even those rare ones that can get there still cannot influence it.

Moreover, the vector vaccine (like the same AstraZeneca) cannot affect the DNA in any way, because it only transfers the coronavirus DNA on the basis of a safe virus.The vaccine cannot cause any changes, except for the immune response.

read also

“A vaccine can lead to infertility”

The same “horror stories” are used by anti-vaccines in relation to other vaccines. Somewhere nearby is a fake that vaccines “can provoke autism.”

The basis of the hypothesis about the alleged danger of the vaccine for women is that the COVID-19 spike protein is similar to the syncytin-1 protein. The production of antibodies against syncytin-1 can cause the body to attack the placenta, that is, lead to infertility.

However, this version does not stand up to criticism. Firstly, the protein similarity is minimal – 0.75%, and secondly, then infertility could be expected not only for the vaccinated, but also for those who had been ill (and for more than a year after the start of the pandemic, the structure of fertility has not changed in any way, there is no evidence of fertility problems ).

The same can be said about the myths that a vaccine can lead to cancer or any other serious illness.

fullscreen

A droplet falls from a syringe after a healthcare worker was given Pfizer / BioNTech vaccine at Providence Women’s and Newborn Hospital, Rhode Island, December 15, 2020

Photo:

AP / David Goldman

Vaccine – voluntary taking mercury “

Another myth, popular among anti-vaccines: the vaccine contains aluminum and mercury, which is sure to have a bad effect on health.

Indeed, mercury or aluminum additional components are often used in preparations. This has been done for more than a decade – and no harm is known from them. The fact is that their number is much less than a person usually consumes, for example, from food or water.

Many of the coronavirus vaccines in use today do not use these components at all.

read also

“You can get sick from a vaccine”

You or your friends have probably heard that the conditional Marya Ivanovna “just got vaccinated and immediately took to the hospital, the doctors say there are a lot of vaccinated people there.”Now, this is impossible. The fact is that there is no live virus in vaccines against coronavirus. Getting infected from the vaccine is like getting pregnant from the shadow of a man.

But you can get infected before vaccination, in between injections and even after two doses. Typically, the “full force” vaccines begin to work in two weeks. It is important to remember that no vaccine in the world guarantees 100% protection.

Therefore, unfortunately, there is a risk of getting sick even after vaccination. But research shows that in vaccinated people, the disease is much easier.This is if you do not take into account the fact that after vaccination, the chance to get infected also approaches the chance to win the lottery.

fullscreen

Nurse administers Pfizer / BioNTech vaccine to a resident of Ikaria nursing home in Barcelona, ​​Spain, February 2, 2021

Photo:

AP / Emilio Morenatti

“Vaccinations cause thrombosis and death”

Many fear thrombosis, facts which has been reported following the use of vector vaccines. The facts were really – such a reaction of the body is possible.But the chances of getting it are lower than an allergic reaction or a temperature after an injection.

Estimate the rarity of these events: By mid-April, there were six cases of thrombosis in the 6.8 million Americans vaccinated by Johnson & Johnson. That is, the risk is less than one in a million. In the UK, of the 18 million vaccinated AstraZeneca, 30 cases were reported – not one in a million, but here the figure is also close to statistical error.

These arguments are used by skeptics who say vaccines have been produced too quickly and are poorly understood.But recall that hundreds of millions of people received various vaccines and scientists did not record massive problems and side effects.

Statistically, the benefits of any existing vaccine outweigh the risks by orders of magnitude, and scientists always emphasize this. Well, again, it’s important to remember: you can die from an aspirin pill.

read also

“If a vaccine does not provide 99% protection, it is bad”

We repeat: there is no vaccine that would give 100% protection.But there is no data on which vaccine is “best”.

For example, studies (not preclinical, but already in practice) of Pfizer have shown that it gives 95% protection for everyone.

But the effectiveness of Johnson & Johnson shows in studies for some reason slightly different results for different regions.

It is even more interesting with it: clinical trials have shown 66.3% effectiveness, but, according to current data, no cases of coronavirus infection are known yet within 4 weeks after its use.

Vaccine efficacy and evaluation figures vary from study to study and depending on the current strains of the coronavirus. The only thing is for sure: they all work and they all significantly reduce the risks of both getting sick with coronavirus and dying from it.

How to get vaccinated?

Ukrainians can get vaccinated against coronavirus at mass vaccination centers, vaccination points and with the help of mobile immunization teams.