Erethism (mad hatter disease)

From Wikipedia, the free encyclopedia

Mercury poisoning, chronic (neurological symptomatology)
Elemental mercury
Specialty	Medical toxicology

Erethism, also known as erethism mercurialis, mad hatter disease, or mad hatter syndrome, is a neurological disorder which affects the whole central nervous system, as well as a symptom complex derived from mercury poisoning. Erethism is characterized by behavioral changes such as irritability, low self-confidence, depression, apathy, shyness and timidity, and in some extreme cases with prolonged exposure to mercury vapors, delirium, personality changes and memory loss. People with erethism often have difficulty with social interactions. Associated physical problems may include a decrease in physical strength, "headaches, general pain, and tremors after exposure to metallic mercury" as well as an irregular heartbeat.

Mercury is an element that is found worldwide in soil, rocks, and water. People who get erethism are often exposed to mercury through their jobs. Higher risk jobs include construction, industrial work, and working in factories. Some elemental and chemical forms of mercury (vapor, methylmercury, inorganic mercury) are more toxic than other forms. The human fetus and medically compromised people (for example, patients with lung or kidney problems) are the most susceptible to the toxic effects of mercury.

Mercury poisoning can also occur outside of occupational exposures including in the home. Inhalation of mercury vapor may stem from cultural and religious rituals where mercury is sprinkled on the floor of a home or car, burned in a candle, or mixed with perfume. Due to widespread use and popular concern, the risk of toxicity from dental amalgam has been exhaustively investigated. It has conclusively been shown to be safe.

Historically, this was common among old England felt-hatmakers who had long-term exposure to vapors from the mercury they used to stabilize the wool in a process called felting, where hair was cut from a pelt of an animal such as a rabbit. The industrial workers were exposed to the mercury vapors, giving rise to the expression "mad as a hatter". Some believe that the character the Mad Hatter in Lewis Carroll's Alice in Wonderland is an example of someone suffering from erethism, but the origin of this account is unclear. The character was almost certainly based on Theophilus Carter, an eccentric furniture dealer who was well known to Carroll.

Signs and symptoms

Acute mercury exposure has given rise to psychotic reactions such as delirium, hallucinations, and suicidal tendency. Occupational exposure has resulted in erethism, with irritability, excitability, excessive shyness, and insomnia as the principal features of a broad-ranging functional disturbance. With continuing exposure, a fine tremor develops, initially involving the hands and later spreading to the eyelids, lips, and tongue, causing violent muscular spasms in the most severe cases. The tremor is reflected in the handwriting which has a characteristic appearance. In milder cases, erethism and tremor regress slowly over a period of years following removal from exposure. Decreased nerve conduction velocity in mercury-exposed workers has been demonstrated. Long-term, low-level exposure has been found to be associated with less pronounced symptoms of erethism, characterized by fatigue, irritability, loss of memory, vivid dreams, and depression (WHO, 1976).

The man affected is easily upset and embarrassed, loses all joy in life and lives in constant fear of being dismissed from his job. He has a sense of timidity and may lose self control before visitors. Thus, if one stops to watch such a man in a factory, he will sometimes throw down his tools and turn in anger on the intruder, saying he cannot work if watched. Occasionally a man is obliged to give up work because he can no longer take orders without losing his temper or, if he is a foreman, because he has no patience with men under him. Drowsiness, depression, loss of memory and insomnia may occur, but hallucinations, delusions and mania are rare.

The most characteristic symptom, though it is seldom the first to appear, is mercurial tremor. It is neither as fine nor as regular as that of hyperthyroidism. It may be interrupted every few minutes by coarse jerky movements. It usually begins in the fingers, but the eyelids, lips and tongue are affected early. As it progresses it passes to the arms and legs, so that it becomes very difficult for a man to walk about the workshop, and he may have to be guided to his bench. At this stage the condition is so obvious that it is known to the layman as "hatter's shakes."

Buckell et al, Chronic Mercury Poisoning (1946)

Effects of chronic occupational exposure to mercury, such as that commonly experienced by affected hatters, include mental confusion, emotional disturbances, and muscular weakness. Severe neurological damage and kidney damage can also occur. Neurological effects include Korsakoff's dementia and erethism (the set of neurological symptoms characteristically associated with mercury poisoning). Signs and symptoms can include red fingers, red toes, red cheeks, sweating, loss of hearing, bleeding from the ears and mouth, loss of appendages such as teeth, hair, and nails, lack of coordination, poor memory, shyness, insomnia, nervousness, tremors, and dizziness. A survey of exposed U.S. hatters revealed predominantly neurological symptomatology, including intention tremor. After chronic exposure to the mercury vapours, hatters tended to develop characteristic psychological traits, such as pathological shyness and marked irritability (box). Such manifestations among hatters prompted several popular names for erethism, including "mad hatter disease", "mad hatter syndrome", "hatter's shakes" and "Danbury shakes".

History among hatters

Some of the steps in the manufacture of felt hats are illustrated in this image from 1858.

 

A man working in hat manufacture with no protective equipment, putting him at risk for mercury poisoning

 

Especially in the 19th century, inorganic mercury in the form of mercuric nitrate was commonly used in the production of felt for hats. During a process called carroting, in which furs from small animals such as rabbits, hares or beavers were separated from their skins and matted together, an orange-colored solution containing mercuric nitrate was used as a smoothing agent. The resulting felt was then repeatedly shaped into large cones, shrunk in boiling water and dried. In treated felts, a slow reaction released volatile free mercury. Hatters (or milliners) who came into contact with vapours from the impregnated felt often worked in confined areas.

Use of mercury in hatmaking is thought to have been adopted by the Huguenots in 17th-century France, at a time when the dangers of mercury exposure were already known. This process was initially kept a trade secret in France, where hatmaking rapidly became a hazardous occupation. At the end of the 17th century the Huguenots carried the secret to England, following the revocation of the Edict of Nantes. During the Victorian era the hatters' malaise became proverbial, as reflected in popular expressions like "mad as a hatter" and "the hatters' shakes".

The first description of symptoms of mercury poisoning among hatters appears to have been made in St Petersburg, Russia, in 1829. In the United States, a thorough occupational description of mercury poisoning among New Jersey hatters was published locally by Addison Freeman in 1860. Adolph Kussmaul's definitive clinical description of mercury poisoning published in 1861 contained only passing references to hatmakers, including a case originally reported in 1845 of a 15-year-old Parisian girl, the severity of whose tremors following two years of carroting prompted opium treatment. In Britain, the toxicologist Alfred Swaine Taylor reported the disease in a hatmaker in 1864.

In 1869, the French Academy of Medicine demonstrated the health hazards posed to hatmakers. Alternatives to mercury use in hatmaking became available by 1874. In the United States, a hydrochloride-based process was patented in 1888 to obviate the use of mercury, but was ignored.

In 1898, legislation was passed in France to protect hatmakers from the risks of mercury exposure. By the turn of the 20th century, mercury poisoning among British hatters had become a rarity.

Picture postcard of a hat factory in Danbury (postmarked 1911)

 

In the United States, the mercury-based process continued to be adopted until as late as 1941, when it was abandoned mainly due to the wartime need for the heavy metal in the manufacture of detonators. Thus, for much of the 20th century mercury poisoning remained common in the U.S. hatmaking industries, including those located in Danbury, Connecticut (giving rise to the expression the "Danbury shakes").

Another 20th-century cohort of affected hatmakers has been studied in Tuscany, Italy.

Hatters of New Jersey

The experience of hatmakers in New Jersey is well documented and has been reviewed by Richard Wedeen. In 1860, at a time when the hatmaking industry in towns such as Newark, Orange and Bloomfield was growing rapidly, a physician from Orange called J. Addison Freeman published an article titled "Mercurial Disease Among Hatters" in the Transactions of the Medical Society of New Jersey. This groundbreaking paper provided a clinical account of the effects of chronic mercury poisoning among the workforce, coupled with an occupational description of the use of mercuric nitrate during carroting and inhalation of mercury vapour later in the process (during finishing, forming and sizing). Freeman concluded that "A proper regard for the health of this class of citizens demands that mercury should not be used so extensively in the manufacture of hats, and that if its use is essential, that the hat finishers' room should be large, with a high ceiling, and well ventilated." Freeman's call for prevention went unheeded. 

In 1878, an inspection of 25 firms around Newark conducted by Dr L. Dennis on behalf of the Essex County Medical Society revealed "mercurial disease" in 25% of 1,589 hatters. Dennis recognized that this prevalence figure was probably an underestimate, given the workers' fear of being fired if they admitted to being diseased. Although Dennis did recommend the use of fans in the workplace he attributed most of the hatters' health problems to alcohol abuse (thus using the stigma of drunkenness in a mainly immigrant workforce to justify the unsanitary working conditions provided by employers).

The surprise is that men can be induced to work at all in such death producing enclosures. It is hard to believe that men of ordinary intelligence could be so indifferent to the ordinary laws of health... It does not seem to have occurred to them that all the efforts to keep up wages... [are] largely offset by the impairment of their health, due to neglect of proper hygienic regulations of their workshops... And when the fact of the workmen in the sizing room, who stand in water, was mentioned, and the simple and inexpensive means by which it could be largely avoided was spoken of, the reply was that it would cost money and hat manufacturers did not care to expend money for such purposes, if they could avoid it. Bishop, Annual Report of the Bureau of Statistics of Labor and Industries of New Jersey (1890)

Some voluntary reductions in mercury exposure were implemented after Lawrence T. Fell, a former journeyman hatter from Orange who had become a successful manufacturer, was appointed Inspector of Factories in 1883. In the late nineteenth century, a pressing health issue among hatters was tuberculosis. This deadly communicable disease was rife in the extremely unhygienic wet and steamy enclosed spaces in which the hatters were expected to work (in its annual report for 1889, the New Jersey Bureau of Labor and Industries expressed incredulity at the conditions—see box). Two-thirds of the recorded deaths of hatters in Newark and Orange between 1873 and 1876 were caused by pulmonary disease, most often in men under 30 years of age, and elevated death rates from tuberculosis persisted into the twentieth century. Consequently, public health campaigns to prevent tuberculosis spreading from the hatters into the wider community tended to eclipse the issue of mercury poisoning. For instance, in 1886 J. W. Stickler, working on behalf of the New Jersey Board of Health, promoted prevention of tuberculosis among hatters, but deemed mercurialism "uncommon", despite having reported tremors in 15–50% of the workers he had surveyed.

While hatters seemed to regard the shakes as an inevitable price to pay for their work rather than a readily preventable disease, their employers professed ignorance of the problem. In a 1901 survey of 11 employers of over a thousand hatters in Newark and Orange, the head of the Bureau of Statistics of New Jersey, William Stainsby, found a lack of awareness of any disease peculiar to hatters apart from tuberculosis and rheumatism (though one employer remarked that "work at the trade develops an inordinate craving for strong drink").

By 1934 the U.S. Public Health Service estimated that 80% of American felt makers had mercurial tremors. Nevertheless, trade union campaigns (led by the United States Hat Finishers Association, originally formed in 1854) never addressed the issue and, unlike in France, no relevant legislation was ever adopted in the United States. Instead, it seems to have been the need for mercury in the war effort that eventually brought to an end the use of mercuric nitrate in U.S. hatmaking; in a meeting convened by the U.S. Public Health Service in 1941, the manufacturers voluntarily agreed to adopt a readily available alternative process using hydrogen peroxide.

"Mad as a hatter"

While the name of Lewis Carroll's Mad Hatter may contain an allusion to the hatters' syndrome, the character itself appears to have been based on an eccentric furniture dealer.

Although the expression "mad as a hatter" was associated with the syndrome, the origin of the phrase is uncertain.

Lewis Carroll's iconic Mad Hatter character in Alice's Adventures in Wonderland displays markedly eccentric behavior, which includes taking a bite out of a teacup. Carroll would have been familiar with the phenomenon of dementia among hatters, but the literary character is thought to be directly inspired by Theophilus Carter, an eccentric furniture dealer who did not show signs of mercury poisoning.

The actor Johnny Depp has said of his portrayal of a carrot-orange haired Mad Hatter in Tim Burton's 2010 film, Alice in Wonderland that the character "was poisoned ... and it was coming out through his hair, through his fingernails and eyes".

Toxic heavy metal

From Wikipedia, the free encyclopedia

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. Testing showed significantly elevated levels of arsenic, copper, barium, cadmium, chromium, lead, mercury, nickel, and thallium in samples of slurry and river water. Cleanup costs may exceed $1.2 billion.

 

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

Heavy metals are found naturally in the earth. They become concentrated as a result of human caused activities and can enter plant, animal, and human tissues via inhalation, diet, and manual handling. Then, they 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 otherwise regarded as toxic heavy metals are essential, in small quantities, for human health.

Contamination sources

Tetraethyl lead is one of the most significant heavy metal contaminants in recent use.

 

Heavy metals are found naturally in the earth, and become concentrated as a result of human activities. Common sources are mining and industrial wastes; vehicle emissions; lead-acid batteries; fertilisers; paints; treated woods; aging water supply infrastructure; and microplastics floating in the world's oceans. Arsenic, cadmium and lead may be present in children's toys at levels that exceed regulatory standards. Lead can be used in toys as a stabilizer, color enhancer, or anti-corrosive agent. Cadmium is sometimes employed as a stabilizer, or to increase the mass and luster of toy jewelry. Arsenic is thought to be used in connection with coloring dyes. Regular imbibers of illegally distilled alcohol may be exposed to arsenic or lead poisoning the source of which is arsenic-contaminated lead used to solder the distilling apparatus. Rat poison used in grain and mash stores may be another source of the arsenic.

Lead is the most prevalent heavy metal contaminant. As a component of tetraethyl lead, (CH
₃CH
₂)
₄Pb, it was used extensively in gasoline during the 1930s–1970s. Lead levels in the aquatic environments of industrialised societies have been estimated to be two to three times those of pre-industrial levels. 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(II) 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.

Entry routes

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. Water sources (groundwater, lakes, streams and rivers) can be polluted by heavy metals leaching from industrial and consumer waste; acid rain can exacerbate this process by releasing heavy metals trapped in soils. Plants are exposed to heavy metals through the uptake of water; animals eat these plants; ingestion of plant- and animal-based foods are the largest sources of heavy metals in humans. Absorption through skin contact, for example from contact with soil, or metal containing toys and jewelry, is another potential source of heavy metal contamination. Toxic heavy metals can bioaccumulate in organisms as they are hard to metabolize.

Detrimental effects

Heavy metals "can bind to vital cellular components, such as structural proteins, enzymes, and nucleic acids, and interfere with their functioning". 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" toxic heavy metals, or chromium (another toxic heavy metal) or arsenic (a metalloid), are shown in the table.

Element	Acute exposure usually a day or less	Chronic exposure often months or years
Cadmium	Pneumonitis (lung inflammation)	Lung cancer Osteomalacia (softening of bones) Proteinuria (excess protein in urine; possible kidney damage)
Mercury	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	Encephalopathy (brain dysfunction) Nausea Vomiting	Anemia Encephalopathy Foot drop/wrist drop (palsy) Nephropathy (kidney disease)
Chromium	Gastrointestinal hemorrhage (bleeding) Hemolysis (red blood cell destruction) Acute renal failure	Pulmonary fibrosis (lung scarring) Lung cancer
Arsenic	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". In 1884, Blake described an apparent connection between toxicity and the atomic weight of an element. The following sections provide historical thumbnails for the "classical" toxic heavy metals (arsenic, mercury and lead) and some more recent examples (chromium and cadmium).

Orpiment, a toxic arsenic mineral used in the tanning industry to remove hair from hides.

Arsenic

Arsenic, as realgar (As
₄S
₄) and orpiment (As
₂S
₃), was known in ancient times. Strabo (64–50 BCE – c. AD 24?), a Greek geographer and historian, 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. 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. Ground water contaminated by arsenic, as of 2014, "is still poisoning millions of people in Asia".

Mercury

Saint Isaac's Cathedral, in Saint Petersburg, Russia. The gold-mercury amalgam used to gild its dome caused numerous casualties among the workers involved.

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. 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. 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. 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. Since the industrial Revolution, mercury levels have tripled in many near-surface seawaters, especially around Iceland and Antarctica.

Dutch Boy white lead paint advertisement, 1912.

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. Dioscorides, a Greek physician who is thought to have lived in the 1st century CE, wrote that lead "makes the mind give way". Lead was used extensively in Roman aqueducts from about 500 BC to 300 AD. 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." During the Mongol period in China (1271−1368 AD), lead pollution due to silver smelting in the Yunnan region exceeded contamination levels from modern mining activities by nearly four times. In 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. In the U.S. city of Flint, Michigan, lead contamination in drinking water has been an issue since 2014. The source of the contamination has been attributed to "corrosion in the lead and iron pipes that distribute water to city residents". 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".

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. In 1890, Newman described the elevated cancer risk of workers in a chromate dye company. Chromate-induced dermatitis was reported in aircraft workers during World War II. 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. 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.

99.999% purity cadmium bar and 1 cm³ cube.

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". In 1955, cadmium was identified as the likely cause and in 1961 the source was directly linked to mining operations in the area. In February 2010, cadmium was found in Walmart exclusive Miley Cyrus jewelry. Wal-Mart continued to sell the jewelry until May, when covert testing organised by Associated Press confirmed the original results. 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.

Remediation

A metal EDTA anion. Pb displaces Ca in Na
₂[CaEDTA] to give Na
₂[PbEDTA], which is passed out of the body in urine.

 

In humans, heavy metal poisoning is generally treated by the administration of chelating agents. 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.

Soils contaminated by heavy metals can be remediated 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.

Benefits

Some elements otherwise 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. A deficiency of these essential metals may increase susceptibility to heavy metal poisoning.

Mercury in fish

From Wikipedia, the free encyclopedia

Nearby anthropogenic sources, such as coal burning and mining of iron, can contaminate water sources with methylmercury, which is efficiently absorbed in the bodies of fish. Through the process of biomagnification, mercury levels in each successive predatory stage increase.

 

Fish and shellfish concentrate mercury in their bodies, often in the form of methylmercury, a highly toxic organomercury compound. Fish products have been shown to contain varying amounts of heavy metals, particularly mercury and fat-soluble pollutants from water pollution. Species of fish that are long-lived and high on the food chain, such as marlin, tuna, shark, swordfish, king mackerel and tilefish (Gulf of Mexico) contain higher concentrations of mercury than others.

Mercury is known to bioaccumulate in humans, so bioaccumulation in seafood carries over into human populations, where it can result in mercury poisoning. Mercury is dangerous to both natural ecosystems and humans because it is a metal known to be highly toxic, especially due to its ability to damage the central nervous system. In human-controlled ecosystems of fish, usually done for market production of wanted seafood species, mercury clearly rises through the food chain via fish consuming small plankton, as well as through non-food sources such as underwater sediment.

The presence of mercury in fish can be a particular health concern for women who are or may become pregnant, nursing mothers, and young children.

Biomagnification

The consumption of fish is by far the most significant source of ingestion-related mercury exposure in humans and animals. Mercury and methyl mercury are present in only very small concentrations in seawater. However, they are absorbed, usually as methyl mercury, by algae at the start of the food chain. This algae is then eaten by fish and other organisms higher in the food chain. Fish efficiently absorb methyl mercury, but excrete it very slowly. Methyl mercury is not soluble and therefore not excreted. Instead, it accumulates, primarily in the viscera, although also in the muscle tissue. This results in the bioaccumulation of mercury, in a buildup in the adipose tissue of successive trophic levels: zooplankton, small nekton, larger fish, and so on. The older that such fish become, the more mercury they may have absorbed. Anything that eats these fish within the food chain also consumes the higher level of mercury that the fish have accumulated. This process explains why predatory fish such as swordfish and sharks or birds like osprey and eagles have higher concentrations of mercury in their tissue than could be accounted for by direct exposure alone. Species on the food chain can amass body concentrations of mercury up to ten times higher than the species they consume. This process is called biomagnification. For example, herring contains mercury levels at about 0.1 parts per million, while shark contains mercury levels greater than 1 part per million.

Legislation

Japan

Since the Minamata disaster, Japan has improved on its mercury regulation. During the 1970s Japan made strides to reduce mercury demand and production. Chief among these efforts was the reduction of inorganic mercury produced by mines. It was halted by 1974, and demand fell from 2,500 tons per year in 1964, its peak, to 10 tons per year in recent years. Since these initial strides, Japan has introduced a list of regulations governing the mercury content of a variety of materials.

Japanese Mercury Regulation

Category	Regulation	Result
Cosmetics	Pharmaceutical Affairs Act	Ban the use of mercury and its compounds
Agriculture	Agricultural Chemicals Control Act	Ban the use of mercury and its compounds as an active ingredient
Household Commodities	Act on Control of Household Products Containing Hazardous Substances	No mercury in household adhesives, household paints, household wax, shoe polish, shoe cream, diapers, bibs, undergarments, gloves, and socks
Pharmaceutical Products	Pharmaceutical Affairs Act	No use of mercury compounds in oral preparations. No use of mercury compounds, other than mercurochrome, as an active ingredient. Mercury as a preservative only if no other option is available.
Air	Air Pollution Control Law	No more than 40 ng/m3
Water	Basic Environment Law and Water Pollution Control Act	Environmental quality standard: no more than 0.0005 mg/L in waterway and ground water. Effluent standard: no more than 0.005 mg/L in effluence.
Soil	Basic Environment Law and Soil Contamination Countermeasures Act	Environmental quality standard: no more than 0.0005 mg/L sample solution. Elution standard: no more than 0.0005 mg/L. Content standard: no more than 15 mg/kg

Regulation of these potential sources of pollution reduces the amount of mercury that ends up in fish and, through biomagnification, in humans. In addition to enacting legislation controlling the mercury levels in potential pollutants, Japan has directly influenced the environment by issuing regulations setting acceptable levels of environmental mercury pollution. 

It is Japan's goal to promote international mercury legislation in hopes of preventing any country from experiencing what it did. Despite Japan's extensive regulation and experience with mercury-based disasters, there is still little information provided to the public. The Japanese Federal Fish Advisory's recommendations are less strict than those in America.

United States of America

Fish advisory chart issued by U.S. Environmental Protection Agency and Food and Drug Administration

The United States is a leader in mercury regulation. A key piece of mercury legislation in the United States is the Mercury and Air Toxics Standards (MATS). This policy was finalized by the Environmental Protection Agency (EPA) on December 16, 2011. This is a federal policy which directly influences mercury in fish, and is the first of its kind in the United States. The facilities targeted by this new policy are the chief sources of mercury in the air. The airborne mercury is dissolved in the oceans, where microorganisms convert waterborne mercury into methyl mercury; mercury thus finds its way into the food chain and into fish. MATS is legislated towards the aim of preventing about 90% of the emissions from power plants from reaching the air. In total the expected health benefits are estimated at $37 billion–$90 billion by 2016. In comparison, the expected economic cost is $9.6 billion annually. Another integral piece of legislation controlling the emission of mercury to the air is the Clean Air Act. Under this act, mercury is classified as a hazardous air pollutant, allowing the EPA to regulate emissions by establishing performance standards.

International

Legislation on a global scale is believed by some to be needed for this issue because mercury pollution is estimated to be so far-reaching. Pollution from one country does not stay localized to that country. Despite the need by some, international regulation has been slow to take off. The first forms of international legislation appeared in the 1970s, beginning as agreements about shared bodies of water. The next step was the Stockholm Declaration, which urged countries to avoid polluting the oceans by dumping. The 1972 Oslo Convention and the 1974 Paris Convention were adopted by parts of Europe. Both lessened polluting the ocean with mercury, the former by banning the dumping of ships and aircraft into the ocean and the latter by obligating participants to reduce land-based pollution on coastlines. The first real global legislation regarding mercury pollution was the Basel Convention of 1989. This convention attempts to reduce the movement of mercury across borders and primarily regulates the import and export of toxic chemicals, including mercury. In 1998 the Convention on Long-Range Transboundary Air Pollution was adopted by most of the European Union, the United States, and Canada. Its primary objective is to cut emissions of heavy metals. The convention is the largest international agreement on mercury established to date. In the early 21st century, the focus of mercury regulation has been on voluntary programs. The next phase in legislation is a global effort, and this appears to be what the Minamata Convention hopes to accomplish. The Minamata Convention, named after the Japanese city that suffered horribly from mercury pollution, has taken four years of negotiation but was finally adopted by delegates from over 140 countries. The convention will come into power after 50 countries have signed it. The Minamata Convention will require all participants to eliminate, where possible, the release of mercury from small-scale gold mining. It will also require a sharp reduction in emission from coal burning.

Levels of contamination

Most-contaminated fish species

The danger level from consuming fish depends on species and size. Size is the best predictor of increased levels of accumulated mercury. Sharks, such as the mako shark, have very high levels of mercury. A study on New Jersey coastal fish indicated that one third of the sampled fish had levels of mercury above 0.5 parts per million, a level that could pose a human health concern for consumers who regularly eat this fish. Another study of marketplace fish caught in waters surrounding Southern Italy showed that, undoubtedly, greater fish weight leads to additional mercury found in fish body tissues. Moreover, the concentration, measured in milligrams of mercury per kilogram of fish, steadily increases with the size of the fish. Anglerfish off the coast of Italy were found with concentrations as high as 2.2 milligrams of mercury per kilogram, higher than the recommended limit of 1 milligram of mercury per kilogram. Annually, Italy catches approximately a third of its fish from the Adriatic Sea, where these anglerfish were found.

Fish that consume their prey in a certain manner may contain much higher concentrations of mercury than other species. Grass carp off the coast of China hold far less internal mercury than do bighead carp. The reason for this is that bighead carp are filter feeders, while grass carp are not. Thus, bighead carp gather more mercury by eating large amounts of small plankton, as well as sucking up sediments that collect a sizable amount of methyl mercury.

US government scientists tested fish in 291 streams around the country for mercury contamination. They found mercury in every fish tested, according to the study by the U.S. Department of the Interior. They found mercury even in fish of isolated rural waterways. Twenty-five percent of the fish tested had mercury levels above the safety levels determined by the U.S. Environmental Protection Agency for people who eat the fish regularly.

Origins of mercury pollution

There are three types of mercury emission: anthropogenic, re-emission, and natural, including volcanoes and geothermal vents. Anthropogenic sources are responsible for 30% of all emissions, while natural sources are responsible for 10%, and re-emission accounts for the other 60%. While re-emission accounts for the largest proportion of emissions, it is likely that the mercury emitted from these sources originally came from anthropogenic sources.

Anthropogenic sources include coal burning, cement production, oil refining, artisan and small-scale gold mining, wastes from consumer products, dental amalgam, the chlor-alkali industry, production of vinyl chloride, and the mining, smelting, and production of iron and other metals. The total amount of mercury released by mankind in 2010 was estimated to be 1,960 metric tons. The majority of this comes from coal burning and gold mining, accounting for 24% and 37% of total anthropogenic output respectively.

Re-emission, the largest emitter, occurs in a variety of ways. It is possible for mercury that has been deposited in soil to be re-emitted into the mercury cycle via floods. A second example of re-emission is a forest fire; mercury that has been absorbed into plant life is re-released into the atmosphere. While it is difficult to estimate the exact extent of mercury re-emission, it is an important field of study. Knowing how easily and how often previously emitted mercury can be released helps us learn how long it will take for a reduction in anthropogenic sources to be reflected in the environment. Mercury that has been released can find its way into the oceans. A 2008 model estimated the total amount of deposition into the oceans that year to be 3,700 metric tons. It is estimated that rivers carry as much as 2,420 metric tons. Much of the mercury deposited in the oceans is re-emitted, however; as much as 300 metric tons is converted into methyl mercury. While only 13% of this finds its way into the food chain, that is still 40 metric tons a year.

Much (an estimated 40%) of the mercury that eventually finds its way into fish originates with coal-burning power plants and chlorine production plants. The largest source of mercury contamination in the United States is coal-fueled power plant emissions. Chlorine chemical plants use mercury to extract chlorine from salt, which in many parts of the world is discharged as mercury compounds in waste water, though this process has been largely replaced by the more economically viable membrane cell process, which does not use mercury. Coal contains mercury as a natural contaminant. When it is fired for electricity generation, the mercury is released as smoke into the atmosphere. Most of this mercury pollution can be eliminated if pollution-control devices are installed.

Mercury in the United States frequently comes from power plants, which release about 50% of the nation's mercury emissions. In other countries, such as Ghana, gold mining requires mercury compounds, leading to workers receiving significant quantities of mercury while performing their jobs. Such mercury from gold mines is specifically known to contribute to biomagnification in aquatic food chains.

The farming of aquatic organisms, known as aquaculture, often involves fish feed that contains mercury. A study by Jardine has found no reliable connection between mercury in fish food affecting aquaculture organisms or aquatic organisms in the wild. Even so, mercury from other sources may still affect organisms grown through aquaculture. In China, farmed fish species, such as bighead carp, mud carp, and Siniperca chuatsi, carried 90% of total mercury content in all of the measured fish in a study by Cheng. This study also concluded that mercury bioaccumulates through food chains even in controlled aquaculture environments. Both total mercury and methyl mercury absorption was found to be derived from sediments containing mercury, not mainly from fish feed.

The Hawaii Institute of Marine Biology has noted that fish feed used in aquaculture often contains heavy metals such as mercury, lead, and arsenic, and has dispatched these concerns to organizations such as the Food and Agriculture Organization of the United Nations. 

Elemental mercury often comes from coal power plants, and oxidized mercury often comes from incinerators. Oil-fired power plants also contribute mercury to the environment. The energy industry therefore is a key player in the introduction of mercury into the environment. When addressing the issue of reducing seafood mercury bioaccumulation on a global scale, it is important to pinpoint major energy producers and consumers whose exchange of energy may be the root of the problem.

Controlling output of mercury pollution sources

A study that was led by scientists from Harvard University and U.S. Geological Survey has determined that in the next several decades there will be a 50 percent increase in mercury levels.^{[citation needed]} The study also shows that the increases are connected through industrial emissions and are not natural as previously thought. However, by decreasing emissions from industrial plants, the possibility of decreasing the high level of mercury remains plausible. Several nations are currently implementing systems that will detect and therefore later be able to control the output of mercury into the atmosphere. Air pollution control devices (APCDs) have been implemented in South Korea as the government is starting to take inventory of mercury sources. Mercury pollution can also be removed by electrostatic precipitators (ESPs). Bag-based filters are also used in factories that may contribute mercury to the environment. Flue-gas desulfurization, normally used to eliminate sulfur dioxide, can also be used in conjunction with APCDs to remove additional mercury before exhausts are released into the environment. Even so, countries such as South Korea have only begun to use inventories of mercury sources, calling into question how fast anti-mercury measures will be put into factories.

Health effects and outcomes

Disparate impacts

Mercury content in fish does not affect all populations equally. Certain ethnic groups, as well as young children, are more likely to suffer the effects of methyl mercury poisoning. In the United States, Wallace gathered data that indicated 16.9% of women who self-identify as Native American, Asian, Pacific Islander, or multiracial exceed the recommended reference dose of mercury. A study done on children of the Faroe Islands near Great Britain showed neurological problems stemming from mothers consuming pilot whale meat during pregnancy.

Regulation and health

While various studies have shown high concentrations of mercury accumulated in fish, medical cases often go unreported and pose a difficulty in correlating mercury in fish with human poisoning. Environmental issues cover a broad range of areas, but medical cases that are associated with pollutants released into the environment by factories or construction areas cause public health issues that affect not only the environment but also human well-being. Substances poisonous to the human body in a particular amount or dose may not cause any symptoms over time. While there are limits to how much of anything the body can have, mercury is a particular poison that produces immediate physical symptoms when the body has been accumulating it over a period of time.

In the United States, the Environmental Protection Agency measures the amount of mercury concentrated in human blood that does not pose fatal health outcomes. The agency is in charge of enforcing regulations and policies that cover a range of environmental topics. Analysis of blood mercury concentrations in childbearing women has proved that exposure to methyl mercury (MeHg) occurs primarily through the consumption of fish. The U.S. FDA highly recommends against pregnant woman and young children consuming raw fish. Pregnant women and young children often lack strong immune systems and are more at risk for foodborne illnesses.

Medical cases and exposure to mercury

In the United States, the EPA serves as an advisory organ to set the levels of mercury that are non-fatal in humans. Symptoms of exposure to high levels of methyl mercury include disturbed vision, hearing, and speech, lack of coordination, and muscle weakness. Medical studies have examined the correlation of fish consumption and health issues. American studies have presented evidence of fish consumption and its effects on child development. Longitudinal studies agree that human activities are what release and accumulate mercury in marine life. Addressing the issues of fish consumption forces health officials to recognize the sources of mercury in the human body. Specific Native American tribes are vulnerable to a high exposure of mercury. Studies have determined that these native peoples in the United States suffer more from mercury poisoning and illness than any other cohort group in the country. This is due to the fact that fish is a main source of protein. Exposure risk was assessed through a medical study, thus raising judicial issues of whether the public health of these groups is a priority in the United States.

Work and exposure

Most cases that arise are due to work exposure or medicinal poisoning. Environmental justice advocates can relate these mercury cases to the unregulated amount of mercury that enters the environment. Workers can be exposed to mercury through the manufacture of fluorescent tubes, chloralkali, or acetaldehyde among other products. Anthropogenic sources and places where mercury is released or used as a solid or vapor puts these has caused fatigue, dizziness, hyperhidrosis, chest congestion, and loss of motor skills. When taken to the hospital, the neurotoxicity levels had already exceeded the maximum amounts. Over-the-counter medicines have been shown to have traces of mercurous chloride. Medical research reported that the children who received doses of these medicines experienced physical symptoms such as "drooling, irregular arm movements, and impaired gait". Exposures to this result in severe physical impairments unregulated chemicals that are put in products. The intake of laxatives that contained about 120 mg of mercurous chloride has also been cases of mercury's toxicity.

Even in countries, such as Sweden, that have phased out mercury in the dental industry and manufacturing, lingering quantities of mercury still exist in lakes and coastal areas. Moreover, global contributions of mercury to the environment also affect that country. A study in Sweden selected 127 women who had a high level of fish consumption. Around 20% of the women selected, after hair and blood samples, were found to have exceeded the EPA's recommended reference dose of 0.1 micrograms of methyl mercury per kilogram of body weight. Additionally, the study concluded that there was "no margin of safety for neuraldevelopmental effects in fetus[es]" without removing the offending species of fish from the diets of the women. This indicates that families intending to raise children should be especially careful about exposing their unborn babies to toxic mercury via fish. 

Children exposed to mercury are particularly susceptible to poisoning since the ratio of food, water, and air intake versus individual body weight is much higher than that of adults. Additionally, children undergo fast growth which causes them to be more susceptible to damaging exposure to methylmercury, as well as the long term consequences of such exposure during childhood development. Young age plays an important role in terms of damage caused by mercury, and much literature on mercury focuses on pregnant women and specific precautions designed to prevent youth mercury exposure. Prenatal methylmercury exposure does cause behavioral problems in infants and worsened cognitive test performance. Additionally, Hughner estimates that 250,000 women may be exposing their unborn babies to levels of methyl mercury above recommended federal levels.

Economically, there does not seem to be a difference in mercury exposure based on socioeconomic bracket and the ability to buy fish from the market. One study shows "no significant differences in mercury levels in tuna, bluefish, and flounder as a function of type of store or economic neighborhood".

By nation

Certain countries have cultural differences that lead to more fish consumption and therefore more possible exposure to seafood methylmercury. In Ghana, the local population traditionally consumes large quantities of fish, leading to potentially dangerous amounts of mercury in the bloodstream. In the Amazonian Basin, during the rainy season, herbivorous fish dominate the diet of 72.2% of the women selected from a particular Amazonian village. Analysis also shows increase of mercury content in the hair of humans who eat fish on a daily basis in the Amazon.

The most serious case of mercury poisoning in recent history was in the Japanese city of Minamata, in the 1950s. Minamata poisoning proves that significant prenatal and postnatal exposure to high levels of methylmercury causes serious neurological problems. Minamata victims also show higher than normal signs of psychiatric diseases, along with those diseases being caused by underlying neurological issues.

A 2014 USGS survey of mercury levels in the United States water system found that methylmercury concentrations in fish were typically highest in wetland areas including the coastal plain streams in the Southeast. Fish methylmercury levels were also high in the Western US, but only in streams that had been mined for mercury or gold.

Seafood consumption benefits

The American College of Obstetricians and Gynecologists note that, considering all the dangers and benefits, the overall result of eating fish in the United States is likely to improve personal health rather than damage it. The college argues that the omega-3 polyunsaturated fatty acids found in fish have a health benefit that outweighs the harm from mercury or polychlorinated biphenyls. Even so, the College also suggests limiting fish consumption for pregnant women. A risk-benefit study weighing the risks of mercury consumption against the benefits derived from fish in Alaska showed that the benefits outweigh the risks when consuming salmon for both cardiovascular health and infant neurological development, and that MeHg data for non-oily fish needs to be of high quality before relative risk can be reliably identified. The Seychelles Child Development Study traced more than seven hundred mother-child pairs for nine years, and found no neurological problems in the children resulting from both prenatal and postnatal methylmercury exposure. A study done with marketed fish in Oman concluded that, except in a few rare cases, the fish available for consumption had lower levels of mercury than limits defined by various health organizations. Clearly, these studies call into question whether or not normal everyday consumption of fish is dangerous in any way, and at very least justify the creation of place-based and culturally relevant consumption advisories. They do not take into account cases of severe mercury poisoning, such as that found in Minamata disease.

Selenium is an element that is known to counteract some of the dangers of ingesting mercury. Multiple studies have been done, such as those in New Jersey and Sweden, that take into account selenium as well as mercury levels. Fish often do contain selenium in conjunction with bioaccumulated mercury, which may offset some of the dangers associated with the mercury ingested.

Current advice

The complexities associated with mercury transport and environmental fate are described by USEPA in their 1997 Mercury Study Report to Congress. Because methyl mercury and high levels of elemental mercury can be particularly toxic to a fetus or young children, organizations such as the U.S. EPA and FDA recommend that women who are pregnant or plan to become pregnant within the next one or two years, as well as young children, avoid eating more than 6 ounces (170g, one average meal) of fish per week.

In the United States, the FDA has an action level for methylmercury in commercial marine and freshwater fish that is 1.0 parts per million (ppm). In Canada, the limit for the total of mercury content is 0.5 ppm. The Got Mercury? website includes a calculator for determining mercury levels in fish.

Species with characteristically low levels of mercury include shrimp, tilapia, salmon, pollock, and catfish (FDA March 2004). The FDA characterizes shrimp, catfish, pollock, salmon, sardines, and canned light tuna as low-mercury seafood, although recent tests have indicated that up to 6 percent of canned light tuna may contain high levels. A study published in 2008 found that mercury distribution in tuna meat is inversely related to the lipid content, suggesting that the lipid concentration within edible tuna tissues has a diluting effect on mercury content. These findings suggest that choosing to consume a type of tuna that has a higher natural fat content may help reduce the amount of mercury intake, compared to consuming tuna with a low fat content. Also, many of the fish chosen for sushi contain high levels of mercury.

According to the US Food and Drug Administration (FDA), the risk from mercury by eating fish and shellfish is not a health concern for most people. However, certain seafood might contain levels of mercury that may cause harm to an unborn baby (and especially its brain development and nervous system). In a young child, high levels of mercury can interfere with the development of the nervous system. The FDA provides three recommendations for young children, pregnant women, and women of child-bearing age:

1. Do not eat shark, swordfish, king mackerel, or tilefish (Gulf of Mexico) because they might contain high levels of mercury.
2. Eat up to 12 ounces (2 average meals of 170 g each) a week of a variety of fish and shellfish that are lower in mercury. Five of the most commonly eaten fish and shellfish that are low in mercury are: shrimp, canned light tuna, salmon, pollock, and catfish. Another commonly eaten fish, albacore or ("white") tuna depending on its origin might have more mercury than canned light tuna. So, when choosing your two meals of fish and shellfish, it is recommended that you should not eat more than up to 6 ounces (one average meal) of albacore tuna per week.
3. Check local advisories about the safety of fish caught by family and friends in your local lakes, rivers, and coastal areas. If no advice is available, eat up to 6 ounces (one average meal of 170 g) per week of fish you catch from local waters, but consume no other fish during that week.

Research suggests that selenium content in fish is protective against the toxic effects of methylmercury content. Fish with higher ratios of selenium to methylmercury (Se:Hg) are better to eat since the selenium binds to the methylmercury allowing it to pass through the body un-absorbed.

In 2012 the European Food Safety Authority (EFSA) reported on chemical contaminants they found in the food of over 20 European countries. They established that fish meat and fish products were primarily responsible for methylmercury in the diet of all age classes. Particularly implicated were swordfish, tuna, cod, pike, whiting and hake. The EFSA recommend a tolerable weekly intake for methylmercury of 1.3 μg/kg body weight.

Background

In the 1950s, inhabitants of the seaside town of Minamata, on Kyushu island in Japan, noticed strange behavior in animals. Cats would exhibit nervous tremors, and dance and scream. Within a few years this was observed in other animals; birds would drop out of the sky. Symptoms were also observed in fish, an important component of the diet, especially for the poor. When human symptoms started to be noticed around 1956 an investigation began. Fishing was officially banned in 1957. It was found that the Chisso Corporation, a petrochemical company and maker of plastics such as vinyl chloride, had been discharging heavy metal waste into the sea for decades. They used mercury compounds as catalysts in their syntheses. It is believed that about 5,000 people were killed and perhaps 50,000 have been to some extent poisoned by mercury. Mercury poisoning in Minamata, Japan, is now known as Minamata disease.