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A 25-foot (7.6 m) wall of coal fly ash contaminated with toxic heavy metals, resulting from the release of 5.4 million cubic yards of coal fly ash slurry into the Emory River, Tennessee, and nearby land and water features, in December 2008.^[1] Testing showed significantly elevated levels of arsenic, copper, barium, cadmium, chromium, lead, mercury, nickel, and thallium in samples of slurry and river water.^[2] Cleanup costs may exceed $1.2 billion.^[3]

A toxic heavy metal is any relatively dense metal or metalloid that is noted for its potential toxicity, especially in environmental contexts.^[4] The term has particular application to cadmium, mercury, lead and arsenic,^[5] all of which appear in the World Health Organisation's list of 10 chemicals of major public concern.^[6] Other examples include chromium, cobalt, nickel, copper, zinc, selenium, silver, antimony and thallium.

Toxic heavy metals are found naturally in the earth, and become concentrated as a result of human caused activities. They enter plant, animal and human tissues via inhalation, diet and manual handling, and can bind to, and interfere with the functioning of vital cellular components. The toxic effects of arsenic, mercury and lead were known to the ancients but methodical studies of the toxicity of some heavy metals appear to date from only 1868. In humans, heavy metal poisoning is generally treated by the administration of chelating agents. Some elements regarded as toxic heavy metals are essential, in small quantities, for human health.

Contamination sources

Tetraethyl lead (CH₃CH₂)₄Pb is probably the most significant toxic heavy metal contaminant in recent use.^[7]

Toxic heavy metals are found naturally in the earth, and become concentrated as a result of human caused activities. Common sources are from mining and industrial wastes; vehicle emissions; lead-acid batteries; fertilisers; paints; treated woods; plastics floating on the world's oceans;^[8] and aging water supply infrastructure.^[9] Lead is the most prevalent toxic heavy metal contaminant.^[10] As a component of tetra-ethyl lead it was used extensively in gasoline during the 1930s-1970s.^[11] Lead levels in the aquatic environments of industrialised societies have been estimated to be two to three times those of pre-industrial levels.^[12] Although the use of leaded gasoline was largely phased out in North America by 1996, soils next to roads built before this time retain high lead concentrations. Lead (from lead azide or lead styphnate used in firearms) gradually accumulates at firearms training grounds, contaminating the local environment and exposing range employees to a risk of lead poisoning.^[13]

Entry routes

Toxic heavy metals enter plant, animal and human tissues via air inhalation, diet and manual handling. Motor vehicle emissions are a major source of airborne contaminants including arsenic, cadmium, cobalt, nickel, lead, antimony, vanadium, zinc, platinum, palladium and rhodium.^[14] Water sources (groundwater, lakes, streams and rivers) can be polluted by toxic heavy metals leaching from industrial and consumer waste; acid rain can exacerbate this process by releasing toxic heavy metals trapped in soils.^[15] Plants are exposed to toxic heavy metals through the uptake of water; animals eat these plants; ingestion of plant- and animal-based foods are the largest sources of toxic heavy metals in humans.^[16] Absorption through skin contact, for example from contact with soil, is another potential source of toxic heavy metal contamination.^[17] Toxic heavy metals can bioaccumulate in organisms as they are hard to metabolize (process and eliminate).^[18]

Detrimental effects

Toxic heavy metals "can bind to vital cellular components, such as structural proteins, enzymes, and nucleic acids, and interfere with their functioning."^[19] Symptoms and effects can vary according to the metal or metal compound, and the dose involved. Broadly, long-term exposure to toxic heavy metals can have carcinogenic, central and peripheral nervous system and circulatory effects. For humans, typical presentations associated with exposure to any of the "classical"^[20] toxic heavy metals, or chromium (another toxic heavy metal) or arsenic (a metalloid), are shown in the table.^[21]

Exposure risk	Acute exposure: Severe harm or death from a single exposure (usually a day or less)	Chronic exposure: Irreversible side effects from long-term exposure (often months or years)
Cadmium poisoning	Pneumonitis (lung inflammation)	Lung cancer Osteomalacia (softening of bones) Proteinuria (excess protein in urine; possible kidney damage)
Mercury poisoning	Diarrhea Fever Vomiting	Stomatitis (inflammation of gums and mouth) Nausea Nephrotic syndrome (nonspecific kidney disorder) Neurasthenia (neurotic disorder) Parageusia (metallic taste) Pink Disease (pain and pink discoloration of hands and feet) Tremor
Lead poisoning	Encephalopathy (brain dysfunction) Nausea Vomiting	Anemia Encephalopathy Foot drop/wrist drop (palsy) Nephropathy (kidney disease)
Chromium toxicity	Gastrointestinal hemorrhage (bleeding) Hemolysis (red blood cell destruction) Acute renal failure	Pulmonary fibrosis (lung scarring) Lung cancer
Arsenic poisoning	Nausea Vomiting Diarrhea Encephalopathy Multi-organ effects Arrhythmia Painful neuropathy	Diabetes Hypopigmentation/Hyperkeratosis Cancer

History

The toxic effects of arsenic, mercury and lead were known to the ancients but methodical studies of the overall toxicity of heavy metals appear to date from only 1868. In that year, Wanklyn and Chapman speculated on the adverse effects of the heavy metals "arsenic, lead, copper, zinc, iron and manganese" in drinking water. They noted an "absence of investigation" and were reduced to "the necessity of pleading for the collection of data."^[22] In 1884, Blake described an apparent connection between toxicity and the atomic weight of an element.^[23] The following sections provide historical thumbnails for the "classical" toxic heavy metals (arsenic, mercury and lead) and some more recent examples (chromium and cadmium).

Arsenic

Arsenic, as realgar (As₄S₄) and orpiment (As₂S₃), was known in ancient times. Strabo (64–50 BCE – c. AD 24?), a Greek geographer and historian,^[24] wrote that only slaves were employed in realgar and orpiment mines since they would inevitably die from the toxic effects of the fumes given off from the ores. Arsenic contaminated beer poisoned over 6,000 people in the Manchester area of England in 1900, and is thought to have killed at least 70 victims.^[25] Clare Luce, American ambassador to Italy from 1953 to 1956, suffered from arsenic poisoning. Its source was traced to flaking arsenic-laden paint on the ceiling of her bedroom. She may also have eaten food contaminated by arsenic in flaking ceiling paint in the embassy dining room.^[26] Ground water contaminated by arsenic, as of 2014, "is still poisoning millions of people in Asia."^[27]

Mercury

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.^[28] 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.^[29] Historically, gold amalgam (an alloy with mercury) 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 workers died from the gilding of the main dome.^[30] 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.^[31] Since the industrial Revolution, mercury levels have tripled in many near-surface seawaters, especially around Iceland and Antarctica.^[32]

Lead

The adverse effects of lead were known to the ancients. In the 2nd century BC the Greek botanist Nicander described the colic and paralysis seen in lead-poisoned people.^[33] Dioscorides, a Greek physician who is thought to have lived in the 1st century CE,^[34] wrote that lead "makes the mind give way". Lead was used extensively in Roman aqueducts from about 500 BC to 300 AD.^[35] Julius Caesar's engineer, Vitruvius, reported, "water is much more wholesome from earthenware pipes than from lead pipes. For it seems to be made injurious by lead, because white lead is produced by it, and this is said to be harmful to the human body."^[36] During the 17th and 18th centuries, people in Devon were afflicted by a condition referred to as Devon colic; this was discovered to be due to the imbibing of lead-contaminated cider. In 2013, the World Health Organization estimated that lead poisoning resulted in 143,000 deaths, and "contribute[d] to 600,000 new cases of children with intellectual disabilities", each year.^[37] In 2015, drinking water lead levels in north-eastern Tasmania, Australia, were reported to reach over 50 times national drinking water guidelines. The source of the contamination was attributed to “a combination of dilapidated drinking water infrastructure, including lead jointed pipelines, end-of-life polyvinyl chloride pipes and household plumbing.”^[38]

Chromium

Potassium chromate, a carcinogen, is used in the dyeing of fabrics, and as a tanning agent to produce leather.

Chromium(III) compounds and chromium metal are not considered a health hazard, while the toxicity and carcinogenic properties of chromium(VI) have been known since at least the late 19th century.^[39] In 1890, Newman described the elevated cancer risk of workers in a chromate dye company.^[40] Chromate-induced dermatitis was reported in aircraft workers during World War II.^[41] In 1963, an outbreak of dermatitis, ranging from erythema to exudative eczema, occurred amongst 60 automobile factory workers in England. The workers had been wet-sanding chromate-based primer paint that had been applied to car bodies.^[42] In Australia, chromium was released from the Newcastle Orica explosives plant on August 8, 2011. Up to 20 workers at the plant were exposed as were 70 nearby homes in Stockton. The town was only notified three days after the release and the accident sparked a major public controversy, with Orica criticised for playing down the extent and possible risks of the leak, and the state Government attacked for their slow response to the incident.^[43]

Cadmium

Cadmium exposure is a phenomenon of the early 20th century, and onwards. In Japan in 1910, the Mitsui Mining and Smelting Company began discharging cadmium into the Jinzugawa river, as a byproduct of mining operations. Residents in the surrounding area subsequently consumed rice grown in cadmium contaminated irrigation water. They experienced softening of the bones and kidney failure. The origin of these symptoms was not clear; possibilities raised at the time included "a regional or bacterial disease or lead poisoning."^[44] In 1955, cadmium was identified as the likely cause and in 1961 the source was directly linked to mining operations in the area.^[45] In February 2010, cadmium was found in Wal-Mart exclusive Miley Cyrus jewelry. Wal-Mart continued to sell the jewelry until May, when covert testing organised by Associated Press confirmed the original results.^[46] In June 2010 cadmium was detected in the paint used on promotional drinking glasses for the movie Shrek Forever After, sold by McDonald's Restaurants, triggering a recall of 12 million glasses.^[47]

Remediation

A metal EDTA anion. Pb displaces Ca in Na₂[CaEDTA] to give Na₂[PbEDTA], which is passed out of the body in urine.^[48]

In humans, heavy metal poisoning is generally treated by the administration of chelating agents.^[49] These are chemical compounds, such as CaNa₂ EDTA (calcium disodium ethylenediaminetetraacetate) that convert heavy metals to chemically inert forms that can be excreted without further interaction with the body. Chelates are not without side effects and can also remove beneficial metals from the body. Vitamin and mineral supplements are sometimes co-administered for this reason.^[50]

Soils contaminated by toxic heavy metals can be re-mediated by one or more of the following technologies: isolation; immobilization; toxicity reduction; physical separation; or extraction. Isolation involves the use of caps, membranes or below-ground barriers in an attempt to quarantine the contaminated soil. Immobilization aims to alter the properties of the soil so as to hinder the mobility of the heavy contaminants. Toxicity reduction attempts to oxidise or reduce the toxic heavy metal ions, via chemical or biological means into less toxic or mobile forms. Physical separation involves the removal of the contaminated soil and the separation of the metal contaminants by mechanical means. Extraction is an on or off-site process that uses chemicals, high-temperature volatization, or electrolysis to extract contaminants from soils. The process or processes used will vary according to contaminant and the characteristics of the site.^[51]

Benefits

Some elements regarded as toxic heavy metals are essential, in small quantities, for human health. These elements include vanadium, manganese, iron, cobalt, copper, zinc, selenium, strontium and molybdenum.^[52] A deficiency of these essential metals may increase susceptibility to heavy metal poisoning.^[53]

Citations

^ Dewan 2008
^ Dewan 2009
^ Poovey 2001
^ Srivastava & Goyal 2010, p. 2
^ Brathwaite & Rabone 1985, p. 363
^ World Health Organisation 2015
^ Wright 2002, p. 288
^ Howell et al. 2012
^ Harvey, Handley & Taylor 2015
^ Di Maio 2001, p. 527
^ Lovei 1998, p. 15
^ Perry & Vanderklein 1996, p. 336
^ Houlton 2014, p. 50
^ Balasubramanian, He & Wang 2009, p. 476
^ Worsztynowicz & Mill 1995, p. 361
^ Radojevic & Bashkin 1999, p. 406
^ Qu et al. 2014, p. 144
^ Pezzarossa, Gorini & Petruzelli 2011, p. 94
^ Lanids, Sofield & Yu 2000, p. 269
^ Neilen & Marvin 2008, p. 10
^ Afal & Wiener 2014
^ Wanklyn & Chapman 1868, pp. 73–8; Cameron 1871, p. 484
^ Blake 1884
^ Dueck 2000, pp. 1–3, 46, 53
^ Dyer 2009
^ Whorton 2011, p. 356
^ Notman 2014
^ Zhao, Zhu & Sui 2006
^ Waldron 1983
^ Emsely 2011, p. 326
^ Davidson, Myers & Weiss 2004, p. 1025
^ New Scientist August 2014, p. 4
^ Pearce 2007; Needleman 2004
^ Rogers 2000, p. 41
^ Gilbert & Weiss 2006
^ Prioreschi 1998, p. 279
^ World Health Organization 2013
^ Harvey, Handley & Taylor 2015
^ Barceloux & Barceloux 1999
^ Newman 1890
^ Haines & Nieboer 1988, p. 504
^ National Research Council 1974, p. 68
^ Tovey 2011; Jones 2011; O'Brien & Aston
^ Vallero & Letcher 2013, p. 240
^ Vallero & Letcher 2013, pp. 239–241
^ Pritchard 2010
^ Mulvihill & Pritchard 2010
^ Cs uros 1997, p. 124
^ Blann & Ahmed 2014, p. 465
^ American Cancer Society 2008; National Capital Poison Center 2010
^ Evanko & Dzombak 1997, pp. 1, 14–40
^ Bánfalvi 2011, p. 12
^ Chowdhury 1987

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[1] Dewan 2008

[2] Dewan 2009

[3] Poovey 2001

[4] Srivastava & Goyal 2010, p. 2

[5] Brathwaite & Rabone 1985, p. 363

[6] World Health Organisation 2015

[7] Wright 2002, p. 288

[8] Howell et al. 2012

[9] Harvey, Handley & Taylor 2015

[10] Di Maio 2001, p. 527

[11] Lovei 1998, p. 15

[12] Perry & Vanderklein 1996, p. 336

[13] Houlton 2014, p. 50

[14] Balasubramanian, He & Wang 2009, p. 476

[15] Worsztynowicz & Mill 1995, p. 361

[16] Radojevic & Bashkin 1999, p. 406

[17] Qu et al. 2014, p. 144

[18] Pezzarossa, Gorini & Petruzelli 2011, p. 94

[19] Lanids, Sofield & Yu 2000, p. 269

[20] Neilen & Marvin 2008, p. 10

[21] Afal & Wiener 2014

[22] Wanklyn & Chapman 1868, pp. 73–8; Cameron 1871, p. 484

[23] Blake 1884

[24] Dueck 2000, pp. 1–3, 46, 53

[25] Dyer 2009

[26] Whorton 2011, p. 356

[27] Notman 2014

[28] Zhao, Zhu & Sui 2006

[29] Waldron 1983

[30] Emsely 2011, p. 326

[31] Davidson, Myers & Weiss 2004, p. 1025

[32] New Scientist August 2014, p. 4

[33] Pearce 2007; Needleman 2004

[34] Rogers 2000, p. 41

[35] Gilbert & Weiss 2006

[36] Prioreschi 1998, p. 279

[37] World Health Organization 2013

[38] Harvey, Handley & Taylor 2015

[39] Barceloux & Barceloux 1999

[40] Newman 1890

[41] Haines & Nieboer 1988, p. 504

[42] National Research Council 1974, p. 68

[43] Tovey 2011; Jones 2011; O'Brien & Aston

[44] Vallero & Letcher 2013, p. 240

[45] Vallero & Letcher 2013, pp. 239–241

[46] Pritchard 2010

[47] Mulvihill & Pritchard 2010

[48] Cs uros 1997, p. 124

[49] Blann & Ahmed 2014, p. 465

[50] American Cancer Society 2008; National Capital Poison Center 2010

[51] Evanko & Dzombak 1997, pp. 1, 14–40

[52] Bánfalvi 2011, p. 12

[53] Chowdhury 1987

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@@ Line 77: / Line 77: @@
 {{refbegin|30em}}
-* <span id="Afal"></span>Afal A & Wiener SW 2014, ''[http://emedicine.medscape.com/article/814960-overview|Heavy Metal Toxicity],'' Medscape.org, viewed 21 April 2014
+* <span id="Afal"></span>{{EMedicine|article|814960|Heavy Metal Toxicity}}
-* <span id="ACS"></span>American Cancer Society 2008, ''[http://www.cancer.org/treatment/treatmentsandsideeffects/complementaryandalternativemedicine/pharmacologicalandbiologicaltreatment/chelation-therapy Chelation Therapy],'' viewed 28 April 2014
+* <span id="ACS"></span>{{cite web |title=Chelation Therapy |date=2008 |publisher=American Cancer Society  |url=http://www.cancer.org/treatment/treatmentsandsideeffects/complementaryandalternativemedicine/pharmacologicalandbiologicaltreatment/chelation-therapy |accessdate=2014-04-28}}
-* <span id="Bala"></span>Balasubramanian R, He J & Wang LK 2009, 'Control, Management, and Treatment of Metal Emissions from Motor Vehicles', in LK Wang, JP Chen, Y Hung & NK Shammas (eds), ''Heavy Metals in the Environment,'' CRC Press, Boca Raton, FL, pp.&nbsp;475–490, ISBN 1420073168
+* <span id="Bala"></span>{{cite book |last=Balasubramanian |first=R |last2=He |first2=J |last3=Wang |first3=LK |chapter=Control, Management, and Treatment of Metal Emissions from Motor Vehicles |chapterurl= |editor-first=LK |editor2-last=Wang |editor2-first=JP |editor3-last=Chen |editor3-first=Y |editor4-last=Hung |editor4-first=NK |editor-last=Shammas  |title=Heavy Metals in the Environment |publisher=CRC Press |year=2009 |isbn=1420073168 |pages=475–490 |url=}}
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 {{refend}}

v t e Wastewater
Sources and types	Acid mine drainage Ballast water Bathroom Blackwater (coal) Blackwater (waste) Boiler blowdown Brine Combined sewer Cooling tower Cooling water Fecal sludge Greywater Infiltration/Inflow Industrial wastewater Ion exchange Leachate Manure Papermaking Produced water Return flow Reverse osmosis Sanitary sewer Septage Sewage Sewage sludge Toilet Urban runoff
Quality indicators	Adsorbable organic halides Biochemical oxygen demand Chemical oxygen demand Coliform index Oxygen saturation Heavy metals pH Salinity Temperature Total dissolved solids Total suspended solids Turbidity Wastewater surveillance
Treatment options	Activated sludge Aerated lagoon Agricultural wastewater treatment API oil–water separator Carbon filtering Chlorination Clarifier Constructed wetland Decentralized wastewater system Extended aeration Facultative lagoon Fecal sludge management Filtration Imhoff tank Industrial wastewater treatment Ion exchange Membrane bioreactor Reverse osmosis Rotating biological contactor Secondary treatment Sedimentation Septic tank Settling basin Sewage sludge treatment Sewage treatment Sewer mining Stabilization pond Trickling filter Ultraviolet germicidal irradiation UASB Vermifilter Wastewater treatment plant
Disposal options	Combined sewer Evaporation pond Groundwater recharge Infiltration basin Injection well Irrigation Marine dumping Marine outfall Reclaimed water Sanitary sewer Septic drain field Sewage farm Storm drain Surface runoff Vacuum sewer
Category: Sewerage