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Sökning: L773:9780128229460

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1.
  • Bergdahl, Ingvar, et al. (författare)
  • Lead
  • 2022. - 5
  • Ingår i: Handbook on the toxicology of metals. - : Elsevier. - 9780128229460 ; , s. 427-493
  • Bokkapitel (refereegranskat)abstract
    • Inorganic lead is the most extensively studied environmental toxin. Today's humans have in the order of 100 times higher lead exposure, compared to prehistoric humans, mainly from food. The exposure was even higher during the 20th century, mainly due to lead addition to gasoline. Today, high exposures occur in many occupations, but also through, for example, contaminated drinking water, traditional drugs, lead paint, and soil and dust in "hotspots" around mines and smelters. Absorbed lead is widely distributed in the body. It accumulates in the skeleton, which, in turn, causes endogenous exposure, especially during pregnancy/lactation and in osteoporosis. Lead passes over the placenta into the fetus, and via breast milk into the infant. The mode(s) of action is not known; different mechanisms might be operating at different concentrations. Toxic effects occur first in the nervous system of fetuses/infants/children, with small cognitive effects already at a mean blood lead concentration (B-Pb) of ≤0.05. μmol/L (≤10. μg/L; which is well below the worldwide mean), without any threshold. Lead effects have also been reported for the cardiovascular system [increase of blood pressure at B-Pb well below 0.5. μmol/L (100. μg/L)], the kidney, post- and prenatal growth, cognition in also adults and elderly, the blood, the immune system, the gastrointestinal tract, and the female and male reproduction. There is important genetic modification of the toxicity. Lead is carcinogenic in animal experiments, but there is only limited evidence in humans.The organolead compounds tetraethyl- and tetramethyllead, earlier used in enormous quantities in leaded gasoline, are easily absorbed at inhalation and through the skin and may cause acute encephalopathia.
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2.
  • Blomqvist, Lennart K., et al. (författare)
  • Gadolinium
  • 2022. - 5
  • Ingår i: Handbook on the toxicology of metals. - : Elsevier. - 9780128229460 ; , s. 267-274
  • Bokkapitel (refereegranskat)abstract
    • Gadolinium (Gd) belongs to the rare-earth elements. Depending on the temperature, Gd is either ferromagnetic or paramagnetic. Gadolinium obtained its name from Johan Gadolin, the Finnish chemist who discovered gadolinite, a mineral that contains gadolinium. The specific properties of Gd make it suitable for certain applications in nuclear reactors as well as in medicine being the base for a chelate administered to patients as a contrast agent in magnetic resonance imaging. Such Gd chelates have been used for more than 30 years. During the past decades, there has been increasing knowledge about the potentially harmful effects of Gd chelates in patients with severe renal dysfunction. In such patients, there is a risk for a potentially life-threatening disease, nephrogenic systemic fibrosis. Precautions, restricting the use of Gd chelates in persons with severely impaired renal function have drastically decreased the occurrence of nephrogenic systemic fibrosis in the last decade. There has also been an increasing awareness of the fact that there is Gd deposition in the body even in patients without renal dysfunction and that this deposition is related partly to the cumulative number of doses given but also the chemical structure of the chelate. In this chapter, the physical and chemical properties of Gd and its related chelates, methods for detection, industrial and medical applications, human exposures, toxicity as well as a further description of potential side effects related to injection of Gd chelates are described.
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3.
  • Gerhardsson, Lars, 1952 (författare)
  • Tellurium
  • 2021
  • Ingår i: Handbook on the Toxicology of Metals (Fifth Edition). Gunnar F. Nordberg and Max Costa (red.). - : Academic Press. - 9780128229460 ; , s. 783-794
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
    • Food (e.g., meat, dairy products, and cereals) is the main source of tellurium exposure in the general population. In the working environment, inhalational exposure predominates. Small amounts of organic tellurium compounds can also be absorbed through the skin. No quantitative data have been published regarding the inhalational absorption of tellurium or tellurium compounds in humans. In experiments on healthy volunteers, a gastrointestinal absorption of 10%-25% has been observed. In animal experiments, a similar absorption has been estimated.The highest tissue concentrations have been observed in the kidneys. Lower concentrations have been observed in heart, lung, and spleen. The main accumulation over time is in bone, which harbors more than 90% of the total body burden, which exceeds 500. mg. Tellurium can pass both the placenta and the blood-brain barrier. Parenterally administered tellurium is predominantly excreted in the urine, whereas orally ingested tellurium salts are transferred through biliary secretion and mainly excreted in the feces. Small amounts, probably approximately 0.1%, of absorbed tellurium are exhaled, presumably as dimethyl telluride. In rat experiments, biological half-times ranging from 9. days in blood to 23. days in the kidney have been reported. The whole-body retention model for humans estimates a biological half-time of approximately 3. weeks. Elimination from bone is slow, with an estimated half-time of approximately 600. days.Acute systemic effects of tellurium toxicity in rats include listlessness, decreased locomotor activity, somnolence, anorexia, weight loss, gastrointestinal disturbances, changes in fur, and occasionally epilation and hind leg paralysis. Long-term studies of chronic effects are sparse. Dominant and critical effects have been reported from the nervous system, including peripheral neuropathy characterized by segmental demyelination and minor axonal degeneration. In the brain, black changes caused by dark tellurium particles localized to lipofuscin granules in the neuronal cytoplasm have been observed. Other effects have been reported from the liver (fatty degeneration and necrosis), kidney (proximal tubular lesions, oliguria, or anuria), and heart (cell necrosis, edema, and congestion).Reproductive effects including, for example, hydrocephalus, edema, exophthalmia, and ocular hemorrhage have been described.Acute exposure to tellurium in occupational settings may cause acute respiratory irritation followed by the development of garlicky odor of the breath and sweat, drowsiness, headache, malaise, lassitude, weakness, and dizziness. Gastrointestinal symptoms such as anorexia, nausea, vomiting, metallic taste, dry mouth, and constipation may appear. Dermatitis and blue-black discoloration of the skin may follow exposure to tellurium hexafluoride. Severe intoxication may lead to depression of the respiratory system and circulatory collapse. No specific antidote for tellurium poisoning has been found. After inhalational exposure, treatment with fresh air, oxygen supply, assisted ventilation, β2-adrenergic agonists, and oral or parenteral corticosteroids can be tried. Reviews of tellurium toxicology have been published by Browning (1969), Izrael'son (1973), Fishbein (1977), Alexander et al. (1988), and Kobayashi (2004). © 2022 Elsevier B.V. All rights reserved.
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4.
  • Hedberg, Yolanda, et al. (författare)
  • Silver
  • 2022. - 5
  • Ingår i: Handbook on the toxicology of metal. - : Elsevier. - 9780128229460 ; , s. 773-782
  • Bokkapitel (refereegranskat)abstract
    • Silver compounds may be absorbed through inhalation, but there are no quantitative human data on the extent of this phenomenon. Silver salts may be absorbed by up to 10%-20% after ingestion. After ingestion in humans, the highest concentrations of silver are usually found in the liver and spleen, but also to some extent in the muscles, skin, and brain. Silver may also be absorbed through dermal exposure, especially via wound care. The biological half-time for silver ranges from a few days for animals up to approximately 50. days for the human liver; it is possible that skin deposits have an even longer half-time, but there are no quantitative data on this for humans. Silver binds to high molecular weight proteins and metallothionein in tissue cytosol fractions. Excretion of silver from the body is primarily biliary. Silver nanoparticles have been shown to be absorbed by both inhalation and oral routes, and only to a minor extent via the dermal route, resulting in deposition in various organ systems. Monitoring of exposure is possible by determinations of levels in whole blood.High-dose repeated exposure of animals to silver and silver compounds may produce anemia, cardiac enlargement, growth retardation, and degenerative changes in the liver.Water-soluble silver compounds such as silver nitrate have a local corrosive effect and may cause fatal poisoning in humans if injected or infused into the uterus. Chronic exposure of humans leads to argyria, a clinical entity characterized by gray-blue pigmentation of the skin and other body viscera. Similar changes in the eye after local treatment with eye drops containing silver compounds are named argyrosis. Allergic contact dermatitis to silver is rare. Genotoxic effects, in terms of direct DNA strand breaks via oxidative stress, have been reported in vitro. Tests indicating genotoxicity (Comet assay) and oxidative stress were positive in one study on silver-workers.
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5.
  • Mann, Koren K., et al. (författare)
  • Tungsten
  • 2022. - 5
  • Ingår i: Handbook on the toxicology of metals. - : Elsevier. - 9780128229460 ; , s. 869-883
  • Bokkapitel (refereegranskat)abstract
    • Tungsten is a rare element with a natural abundance thought to be around 1.5 parts per million. It is remarkable for its robust physical properties, making it useful for many industrial applications. Tungsten is the heaviest metal to have a known biological role as it is essential as a cofactor for oxidoreductases in some thermophilic prokaryotes. In animal models, ingested and inhaled tungsten is rapidly absorbed and excreted in the urine. The remaining tungsten in the body is distributed mainly to the spleen, kidney, and bone, with the highest tungsten accumulation in the bone. Tungsten metabolism closely resembles molybdenum in chemical properties. Occupational inhalation exposure to tungsten carbide dust has been linked to cases of pulmonary fibrosis, a hard metal disease, although the contribution of tungsten carbide versus cobalt coexposure is unclear. Small quantities of tungsten are present in food and water and trace quantities, related to industrial emissions, are found in the general atmosphere. Tungsten is also present in human serum, urine, and feces, with elimination approximately balancing intake of the metal in the few nonindustrially exposed subjects studied. Industrial, medical, and military uses of tungsten have been expanding rapidly; therefore, the potential for tungsten spreading into the environment is rapidly increasing.
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6.
  • Nordberg, Gunnar, et al. (författare)
  • Cadmium
  • 2022. - 5
  • Ingår i: Handbook on the toxicology of metals. - : Elsevier. - 9780128229460 ; , s. 141-196
  • Bokkapitel (refereegranskat)abstract
    • Cadmium (Cd) occurs with zinc and lead in sulfide ores. Elevated concentrations in air, water, and soil may occur close to nonferrous mining and metal refining industries. Cadmium metal has been used as an anticorrosive when electroplated onto steel. Cd compounds are used in batteries, as pigments and in solar panels. Between 10% and 50% of inhaled Cd will be absorbed and 5%-10% of ingested Cd. The accumulation of Cd in humans occurs in many tissues, with particularly long half-lives (10-30 years) in muscle, bone, kidney, and liver. Cd bound to metallothionein in plasma is filtered through the renal glomeruli and reabsorbed in the tubuli, where the metal ion is released and toxic effects occur. The average amount of Cd ingested in Japan and most European and North American countries is. <10-20. μg/day. The corresponding average urinary excretion of Cd is. <0.5-1.0. μg/day and the blood concentration is 0.2-0.7. μg/L in nonsmokers; it is twice as high in smokers. Acute inhalation of Cd in air, for example, from soldering or welding fumes, may lead to severe chemical pneumonitis. Long-term exposure to low air levels may lead to chronic obstructive lung disease and possibly to lung cancer. Long-term excessive exposure from the air or food leads to renal tubular dysfunction with low molecular weight proteinuria. It may also lead to disturbance of calcium metabolism, osteoporosis, and osteomalacia, mainly among postmenopausal women. A disease exhibiting these features. -called itai-itai disease. -occurred in the 1950s in a Cd-polluted area of Japan. Cd-induced cancer of the lungs, prostate, and other organs in animals and increased rates of cancer of the lungs and other organs in humans. The International Agency for Research on Cancer (IARC) classified Cd as a human carcinogen (Group 1). Adverse kidney effects occur in sensitive occupational groups, as well as in general population groups, after lifelong exposures giving rise to urinary Cd (UCd) of 2-4. μg/g creatinine. At such exposures, bone effects including osteoporosis and fractures may also occur in sensitive groups. Adverse bone and kidney effects may occur in a small but sensitive population group as a result of lifelong cadmium exposure with UCd of approximately 1. μg/g creatinine and higher, but the evidence is still inconclusive. This level of exposure occurs within general population groups in many countries. Osteomalacia is treated with large doses of vitamin D, but there is no effective treatment for other Cd-related effects. Because of the long half-life of Cd and the irreversibility of bone effects and some kidney effects, primary prevention is essential. The toxicological and environmental aspects of Cd have been reviewed in detail by Friberg et al. (1974, 1985, 1986), Tsuchiya (1978), Nriagu (1980, 1981), the WHO/IPCS (1992), the IARC (1993, 2012), Järup et al. (1998c), the Agency for Toxic Substances and Disease Registry (. ATSDR, 1999), Nordberg and Nordberg (2002), the European Union (. EU, 2003, 2007; ECHA 2020), Satarug and Moore (2004), and the World Health Organization Food and Agriculture Organization (. JECFA, 2004, 2012), the European Food Safety Authority (. EFSA, 2009, 2012), Akesson et al. (2014), the Scientific Committee on Occupational Exposure Limits (. SCOEL, 2017), and the International Union of Pure and Applied Chemistry (. Nordberg et al., 2018).
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7.
  • Nordberg, Gunnar, et al. (författare)
  • Preface
  • 2022. - 5
  • Ingår i: Handbook on the toxicology of metals. - : Elsevier. - 9780128229460 ; , s. xxxix-xxxix
  • Bokkapitel (refereegranskat)
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8.
  • Oskarsson, Agneta (författare)
  • Molybdenum
  • 2022
  • Ingår i: Handbook on the Toxicology of Metals : Volume II: Specific Metals. - 9780128229460 ; 2, s. 601-614
  • Bokkapitel (refereegranskat)abstract
    • Molybdenum is an essential element, required as a component of enzymes involved in, that is, the catabolism of sulfur amino acids and nucleotides. Dietary recommendations have been established and human intake is usually within the range of the recommendations. Soluble molybdenum compounds are readily absorbed when ingested, and data supporting absorption after inhalation have also been presented in experimental animals and occupationally exposed humans. The highest molybdenum concentrations are found in the kidneys and liver. Excretion, primarily through the urine, is rapid. The biological half-life in blood ranges from a few hours to a few days.The metabolism of molybdenum is affected by copper and sulfur intake. In livestock, chronic molybdenum poisoning (known as teart disease) is caused by feed high in molybdenum and low in copper. Symptoms include anemia, gastrointestinal disturbances, bone disorders, and growth retardation.In laboratory animals, excessive molybdenum may give rise to morphological and functional changes in the kidneys. Reproductive toxicity of molybdenum has been reported, but not reproduced in more recent OECD guideline studies. Molybdenum trioxide was carcinogenic to animals (mice and rats) in long-term GLP studies. Lung fibrosis was observed at high doses.Increased blood uric acid values and gout-like symptoms have been reported among exposed workers, as well as among the general population living in an area with a high-molybdenum and low-copper content in the soil and vegetables. Epidemiological studies indicate an accelerated decline in glomerular filtration rate, also impaired semen quality and an increased risk for stroke have been reported but remain to be confirmed.Molybdenum toxicity and essentiality have been reviewed, that is, by Novotny (2011), World Health Organization (WHO, 2011), Mendel and Kruse (2012), EFSA (2013), IARC (2019), and ATSDR (2020).
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