Environmental impact of the coal industry

From Wikipedia, the free encyclopedia

A coal surface mining site in Bihar, India

 

A mountaintop removal mining operation in the United States

The environmental impact of the coal industry includes issues such as land use, waste management, water and air pollution, caused by the coal mining, processing and the use of its products. In addition to atmospheric pollution, coal burning produces hundreds of millions of tons of solid waste products annually, including fly ash, bottom ash, and flue-gas desulfurization sludge, that contain mercury, uranium, thorium, arsenic, and other heavy metals.

There are severe health effects caused by burning coal. According to a report by the World Health Organization in 2008, coal particulates pollution are estimated to shorten approximately 1,000,000 lives annually worldwide. A 2004 study commissioned by environmental groups, but contested by the US EPA, concluded that coal burning costs 24,000 lives a year in the United States. More recently, an academic study estimated that the premature deaths from coal related air pollution was about 52,000. When compared to electricity produced from natural gas via hydraulic fracturing, coal electricity is 10-100 times more toxic, largely due to the amount of particulate matter emitted during combustion. When coal is compared to solar photovoltaic generation, the latter could save 51,999 American lives per year if solar were to replace coal generation in the U.S. In addition, the list of historical coal mining disasters is a long one, although work related coal deaths has declined substantially as safety measures have been enacted and underground mining has given up market share to surface mining. Underground mining hazards include suffocation, gas poisoning, roof collapse and gas explosions. Open cut hazards are principally mine wall failures and vehicle collisions. In the United States, an average of 26 coal miners per year died in the decade 2005–2014.

Land use management

Impact to land and surroundings

Strip mining severely alters the landscape, which reduces the value of the natural environment in the surrounding land. The land surface is dedicated to mining activities until it can be reshaped and reclaimed. If mining is allowed, resident human populations must be resettled off the mine site; economic activities, such as agriculture or hunting and gathering food and medicinal plants are interrupted. What becomes of the land surface after mining is determined by the manner in which the mining is conducted. Usually reclamation of disturbed lands to a land use condition is not equal to the original use. Existing land uses (such as livestock grazing, crop and timber production) are temporarily eliminated mining area. High-value, intensive-land-use areas like urban and transportation systems are not usually affected by mining operations. If mineral values are sufficient, these improvements may be removed to an adjacent area. 

Strip mining eliminates existing vegetation, destroys the genetic soil profile, displaces or destroys wildlife and habitat, alters current land uses, and to some extent permanently changes the general topography of the area mined. Adverse impacts on geological features of human interest may occur in a coal strip mine. Geomorphic and geophysical features and outstanding scenic resources may be sacrificed by indiscriminate mining. Paleontological, cultural, and other historic values may be endangered due to the disruptive activities of blasting, ripping, and excavating coal. Stripping of overburden eliminates and destroys archeological and historic features, unless they are removed beforehand.

The removal of vegetative cover and activities associated with the construction of haul roads, stockpiling of topsoil, displacement of overburden and hauling of soil and coal increase the quantity of dust around mining operations. Dust degrades air quality in the immediate area, has an adverse impact on vegetative life, and constitutes health and safety hazards for mine workers and nearby residents.

Surface mining disrupts virtually all aesthetic elements of the landscape. Alteration of land forms often imposes unfamiliar and discontinuous configurations. New linear patterns appear as material is extracted and waste piles are developed. Different colors and textures are exposed as vegetative cover is removed and overburden dumped to the side. Dust, vibration, and diesel exhaust odors are created (affecting sight, sound, and smell). Residents of local communities often find such impacts disturbing or unpleasant. In case of mountaintop removal, tops are removed from mountains or hills to expose thick coal seams underneath. The soil and rock removed is deposited in nearby valleys, hollows and depressions, resulting in blocked (and contaminated) waterways.

Removal of soil and rock overburden covering the coal resource may cause burial and loss of topsoil, exposes parent material, and creates large infertile wastelands. Soil disturbance and associated compaction result in conditions conducive to erosion. Soil removal from the area to be surface-mined alters or destroys many natural soil characteristics, and reduces its biodiversity and productivity for agriculture. Soil structure may be disturbed by pulverization or aggregate breakdown.

Mine collapses (or mine subsidences) have the potential to produce major effects above ground, which are especially devastating in developed areas. German underground coal-mining (especially in North Rhine-Westphalia) has damaged thousands of houses, and the coal-mining industries have set aside large sums in funding for future subsidence damages as part of their insurance and state-subsidy schemes. In a particularly spectacular case in the German Saar region (another historical coal-mining area), a suspected mine collapse in 2008 created an earthquake measuring 4.0 on the Richter magnitude scale, causing some damage to houses. Previously, smaller earthquakes had become increasingly common and coal mining was temporarily suspended in the area.

In response to negative land effects of coal mining and the abundance of abandoned mines in the US the federal government enacted the Surface Mining Control and Reclamation Act of 1977, which requires reclamation plans for future coal mining sites. These plans must be approved by federal or state authorities before mining begins.

Water management

Surface mining may impair groundwater in numerous ways: by drainage of usable water from shallow aquifers; lowering of water levels in adjacent areas and changes in flow direction within aquifers; contamination of usable aquifers below mining operations due to infiltration (percolation) of poor-quality mine water; and increased infiltration of precipitation on spoil piles. Where coal or carbonaceous shale is present, increased infiltration may result in: increased runoff of poor-quality water and erosion from spoil piles, recharge of poor-quality water to shallow groundwater aquifers and poor-quality water flow to nearby streams.

The contamination of both groundwater and nearby streams may be for long periods of time. Deterioration of stream quality results from acid mine drainage, toxic trace elements, high content of dissolved solids in mine drainage water, and increased sediment loads discharged to streams. When coal surfaces are exposed, pyrite comes in contact with water and air and forms sulfuric acid. As water drains from the mine, the acid moves into the waterways; as long as rain falls on the mine tailings the sulfuric-acid production continues, whether the mine is still operating or not. Also waste piles and coal storage piles can yield sediment to streams. Surface waters may be rendered unfit for agriculture, human consumption, bathing, or other household uses.

To anticipate these problems, water is monitored at coal mines. The five principal technologies used to control water flow at mine sites are: diversion systems, containment ponds, groundwater pumping systems, subsurface drainage systems and subsurface barriers.

River water pollution

Coal-fired boilers / power plants when using coal or lignite rich in limestone produces ash containing calcium oxide (CaO). CaO readily dissolves in water to form slaked lime / Ca(OH)₂ and carried by rain water to rivers / irrigation water from the ash dump areas. Lime softening process precipitates Ca and Mg ions / removes temporary hardness in the water and also converts sodium bicarbonates in river water into sodium carbonate. Sodium carbonate (washing soda) further reacts with the remaining Ca and Mg in the water to remove / precipitate the total hardness. Also water-soluble sodium salts present in the ash enhance the sodium content in water further. Thus river water is converted into soft water by eliminating Ca and Mg ions and enhancing Na ions by coal-fired boilers. Soft water application in irrigation (surface or ground water) converts the fertile soils into alkaline sodic soils. River water alkalinity and sodicity due to accumulation of salts in the remaining water after meeting various transpiration and evaporation losses, become acute when many coal-fired boilers and power stations are installed in a river basin. River water sodicity affects downstream cultivated river basins located in China, India, Egypt, Pakistan, west Asia, Australia, western US, etc.

Waste management

Aerial photograph of Kingston Fossil Plant coal fly ash slurry spill site taken the day after the event (December 23, 2008)

 

The burning of coal leaves substantial quantities of fly ash, which is usually stored in impoundment ponds. In the low-coal-content areas waste forms spoil tip. The U.S. EPA classified the 44 sites as potential hazards to communities (which means the waste sites could cause death and significant property damage if an event such as a storm, a terrorist attack or a structural failure caused a spill). The U.S. EPA estimated that about 300 dry landfills and wet storage ponds are used around the country to store ash from coal-fired power plants. The storage facilities hold the noncombustible ingredients of coal and the ash trapped by equipment designed to reduce air pollution.

Wildlife

Surface mining of coal causes direct and indirect damage to wildlife. The impact on wildlife stems primarily from disturbing, removing and redistributing the land surface. Some impacts are short-term, and confined to the mine site however others have far-reaching, long-term effects.

The most direct effect on wildlife is destruction or displacement of species in areas of excavation and spoil piling. Pit and spoil areas are not capable of providing food and cover for most species of wildlife. Mobile wildlife species like game animals, birds, and predators leave these areas. More sedentary animals like invertebrates, reptiles, burrowing rodents and small mammals may be destroyed. The community of microorganisms and nutrient-cycling processes are upset by movement, storage, and redistribution of soil. 

Degradation of aquatic habitats is a major impact by surface mining, and may be apparent many miles from a mining site. Sediment contamination of surface water is common with surface mining. Sediment yields may increase a thousand times their former level as a result of strip mining.

The effects of sediment on aquatic wildlife vary with the species and the amount of contamination. High sediment levels can kill fish directly, bury spawning beds, reduce light transmission, alter temperature gradients, fill in pools, spread stream flows over wider, shallower areas, and reduce production of aquatic organisms used as food by other species. These changes destroy the habitat of valued species, and may enhance habitat for less-desirable species. Existing conditions are already marginal for some freshwater fish in the United States, and the sedimentation of their habitat may result in their extinction. The heaviest sediment pollution of a drainage normally comes within 5 to 25 years after mining. In some areas, unvegetated spoil piles continue to erode even 50 to 65 years after mining.

The presence of acid-forming materials exposed as a result of surface mining can affect wildlife by eliminating habitat and by causing direct destruction of some species. Lesser concentrations can suppress productivity, growth rate and reproduction of many aquatic species. Acids, dilute concentrations of heavy metals, and high alkalinity can cause severe damage to wildlife in some areas. The duration of acidic-waste pollution can be long; estimates of the time required to leach exposed acidic materials in the Eastern United States range from 800 to 3,000 years.

Air pollution

Air emissions

“	In northern China, air pollution from the burning of fossil fuels, principally coal, is causing people to die on average 5.5 years sooner than they otherwise might.	”
— Tim Flannery, Atmosphere of Hope, 2015.

Coal and coal waste products (including fly ash, bottom ash and boiler slag) release approximately 20 toxic-release chemicals, including arsenic, lead, mercury, nickel, vanadium, beryllium, cadmium, barium, chromium, copper, molybdenum, zinc, selenium and radium, which are dangerous if released into the environment. While these substances are trace impurities, enough coal is burned that significant amounts of these substances are released.

During combustion, the reaction between coal and the air produces oxides of carbon, including carbon dioxide (CO₂, an important greenhouse gas), oxides of sulfur (mainly sulfur dioxide, SO₂), and various oxides of nitrogen (NO_x). Because of the hydrogenous and nitrogenous components of coal, hydrides and nitrides of carbon and sulfur are also produced during the combustion of coal in air. These include hydrogen cyanide (HCN), sulfur nitrate (SNO₃) and other toxic substances.

SO₂ and nitrogen oxide react in the atmosphere to form fine particles and ground-level ozone and are transported long distances, making it difficult for other states to achieve healthy levels of pollution control.

The wet cooling towers used in coal-fired power stations, etc. emit drift and fog which are also an environmental concern. The drift contains Respirable suspended particulate matter. In case of cooling towers with sea water makeup, sodium salts are deposited on nearby lands which would convert the land into alkali soil, reducing the fertility of vegetative lands and also cause corrosion of nearby structures. 

Fires sometimes occur in coal beds underground. When coal beds are exposed, the fire risk is increased. Weathered coal can also increase ground temperatures if it is left on the surface. Almost all fires in solid coal are ignited by surface fires caused by people or lightning. Spontaneous combustion is caused when coal oxidizes and airflow is insufficient to dissipate heat; this more commonly occurs in stockpiles and waste piles, rarely in bedded coal underground. Where coal fires occur, there is attendant air pollution from emission of smoke and noxious fumes into the atmosphere. Coal seam fires may burn underground for decades, threatening destruction of forests, homes, roadways and other valuable infrastructure. The best-known coal-seam fire may be the one which led to the permanent evacuation of Centralia, Pennsylvania, United States.

Approximately 75 Tg/S per year of Sulfur Dioxide (SO₂) is released from burning coal. After release, the Sulfur Dioxide is oxidized to gaseous H₂SO₂ which scatters solar radiation, hence their increase in the atmosphere exerts a cooling effect on climate that masks some of the warming caused by increased greenhouse gases. Release of SO₂ also contributes to the widespread acidification of ecosystems.

Mercury emissions

In New York State winds deposit mercury from the coal-fired power plants of the Midwest, contaminating the waters of the Catskill Mountains. Mercury is concentrated up the food chain, as it is converted into methylmercury, a toxic compound which harms both wildlife and people who consume freshwater fish. The mercury is consumed by worms, which are eaten by fish, which are eaten by birds (including bald eagles). As of 2008, mercury levels in bald eagles in the Catskills had reached new heights. "People are exposed to methylmercury almost entirely by eating contaminated fish and wildlife that are at the top of aquatic food chains." Ocean fish account for the majority of human exposure to methylmercury; the full range of sources of methylmercury in ocean fish is not well understood.

In February 2012, the U.S. EPA issued Mercury and Air Toxics Standards (MATS), which require all coal plants to substantially reduce mercury emissions.

Today [2011], more than half of all coal-fired power plants already deploy pollution control technologies that will help them meet these achievable standards. Once final, these standards will level the playing field by ensuring the remaining plants – about 40 percent of all coal-fired power plants – take similar steps to decrease dangerous pollutants.

Annual excess mortality and morbidity

In 2008 the World Health Organization (WHO) and other organizations calculated that coal particulates pollution cause approximately one million deaths annually across the world, which is approximately one third of all premature deaths related to all air pollution sources, for example in Istanbul by lung diseases and cancer.

Pollutants emitted by burning coal include fine particulates (PM2.5) and ground level ozone. Every year, the burning of coal without the use of available pollution control technology causes thousands of preventable deaths in the United States. A study commissioned by the Maryland nurses association in 2006 found that emissions from just six of Maryland's coal-burning plants caused 700 deaths per year nationwide, including 100 in Maryland. Since installation of pollution abatement equipment on one of these six, the Brandon Shores plant, now "produces 90 percent less nitrogen oxide, an ingredient of smog; 95 percent less sulfur, which causes acid rain; and vastly lower fractions of other pollutants."

Economic costs

A 2001 EU-funded study known as ExternE, or Externalities of Energy, over the decade from 1995 to 2005 found that the cost of producing electricity from coal would double over its present value, if external costs were taken into account. These external costs include damage to the environment and to human health from airborne particulate matter, nitrogen oxides, chromium VI and arsenic emissions produced by coal. It was estimated that external, downstream, fossil fuel costs amount up to 1–2% of the EU’s entire Gross Domestic Product (GDP), with coal being the main fossil fuel accountable, and this was before the external cost of global warming from these sources was even included. The study found that environmental and health costs of coal alone were €0.06/kWh, or 6 cents/kWh, with the energy sources of the lowest external costs being nuclear power €0.0019/kWh, and wind power at €0.0009/kWh.

High rates of motherboard failures in China and India appear to be due to "sulfurous air pollution produced by coal that’s burned to generate electricity. It corrodes the copper circuitry," according to Intel researchers.

Greenhouse gas emissions

The combustion of coal is the largest contributor to the human-made increase of CO₂ in the atmosphere. Electric generation using coal burning produces approximately twice the greenhouse gasses per kilowatt compared to generation using natural gas.

Coal mining releases methane, a potent greenhouse gas. Methane is the naturally occurring product of the decay of organic matter as coal deposits are formed with increasing depths of burial, rising temperatures, and rising pressure over geological time. A portion of the methane produced is absorbed by the coal and later released from the coal seam (and surrounding disturbed strata) during the mining process. Methane accounts for 10.5 percent of greenhouse-gas emissions created through human activity. According to the Intergovernmental Panel on Climate Change, methane has a global warming potential 21 times greater than that of carbon dioxide over a 100-year timeline. The process of mining can release pockets of methane. These gases may pose a threat to coal miners, as well as a source of air pollution. This is due to the relaxation of pressure and fracturing of the strata during mining activity, which gives rise to safety concerns for the coal miners if not managed properly. The buildup of pressure in the strata can lead to explosions during (or after) the mining process if prevention methods, such as "methane draining", are not taken.

In 2008 James E. Hansen and Pushker Kharecha published a peer-reviewed scientific study analyzing the effect of a coal phase-out on atmospheric CO₂ levels. Their baseline mitigation scenario was a phaseout of global coal emissions by 2050. Under the Business as Usual scenario, atmospheric CO₂ peaks at 563 parts per million (ppm) in the year 2100. Under the four coal phase-out scenarios, atmospheric CO₂ peaks at 422–446 ppm between 2045 and 2060 and declines thereafter.

Radiation exposure

Coal also contains low levels of uranium, thorium, and other naturally occurring radioactive isotopes which, if released into the environment, may lead to radioactive contamination. Coal plants emit radiation in the form of radioactive fly ash, which is inhaled and ingested by neighbours, and incorporated into crops. A 1978 paper from Oak Ridge National Laboratory estimated that coal-fired power plants of that time may contribute a whole-body committed dose of 19 µSv/a to their immediate neighbours in a 500 m radius. The United Nations Scientific Committee on the Effects of Atomic Radiation's 1988 report estimated the committed dose 1 km away to be 20 µSv/a for older plants or 1 µSv/a for newer plants with improved fly ash capture, but was unable to confirm these numbers by test.

Excluding contained waste and unintentional releases from nuclear plants, coal-plants carry more radioactive wastes into the environment than nuclear plants per unit of produced energy. Plant-emitted radiation carried by coal-derived fly ash delivers 100 times more radiation to the surrounding environment than does the normal operation of a similarly productive nuclear plant. This comparison does not consider the rest of the fuel cycle, i.e., coal and uranium mining and refining and waste disposal. The operation of a 1000-MWe coal-fired power plant results in a nuclear radiation dose of 490 person-rem/year, compared to 136 person-rem/year, for an equivalent nuclear power plant including uranium mining, reactor operation and waste disposal.

Dangers to miners

Historically, coal mining has been a very dangerous activity, and the list of historical coal mining disasters is long. The principal hazards are mine wall failures and vehicle collisions; underground mining hazards include suffocation, gas poisoning, roof collapse and gas explosions. Chronic lung diseases, such as pneumoconiosis (black lung) were once common in miners, leading to reduced life expectancy. In some mining countries black lung is still common, with 4,000 new cases of black lung every year in the US (4 percent of workers annually) and 10,000 new cases every year in China (0.2 percent of workers). Rates may be higher than reported in some regions.

In the United States, an average of 23 coal miners per year died in the decade 2007–2016. Recent U.S. coal-mining disasters include the Sago Mine disaster of January 2006. In 2007, a mine accident in Utah's Crandall Canyon Mine killed nine miners, with six entombed. The Upper Big Branch Mine disaster in West Virginia killed 29 miners in April 2010.

However, in lesser developed countries and some developing countries, many miners continue to die annually, either through direct accidents in coal mines or through adverse health consequences from working under poor conditions. China, in particular, has the highest number of coal mining related deaths in the world, with official statistics claiming that 6,027 deaths in 2004. To compare, 28 deaths were reported in the US in the same year. Coal production in China is twice that in the US, while the number of coal miners is around 50 times that of the US, making deaths in coal mines in China 4 times as common per worker (108 times as common per unit output) as in the US. 

The Farmington coal mine disaster kills 78. West Virginia, US, 1968.

 

Build-ups of a hazardous gas are known as damps:

• Black damp: a miture of carbon dioxide and nitrogen in a mine can cause suffocation. The anoxic condition results of depletion of oxygen in enclosed spaces, e.g. by corrosion.
• After damp: similar to black damp, after damp consists of carbon monoxide, carbon dioxide and nitrogen and forms after a mine explosion.
• Fire damp: consists of mostly methane, a highly flammable gas that explodes between 5% and 15% – at 25% it causes asphyxiation.
• Stink damp: so named for the rotten egg smell of the hydrogen sulphide gas, stink damp can explode and is also very toxic.
• White damp: air containing carbon monoxide which is toxic, even at low concentrations

Firedamp explosions can trigger the much more dangerous coal dust explosions, which can engulf an entire pit. Most of these risks can be greatly reduced in modern mines, and multiple fatality incidents are now rare in some parts of the developed world. Modern mining in the US results in approximately 30 deaths per year due to mine accidents.

Mercury poisoning

From Wikipedia, the free encyclopedia

Mercury poisoning
Synonyms	Mercury toxicity, mercury overdose, mercury intoxication, hydrargyria, mercurialism
Elemental mercury
Specialty	Toxicology
Symptoms	Muscle weakness, poor coordination, numbness in the hands and feet
Complications	Kidney problems, decreased intelligence
Causes	Exposure to mercury
Diagnostic method	Difficult
Prevention	Decreasing use of mercury, low mercury diet
Medication	Acute poisoning: dimercaptosuccinic acid (DMSA), dimercaptopropane sulfonate (DMPS)

Mercury poisoning is a type of metal poisoning due to exposure to mercury. Symptoms depend upon the type, dose, method, and duration of exposure. They may include muscle weakness, poor coordination, numbness in the hands and feet, skin rashes, anxiety, memory problems, trouble speaking, trouble hearing, or trouble seeing. High level exposure to methylmercury is known as Minamata disease. Methylmercury exposure in children may result in acrodynia (pink disease) in which the skin becomes pink and peels. Long-term complications may include kidney problems and decreased intelligence. The effects of long-term low-dose exposure to methylmercury are unclear.

Forms of mercury exposure include metal, vapor, salt, and organic compound. Most exposure is from eating fish, amalgam based dental fillings, or exposure at work. In fish, those higher up in the food chain generally have higher levels of mercury. Less commonly, poisoning may occur as a method of attempted suicide. Human activities that release mercury into the environment include the burning of coal and mining of gold. Tests of the blood, urine, and hair for mercury are available but do not relate well to the amount in the body.

Prevention includes eating a diet low in mercury, removing mercury from medical and other devices, proper disposal of mercury, and not mining further mercury. In those with acute poisoning from inorganic mercury salts, chelation with either dimercaptosuccinic acid (DMSA) or dimercaptopropane sulfonate (DMPS) appears to improve outcomes if given within a few hours of exposure. Chelation for those with long-term exposure is of unclear benefit. In certain communities that survive on fishing, rates of mercury poisoning among children have been as high as 1.7 per 100.

Signs and symptoms

Common symptoms of mercury poisoning include peripheral neuropathy, presenting as paresthesia or itching, burning, pain, or even a sensation that resembles small insects crawling on or under the skin (formication); skin discoloration (pink cheeks, fingertips and toes); swelling; and desquamation (shedding or peeling of skin). 

Mercury irreversibly inhibits selenium-dependent enzymes (see below) and may also inactivate S-adenosyl-methionine, which is necessary for catecholamine catabolism by catechol-O-methyl transferase. Due to the body's inability to degrade catecholamines (e.g. epinephrine), a person suffering from mercury poisoning may experience profuse sweating, tachycardia (persistently faster-than-normal heart beat), increased salivation, and hypertension (high blood pressure). 

Affected children may show red cheeks, nose and lips, loss of hair, teeth, and nails, transient rashes, hypotonia (muscle weakness), and increased sensitivity to light. Other symptoms may include kidney dysfunction (e.g. Fanconi syndrome) or neuropsychiatric symptoms such as emotional lability, memory impairment, or insomnia. 

Thus, the clinical presentation may resemble pheochromocytoma or Kawasaki disease. Desquamation (skin peeling) can occur with severe mercury poisoning acquired by handling elemental mercury.

Causes

The consumption of fish is by far the most significant source of ingestion-related mercury exposure in humans, although plants and livestock also contain mercury due to bioconcentration of mercury from seawater, freshwater, marine and lacustrine sediments, soils, and atmosphere, and due to biomagnification by ingesting other mercury-containing organisms. Exposure to mercury can occur from breathing contaminated air, from eating foods that have acquired mercury residues during processing, from exposure to mercury vapor in mercury amalgam dental restorations, and from improper use or disposal of mercury and mercury-containing objects, for example, after spills of elemental mercury or improper disposal of fluorescent lamps.

All of these, except elemental liquid mercury produce toxicity or death with less than a gram. Mercury's zero oxidation state (Hg⁰) exists as vapor or as liquid metal, its mercurous state (Hg⁺) exists as inorganic salts, and its mercuric state (Hg²⁺) may form either inorganic salts or organomercury compounds.

Consumption of whale and dolphin meat, as is the practice in Japan, is a source of high levels of mercury poisoning. Tetsuya Endo, a professor at the Health Sciences University of Hokkaido, has tested whale meat purchased in the whaling town of Taiji and found mercury levels more than 20 times the acceptable Japanese standard.

Human-generated sources, such as coal-burning power plants emit about half of atmospheric mercury, with natural sources such as volcanoes responsible for the remainder. An estimated two-thirds of human-generated mercury comes from stationary combustion, mostly of coal. Other important human-generated sources include gold production, nonferrous metal production, cement production, waste disposal, human crematoria, caustic soda production, pig iron and steel production, mercury production (mostly for batteries), and biomass burning.

Small independent gold-mining operation workers are at higher risk of mercury poisoning because of crude processing methods. Such is the danger for the galamsey in Ghana and similar workers known as orpailleurs in neighboring francophone countries. While no official government estimates of the labor force have been made, observers believe 20,000–50,000 work as galamseys in Ghana, a figure including many women, who work as porters. Similar problems have been reported amongst the gold miners of Indonesia.

Some mercury compounds, especially organomercury compounds, can also be readily absorbed through direct skin contact. Mercury and its compounds are commonly used in chemical laboratories, hospitals, dental clinics, and facilities involved in the production of items such as fluorescent light bulbs, batteries, and explosives.

Many traditional medicines, including Ayurvedic medicine and Traditional Chinese medicine contain mercury and other heavy metals.

No scientific data support the claim that mercury compounds in vaccine preservatives cause autism or its symptoms.

Sources

Compounds of mercury tend to be much more toxic than either the elemental form or the salts. These compounds have been implicated in causing brain and liver damage. The most dangerous mercury compound, dimethylmercury, is so toxic that even a few microliters spilled on the skin, or even on a latex glove, can cause death.

Methylmercury and related organomercury compounds

Methylmercury is the major source of organic mercury for all individuals. Due to bioaccumulation it works its way up through the food web and thus biomagnifies, resulting in high concentrations among populations of some species. Top predatory fish, such as tuna or swordfish, are usually of greater concern than smaller species. The US FDA and the EPA advise women of child-bearing age, nursing mothers, and young children to completely avoid swordfish, shark, king mackerel and tilefish from the Gulf of Mexico, and to limit consumption of albacore ("white") tuna to no more than 170 g (6 oz) per week, and of all other fish and shellfish to no more than 340 g (12 oz) per week. A 2006 review of the risks and benefits of fish consumption found, for adults, the benefits of one to two servings of fish per week outweigh the risks, even (except for a few fish species) for women of childbearing age, and that avoidance of fish consumption could result in significant excess coronary heart disease deaths and suboptimal neural development in children.

The period between exposure to methylmercury and the appearance of symptoms in adult poisoning cases is long. The longest recorded latent period is five months after a single exposure, in the Dartmouth case (see History); other latent periods in the range of weeks to months have also been reported. No explanation for this long latent period is known. When the first symptom appears, typically paresthesia (a tingling or numbness in the skin), it is followed rapidly by more severe effects, sometimes ending in coma and death. The toxic damage appears to be determined by the peak value of mercury, not the length of the exposure.

Methylmercury exposure during rodent gestation, a developmental period that approximately models human neural development during the first two trimesters of gestation, has long-lasting behavioral consequences that appear in adulthood and, in some cases, may not appear until aging. Prefrontal cortex or dopamine neurotransmission could be especially sensitive to even subtle gestational methylmercury exposure and suggests that public health assessments of methylmercury based on intellectual performance may underestimate the impact of methylmercury in public health. 

Ethylmercury is a breakdown product of the antibacteriological agent ethylmercurithiosalicylate, which has been used as a topical antiseptic and a vaccine preservative (further discussed under Thiomersal below). Its characteristics have not been studied as extensively as those of methylmercury. It is cleared from the blood much more rapidly, with a half-life of seven to 10 days, and it is metabolized much more quickly than methylmercury. It is presumed not to have methylmercury's ability to cross the blood–brain barrier via a transporter, but instead relies on simple diffusion to enter the brain. Other exposure sources of organic mercury include phenylmercuric acetate and phenylmercuric nitrate. These compounds were used in indoor latex paints for their antimildew properties, but were removed in 1990 because of cases of toxicity.

Inorganic mercury compounds

Mercury occurs as salts such as mercuric chloride (HgCl₂) and mercurous chloride (Hg₂Cl₂), the latter also known as calomel. Because they are more soluble in water, mercuric salts are usually more acutely toxic than mercurous salts. Their higher solubility lets them be more readily absorbed from the gastrointestinal tract. Mercury salts affect primarily the gastrointestinal tract and the kidneys, and can cause severe kidney damage; however, as they cannot cross the blood–brain barrier easily, these salts inflict little neurological damage without continuous or heavy exposure. Mercuric cyanide (Hg(CN)₂) is a particularly toxic mercury compound that has been used in murders, as it contains not only mercury but also cyanide, leading to simultaneous cyanide poisoning. The drug n-acetyl penicillamine has been used to treat mercury poisoning with limited success.

Elemental mercury

Quicksilver (liquid metallic mercury) is poorly absorbed by ingestion and skin contact. Its vapor is the most hazardous form. Animal data indicate less than 0.01% of ingested mercury is absorbed through the intact gastrointestinal tract, though it may not be true for individuals suffering from ileus. Cases of systemic toxicity from accidental swallowing are rare, and attempted suicide via intravenous injection does not appear to result in systemic toxicity, though it still causes damage by physically blocking blood vessels both at the site of injection and the lungs. Though not studied quantitatively, the physical properties of liquid elemental mercury limit its absorption through intact skin and in light of its very low absorption rate from the gastrointestinal tract, skin absorption would not be high. Some mercury vapor is absorbed dermally, but uptake by this route is only about 1% of that by inhalation.

In humans, approximately 80% of inhaled mercury vapor is absorbed via the respiratory tract, where it enters the circulatory system and is distributed throughout the body. Chronic exposure by inhalation, even at low concentrations in the range 0.7–42 μg/m³, has been shown in case–control studies to cause effects such as tremors, impaired cognitive skills, and sleep disturbance in workers.

Acute inhalation of high concentrations causes a wide variety of cognitive, personality, sensory, and motor disturbances. The most prominent symptoms include tremors (initially affecting the hands and sometimes spreading to other parts of the body), emotional lability (characterized by irritability, excessive shyness, confidence loss, and nervousness), insomnia, memory loss, neuromuscular changes (weakness, muscle atrophy, muscle twitching), headaches, polyneuropathy (paresthesia, stocking-glove sensory loss, hyperactive tendon reflexes, slowed sensory and motor nerve conduction velocities), and performance deficits in tests of cognitive function.

Mechanism

The toxicity of mercury sources can be expected to depend on its nature, i.e., salts vs. organomercury compounds vs. elemental mercury. 

One mechanism of mercury toxicity involves its irreversible inhibition of selenoenzymes, such as thioredoxin reductase (IC50 = 9 nM). Although it has many functions, thioredoxin reductase restores vitamins C and E, as well as a number of other important antioxidant molecules, back into their reduced forms, enabling them to counteract oxidative damage. Since the rate of oxygen consumption is particularly high in brain tissues, production of reactive oxygen species (ROS) is accentuated in these vital cells, making them particularly vulnerable to oxidative damage and especially dependent upon the antioxidant protection provided by selenoenzymes. High mercury exposures deplete the amount of cellular selenium available for the biosynthesis of thioredoxin reductase and other selenoenzymes that prevent and reverse oxidative damage, which, if the depletion is severe and long lasting, results in brain cell dysfunctions that can ultimately cause death. 

Mercury in its various forms is particularly harmful to fetuses as an environmental toxin in pregnancy, as well as to infants. Women who have been exposed to mercury in substantial excess of dietary selenium intakes during pregnancy are at risk of giving birth to children with serious birth defects. Mercury exposures in excess of dietary selenium intakes in young children can have severe neurological consequences, preventing nerve sheaths from forming properly. 

Exposure to methylmercury causes increased levels of antibodies sent to myelin basic protein (MBP), which is involved in the myelination of neurons, and glial fibrillary acidic protein (GFAP), which is essential to many central nervous system (CNS). This causes an autoimmmune response against MBP and GFAP and results in the degradation of neural myelin and general decline in function of the CNS.

Diagnosis

Diagnosis of elemental or inorganic mercury poisoning involves determining the history of exposure, physical findings, and an elevated body burden of mercury. Although whole-blood mercury concentrations are typically less than 6 μg/L, diets rich in fish can result in blood mercury concentrations higher than 200 μg/L; it is not that useful to measure these levels for suspected cases of elemental or inorganic poisoning because of mercury's short half-life in the blood. If the exposure is chronic, urine levels can be obtained; 24-hour collections are more reliable than spot collections. It is difficult or impossible to interpret urine samples of patients undergoing chelation therapy, as the therapy itself increases mercury levels in the samples.

Diagnosis of organic mercury poisoning differs in that whole-blood or hair analysis is more reliable than urinary mercury levels.

Prevention

Mercury poisoning can be prevented or minimized by eliminating or reducing exposure to mercury and mercury compounds. To that end, many governments and private groups have made efforts to heavily regulate the use of mercury, or to issue advisories about its use. For example, the export from the European Union of mercury and some mercury compounds has been prohibited since 15 March 2010.

Country	Regulating agency	Regulated activity	Medium	Type of mercury compound	Type of limit	Limit
US	Occupational Safety and Health Administration	occupational exposure	air	elemental mercury	Ceiling (not to exceed)	0.1 mg/m³
US	Occupational Safety and Health Administration	occupational exposure	air	organic mercury	Ceiling (not to exceed)	0.05 mg/m³
US	Food and Drug Administration	eating	sea food	methylmercury	Maximum allowable concentration	1 ppm (1 mg/L)
US	Environmental Protection Agency	drinking	water	inorganic mercury	Maximum contaminant level	2 ppb (0.002 mg/L)

The United States Environmental Protection Agency (EPA) issued recommendations in 2004 regarding exposure to mercury in fish and shellfish. The EPA also developed the "Fish Kids" awareness campaign for children and young adults  on account of the greater impact of mercury exposure to that population.

Cleaning spilled mercury

EPA workers clean up residential mercury spill in 2004

 

Mercury thermometers and mercury light bulbs are not as common as they used to be, and the amount of mercury they contain is unlikely to be a health concern if handled carefully. However, broken items still require careful cleanup, as mercury can be hard to collect and it is easy to accidentally create a much larger exposure problem. If available, powdered sulfur may be applied to the spill, in order to create a solid compound that is more easily removed from surfaces than liquid mercury.

Treatment

Identifying and removing the source of the mercury is crucial. Decontamination requires removal of clothes, washing skin with soap and water, and flushing the eyes with saline solution as needed.

Chelation therapy

Chelation therapy for acute inorganic mercury poisoning can be done with DMSA, 2,3-dimercapto-1-propanesulfonic acid (DMPS), D-penicillamine (DPCN), or dimercaprol (BAL). Only DMSA is FDA-approved for use in children for treating mercury poisoning. However, several studies found no clear clinical benefit from DMSA treatment for poisoning due to mercury vapor. No chelator for methylmercury or ethylmercury is approved by the FDA; DMSA is the most frequently used for severe methylmercury poisoning, as it is given orally, has fewer side-effects, and has been found to be superior to BAL, DPCN, and DMPS. α-Lipoic acid (ALA) has been shown to be protective against acute mercury poisoning in several mammalian species when it is given soon after exposure; correct dosage is required, as inappropriate dosages increase toxicity. Although it has been hypothesized that frequent low dosages of ALA may have potential as a mercury chelator, studies in rats have been contradictory. Glutathione and N-acetylcysteine (NAC) are recommended by some physicians, but have been shown to increase mercury concentrations in the kidneys and the brain.

Chelation therapy can be hazardous if administered incorrectly. In August 2005, an incorrect form of EDTA (edetate disodium) used for chelation therapy resulted in hypocalcemia, causing cardiac arrest that killed a five-year-old autistic boy.

Other

Experimental findings have demonstrated an interaction between selenium and methylmercury, but epidemiological studies have found little evidence that selenium helps to protect against the adverse effects of methylmercury.

Prognosis

Some of the toxic effects of mercury are partially or wholly reversible, either through specific therapy or through natural elimination of the metal after exposure has been discontinued. Autopsy findings point to a half-life of inorganic mercury in human brains of 27.4 years. Heavy or prolonged exposure can do irreversible damage, in particular in fetuses, infants, and young children. Young's syndrome is believed to be a long-term consequence of early childhood mercury poisoning.

Mercuric chloride may cause cancer as it has caused increases in several types of tumors in rats and mice, while methyl mercury has caused kidney tumors in male rats. The EPA has classified mercuric chloride and methyl mercury as possible human carcinogens (ATSDR, EPA)

Detection in biological fluids

Mercury may be measured in blood or urine to confirm a diagnosis of poisoning in hospitalized people or to assist in the forensic investigation in a case of fatal overdosage. Some analytical techniques are capable of distinguishing organic from inorganic forms of the metal. The concentrations in both fluids tend to reach high levels early after exposure to inorganic forms, while lower but very persistent levels are observed following exposure to elemental or organic mercury. Chelation therapy can cause a transient elevation of urine mercury levels.

History

• Several Chinese emperors and other Chinese nobles are known or suspected to have died or been sickened by mercury poisoning after alchemists administered them "elixirs" to promote health, longevity, or immortality that contained either elemental mercury or (more commonly) cinnabar. Among the most prominent examples:
  • The first emperor of unified China, Qin Shi Huang, it is reported, died of ingesting mercury pills that were intended to give him eternal life.
  • Emperor Xuānzong of Tang, one of the emperors of the late Tang dynasty of China, was prescribed "cinnabar that had been treated and subdued by fire" to achieve immortality. Concerns that the prescription was having ill effects on the emperor's health and sanity were waved off by the imperial alchemists, who cited to medical texts listing a number of the emperor's conditions (including itching, formication, swelling, and muscle weakness), today recognized as signs and symptoms of mercury poisoning, as evidence that the elixir was effectively treating the emperor's latent ailments. Xuānzong became irritable and paranoid, and he seems to have ultimately died from the poisoning.
• During the Spanish conquest of the New World in the 16th and 17th centuries, slave mining of mercury deposits was common because the metal was used to purify the rich silver deposits in Central America before being shipped back to Spain. To avoid the effects of mercury poisoning on their children, parents were known to purposefully maim or dismember their children to make them unable to work in the mines.
• The phrase mad as a hatter is likely a reference to mercury poisoning among milliners (so-called "mad hatter disease"), as mercury-based compounds were once used in the manufacture of felt hats in the 18th and 19th century. (The Mad Hatter character of Alice in Wonderland was, it is presumed, inspired by an eccentric furniture dealer named Theophilus Carter. Carter was not a victim of mad hatter disease although Lewis Carroll would have been familiar with the phenomenon of dementia that occurred among hatters.)
• In 1810, two British ships, HMS Triumph and HMS Phipps, salvaged a large load of elemental mercury from a wrecked Spanish vessel near Cadiz, Spain. The bladders containing the mercury soon ruptured. The element spread about the ships in liquid and vapor forms. The sailors presented with neurologic compromises: tremor, paralysis, and excessive salivation as well as tooth loss, skin problems, and pulmonary complaints. In 1823 William Burnet, MD published a report on the effects of Mercurial vapor. The Triumph’s surgeon, Henry Plowman, had concluded that the ailments had arisen from inhaling the mercurialized atmosphere. His treatment was to order the lower deck gun ports to be opened, when it was safe to do so; sleeping on the orlop was forbidden; and no men slept in the lower deck if they were at all symptomatic. Windsails were set to channel fresh air into the lower decks day and night.
• Historically, gold amalgam was widely used in gilding, leading to numerous casualties among the workers. It is estimated that during the construction of Saint Isaac's Cathedral alone, 60 men died from the gilding of the main dome.
• For years, including the early part of his presidency, Abraham Lincoln took a common medicine of his time called "blue mass," which contained significant amounts of mercury.
• On September 5, 1920, silent movie actress Olive Thomas ingested mercury capsules dissolved in an alcoholic solution at the Hotel Ritz in Paris. There is still controversy over whether it was suicide, or whether she consumed the external preparation by mistake. Her husband, Jack Pickford (the brother of Mary Pickford), had syphilis, and the mercury was used as a treatment of the venereal disease at the time. She died a few days later at the American Hospital in Neuilly.
• An early scientific study of mercury poisoning was in 1923–6 by the German inorganic chemist, Alfred Stock, who himself became poisoned, together with his colleagues, by breathing mercury vapor that was being released by his laboratory equipment—diffusion pumps, float valves, and manometers—all of which contained mercury, and also from mercury that had been accidentally spilt and remained in cracks in the linoleum floor covering. He published a number of papers on mercury poisoning, founded a committee in Berlin to study cases of possible mercury poisoning, and introduced the term micromercurialism.
• The term Hunter-Russell syndrome derives from a study of mercury poisoning among workers in a seed packing factory in Norwich, England in the late 1930s who breathed methylmercury that was being used as a seed disinfectant and preservative.
• Outbreaks of methylmercury poisoning occurred in several places in Japan during the 1950s due to industrial discharges of mercury into rivers and coastal waters. The best-known instances were in Minamata and Niigata. In Minamata alone, more than 600 people died due to what became known as Minamata disease. More than 21,000 people filed claims with the Japanese government, of which almost 3000 became certified as having the disease. In 22 documented cases, pregnant women who consumed contaminated fish showed mild or no symptoms but gave birth to infants with severe developmental disabilities.
• Mercury poisoning of two First Nation communities in Ontario, Canada occurred in the late 1960s due to industrial chemical waste released into the waterways and air.
• Widespread mercury poisoning occurred in rural Iraq in 1971–1972, when grain treated with a methylmercury-based fungicide that was intended for planting only was used by the rural population to make bread, causing at least 6530 cases of mercury poisoning and at least 459 deaths (see Basra poison grain disaster).
• On August 14, 1996, Karen Wetterhahn, a chemistry professor working at Dartmouth College, spilled a small amount of dimethylmercury on her latex glove. She began experiencing the symptoms of mercury poisoning five months later and, despite aggressive chelation therapy, died a few months later from brain malfunction due to mercury intoxication.
• In April 2000, Alan Chmurny attempted to kill a former employee, Marta Bradley, by pouring mercury into the ventilation system of her car.
• On March 19, 2008, Tony Winnett, 55, inhaled mercury vapors while trying to extract gold from computer parts (by using liquid mercury to separate gold from the rest of the alloy), and died ten days later. His Oklahoma residence became so contaminated that it had to be gutted.
• In December 2008, actor Jeremy Piven was diagnosed with mercury poisoning possibly resulting from eating sushi twice a day for twenty years or herbal remedies he was also taking.
• In India, a study by Centre for Science and Environment and Indian Institute of Toxicology Research has found that in the country's energy capital Singrauli, mercury is slowly entering people's homes, food, water and even blood.

Infantile acrodynia

Infantile acrodynia (also known as "calomel disease", "erythredemic polyneuropathy", and "pink disease") is a type of mercury poisoning in children characterized by pain and pink discoloration of the hands and feet. The word is derived from the Greek, where άκρο means end or extremity, and οδυνη means pain. Acrodynia resulted primarily from calomel in teething powders and decreased greatly after calomel was excluded from most teething powders in 1954.

Acrodynia is difficult to diagnose, "it is most often postulated that the etiology of this syndrome is an idiosyncratic hypersensitivity reaction to mercury because of the lack of correlation with mercury levels, many of the symptoms resemble recognized mercury poisoning."

Medicine

Mercury was once prescribed as a purgative. Many mercury-containing compounds were once used in medicines. These include calomel (mercurous chloride), and mercuric chloride.

Thiomersal

In 1999, the Centers for Disease Control (CDC) and the American Academy of Pediatrics (AAP) asked vaccine makers to remove the organomercury compound thiomersal (spelled "thimerosal" in the US) from vaccines as quickly as possible, and thiomersal has been phased out of US and European vaccines, except for some preparations of influenza vaccine. The CDC and the AAP followed the precautionary principle, which assumes that there is no harm in exercising caution even if it later turns out to be unwarranted, but their 1999 action sparked confusion and controversy that Thiomersal was the cause of autism.

Since 2000, the thiomersal in child vaccines has been alleged to contribute to autism, and thousands of parents in the United States have pursued legal compensation from a federal fund. A 2004 Institute of Medicine (IOM) committee favored rejecting any causal relationship between thiomersal-containing vaccines and autism. Autism incidence rates increased steadily even after thiomersal was removed from childhood vaccines. Currently there is no accepted scientific evidence that exposure to thiomersal is a factor in causing autism.

Dental amalgam toxicity

Dental amalgam is a possible cause of low-level mercury poisoning due to its use in dental fillings. Discussion on the topic includes debates on whether amalgam should be used, with critics arguing that its toxic effects make it unsafe.

Cosmetics

Some skin whitening products contain the toxic mercury(II) chloride as the active ingredient. When applied, the chemical readily absorbs through the skin into the bloodstream. The use of mercury in cosmetics is illegal in the United States. However, cosmetics containing mercury are often illegally imported. Following a certified case of mercury poisoning resulting from the use of an imported skin whitening product, the United States Food and Drug Administration warned against the use of such products. Symptoms of mercury poisoning have resulted from the use of various mercury-containing cosmetic products. The use of skin whitening products is especially popular among Asian women. In Hong Kong in 2002, two products were discovered to contain between 9,000 and 60,000 times the recommended dose.

Fluorescent lamps

Fluorescent lamps contain mercury, which is released when bulbs break. Mercury in bulbs is typically present as either elemental mercury liquid, vapor, or both, since the liquid evaporates at ambient temperature. When broken indoors, bulbs may emit sufficient mercury vapor to present health concerns, and the U.S. Environmental Protection Agency recommends evacuating and airing out a room for at least 15 minutes after breaking a fluorescent light bulb. Breakage of multiple bulbs presents a greater concern. A 1987 report described a 23-month-old toddler who suffered anorexia, weight loss, irritability, profuse sweating, and peeling and redness of fingers and toes. This case of acrodynia was traced to exposure of mercury from a carton of 8-foot fluorescent light bulbs that had broken in a potting shed adjacent to the main nursery. The glass was cleaned up and discarded, but the child often used the area to play in .

Assassination attempts

Mercury has, allegedly, been used at various times to assassinate people. In 2008, Russian lawyer Karinna Moskalenko claimed to have been poisoned by mercury left in her car, while in 2010 journalists Viktor Kalashnikov and Marina Kalashnikova accused Russia's FSB of trying to poison them.