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CHEMICAL HAZARD - Arsenic poisoning

Photo: Credit to Valerie Dumar, Austin Acuff, Max Laider and Casey King

Arsenic poisoning

From Wikipedia, the free encyclopedia

Arsenic poisoning is a medical condition caused by elevated levels of arsenic in the body. The dominant basis of arsenic poisoning is from ground water that naturally contains high concentrations of arsenic. A 2007 study found that over 137 million people in more than 70 countries are probably affected by arsenic poisoning from drinking water.

Signs and symptoms

Symptoms of arsenic poisoning begin with headaches, confusion, severe diarrhea, and drowsiness. As the poisoning develops, convulsions and changes in fingernail pigmentation called leukonychia striata may occur. Aldrich Mee’s lines (leuchoparonychia) on nails are also seen. When the poisoning becomes acute, symptoms may include diarrhea, vomiting, blood in the urine, cramping muscles, hair loss, stomach pain, and more convulsions. The organs of the body that are usually affected by arsenic poisoning are the lungs, skin, kidneys, and liver. The final result of arsenic poisoning is coma and death.

Arsenic is related to heart disease (hypertension related cardiovascular), cancer, stroke (cerebrovascular diseases), chronic lower respiratory diseases, and diabetes.

Night blindness

Chronic exposure to arsenic is related to vitamin A deficiency which is related to heart disease and night blindness.

Inorganic arsenites (arsenic(III)) in drinking water have a much higher acute toxicity than organic arsenates (arsenic(V)). The acute minimal lethal dose of arsenic in adults is estimated to be 70 to 200 mg or 1 mg/kg/day.

Causes

Drinking water

Main article: Arsenic contamination of groundwater

Chronic arsenic poisoning results from drinking contaminated well water over a long period of time. Many aquifers contain high concentration of arsenic salts. TheWorld Health Organization recommends a limit of 0.01 mg/L (10ppb) of arsenic in drinking water. This recommendation was established based on the limit of detection for most laboratories testing equipment at the time of publication of the WHO water quality guidelines. More recent findings show that consumption of water with levels as low as 0.00017 mg/L (0.17ppb) over long periods of time can lead to arsenicosis.

From a 1988 study in China, the US protection agency quantified the lifetime exposure of arsenic in drinking water at concentrations of 0.0017 mg/L, 0.00017 mg/L, and 0.000017 mg/L are associated with a lifetime skin cancer risk of 1 in 10,000, 1 in 100,000, and 1 in 1,000,000 respectively. The World Health Organization asserts that a level of 0.01 mg/L poses a risk of 6 in 10000 chance of lifetime skin cancer risk and contends that this level of risk is acceptable.

One of the worst incidents of arsenic poisoning via well water occurred in Bangladesh, which the World Health Organization called the "largest mass poisoning of a population in history."

Mining techniques such as hydraulic fracturing may mobilize arsenic in groundwater and aquifers due to enhanced methane transport and resulting changes in redox conditions, and inject fluid containing additional arsenic.

Occupational exposures

Main article: Arsenic § Applications

Because of its high toxicity, arsenic is little used in the Western world, although in Asia is still a popular pesticide. Arsenic is mainly encountered occupationally in the smelting of zinc and copper ores.

Food

It has been found that rice is particularly susceptible to accumulation of arsenic from soil. Rice grown in the US has an average 260 ppb of arsenic according to a study, but U.S. arsenic intake remains far below WHO recommended limits. China has set a standard for arsenic limits in food (150 ppb), as levels in rice exceed those in water.

In the United States, levels of arsenic that are above natural levels, but still well below danger levels set in federal safety standards, have been detected in commercially grown chickens. The source of the arsenic appears to be the feed additives roxarsone and nitarsone, which are used to control the parasitic infection coccidiosis as well as to increase weight and skin coloring of the poultry.

Pathophysiology

Main article: Arsenic toxicity

Arsenic interferes with cellular longevity by allosteric inhibition of an essential metabolic enzyme pyruvate dehydrogenase (PDH) complex, which catalyzes the oxidation of pyruvate to acetyl-CoA by NAD⁺. With the enzyme inhibited, the energy system of the cell is disrupted resulting in a cellular apoptosis episode. Biochemically, arsenic prevents use of thiamine resulting in a clinical picture resembling thiamine deficiency. Poisoning with arsenic can raise lactate levels and lead to lactic acidosis. Low potassium levels in the cells increases the risk of experiencing a life-threatening heart rhythm problem from arsenic trioxide. Arsenic in cells clearly stimulates the production of hydrogen peroxide (H₂O₂). When the H₂O₂ reacts with certain metals such as iron or manganese it produces a highly reactive hydroxyl radical. Inorganic arsenic trioxide found in ground water particularly affects voltage-gated potassium channels, disrupting cellular electrolytic function resulting in neurological disturbances, cardiovascular episodes such as prolonged QT interval, neutropenia, high blood pressure, central nervous system dysfunction, anemia, and death. Arsenic is a ubiquitous element present in American drinking water.

Arsenic exposure plays a key role in the pathogenesis of vascular endothelial dysfunction as it inactivates endothelial nitric oxide synthase, leading to reduction in the generation and bioavailability of nitric oxide. In addition, the chronic arsenic exposure induces high oxidative stress, which may affect the structure and function of cardiovascular system. Further, the arsenic exposure has been noted to induce atherosclerosis by increasing the platelet aggregation and reducing fibrinolysis. Moreover, arsenic exposure may cause arrhythmia by increasing the QT interval and accelerating the cellular calcium overload. The chronic exposure to arsenic upregulates the expression of tumor necrosis factor-α, interleukin-1, vascular cell adhesion molecule and vascular endothelial growth factor to induce cardiovascular pathogenesis.

—Pitchai Balakumar1 and Jagdeep Kaur, "Arsenic Exposure and Cardiovascular Disorders: An Overview", Cardiovascular Toxicology, December 2009

Tissue culture studies have shown that arsenic compounds block both IKr and Iks channels and, at the same time, activates IK-ATP channels. Arsenic compounds also disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. These metabolic interferences lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. A post mortem reveals brick red colored mucosa, due to severe hemorrhage. Although arsenic causes toxicity, it can also play a protective role.

Diagnosis

Arsenic may be measured in blood or urine to monitor excessive environmental or occupational exposure, confirm a diagnosis of poisoning in hospitalized victims or to assist in the forensic investigation in a case of fatal over dosage. Some analytical techniques are capable of distinguishing organic from inorganic forms of the element. Organic arsenic compounds tend to be eliminated in the urine in unchanged form, while inorganic forms are largely converted to organic arsenic compounds in the body prior to urinary excretion. The current biological exposure index for U.S. workers of 35 µg/L total urinary arsenic may easily be exceeded by a healthy person eating a seafood meal.

Tests are available to diagnose poisoning by measuring arsenic in blood, urine, hair, and fingernails. The urine test is the most reliable test for arsenic exposure within the last few days. Urine testing needs to be done within 24–48 hours for an accurate analysis of an acute exposure. Tests on hair and fingernails can measure exposure to high levels of arsenic over the past 6–12 months. These tests can determine if one has been exposed to above-average levels of arsenic. They cannot predict, however, whether the arsenic levels in the body will affect health. Chronic arsenic exposure can remain in the body systems for a longer period of time than a shorter term or more isolated exposure and can be detected in a longer time frame after the introduction of the arsenic, important in trying to determine the source of the exposure.

Hair is a potential bioindicator for arsenic exposure due to its ability to store trace elements from blood. Incorporated elements maintain their position during growth of hair. Thus for a temporal estimation of exposure, an assay of hair composition needs to be carried out with a single hair which is not possible with older techniques requiring homogenization and dissolution of several strands of hair. This type of biomonitoring has been achieved with newer microanalytical techniques like Synchrotron radiation based X ray fluorescence (SXRF) spectroscopy and Microparticle induced X ray emission (PIXE).The highly focused and intense beams study small spots on biological samples allowing analysis to micro level along with the chemical speciation. In a study, this method has been used to follow arsenic level before, during and after treatment with Arsenious oxide in patients with Acute Promyelocytic Leukemia.

Treatment

Chelation

Chemical and synthetic methods are used to treat arsenic poisoning. Dimercaprol and dimercaptosuccinic acid are chelating agents that sequester the arsenic away from blood proteins and are used in treating acute arsenic poisoning. The most important side effect is hypertension. Dimercaprol is considerably more toxic than succimer. DMSA monoesters, e.g. MiADMSA, are promising antidotes for arsenic poisoning. Calcium sodium edetate is also used.

Nutrition

Supplemental potassium decreases the risk of experiencing a life-threatening heart rhythm problem from arsenic trioxide.

Removal

Various techniques have been evolved for arsenic removal, most frequently using absorbents such as activated carbon, aluminum oxide, co-operative with iron oxide to form sludges, adsorption onto iron-oxide-coated polymeric materials, and electrocoagulation by nanoparticle. To remove the stress of heavy and toxic metals, an environment-friendly approach must be applied and the use of naturally occurring microbe must be emphasized. Bacteria, yeast, fungi, algae—all of them can be used for remediation processes and it is always recommended that microbe used for bioremediation must have natural decontamination process and the method should be cost-effective.

History

In addition to its presence as a poison, for centuries arsenic was used medicinally. It has been used for over 2,400 years as a part of traditional Chinese medicine. In the western world, arsenic compounds, such as salvarsan, were used extensively to treat syphilis before penicillin was introduced. It was eventually replaced as a therapeutic agent by sulfa drugs and then by other antibiotics. Arsenic was also an ingredient in many tonics (or "patent medicines").

In addition, during the Elizabethan era, some women used a mixture of vinegar, chalk, and arsenic applied topically to whiten their skin. This use of arsenic was intended to prevent aging and creasing of the skin, but some arsenic was inevitably absorbed into the blood stream.

Some pigments, most notably the popular Emerald Green (known also under several other names), were based on arsenic compounds. Overexposure to these pigments was a frequent cause of accidental poisoning of artists and craftsmen.

Arsenic became a favored method for murder of the Middle Ages and Renaissance, particularly among ruling classes in Italy allegedly. Because the symptoms are similar to those of cholera, which was common at the time, arsenic poisoning often went undetected. By the 19th century, it had acquired the nickname "inheritance powder," perhaps because impatient heirs were known or suspected to use it to ensure or accelerate their inheritances.

In ancient Korea, and particularly in Joseon Dynasty, arsenic-sulfur compounds have been used as a major ingredient of sayak (사약; 賜藥), which was a poison cocktail used in capital punishment of high-profile political figures and members of the royal family.  Due to social and political prominence of the condemned, many of these events were well-documented, often in the Annals of Joseon Dynasty; they are sometimes portrayed in historical television miniseries because of their dramatic nature.

Notable cases

Arsenic poisoning, accidental or deliberate, has been implicated in the illness and death of a number of prominent people throughout history.

Francesco I de' Medici, Grand Duke of Tuscany

Recent forensic evidence uncovered by Italian scientists suggests that Francesco (1541-1587) and his wife were poisoned, possibly by his brother and successor Ferdinando.

George III of Great Britain

George III's (1738–1820) personal health was a concern throughout his long reign. He suffered from periodic episodes of physical and mental illness, five of them disabling enough to require the King to withdraw from his duties. In 1969, researchers asserted that the episodes of madness and other physical symptoms were characteristic of the disease porphyria, which was also identified in members of his immediate and extended family. In addition, a 2004 study of samples of the King's hair revealed extremely high levels of arsenic, which is a possible trigger of disease symptoms. A 2005 article in the medical journal The Lancet suggested the source of the arsenic could be the antimony used as a consistent element of the King's medical treatment. The two minerals are often found in the same ground, and mineral extraction at the time was not precise enough to eliminate arsenic from compounds containing antimony.

Theodor Ursinus

Theodor Gottlieb Ursinus (1749–1800), a high-ranking Prussian civil servant and justice official, was poisoned by his wife Charlotte Ursinus (1760–1836). At the time, his death was ruled a stroke, but soon after the widow was found to have poisoned, between 1797 and 1801, not only her husband, but also her aunt and her lover, as well as to have attempted to poison her servant in 1803. Her sensational trial led to the first reliable method of identifying arsenic poisoning.

Napoleon Bonaparte

It has been suggested that Napoleon Bonaparte (1769–1821) suffered and died from arsenic poisoning during his imprisonment on the island of Saint Helena. Forensic samples of his hair did show high levels, 13 times the normal amount, of the element. This, however, does not prove deliberate poisoning by Napoleon's enemies:copper arsenite has been used as a pigment in some wallpapers, and microbiological liberation of the arsenic into the immediate environment would be possible. The case is equivocal in the absence of clearly authenticated samples of the wallpaper. Samples of hair taken during Napoleon's lifetime also show levels of arsenic, so that arsenic from the soil could not have polluted the post-mortem sample. Even without contaminated wallpaper or soil, commercial use of arsenic at the time provided many other routes by which Napoleon could have consumed enough arsenic to leave this forensic trace.

Simón Bolívar

South American independence leader Simón Bolívar (1783–1830), according to Paul Auwaerter from the Division of Infectious Diseases in the Department of Medicine at the Johns Hopkins University School of Medicine, may have died due to chronic arsenic poisoning further complicated by bronchiectasis and lung cancer.Auwaerter has considered murder and acute arsenic poisoning unlikely, arguing that gradual "environmental contact with arsenic would have been entirely possible" as a result of drinking contaminated water in Peru or through the medicinal use of arsenic (which was common at the time) as Bolívar had reportedly resorted to it during the treatment for some of his illnesses.

Charles Francis Hall

American explorer Charles Francis Hall (1821–1871) died unexpectedly during his third Arctic expedition aboard the ship Polaris. After returning to the ship from a sledging expedition Hall drank a cup of coffee and fell violently ill. He collapsed in what was described as a fit. He suffered from vomiting and delirium for the next week, then seemed to improve for a few days. He accused several of the ship's company, including ship's physician Emil Bessels with whom he had longstanding disagreements, of having poisoned him. Shortly thereafter, Hall again began suffering the same symptoms, died, and was taken ashore for burial. Following the expedition's return a US Navy investigation ruled that Hall had died from apoplexy.

In 1968, however, Hall's biographer Chauncey C. Loomis, a professor at Dartmouth College, traveled to Greenland to exhume Hall's body. Due to the permafrost, Hall's body, flag shroud, clothing and coffin were remarkably well preserved. Tissue samples of bone, fingernails and hair showed that Hall died of poisoning from large doses of arsenic in the last two weeks of his life, consistent with the symptoms party members reported. It is possible that Hall dosed himself with quack medicines which included the poison, but it is possible that he was murdered by Bessels or one of the other members of the expedition.

Clare Boothe Luce

Clare Boothe Luce (1903–1987), the American ambassador to Italy from 1953 to 1956, did not die from arsenic poisoning, but suffered an increasing variety of physical and psychological symptoms until arsenic was implicated. Its source was traced to the 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.

Emperor Guangxu

In 2008, testing in the People's Republic of China confirmed that China's second-to-last emperor was poisoned with a massive dose of arsenic; suspects include his dying aunt, the Empress Dowager Cixi, and her strongman, Yuan Shikai.

Phar Lap

The famous and largely successful New Zealand bred racehorse Phar Lap died suddenly in 1932. Poisoning was considered as a cause of death and several forensic examinations were completed at the time of death. In a recent examination, 75 years after his death, forensic scientists determined that the horse had ingested a massive dose of arsenic shortly before his death.

King Faisal I of Iraq

According to his British nurse, Lady Badget, King Faisal I of Iraq suffered from symptoms similar to those of arsenic poisoning during his last visit to Switzerland for treatment in 1933, at the age of 48. His Swiss doctors found him in a very healthy situation a day before.

Source: http://en.wikipedia.org/

CHEMICAL HAZARD - Arsenic

Arsenic

Fact sheet N°372
December 2012

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Key facts

• Arsenic is naturally present at high levels in the groundwater of a number of countries.
• Arsenic is highly toxic in its inorganic form.
• Contaminated water used for drinking, food preparation and irrigation of food crops poses the greatest threat to public health from arsenic.
• Long-term exposure to arsenic from drinking-water and food can cause cancer and skin lesions. It has also been associated with developmental effects, cardiovascular disease, neurotoxicity and diabetes.
• The most important action in affected communities is the prevention of further exposure to arsenic by provision of a safe water supply.

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Sources of exposure

Arsenic is a natural component of the earth’s crust and is widely distributed throughout the environment in the air, water and land. It is highly toxic in its inorganic form.

People are exposed to elevated levels of inorganic arsenic through drinking contaminated water, using contaminated water in food preparation and irrigation of food crops, industrial processes, eating contaminated food and smoking tobacco.

Long-term exposure to inorganic arsenic, mainly through drinking of contaminated water, eating of food prepared with this water and eating food irrigated with arsenic-rich water, can lead to chronic arsenic poisoning. Skin lesions and skin cancer are the most characteristic effects.

Drinking-water and food

The greatest threat to public health from arsenic originates from contaminated groundwater. Inorganic arsenic is naturally present at high levels in the groundwater of a number of countries, including Argentina, Bangladesh, Chile, China, India, Mexico, and the United States of America. Drinking-water, crops irrigated with contaminated water and food prepared with contaminated water are the sources of exposure.

Fish, shellfish, meat, poultry, dairy products and cereals can also be dietary sources of arsenic, although exposure from these foods is generally much lower compared to exposure through contaminated groundwater. In seafood, arsenic is mainly found in its less toxic organic form.

Industrial processes

Arsenic is used industrially as an alloying agent, as well as in the processing of glass, pigments, textiles, paper, metal adhesives, wood preservatives and ammunition. Arsenic is also used in the hide tanning process and, to a limited extent, in pesticides, feed additives and pharmaceuticals.

Tobacco

People who smoke tobacco can also be exposed to the natural inorganic arsenic content of tobacco because tobacco plants essentially take up arsenic naturally present in the soil. Also, in the past, the potential for elevated arsenic exposure was much greater when tobacco plants used to be treated with lead arsenate insecticide.

Health effects

Arsenic occurs in inorganic and organic forms. Inorganic arsenic compounds (such as those found in water) are highly toxic while organic arsenic compounds (such as those found in seafood) are less harmful to health.

Acute effects

The immediate symptoms of acute arsenic poisoning include vomiting, abdominal pain and diarrhoea. These are followed by numbness and tingling of the extremities, muscle cramping and death, in extreme cases.

Long-term effects

The first symptoms of long-term exposure to high levels of inorganic arsenic (e.g. through drinking-water and food) are usually observed in the skin, and include pigmentation changes, skin lesions and hard patches on the palms and soles of the feet (hyperkeratosis). These occur after a minimum exposure of approximately five years and may be a precursor to skin cancer.

In addition to skin cancer, long-term exposure to arsenic may also cause cancers of the bladder and lungs. The International Agency for Research on Cancer (IARC) has classified arsenic and arsenic compounds as carcinogenic to humans, and has also stated that arsenic in drinking-water is carcinogenic to humans.

Other adverse health effects that may be associated with long-term ingestion of inorganic arsenic include developmental effects, neurotoxicity, diabetes and cardiovascular disease. In China (Province of Taiwan), arsenic exposure has been linked to “blackfoot disease”, which is a severe disease of blood vessels leading to gangrene. However, this disease has not been observed in other parts of the world, and it is possible that malnutrition contributes to its development.

Magnitude of the problem

Arsenic contamination of groundwater is widespread and there are a number of regions where arsenic contamination of drinking-water is significant.

Arsenic in Bangladesh has attracted much attention since recognition in the 1990s of its wide occurrence in well-water in that country. Since this time, significant progress has since been made and the number of people exposed to arsenic exceeding the Bangladesh drinking-water quality standard has decreased by approximately 40%. Despite these efforts, it is estimated that about 20 million and 45 million people in Bangladesh are at risk of being exposed to arsenic concentrations that are greater than the national standard of 50 μg/litre and the WHO guideline value of 10 μg/litre respectively1.

The symptoms and signs caused by long-term elevated exposure to inorganic arsenic differ between individuals, population groups and geographical areas. Thus, there is no universal definition of the disease caused by arsenic. This complicates the assessment of the burden on health of arsenic.

Similarly, there is no method to distinguish cases of cancer caused by arsenic from cancers induced by other factors. As a result, there is no reliable estimate of the magnitude of the problem worldwide.

In 2010, the Joint FAO/WHO Expert Committee on Food Additives (JECFA) re-evaluated the effects of arsenic on human health, taking new data into account. JECFA concluded that for certain regions of the world where concentrations of inorganic arsenic in drinking-water exceed 50–100 μg/litre, there is some evidence of adverse effects. In other areas, where arsenic concentrations in water are elevated (10–50 μg/litre), JECFA concluded that while there is a possibility of adverse effects, these would be at a low incidence that would be difficult to detect in epidemiological studies.

Prevention and control

The most important action in affected communities is the prevention of further exposure to arsenic by the provision of a safe water supply for drinking, food preparation and irrigation of food crops. There are a number of options to reduce levels of arsenic in drinking-water.

• Substitute high-arsenic sources such as groundwater, with low-arsenic, microbiologically safe sources such as rain water and treated surface water. Low-arsenic water can be used for drinking, cooking and irrigation purposes, whereas arsenic-rich water can be used for other purposes such as bathing and washing clothes.
• Discriminate between high-arsenic and low-arsenic sources. For example, test water for arsenic levels and paint tube wells or hand pumps different colours. This can be an effective and low-cost means to rapidly reduce exposure to arsenic when accompanied by effective education.
• Blend low-arsenic water with higher-arsenic water to achieve an acceptable arsenic concentration level.
• Install arsenic removal systems – either centralized or domestic – and ensure the appropriate disposal of the removed arsenic. Technologies for arsenic removal include oxidation, coagulation–precipitation, absorption, ion exchange and membrane techniques. There is an increasing number of effective and low-cost options for removing arsenic from small or household supplies.

Long-term actions are also required to reduce occupational exposure from industrial processes.

Education and community engagement are key factors for ensuring successful interventions. There is a need for community members to understand the risks of high arsenic exposure and the sources of arsenic exposure, including the intake of arsenic by crops (e.g. rice) from irrigation water and the intake of arsenic into food from cooking water.

High-risk populations should also be monitored for early signs of arsenic poisoning – usually skin problems.

Source: http://www.who.int/

CHEMICAL HAZARD - Cadmium poisoning

Cadmium poisoning

From Wikipedia, the free encyclopedia


Cadmium is an extremely toxic metal commonly found in industrial workplaces. Due to its low permissible exposure limit, overexposures may occur even in situations where trace quantities of cadmium are found. Cadmium is used extensively in electroplating, although the nature of the operation does not generally lead to overexposures. Cadmium is also found in some industrial paints and may represent a hazard when sprayed. Operations involving removal of cadmium paints by scraping or blasting may pose a significant hazard. Cadmium is also present in the manufacturing of some types of batteries. Exposures to cadmium are addressed in specific standards for the general industry, shipyard employment, construction industry, and the agricultural industry.

Sources of exposure

In the 1950s and 1960s industrial exposure to cadmium was high, but as the toxic effects of cadmium became apparent, industrial limits on cadmium exposure have been reduced in most industrialized nations and many policy makers agree on the need to reduce exposure further. While working with cadmium it is important to do so under a fume hood to protect against dangerous fumes. Brazing fillers which contain cadmium should be handled with care. Serious toxicity problems have resulted from long-term exposure to cadmium plating baths.

Buildup of cadmium levels in the water, air, and soil has been occurring particularly in industrial areas. Environmental exposure to cadmium has been particularly problematic in Japan where many people have consumed rice that was grown in cadmium contaminated irrigation water. This phenomenon is known under the name itai-itai disease.

Food is another source of cadmium. Plants may only contain small or moderate amounts in non-industrial areas, but high levels may be found in the liver and kidneys of adult animals. The daily intake of cadmium through food varies by geographic region. Intake is reported to be approximately 8 to 30mcg in Europe and the United States versus 59 to 113 mcg in various areas of Japan.

Cigarettes are also a significant source of cadmium exposure. Although there is generally less cadmium in tobacco than in food, the lungs absorb cadmium more efficiently than the stomach.

Aside from tobacco smokers, people who live near hazardous waste sites or factories that release cadmium into the air have the potential for exposure to cadmium in air. However, numerous state and federal regulations in the United States control the amount of cadmium that can be released to the air from waste sites and incinerators so that properly regulated sites are not hazardous. The general population and people living near hazardous waste sites may be exposed to cadmium in contaminated food, dust, or water from unregulated releases or accidental releases. Numerous regulations and use of pollution controls are enforced to prevent such releases.

Workers can be exposed to cadmium in air from the smelting and refining of metals, or from the air in plants that make cadmium products such as batteries, coatings, or plastics. Workers can also be exposed when soldering or welding metal that contains cadmium. Approximately 512,000 workers in the United States are in environments each year where a cadmium exposure may occur. Regulations that set permissible levels of exposure, however, are enforced to protect workers and to make sure that levels of cadmium in the air are considerably below levels thought to result in harmful effects.

Artists who work with cadmium pigments, which are commonly used in strong oranges, reds, and yellows, can easily accidentally ingest dangerous amounts, particularly if they use the pigments in dry form, as with chalk pastels, or in mixing their own paints.

Some sources of phosphate in fertilizers contain cadmium in amounts of up to 100 mg/kg, which can lead to an increase in the concentration of cadmium in soil (for example in New Zealand). Nickel-cadmium batteries are one of the most popular and most common cadmium-based products, and this soil can be mined for use in them.

An experiment during the early 1960s involving the spraying of cadmium over Norwich has recently been declassified by the UK government, as documented in a BBC News article.

In February 2010, cadmium was found in an entire line of Wal-Mart exclusive Miley Cyrus jewelry. The charms were tested at the behest of the Associated Press and were found to contain high levels of cadmium. Wal-Mart did not stop selling the jewelry until May 12 because "it would be too difficult to test products already on its shelves". On June 4 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.

Clinical effects

Acute exposure to cadmium fumes may cause flu like symptoms including chills, fever, and muscle ache sometimes referred to as "the cadmium blues." Symptoms may resolve after a week if there is no respiratory damage. More severe exposures can cause tracheo-bronchitis, pneumonitis, and pulmonary edema. Symptoms of inflammation may start hours after the exposure and include cough, dryness and irritation of the nose and throat, headache, dizziness, weakness, fever, chills, and chest pain.

Inhaling cadmium-laden dust quickly leads to respiratory tract and kidney problems which can be fatal (often from renal failure). Ingestion of any significant amount of cadmium causes immediate poisoning and damage to the liver and the kidneys. Compounds containing cadmium are also carcinogenic.

The bones become soft (osteomalacia), lose bone mineral density (osteoporosis) and become weaker. This causes the pain in the joints and the back, and also increases the risk of fractures. In extreme cases of cadmium poisoning, mere body weight causes a fracture.

The kidneys lose their function to remove acids from the blood in proximal renal tubular dysfunction. The kidney damage inflicted by cadmium poisoning is irreversible. The proximal renal tubular dysfunction creates low phosphate levels in the blood (hypophosphatemia), causing muscle weakness and sometimes coma. The dysfunction also causes gout, a form of arthritis due to the accumulation of uric acid crystals in the joints because of high acidity of the blood (hyperuricemia). Another side effect is increased levels of chloride in the blood (hyperchloremia). The kidneys can also shrink up to 30%. Cadmium exposure is also associated with the development of kidney stones.

Other patients lose their sense of smell (anosmia).

Biological or biochemical mechanisms for toxicity

Cadmium acts as a catalyst in forming reactive oxygen species. It increases lipid peroxidation, in addition it depletes antioxidants, glutathione and protein-bound sulfhydryl groups. It also promotes the production of inflammatory cytokines.

Biomarkers of excessive exposure

Increased concentrations of urinary beta-2 microglobulin can be an early indicator of renal dysfunction in persons chronically exposed to low but excessive levels of environmental cadmium. The urinary beta-2 microglobulin test is an indirect method of measuring cadmium exposure. Under some circumstances, the Occupational Health and Safety Administration requires screening for renal damage in workers with long-term exposure to high levels of cadmium. Blood or urine cadmium concentrations provide a better index of excessive exposure in industrial situations or following acute poisoning, whereas organ tissue (lung, liver, kidney) cadmium concentrations may be useful in fatalities resulting from either acute or chronic poisoning. Cadmium concentrations in healthy persons without excessive cadmium exposure are generally less than 1 μg/L in either blood or urine. The ACGIH biological exposure indices for blood and urine cadmium levels are 5 μg/L and 5 μg/g creatinine, respectively, in random specimens. Persons who have sustained renal damage due to chronic cadmium exposure often have blood or urine cadmium levels in a range of 25-50 μg/L or 25-75 μg/g creatinine, respectively. These ranges are usually 1000-3000 μg/L and 100-400 μg/L, respectively, in survivors of acute poisoning and may be substantially higher in fatal cases.

Source: http://en.wikipedia.org/

CHEMICAL HAZARD - Cadmium

Summary

Cadmium is a metal used in the manufacture of batteries, and is also found in cigarette smoke. Ongoing exposure to cadmium can lead to adverse health effects, including certain kidney and lung conditions. Occupations at risk of cadmium exposure include battery manufacturing, welding or soldering, smelting, textile working and manufacturing. Some fertilised soils may contain high levels of cadmium.

Cadmium is a heavy metal that is produced during the smelting of other metals, such as zinc lead and copper. Cadmium is most frequently used in the manufacture of nickel-cadmium rechargeable batteries found in mobile phones and cordless equipment. It is also used in metal plating, some paints, plastics and fertilisers, and is found in cigarette smoke.

Exposure to cadmium occurs mostly in the workplace where cadmium products are made. The general population can be exposed to cadmium from cigarette smoke or eating cadmium-contaminated foods. Cadmium can affect the kidneys, lungs, and bones.

High-risk occupations and hobbies for cadmium

Some of the occupations that directly involve cadmium and carry a higher risk of exposure include:

• battery manufacture
• jobs involving welding or soldering
• smelting
• mining
• textile work
• cadmium alloy manufacture or use
• manufacture of materials that contain cadmium, such as certain paints and plastics
• jewellery making
• stained glass window making
• municipal solid waste recovery workers.

Other sources of exposure to cadmium

Other ways people may be exposed to cadmium include:

• cigarette smoking – cigarettes contain cadmium and smokers inhale cadmium when they smoke. Smokers may receive twice the daily dose of cadmium as non-smokers. People breathing cigarette smoke can also inhale cadmium.
• food – vegetables, like potatoes and leafy vegetables, and cereal grains grown in contaminated soils with high levels of cadmium may contain small amounts of cadmium. Kidneys and livers of animals and shellfish can contain higher levels of cadmium than other foods.
• industrial areas – some industrial processes, such as metal smelting, release cadmium into the air. Controls are placed on industry to limit emission levels and ensure protection of public health.
• fertilised soils – in agricultural areas, phosphate fertilised soils may contain higher levels of cadmium than unfertilised soils.

Health effects of exposure to cadmium

It is unlikely that the general population would be exposed to a level of cadmium high enough to cause adverse health effects.

The health effects associated with cadmium exposure depend on the way people are exposed to cadmium, how much has entered the person’s body, how long the person has been exposed for and how the person’s body responds to the exposure. Once cadmium enters the body, it is stored in the liver and kidneys, and then slowly excreted in urine.

Inhalation of cadmium

Inhalation is the main way workers are exposed to cadmium. Safe levels and standards of exposure are enforced to protect workers’ health. These standards are set below levels which are thought to cause adverse effects.

Breathing air with high levels of cadmium over a short period of time is initially like the flu with chills, fever and muscle pain, then later can cause lung damage, shortness of breath, chest pain and cough, which may lead to death in severe cases.

Breathing lower levels of cadmium over a longer period of time can lead to kidney disease and cause bones to become weaker.

Ingestion of cadmium

Eating food or drink contaminated with high levels of cadmium can cause stomach irritation, abdominal cramps, nausea, vomiting and diarrhoea. Headaches and flu-like symptoms, swelling of the throat and tingling hands may also occur.

Only a small amount of cadmium remains in the body after eating food contaminated with cadmium, but if consumed over a long period of time, cadmium can lead to kidney disease and cause bones to become weaker.

Large amounts of cadmium can damage the kidney, liver and heart and in severe cases may cause death.

Effects of cadmium exposure on children and babies

Children exposed to cadmium should have the same symptoms as adults. Small amounts of cadmium may be found in the breastmilk of women who were exposed to high cadmium levels.

Mothers exposed to high levels of cadmium in their workplace may have children with lower birth weights. Exposure to cadmium at normal environmental levels is not likely to cause mothers to have babies with low birth weights.

Carcinogenicity

Cadmium and its compounds are classified as causing cancer, but there is no evidence that cadmium causes cancer at the low levels normally found in the environment. Breathing cadmium in the air can cause lung cancer, but ingesting contaminated food or drink is not thought to cause cancer.

Testing and treatment for cadmium

If you think you have been exposed to high levels of cadmium, you should seek advice from your doctor.

Urine or blood tests can measure cadmium levels in the body. Tests are also available to check the health of the kidneys and liver. The accuracy of hair and nail tests in measuring the extent of cadmium exposure has not been determined. 

There is no specific treatment for cadmium poisoning, but supportive medical care may be required. Reducing the risk of further exposure is the most important step in managing people exposed to lower levels of cadmium over a longer period of time.

Reducing the risk of exposure

Suggestions to reduce the risk of exposure to cadmium include:

• Stop smoking. Cigarette smoke contains cadmium that can be absorbed through the lungs.
• Try to avoid inhaling other people’s cigarette smoke.
• Eat a healthy balanced diet with only moderate amounts of shellfish and organ meats.
• If your job or hobbies involve handling cadmium, always use appropriate personal protective equipment and consider having your cadmium levels checked regularly by your doctor.

Cadmium batteries

Common alkaline batteries do not contain cadmium. However, nickel-cadmium rechargeable batteries used in mobile phones, cordless tools, laptop computers and digital cameras do contain cadmium. These batteries and equipment should be disposed of at appropriate waste disposal sites.

Where to get help

• Your doctor
• WorkSafe Victoria, Tel. (03) 9641 1444 or 1800 136 089 (toll free) – for general enquiries regarding cadmium in workplaces
• Department of Health, Environmental Health Unit, Tel. 1300 761 874 – for health information regarding cadmium
• Environment Protection Authority Victoria, Tel. (03) 9695 2722 – for information regarding the environmental impacts and disposal of cadmium

Things to remember

• Cadmium is a heavy metal with many uses, including the manufacture of rechargeable batteries.
• Exposure to cadmium can affect the kidneys, lungs and bones.
• Cigarette smoke contains high levels of cadmium.
• Blood and urine tests can measure the amount of cadmium present in the body.

Source: http://www.betterhealth.vic.gov.au/