Habitat fragmentation

From Wikipedia, the free encyclopedia

Fragmentation and destruction of Great Ape habitat in Central Africa, from the GLOBIO and GRASP projects. Areas shown in black and red delineate areas of severe and moderate habitat loss, respectively.

 

Habitat fragmentation describes the emergence of discontinuities (fragmentation) in an organism's preferred environment (habitat), causing population fragmentation and ecosystem decay. Causes of habitat fragmentation include geological processes that slowly alter the layout of the physical environment (suspected of being one of the major causes of speciation),and human activity such as land conversion, which can alter the environment much faster and causes the extinction of many species. 

Deforestation and increased road-building in the Amazon Rainforest are a significant concern because of increased human encroachment upon wild areas, increased resource-extraction and further threats to biodiversity.

Definition

The term habitat fragmentation includes five discrete phenomena:

• Reduction in the total area of the habitat
• Decrease of the interior: edge ratio
• Isolation of one habitat fragment from other areas of habitat
• Breaking up of one patch of habitat into several smaller patches
• Decrease in the average size of each patch of habitat

"fragmentation ... not only causes loss of the amount of habitat, but by creating small, isolated patches it also changes the properties of the remaining habitat" (van den Berg et al. 2001). Habitat fragmentation is the landscape level of the phenomenon, and patch level process. Thus meaning, it covers; the patch areas, edge effects, and patch shape complexity.

In scientific literature, there is some debate whether the term "habitat fragmentation" applies in cases of habitat loss, or whether the term primarily applies to the phenomenon of habitat being cut into smaller pieces without significant reduction in habitat area. Scientists who use the stricter definition of "habitat fragmentation" per se would refer to loss of habitat area as "habitat loss" and explicitly mention both terms if describing a situation where the habitat becomes less connected and there is less overall habitat.

Causes

Natural causes

Evidence of habitat destruction through natural processes such as volcanism, fire, and climate change is found in the fossil record. For example, habitat fragmentation of tropical rainforests in Euramerica 300 million years ago led to a great loss of amphibian diversity, but simultaneously the drier climate spurred on a burst of diversity among reptiles.

Human causes

Habitat fragmentation is frequently caused by humans when native plants is cleared for human activities such as agriculture, rural development, urbanization and the creation of hydroelectric reservoirs. Habitats which were once continuous become divided into separate fragments. After intensive clearing, the separate fragments tend to be very small islands isolated from each other by cropland, pasture, pavement, or even barren land. The latter is often the result of slash and burn farming in tropical forests. In the wheat belt of central western New South Wales, Australia, 90% of the native vegetation has been cleared and over 99% of the tall grass prairie of North America has been cleared, resulting in extreme habitat fragmentation.

Endogenous vs. exogenous

There are two types of processes that can lead to habitat fragmentation. There are exogenous processes and endogenous processes. Endogenous are process that develop as a part of a species biology so they typically include changes in biology, behavior and interactions within or between species. Endogenous threats can result in changes to breeding patterns or migration patterns and are often triggered by exogenous processes. Exogenous processes are independent of species biology and can include habitat degradation, habitat subdivision or habitat isolation. These processes can have a substantial impact on endogenous processes by fundamentally altering species behavior. Habitat subdivision or isolation can lead to changes in dispersal or movement of species including changes to seasonal migration. These changes can lead to decrease in a density of species, increased competition or even increased predation.

Implications

Habitat Loss and Biodiversity

One of the major ways that habitat fragmentation affects biodiversity is by reducing the amount of suitable habitat available for organisms. Habitat fragmentation often involves both habitat destruction and the subdivision of previously continuous habitat. Plants and other sessile organisms are disproportionately affected by some types of habitat fragmentation because they cannot respond quickly to the altered spatial configuration of the habitat.

Habitat loss, which can occur through the process of habitat fragmentation, is considered to be the greatest threat to species. But, the effect of the configuration of habitat patches within the landscape, independent of the effect of the amount of habitat within the landscape (referred to as fragmentation per se), has been suggested to be small. A review of empirical studies found that, of the 381 reported significant effect of habitat fragmentation per se on species occurrences, abundances or diversity in the scientific literature, 76% were positive whereas 24% were negative. Despite these results, the scientific literature tends to emphasize negative effects more than positive effects. Positive effects of habitat fragmentation per se imply that several small patches of habitat can have higher conservation value than a single large patch of equivalent size. Land sharing strategies could therefore have more positive impacts on species than land sparing strategies.

Habitat fragmented by numerous roads near the Indiana Dunes National Lakeshore.

 

Area is the primary determinant of the number of species in a fragment and the relative contributions of demographic and genetic processes to the risk of global population extinction depend on habitat configuration, stochastic environmental variation and species features. Minor fluctuations in climate, resources, or other factors that would be unremarkable and quickly corrected in large populations can be catastrophic in small, isolated populations. Thus fragmentation of habitat is an important cause of species extinction. Population dynamics of subdivided populations tend to vary asynchronously. In an unfragmented landscape a declining population can be "rescued" by immigration from a nearby expanding population. In fragmented landscapes, the distance between fragments may prevent this from happening. Additionally, unoccupied fragments of habitat that are separated from a source of immigrants by some barrier are less likely to be repopulated than adjoining fragments. Even small species such as the Columbia spotted frog are reliant on the rescue effect. Studies showed 25% of juveniles travel a distance over 200m compared to 4% of adults. Of these, 95% remain in their new locale, demonstrating that this journey is necessary for survival.

Additionally, habitat fragmentation leads to edge effects. Microclimatic changes in light, temperature and wind can alter the ecology around the fragment, and in the interior and exterior portions of the fragment. Fires become more likely in the area as humidity drops and temperature and wind levels rise. Exotic and pest species may establish themselves easily in such disturbed environments, and the proximity of domestic animals often upsets the natural ecology. Also, habitat along the edge of a fragment has a different climate and favours different species from the interior habitat. Small fragments are therefore unfavourable for species which require interior habitat. The percentage preservation of contiguous habitats is closely related to both genetic and species biodiversity preservation. Generally a 10% remnant contiguous habitat will result in a 50% biodiversity loss.

Informed Conservation

Habitat fragmentation is often a cause of species becoming threatened or endangered. The existence of viable habitat is critical to the survival of any species, and in many cases the fragmentation of any remaining habitat can lead to difficult decisions for conservation biologists. Given a limited amount of resources available for conservation is it preferable to protect the existing isolated patches of habitat or to buy back land to get the largest possible continuous piece of land. In rare cases a conservation reliant species may gain some measure of disease protection by being distributed in isolated habitats. This ongoing debate is often referred to as SLOSS (Single Large or Several Small).

One solution to the problem of habitat fragmentation is to link the fragments by preserving or planting corridors of native vegetation. In some cases, a bridge or underpass may be enough to join two fragments. This has the potential to mitigate the problem of isolation but not the loss of interior habitat. 

Another mitigation measure is the enlargement of small remnants in order to increase the amount of interior habitat. This may be impractical since developed land is often more expensive and could require significant time and effort to restore. 

The best solution is generally dependent on the particular species or ecosystem that is being considered. More mobile species, like most birds, do not need connected habitat while some smaller animals, like rodents, may be more exposed to predation in open land. These questions generally fall under the headings of metapopulations island biogeography.

Genetic Risks

As the remaining habitat patches are smaller, they tend to support smaller populations of fewer species. Small populations are at an increased risk of a variety of genetic consequences that influence their long-term survival. Remnant populations often contain only a subset of the genetic diversity found in the previously continuous habitat. In these cases, processes that act upon underlying genetic diversity, such as adaptation, have a smaller pool of fitness-maintaining alleles to survive in the face of environmental change. However in some scenarios, where subsets of genetic diversity are partitioned among multiple habitat fragments, almost all original genetic diversity can be maintained despite each individual fragment displaying a reduced subset of diversity.

Gene Flow and Inbreeding

Gene flow occurs when individuals of the same species exchange genetic information through reproduction. Populations can maintain genetic diversity through migration. When a habitat becomes fragmented and reduced in area, gene flow and migration is typically reduced. Fewer individuals will migrate into the remaining fragments, and small disconnected populations that may have once been part of a single large population will become reproductively isolated. Scientific evidence that gene flow is reduced due to fragmentation depends on the study species. While trees that have long-range pollination and dispersal mechanisms may not experience reduced gene flow following fragmentation, most species are at risk of reduced gene flow following habitat fragmentation.

Reduced gene flow, and reproductive isolation can result in inbreeding between related individuals. Inbreeding does not always result in negative fitness consequences, but when inbreeding is associated with fitness reduction it is called inbreeding depression. Inbreeding becomes of increasing concern as the level of homozygosity increases, facilitating the expression of deleterious alleles that reduce the fitness. Habitat fragmentation can lead to inbreeding depression for many species due to reduced gene flow. Inbreeding depression is associated with conservation risks, like local extinction.

Genetic Drift

Small populations are more susceptible to genetic drift. Genetic drift is random changes to the genetic make up of populations and always leads to reductions in genetic diversity. The smaller the population is, the more likely genetic drift will be a driving force of evolution rather than natural selection. Because genetic drift is a random process, it does not allow species to become more adapted to their environment. Habitat fragmentation is associated with increases to genetic drift in small populations which can have negative consequences for the genetic diversity of the populations. However, research suggests that some tree species may be resilient to the negative consequences of genetic drift until population size is as small as ten individuals or less.

Adaptation

In order for populations to evolve in response to natural selection, they must be large enough that natural selection is a stronger evolutionary force than genetic drift. Recent studies on the impacts of habitat fragmentation on adaptation in some plant species have suggested that organisms in fragmented landscapes may be able to adapt to fragmentation. However, there are also many cases where fragmentation reduces adaptation capacity because of small population size.

Examples of Impacted Species

Some species that have experienced genetic consequences due to habitat fragmentation are listed below:

Macquarie perch

• Macquaria australasica
• Fagus sylvatica 
• Betula nana
• Rhinella ornata 
• Ochotona princeps
• Uta stansburiana
• Plestiodon skiltonianus
• Sceloporus occidentalis
• Chamaea fasciata

Effect on Animal Behaviours

Although the way habitat fragmentation affects the genetics and extinction rates of species has been heavily studied, fragmentation has also been shown to affect species' behaviours and cultures as well. This is important because social interactions have the ability to determine and have an effect on a species' fitness and survival. Habitat fragmentation alters the resources available and the structure of habitats, as a result alters the behaviours of species and the dynamics between differing species. Behaviours affected can be within a species such as reproduction, mating, foraging, species dispersal, communication and movement patterns or can be behaviours between species such as predator prey relationships.

Predation Behaviours

Habitat fragmentation due to anthropogenic activities has been shown to greatly affect the predator-prey dynamics of many species by altering the amount of species and the members of those species. This affects the natural predator-prey relationships between animals in a given community and forces them to alter their behaviours and interactions, therefore resetting the so called "behavioral space race". The way in which fragmentation changes and re-shapes these interactions can occur in many different forms. Most prey species have patches of land that are refuge from their predators, allowing them the safety to reproduce and raise their young. Human introduced structures such as roads and pipelines alter these areas by facilitating predator activity in these refuges, increasing predator-prey overlap. The opposite could also occur in the favour of prey, increasing prey refuge and subsequently decreasing predation rates. Fragmentation may also increase predator abundance or predator efficiency and therefore increase predation rates in this manner. Several other factors can also increase or decrease the extent to which the shifting predator-prey dynamics affect certain species, including how diverse a predators diet is and how flexible habitat requirements are for predators and prey. Depending on which species are affected and these other factors, fragmentation and its resulting effects on predator-prey dynamics may contribute to a species extinction. In response to these new environmental pressures, new adaptive behaviours may be developed. Prey species may adapt to increased risk of predation with strategies such as altering mating tactics or changing behaviours and activities related to food and foraging.

Boreal Woodland Caribous

In the boreal woodland caribous of British Columbia the effects of fragmentation are clearly demonstrated. The species refuge area is peatland bog which has been interrupted by linear features such as roads and pipelines. These features have allowed their natural predators, the wolf and the black bear to more efficiently travel over landscapes and between patches of land. Since their predators can more easily access the caribous' refuge, the females of the species attempt to avoid the area, affecting their reproductive behaviours and offspring produced.

Communication Behaviours

Fragmentation affecting the communication behaviours of birds has been well studied in Dupont's Lark. The Larks primarily reside in regions of Spain and are a small passerine bird which use songs as a means of cultural transmission between members of the species. The Larks have two distinct vocalizations, the song and the territorial call. The territorial call is used by males to defend and signal territory from other male Larks and is shared between neighbouring territories when males respond to a rivals song. Occasionally it is used as a threat signal to signify an impending attack on territory. A large song repertoire can enhance a males ability to survive and reproduce as he has a greater ability to defend his territory from other males, and a larger number of males in the species means a larger variety of songs being transmitted. Fragmentation of the Dupont's Lark territory from agriculture, forestry and urbanization appears to have a large effect on their communication structures. Males only perceive territories of a certain distance to be rivals and so isolation of territory from others due to fragmentation leads to a decrease in territorial calls as the males no longer have any reason to use it or have any songs to match.

Forest fragmentation

Forest fragmentation is a form of habitat fragmentation where forests are reduced (either naturally or man-made) to relatively small, isolated patches of forest known as forest fragments or forest remnants. The intervening matrix that separates the remaining woodland patches can be natural open areas, farmland, or developed areas. Following the principles of island biogeography, remnant woodlands act like islands of forest in a sea of pastures, fields, subdivisions, shopping malls, etc. These fragments will then begin to undergo the process of ecosystem decay. 

Forest fragmentation also includes less subtle forms of discontinuities such as utility right-of-ways (ROWs). Utility ROWs are of ecological interest because they have become pervasive in many forest communities, spanning areas as large as 5 million acres in the United States. Utility ROWs include electricity transmission ROWs, gas pipeline and telecommunication ROWs. Electricity transmission ROWs are created to prevent vegetation interference with transmission lines. Some studies have shown that electricity transmission ROWs harbor more plant species than adjoining forest areas, due to alterations in the microclimate in and around the corridor. Discontinuities in forest areas associated with utility right-of-ways can serve as biodiversity havens for native bees and grassland species, as the right-of-ways are preserved in an early successional stage.

Implications

Forest fragmentation is one of the greatest threats to biodiversity in forests, especially in the tropics. The problem of habitat destruction that caused the fragmentation in the first place is compounded by

• the inability of individual forest fragments to support viable populations, especially of large vertebrates
• the local extinction of species that do not have at least one fragment capable of supporting a viable population
• edge effects that alter the conditions of the outer areas of the fragment, greatly reducing the amount of true forest interior habitat.

The effect of fragmentation on the flora and fauna of a forest patch depends on a) the size of the patch, and b) its degree of isolation. Isolation depends on the distance to the nearest similar patch, and the contrast with the surrounding areas. For example, if a cleared area is reforested or allowed to regenerate, the increasing structural diversity of the vegetation will lessen the isolation of the forest fragments. However, when formerly forested lands are converted permanently to pastures, agricultural fields, or human-inhabited developed areas, the remaining forest fragments, and the biota within them, are often highly isolated.

Forest patches that are smaller or more isolated will lose species faster than those that are larger or less isolated. A large number of small forest "islands" typically cannot support the same biodiversity that a single contiguous forest would hold, even if their combined area is much greater than the single forest. However, forest islands in rural landscapes greatly increase their biodiversity.

Approaches to understanding habitat fragmentation

Two approaches that are typically used to understand habitat fragmentation and its ecological impacts.

Species-oriented approach

The species-oriented approach focuses specifically on individual species and how they each respond to their environment and habitat changes with in it. This approach can be limited because it does only focus on individual species and does not allow for a broad view of the impacts of habitat fragmentation across species.

Pattern-oriented approach

The pattern-oriented approach is based on land cover and its patterning in correlation with species occurrences. One model of study for landscape patterning is the patch-matrix-corridor model developed by Richard Forman The pattern-oriented approach focuses on land cover defined by human means and activities. This model has stemmed from island biogeography and tries to infer causal relationships between the defined landscapes and the occurrence of species or groups of species within them. The approach has limitations in its collective assumptions across species or landscapes which may not account for variations amongst them.

Variegation Model

The other model is the variegation model. Variegated landscapes retain much of their natural vegetation but are intermixed with gradients of modified habitat.  This model of habitat fragmentation typically applies to landscapes that are modified by agriculture. In contrast to the fragmentation model that is denoted by isolated patches of habitat surrounded by unsuitable landscape environments, the variegation model applies to landscapes modified by agriculture where small patches of habitat remain near the remnant original habitat. In between these patches are a matrix of grassland that are often modified versions of the original habitat. These areas do not present as much of a barrier to native species.

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.