Arsenic poisoning is a medical condition that occurs due to elevated levels of arsenic in the body. If arsenic poisoning occurs over a brief period of time symptoms may include vomiting, abdominal pain, encephalopathy, and watery diarrhea that contains blood. Long-term exposure can result in thickening of the skin, darker skin, abdominal pain, diarrhea, heart disease, numbness, and cancer.
The most common reason for long-term exposure is contaminated drinking water. Groundwater most often becomes contaminated naturally; however, contamination may also occur from mining or agriculture. It may also be found in the soil and air. Recommended levels in water are less than 10–50 µg/L (10–50 parts per billion). Other routes of exposure include toxic waste sites and traditional medicines. Most cases of poisoning are accidental. Arsenic acts by changing the functioning of around 200 enzymes. Diagnosis is by testing the urine, blood, or hair.
Prevention is by using water that does not contain high levels of arsenic. This may be achieved by the use of special filters or using rainwater. There is not good evidence to support specific treatments for long-term poisoning. For acute poisonings treating dehydration is important. Dimercaptosuccinic acid (DMSA) or dimercaptopropane sulfonate (DMPS) may be used while dimercaprol (BAL) is not recommended. Hemodialysis may also be used.
Through drinking water, more than 200 million people globally are exposed to higher than safe levels of arsenic. The areas most affected are Bangladesh and West Bengal. Exposure is also more common in people of low income and minorities. Acute poisoning is uncommon. The toxicity of arsenic has been described as far back as 1500 BC in the Ebers papyrus.
|Synonyms||Arsenic toxicity, arsenic overdose|
|Areas of the world with high naturally occurring arsenic levels in the groundwater.|
|Symptoms||Acute: vomiting, abdominal pain, watery diarrhea|
Chronic: thickened skin, darker skin, cancer
|Diagnostic method||Urine, blood, or hair testing|
|Prevention||Drinking water without arsenic|
|Treatment||Dimercaptosuccinic acid, dimercaptopropane sulfonate|
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 (Mees's lines, or Aldrich-Mees's lines) may occur. When the poisoning becomes acute, symptoms may include diarrhea, vomiting, vomiting blood, 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 disease), cancer, stroke (cerebrovascular diseases), chronic lower respiratory diseases, and diabetes. Skin effects can include skin cancer in the long-term but often prior to skin cancer are different skin lesions. Other effects may include darkening of skin and thickening of skin.
Chronic exposure to arsenic is related to vitamin A deficiency, which is related to heart disease and night blindness. The acute minimal lethal dose of arsenic in adults is estimated to be 70 to 200 mg or 1 mg/kg/day.
Its comutagenic effects may be explained by interference with base and nucleotide excision repair, eventually through interaction with zinc finger structures. Dimethylarsinic acid, DMA(V), caused DNA single strand breaks resulting from inhibition of repair enzymes at levels of 5 to 100 mM in human epithelial type II cells.
MMA(III) and DMA(III) were also shown to be directly genotoxic by effectuating scissions in supercoiled ΦX174 DNA. Increased arsenic exposure is associated with an increased frequency of chromosomal aberrations, micronuclei and sister-chromatid exchanges. An explanation for chromosomal aberrations is the sensitivity of the protein tubulin and the mitotic spindle to arsenic. Histological observations confirm effects on cellular integrity, shape and locomotion.
DMA(III) is able to form reactive oxygen species (ROS) by reaction with molecular oxygen. Resulting metabolites are the dimethylarsenic radical and the dimethylarsenic peroxyl radical. Both DMA(III) and DMA(V) were shown to release iron from horse spleen as well as from human liver ferritin if ascorbic acid was administered simultaneously. Thus, formation of ROS can be promoted. Moreover, arsenic could cause oxidative stress by depleting the cell's antioxidants, especially the ones containing thiol groups. The accumulation of ROS like the cited above and hydroxyl radicals, superoxide radicals and hydrogen peroxides causes aberrant gene expression at low concentrations and lesions of lipids, proteins and DNA in higher concentrations which eventually lead to cellular death. In a rat animal model, urine levels of 8-hydroxy-2’-desoxyguanosine (as a biomarker of ROS DNA damage) were measured after treatment with DMA(V). In comparison to control levels, they turned out to be significantly increased. This theory is further supported by a cross-sectional study which found elevated mean serum lipid peroxides (LPO) in the As exposed individuals which correlated with blood levels of inorganic arsenic and methylated metabolites and inversely correlated with nonprotein sulfhydryl (NPSH) levels in whole blood. Another study found an association of As levels in whole blood with the level of reactive oxidants in plasma and an inverse relationship with plasma antioxidants. A finding of the latter study indicates that methylation might in fact be a detoxification pathway with regard to oxidative stress: the results showed that the lower the As methylation capacity was, the lower the level of plasma antioxidant capacity. As reviewed by Kitchin (2001), the oxidative stress theory provides an explanation for the preferred tumor sites connected with arsenic exposure. Considering that a high partial pressure of oxygen is present in lungs and DMA(III) is excreted in gaseous state via the lungs this seems to be a plausible mechanism for special vulnerability. The fact that DMA is produced by methylation in the liver, excreted via the kidneys and latter on stored in the bladder accounts for the other tumor localizations.
Regarding DNA methylation, some studies suggest interaction of As with methyltransferases which leads to an inactivation of tumor suppressor genes through hypermethylation, others state that hypomethylation might occur due to a lack of SAM resulting in aberrant gene activation. An experiment by Zhong et al. (2001) with arsenite-exposed human lung A549, kidney UOK123, UOK109 and UOK121 cells isolated eight different DNA fragments by methylation-sensitive arbitrarily primed PCR. It turned out that six of the fragments were hyper- and two of them were hypomethylated. Higher levels of DNA methltransferase mRNA and enzyme activity were found.
Kitchin (2001) proposed a model of altered growth factors which lead to cell proliferation and thus to carcinogenesis. From observations, it is known that chronic low-dose arsenic poisoning can lead to increased tolerance to its acute toxicity. MRP1-overexpressing lung tumor GLC4/Sb30 cells poorly accumulate arsenite and arsenate. This is mediated through MRP-1 dependent efflux. The efflux requires GSH, but no As-GSH complex formation.
Although many mechanisms have been proposed, no definite model can be given for the mechanisms of chronic arsenic poisoning. The prevailing events of toxicity and carcinogenicity might be quite tissue-specific. Current consensus on the mode of carcinogenesis is that it acts primarily as a tumor promoter. Its co-carcinogenicity has been demonstrated in several models. However, the finding of several studies that chronically arsenic-exposed Andean populations (as most extremely exposed to UV-light) do not develop skin cancer with chronic arsenic exposure, is puzzling.
Organic arsenic is less harmful than inorganic arsenic. Seafood is a common source of the less toxic organic arsenic in the form of arsenobetaine. The arsenic reported in 2012 in fruit juice and rice by Consumer Reports was primarily inorganic arsenic. Because of its high toxicity, arsenic is seldom used in the Western world, although in Asia it is still a popular pesticide. Arsenic is mainly encountered occupationally in the smelting of zinc and copper ores.
Arsenic is naturally found in groundwater and presents serious health threats when high amounts exist. Chronic arsenic poisoning results from drinking contaminated well water over a long period of time. Many aquifers contain high concentration of arsenic salts. The World Health Organization (WHO) Guidelines for drinking water quality established in 1993 a provisional guideline value of 0.01 mg/L (10 parts per billion) for maximum contaminant levels 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 (0.17 parts per billion) 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 (1.7 ppb), 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. WHO asserts that a water level of 0.01 mg/L (10 ppb) 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" recognized as a major public health concern. The contamination in the Ganga- Brahmaputra fluvial plains in India and Padma-Meghna fluvial plains in Bangladesh demonstrated adverse impacts on human health.
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.
In the US, the U.S. Geological Survey estimates that the median groundwater concentration is 1 μg/L or less, although some groundwater aquifers, particularly in the western United States, can contain much higher levels. For example, median levels in Nevada were about 8 μg/L but levels of naturally occurring arsenic as high as 1000 μg/L have been measured in the United States in drinking water.
Geothermally active zones occur at hotspots where mantle-derived plumes ascend, such as in Hawaii and Yellowstone National Park, USA. Arsenic is an incompatible element ( do not fit easily into the lattices of common rock-forming minerals). Concentrations of arsenic are high mainly in geothermal waters that leach continental rocks. Arsenic in hot geothermal fluids was shown to be derived mainly from leaching of host rocks at Yellowstone National Park, in Wyoming, USA, rather than from magmas.
In the western USA, there are As (arsenic) inputs to groundwater and surface water from geothermal fluids in and near Yellowstone National Park, and in other western mineralized areas. Groundwater associated with volcanics in California contain As at concentrations ranging up to 48,000 μg/L, with As-bearing sulfide minerals as the main source. Geothermal waters on Dominica in the Lesser Antilles also contain concentrations of As >50 μg/L.
In general, because arsenic is an incompatible element, it accumulates in differentiated magmas, and in other western mineralized areas. Weathering of pegmatite veins in Connecticut, USA, was thought to contribute As to groundwater.
In Pennsylvania, As concentrations in water discharging from abandoned anthracite mines ranged from <0.03 to 15 μg/L and from abandoned bituminous mines, from 0.10 to 64 μg/L, with 10% of samples exceeding the United States Environmental Protection Agency MLC of 10 μg/L/
In the Piedmont of Pennsylvania and New Jersey, groundwater in Mesozoic age aquifers contains elevated levels of As—domestic well waters from Pennsylvania contained up to 65 μg/L, whereas in New Jersey the highest concentration measured recently was 215 μg/L.
Food also contains many organic arsenic compounds. The key organic arsenic compounds that can be routinely found in food (depending on food type) include monomethylarsonic acid (MMAsV), Dimethylearsenoicacid (DMAsV ), arsenobetaine, arsenocholine, arsenosugars, and arsenolipids. DMAsV or MMAsV can be found in various types of fin fish, crabs, and mollusks, but often at very low levels.
Arsenobetaine is the major form of arsenic in marine animals, and, by all accounts, it is considered a compound that is nontoxic under conditions of human consumption. Arsenocholine, which is mainly found in shrimp, is chemically similar to arsenobetaine, and is considered to be “essentially nontoxic”. Although arsenobetaine is little studied, available information indicates it is not mutagenic, immunotoxic, or embryotoxic.
Arsenosugars and arsenolipids have recently been identified. Exposure to these compounds and toxicological implications are currently being studied. Arsenosugars are detected mainly in seaweed but are also found to a lesser extent in marine mollusks. Studies addressing arsenosugar toxicity, however, have largely been limited to in vitro studies, which show that arsenosugars are significantly less toxic than both inorganic arsenic and trivalent methylated arsenic metabolites.
It has been found that rice is particularly susceptible to accumulation of arsenic from soil. Rice grown in the U.S. has an average 260 ppb of arsenic, according to a study; but U.S. arsenic intake remains far below World Health Organization-recommended limits. China has set a standard for arsenic limits in food (150 ppb), as levels in rice exceed those in water.
Arsenic is a ubiquitous element present in American drinking 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 raised 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.
High levels of inorganic arsenic were reportedly found in 83 California wines in 2015.
Exposure to arsenic in soil can occur through multiple pathways. Compared with the intake of naturally occurring arsenic from water and the diet, soil arsenic constitutes only a small fraction of intake.
The European Commission (2000) reports that levels of arsenic in air range 0–1 ng/m3 in remote areas, 0.2–1.5 ng/m3 in rural areas, 0.5–3 ng/m3 in urban areas, and up to about 50 ng/m3 in the vicinity of industrial sites. Based on these data, the European Commission (2000) estimated that in relation to food, cigarette smoking, water, and soil, air contributes less than 1% of total arsenic exposure.
The use of lead arsenate pesticides has been effectively eliminated for over 50 years. However, because of the pesticide's environmental persistence, it is estimated that millions of acres of land are still contaminated with lead arsenate residues. This presents a potentially significant public health concern in some areas of the United States (e.g., New Jersey, Washington, and Wisconsin), where large areas of land used historically as orchards have been converted into residential developments.
Some modern uses of arsenic-based pesticides still exist. Chromated copper arsenate (CCA) has been registered for use in the United States since the 1940s as a wood preservative, protecting wood from insects and microbial agents. In 2003, CCA manufacturers instituted a voluntary recall of residential uses of CCA-treated wood. the EPA 2008 final report stated that CCA is still approved for use in nonresidential applications, such as in marine facilities (pilings and structures), utility poles, and sand highway structures.
Exposure studies in the copper smelting industry are much more extensive and have established definitive links between arsenic, a by-product of copper smelting, and lung cancer via inhalation. Dermal and neurological effects were also increased in some of these studies. Although as time went on, occupational controls became more stringent and workers were exposed to reduced arsenic concentrations, the arsenic exposures measured from these studies ranged from about 0.05 to 0.3 mg/m3 and are significantly higher than airborne environmental exposures to arsenic (which range from 0 to 0.000003 mg/m3).
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 cellular apoptosis. 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 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.
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.
Arsenite inhibits not only the formation of acetyl-CoA but also the enzyme succinic dehydrogenase. Arsenate can replace phosphate in many reactions. It is able to form Glc-6-Arsenate in vitro; therefore it has been argued that hexokinase could be inhibited. (Eventually this may be a mechanism leading to muscle weakness in chronic arsenic poisoning.) In the glyceraldehyde 3-phosphate dehydrogenase reaction arsenate attacks the enzyme-bound thioester. The formed 1-arseno-3-phosphoglycerate is unstable and hydrolyzes spontaneously. Thus, ATP formation in Glycolysis is inhibited while bypassing the phosphoglycerate kinase reaction. (Moreover, the formation of 2,3-bisphosphoglycerate in erythrocytes might be affected, followed by a higher oxygen affinity of hemoglobin and subsequently enhanced cyanosis) As shown by Gresser (1981), submitochondrial particles synthesize Adenosine-5’-diphosphate-arsenate from ADP and arsenate in presence of succinate. Thus, by a variety of mechanisms arsenate leads to an impairment of cell respiration and subsequently diminished ATP formation. This is consistent with observed ATP depletion of exposed cells and histopathological findings of mitochondrial and cell swelling, glycogen depletion in liver cells and fatty change in liver, heart and kidney.
Experiments demonstrated enhanced arterial thrombosis in a rat animal model, elevations of serotonin levels, thromboxane A and adhesion proteins in platelets, while human platelets showed similar responses. The effect on vascular endothelium may eventually be mediated by the arsenic-induced formation of nitric oxide. It was demonstrated that +3 As concentrations substantially lower than concentrations required for inhibition of the lysosomal protease cathepsin L in B cell line TA3 were sufficient to trigger apoptosis in the same B cell line, while the latter could be a mechanism mediating immunosuppressive effects.
The two forms of inorganic arsenic, reduced (trivalent As(III)) and oxidized (pentavalent As(V)), can be absorbed, and accumulated in tissues and body fluids. In the liver, the metabolism of arsenic involves enzymatic and non-enzymatic methylation, the most frequently excreted metabolite (≥ 90%) in the urine of mammals is dimethylarsinic acid or cacodylic acid, DMA(V). Dimethylarsenic acid is also known as Agent Blue and was used as herbicide in the American war in Vietnam.
In humans inorganic arsenic is reduced nonenzymatically from pentoxide to trioxide, using glutathione (GSH) or it is mediated by enzymes. Reduction of arsenic pentoxide to arsenic trioxide increases its toxicity and bio availability, Methylation occurs through methyltransferase enzymes. S-adenosylmethionine (SAM) may serve as methyl donor. Various pathways are used, the principal route being dependent on the current environment of the cell. Resulting metabolites are monomethylarsonous acid, MMA(III), and dimethylarsinous acid, DMA(III).
Methylation had been regarded as a detoxification process, but reduction from +5 As to +3 As may be considered as a bioactivation instead. Another suggestion is that methylation might be a detoxification if "As[III] intermediates are not permitted to accumulate" because the pentavalent organoarsenics have a lower affinity to thiol groups than inorganic pentavalent arsenics. Gebel (2002) stated that methylation is a detoxification through accelerated excretion. With regard to carcinogenicity it has been suggested that methylation should be regarded as a toxification.
Arsenic, especially +3 As, binds to single, but with higher affinity to vicinal sulfhydryl groups, thus reacts with a variety of proteins and inhibits their activity. It was also proposed that binding of arsenite at nonessential sites might contribute to detoxification. Arsenite inhibits members of the disulfide oxidoreductase family like glutathione reductase and thioredoxin reductase.
The remaining unbound arsenic (≤ 10%) accumulates in cells, which over time may lead to skin, bladder, kidney, liver, lung, and prostate cancers. Other forms of arsenic toxicity in humans have been observed in blood, bone marrow, cardiac, central nervous system, gastrointestinal, gonadal, kidney, liver, pancreatic, and skin tissues.
Another aspect is the similarity of arsenic effects to the heat shock response. Short-term arsenic exposure has effects on signal transduction inducing heat shock proteins with masses of 27,60,70,72,90,110 kDa as well as metallotionein, ubiquitin, mitogen-activated [MAP] kinases, extracellular regulated kinase [ERK], c-jun terminal kinases [JNK] and p38. Via JNK and p38 it activates c-fos, c-jun and egr-1 which are usually activated by growth factors and cytokines. The effects are largely dependent on the dosing regime and may be as well inversed.
As shown by some experiments reviewed by Del Razo (2001), ROS induced by low levels of inorganic arsenic increase the transcription and the activity of the activator protein 1 (AP-1) and the nuclear factor-κB (NF-κB) (maybe enhanced by elevated MAPK levels), which results in c-fos/c-jun activation, over-secretion of pro-inflammatory and growth promoting cytokines stimulating cell proliferation. Germolec et al. (1996) found an increased cytokine expression and cell proliferation in skin biopsies from individuals chronically exposed to arsenic-contaminated drinking water.
Increased AP-1 and NF-κB obviously also result in an up-regulation of mdm2 protein, which decreases p53 protein levels. Thus, taking into account p53's function, a lack of it could cause a faster accumulation of mutations contributing to carcinogenesis. However, high levels of inorganic arsenic inhibit NF-κB activation and cell proliferation. An experiment of Hu et al. (2002) demonstrated increased binding activity of AP-1 and NF-κB after acute (24 h) exposure to +3 sodium arsenite, whereas long-term exposure (10–12 weeks) yielded the opposite result. The authors conclude that the former may be interpreted as a defense response while the latter could lead to carcinogenesis. As the contradicting findings and connected mechanistic hypotheses indicate, there is a difference in acute and chronic effects of arsenic on signal transduction which is not clearly understood yet.
Studies have demonstrated that the oxidative stress generated by arsenic may disrupt the signal transduction pathways of the nuclear transcriptional factors PPAR's, AP-1, and NF-κB, as well as the pro-inflammatory cytokines IL-8 and TNF-α. The interference of oxidative stress with signal transduction pathways may affect physiological processes associated with cell growth, metabolic syndrome X, glucose homeostasis, lipid metabolism, obesity, insulin resistance, inflammation, and diabetes-2. Recent scientific evidence has elucidated the physiological roles of the PPAR's in the ω- hydroxylation of fatty acids and the inhibition of pro-inflammatory transcription factors (NF-κB and AP-1), pro-inflammatory cytokines (IL-1, -6, -8, -12, and TNF-α), cell4 adhesion molecules (ICAM-1 and VCAM-1), inducible nitric oxide synthase, proinflammatory nitric oxide (NO), and anti-apoptotic factors.
Epidemiological studies have suggested a correlation between chronic consumption of drinking water contaminated with arsenic and the incidence of Type 2-diabetes. The human liver after exposure to therapeutic drugs may exhibit hepatic non-cirrhotic portal hypertension, fibrosis, and cirrhosis. However, the literature provides insufficient scientific evidence to show cause and effect between arsenic and the onset of diabetes mellitus Type 2.
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.
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.
Supplemental potassium decreases the risk of experiencing a life-threatening heart rhythm problem from arsenic trioxide.
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.
During the Victorian era (late 19th Century) in the United States, U.S. Newspapers advertised "Arsenic Complexion Wafers". These wafers promised to help get rid of blemishes on the face such as moles and pimples.
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.:63 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.:21 It was also a common murder technique in the 19th century in domestic violence situations, such as the case of Rebecca Copin, who attempted to poison her husband by "putting arsenic in his coffee".
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.
In U.S 1975, under the authority of the Safe Drinking Water Act (SDWA), U.S. Environment Protection Agency determined the National Interim Primary Drinking Water Regulation levels of arsenic (inorganic contaminant - IOCs) to be 0.05 mg/L (50 parts per billion - ppb).
Throughout the years, many studies reported dose-dependent effects of arsenic in drinking water and skin cancer. In other to prevent new cases and death from cancerous and non-cancerous diseases, SDWA directed EPA to revise arsenic's levels and specified the maximum contaminant level (MCL). MCLs are set as close to the health goals as possible, considering cost, benefits and the ability of public water systems to detect and remove contaminants using suitable treatment technologies.
In 2001, EPA adopted a lower standard of MCL 0.01 mg/L (10 ppb) for arsenic in drinking water that applies to both community water systems and non-transient non-community water systems.
In some other countries, when developing national drinking water standards based on the guideline values, it is necessary to take account of a variety of geographical, socio-economic, dietary and other conditions affecting potential exposure. These factors lead to national standards that differ appreciably from the guideline values. That is the case of countries such as India and Bangladesh, where the permissible limit of arsenic in absence of an alternative source of water is 0.05 mg/L.
Arsenic removal technologies are traditional treatment processes which have been tailored to improve removal of arsenic from drinking water. Although some of the removal processes, such as precipitative processes, adsorption processes, ion exchange processes, and separation (membrane) processes, may be technically feasible, their cost may be prohibitive.
For underdeveloped countries, the challenge is finding the means to fund such technologies. EPA, for example, has estimated the total national annualized cost of treatment, monitoring, reporting, record keeping, and administration for reinforce the MCL rule to be approximately $181 million. Most of the cost is due to the installation and operation of the treatment technologies needed to reduce arsenic in public water system.
Arsenic exposure through groundwater is highly concerning throughout the perinatal period. Pregnant women are a high-risk population because not only are the mothers at risk for adverse outcomes, but in-utero exposure also poses health risks to the infant. There is a dose-dependent relationship between maternal exposure to arsenic and infant mortality, meaning that infants born to women exposed to higher concentrations, or exposed for longer periods of time, have a higher mortality rate.
Studies have shown that ingesting arsenic through groundwater during pregnancy poses dangers to the mother including, but not limited to abdominal pain, vomiting, diarrhea, skin pigmentation changes, and cancer. Research has also demonstrated that arsenic exposure also causes low birth weight, low birth size, infant mortality, and a variety of other outcomes in infants. Some of these effects, like lower birth-rate and size may be due to the effects of arsenic on maternal weight gain during pregnancy.
The 1858 Bradford sweets poisoning was the arsenic poisoning of more than 200 people in Bradford, England, when sweets accidentally made with arsenic were sold from a market stall. Twenty-one victims died as a result. The event contributed to the passage of the Pharmacy Act 1868 in the United Kingdom and legislation regulating the adulteration of foodstuffs.1900 English beer poisoning
In 1900, more than 6,000 people in England were poisoned by arsenic-tainted beer, with more than 70 of the afflicted dying as a result. The food safety crisis was caused by arsenic entering the supply chain through impure sugar which had been made with contaminated sulphuric acid. The illness was prevalent across the Midlands and North West England, with Manchester being the most heavily affected.Originally misdiagnosed as alcoholic neuropathy, the main epidemic was only recognised after several months. Additionally, investigation into the outbreak found other sources of arsenic in beer, which had been unknowingly poisoning thousands in decades preceding the outbreak.2007 Carancas impact event
The Carancas impact event refers to the fall of the Carancas chondritic meteorite on September 15, 2007, near the village of Carancas in Peru, close to the Bolivian border and Lake Titicaca. The impact created a crater and scorched earth around its location. A local official, Marco Limache, said that "boiling water started coming out of the crater, and particles of rock and cinders were found nearby", as "fetid, noxious" gases spewed from the crater. Surface impact occurred above 3,800 metres (12,500 ft).
After the impact, villagers who had approached the impact site grew sick from a then-unexplained illness, with a wide array of symptoms. Two days later, Peruvian scientists confirmed that there had indeed been a meteorite strike, quieting widespread speculation that it may have been a geophysical rather than a celestial event. At that point, no further information on the cause of the mystery illness was known. The ground water in the local area is known to contain arsenic compounds, and the illness is now believed to have been caused by arsenic poisoning incurred when residents of the area inhaled the vapor of the boiling arsenic-contaminated water.Arsenic contamination of groundwater
Arsenic contamination of groundwater is a form of groundwater pollution which is often due to naturally occurring high concentrations of arsenic in deeper levels of groundwater. It is a high-profile problem due to the use of deep tubewells for water supply in the Ganges Delta, causing serious arsenic poisoning to large numbers of people. A 2007 study found that over 137 million people in more than 70 countries are probably affected by arsenic poisoning of drinking water. The problem became serious health concern after mass poisoning of water in Bangladesh. Arsenic contamination of ground water is found in many countries throughout the world, including the US.Approximately 20 major incidents of groundwater floarsenic contamination have been reported. Of these, four major incidents occurred in Asia, in Thailand, Taiwan, and Mainland China. Locations of potentially hazardous wells have been mapped in China.Arsenic poisoning 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.Eric XIV of Sweden
Towards the end of his life, king Eric XIV (1533–1577) was held prisoner in many different castles in both Sweden and Finland. He died in prison in Örbyhus Castle: according to a tradition starting with Johannes Messenius, his final meal was a poisoned bowl of pea soup. A document signed by his brother, John III of Sweden, and a nobleman, Bengt Bengtsson Gylta (1514–74), gave Eric's guards in his last prison authorization to poison him if anyone tried to release him. His body was exhumed in 1958 and modern forensic analysis revealed evidence of lethal arsenic poisoning.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 journey to the Arctic, the Polaris expedition. 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 the 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 U.S. 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 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.Guangxu Emperor
In 2008, testing in the People's Republic of China confirmed that the Guangxu Emperor (1871–1908) was poisoned with a massive dose of arsenic; suspects include his dying aunt, 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.Anderson Mazoka
The popular opposition leader in Zambia, Anderson Mazoka, whose health deteriorated after the 2001 presidential elections, repeatedly accused government agents of poisoning him. His daughter, Mutinta, confirmed after his death on 24 May 2006 that arsenic was found in his body after he died from kidney complications.Munir Said Thalib
Munir Said Thalib, an Indonesian human right and anti-corruption activist, was poisoned with arsenic onboard Garuda Indonesia flight from Jakarta to Amsterdam on September 7, 2004. The Netherlands Forensic Institute revealed that Munir's body contained a level of arsenic almost three times the lethal dose. Pollycarpus Budihari Priyanto, an active pilot at the time of the assassination, was found guilty of murder. Despite the guilty verdict, the circumstances surrounding the case remained unclear.Emmerson Mnangagwa
Robert Mugabe's successor as President of Zimbabwe, Emmerson Mnangagwa has claimed he was poisoned with arsenic at a rally. His entourage has suggested that supporters of Grace Mugabe were responsible.Moriku Joyce
State minister for primary health care, Dr. Moriku Joyce, revealed to the Daily Monitor that unknown people had poisoned her. This was after toxicological investigations in Ugandan and South African laboratories confirmed the presence of arsenic poison in her body.Arsenicum album
In homeopathy, arsenicum album (Arsen. alb.) is a solution prepared by diluting aqueous arsenic trioxide generally until there is little or no arsenic remaining in the solution. It is used by homeopaths to treat a range of symptoms that include digestive disorders and, as an application of the homeopathic Law of Similars has been suggested by homeopaths as a treatment for arsenic poisoning. Since the arsenic oxide in a homeopathic preparation is normally non-existent, it is considered generally safe, although cases of arsenic poisoning from poorly prepared homeopathic treatments sold in India have been reported. When properly prepared, however, the extreme dilutions, typically to at least 1 in 1024, or 12C in homeopathic notation, mean that statistically it is extremely unlikely that any pill contains even a molecule of the original arsenic used. While some small, unblinded studies have claimed an effect on reducing arsenic toxicity, they do not recommend its large-scale use, and studies of homeopathic remedies have been shown to generally have problems that prevent them from being considered unambiguous evidence. There is no known mechanism for how arsenicum album could remove arsenic from a body, and there is insufficient evidence for it to be considered effective medicine (for any condition) by the scientific community.Christine Young
Christine Young is an American investigative journalist and author of the book A Bitter Brew: Faith, Power and Poison in a Small New England Town, which documented the largest case of criminal arsenic poisoning in American history.Eric XIV of Sweden
Eric XIV (Swedish: Erik XIV; 13 December 1533 – 26 February 1577) was King of Sweden from 1560 until he was deposed in 1568. Eric XIV was the eldest son of Gustav I (1496–1560) and Catherine of Saxe-Lauenburg (1513–35). He was also ruler of Estonia, after its conquest by Sweden in 1561.
While he has been regarded as intelligent and artistically skilled, as well as politically ambitious, early in his reign he showed signs of mental instability, a condition that eventually led to insanity. Some scholars claim that his illness began early during his reign, while others believe that it first manifested with the Sture Murders.
Eric, having been deposed and imprisoned, was most likely murdered. An examination of his remains in 1958 confirmed that he probably died of arsenic poisoning.John Cassin
John Cassin (September 6, 1813 – January 10, 1869) was an American ornithologist. A Pennsylvania Quaker and businessman, he took up an unpaid position as curator of the Philadelphia Academy of Natural Sciences and published several books, and described numerous species of bird.
Cassin was born in Upper Providence Township, Delaware County, Pennsylvania near Philadelphia on September 6, 1813. Though his ancestors were Quakers, several had distinguished themselves in military and naval service.
A careful and talented taxonomist, Cassin named 198 birds not described in the works of his predecessors Alexander Wilson and John James Audubon. He is commemorated himself in the names of a number of birds from western North America, including the Cassin's auklet, Cassin's kingbird, Cassin's vireo, Cassin's sparrow, and Cassin's finch. The periodic cicada Magicicada cassini is also named for him.
Cassin drew, engraved, and colored many of the illustrations published in the Pacific Railroad Surveys.
Named curator of the Philadelphia Academy of Natural Sciences in 1842, Cassin described many new bird species and revised a number of families in the Academy's publications. His more extensive publications include Birds of California, with descriptions and colored engravings of fifty species not given by Audubon; Synopsis of the Birds of North America; Ornithology of the United States Exploring Expedition; Ornithology of the Japan Expedition; Ornithology of Gillis's Astronomical Expedition to Chile; and chapters on raptorial birds and waders in Ornithology of the Pacific Railroad Explorations and Surveys.
Only one volume appeared of the most ambitious of Cassin's works, the Illustrations of the Birds of California, Texas, Oregon, British and Russian America (1853–56). He also served as co-author, with Spencer Fullerton Baird and George Newbold Lawrence, of Birds of North America (1860).
He died in 1869 of arsenic poisoning caused by his handling of bird skins preserved with arsenic. His collection, some 4300 birds, was purchased for $500 by John Whipple Potter Jenks for Brown University's new museum of natural history.Judy Buenoano
Judias V. “Judy” Buenoano (born Judias Welty, also known as Judias Goodyear and Judias Morris) (April 4, 1943 – March 30, 1998) was an American convicted murderer who was executed for the 1971 murder of her husband James Goodyear. She was also convicted for the 1980 murder of her son Michael Buenoano and of the 1983 attempted murder of her fiancé John Gentry. Buenoano is also acknowledged to have been responsible for the 1978 death of her boyfriend Bobby Joe Morris in Colorado; however, by the time authorities made the connection between Buenoano and Morris, she had already been sentenced to death in the state of Florida.Buenoano is also believed to have been involved in a 1974 murder in Alabama, and in the 1980 death of her boyfriend Gerald Dossett. After her arrest, Dossett's body was exhumed and analysed for signs of arsenic poisoning. No charges were laid in that case. Buenoano was the first woman to be executed in Florida since 1848, and was only the third woman to be executed in the U.S. since the reinstatement of capital punishment in 1976. Nationally, she was the first woman executed in the electric chair since 1957, when Rhonda Belle Martin was electrocuted in Alabama.Leukonychia
Leukonychia (or leuconychia), also known as white nails or milk spots, is a medical term for white discolouration appearing on nails. It is derived from the Greek words leuko ("white") and onyx ("nail"). The most common cause is injury to the base of the nail (the matrix) where the nail is formed.
It is harmless and most commonly caused by minor injuries, such as nail biting, which occur while the nail is growing. Leukonychia occurs most commonly in healthy individuals, and is unrelated to any known nutritional or physiological deficiency. When caused by injury the marks will disappear as the nail grows outwards. While there are various sources that link dietary needs or vitamin deficiency with recurrent leukonychia, this notion has been challenged by some medical researchers.Other possible reasons for this problem with nail colour can be linked to:
Psoriasis as well as eczema
Iron deficiencyLodovico Ferrari
Lodovico de Ferrari (2 February 1522 – 5 October 1565) was an Italian mathematician.
Born in Bologna, Italy, Lodovico's grandfather, Bartholomew de Ferrari, was forced out of Milan to Bologna. Lodovico settled in Bologna, Italy and he began his career as the servant of Gerolamo Cardano. He was extremely bright, so Cardano started teaching him mathematics. Ferrari aided Cardano on his solutions for quadratic equations and cubic equations, and was mainly responsible for the solution of quartic equations that Cardano published. While still in his teens, Ferrari was able to obtain a prestigious teaching post in Rome after Cardano resigned from it and recommended him. Ferrari retired when young at 42 years old, and wealthy. He then moved back to his home town of Bologna where he lived with his widowed sister Maddalena to take up a professorship of mathematics at the University of Bologna in 1565. Shortly thereafter, he died of white arsenic poisoning, according to a legend - because of his sisters.Lyda Southard
Lyda Southard (also known as Lyda Anna Mae Trueblood) was born on October 16, 1892, and died on February 5, 1958, of a heart attack. She is considered one of America's first known female serial killers, preceded by Jane Toppan. It was suspected that she had killed her four husbands, a brother-in-law, and her daughter by using arsenic poisoning derived from flypaper to poison them in order to attain life insurance money.Lynchings of Benjamin and Mollie French
The lynching of the Frenches of Warsaw took place in Warsaw, Gallatin County, Kentucky on May 3, 1876 between 1am–2am on a Wednesday morning. Benjamin and Mollie French, African Americans, were lynched by a white mob for the murder of another African American, which was unusual for this period. Lake Jones was an elderly black man who had faithfully served a white family named Howard, both before and after his emancipation from slavery. The Frenches killed Lake Jones by arsenic poisoning, intending to steal his money.The Ku Klux Klan lynched the Frenches because, they said, Lake Jones was "the best nigger in the country." The KKK broke into the jail, took the Frenches about a mile north of Warsaw, and hanged them both from a tree on J.H. McDaniels' (McDonnell's in another account) farm.Metal toxicity
Metal toxicity or metal poisoning is the toxic effect of certain metals in certain forms and doses on life. Some metals are toxic when they form poisonous soluble compounds. Certain metals have no biological role, i.e. are not essential minerals, or are toxic when in a certain form. In the case of lead, any measurable amount may have negative health effects. Often heavy metals are thought as synonymous, but lighter metals may also be toxic in certain circumstances, such as beryllium and lithium. Not all heavy metals are particularly toxic, and some are essential, such as iron. The definition may also include trace elements when in abnormally high doses may be toxic. An option for treatment of metal poisoning may be chelation therapy, which is a technique which involves the administration of chelation agents to remove metals from the body.
Toxic metals sometimes imitate the action of an essential element in the body, interfering with the metabolic process resulting in illness. Many metals, particularly heavy metals are toxic, but some heavy metals are essential, and some, such as bismuth, have a low toxicity. Most often the definition of toxic metals includes at least cadmium, manganese, lead, mercury and the radioactive metals. Metalloids (arsenic, polonium) may be included in the definition. Radioactive metals have both radiological toxicity and chemical toxicity. Metals in an oxidation state abnormal to the body may also become toxic: chromium(III) is an essential trace element, but chromium(VI) is a carcinogen.
Toxicity is a function of solubility. Insoluble compounds as well as the metallic forms often exhibit negligible toxicity. The toxicity of any metal depends on its ligands. In some cases, organometallic forms, such as methylmercury and tetraethyl lead, can be extremely toxic. In other cases, organometallic derivatives are less toxic such as the cobaltocenium cation.
Decontamination for toxic metals is different from organic toxins: because toxic metals are elements, they cannot be destroyed. Toxic metals may be made insoluble or collected, possibly by the aid of chelating agents, or through bioremediation. Alternatively, they can be diluted into a sufficiently large reservoir, such as the sea, because immediate toxicity is a function of concentration rather than amount.
Toxic metals can bioaccumulate in the body and in the food chain. Therefore, a common characteristic of toxic metals is the chronic nature of their toxicity. This is particularly notable with radioactive heavy metals such as radium, which imitates calcium to the point of being incorporated into human bone, although similar health implications are found in lead or mercury poisoning. The exceptions to this are barium and aluminium, which can be removed efficiently by the kidneys.Morinaga Milk arsenic poisoning incident
The Morinaga Milk arsenic poisoning incident occurred in 1955 in Japan and is believed to have resulted in the deaths of over 100 infants. The incident occurred when arsenic was inadvertently added to dried milk via an industrial grade of monosodium phosphate additive. This incident also led to negative health effects for thousands of other infants and individuals, which has had lingering health effects.To Keep My Love Alive
"To Keep My Love Alive" is a 1943 popular song composed by Richard Rodgers, with lyrics by Lorenz Hart for the 1943 revival of the 1927 musical A Connecticut Yankee, where it was introduced by Vivienne Segal. It was written especially for Segal. (R&H Theatricals background) It was the last song that Hart wrote before his death from pneumonia.
The song outlines the many ways the singer "bumped off" her fifteen husbands in order to avoid being unfaithful to any of them. Some of her methods are arsenic poisoning, stabbing and appendectomy.Toroku arsenic disease
Toroku arsenic disease (土呂久砒素公害, Toroku hiso kōgai) was a disease resulting from air and water pollution from a refinery at a mine at Toroku, located in Takachiho, Nishiusuki District, Miyazaki, Japan.
It emitted arsenic-containing air, resulting in patients with chronic arsenic poisoning producing skin changes, skin cancers and sometimes lung cancer. The Sumitomo Metal Mining Co., Ltd., which bought the right of mining was sued by the patients for health damage, but 15 years later, the lawsuit ended with a compromise.Örbyhus
Örbyhus is a locality situated in Tierp Municipality, Uppsala County, Sweden with 1,984 inhabitants in 2010.Örbyhus Castle, located a few kilometers from the village, is where king Eric XIV of Sweden was imprisoned until his death from arsenic poisoning on 26 February 1577.