The Experts below are selected from a list of 249 Experts worldwide ranked by ideXlab platform
R. Steven Pappas - One of the best experts on this subject based on the ideXlab platform.
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Cadmium and Cadmium/Zinc Ratios and Tobacco-Related Morbidities.
International Journal of Environmental Research and Public Health, 2017Co-Authors: Patricia Richter, Obaid Faroon, R. Steven PappasAbstract:Metals are one of five major categories of carcinogenic or toxic constituents in tobacco and tobacco smoke. Cadmium is highly volatile and a higher percentage of the total tobacco Cadmium content is efficiently transferred to mainstream tobacco smoke than many other toxic metals in tobacco. Inhaled Cadmium bioaccumulates in the lungs and is distributed beyond the lungs to other tissues, with a total body biological half-life of one to two decades. Chronic Cadmium exposure through tobacco use elevates blood and urine Cadmium concentrations. Cadmium is a carcinogen, and an inducer of proinflammatory immune responses. Elevated exposure to Cadmium is associated with reduced pulmonary function, obstructive lung disease, bronchogenic carcinoma, cardiovascular diseases including myocardial infarction, peripheral arterial disease, prostate cancer, cervical cancer, pancreatic cancer, and various oral pathologies. Cadmium and zinc have a toxicologically inverse relationship. Zinc is an essential element and is reportedly antagonistic to some manifestations of Cadmium toxicity. This review summarizes associations between blood, urine, and tissue Cadmium concentrations with emphasis on Cadmium exposure due to tobacco use and several disease states. Available data about zinc and Cadmium/zinc ratios and tobacco-related diseases is summarized from studies reporting smoking status. Collectively, data suggest that blood, urine, and tissue Cadmium and Cadmium/zinc ratios are often significantly different between smokers and nonsmokers and they are also different in smokers for several diseases and cancers. Additional biomonitoring data such as blood or serum and urine zinc and Cadmium levels and Cadmium/zinc ratios in smokers may provide further insight into the development and progression of diseases of the lung, cardiovascular system, and possibly other organs.
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Cadmium and Cadmium/zinc ratios and tobacco‐related morbidities
International Journal of Environmental Research and Public Health, 2017Co-Authors: Patricia Richter, Obaid Faroon, R. Steven PappasAbstract:Metals are one of five major categories of carcinogenic or toxic constituents in tobacco and tobacco smoke. Cadmium is highly volatile and a higher percentage of the total tobacco Cadmium content is efficiently transferred to mainstream tobacco smoke than many other toxic metals in tobacco. Inhaled Cadmium bioaccumulates in the lungs and is distributed beyond the lungs to other tissues, with a total body biological half-life of one to two decades. Chronic Cadmium exposure through tobacco use elevates blood and urine Cadmium concentrations. Cadmium is a carcinogen, and an inducer of proinflammatory immune responses. Elevated exposure to Cadmium is associated with reduced pulmonary function, obstructive lung disease, bronchogenic carcinoma, cardiovascular diseases including myocardial infarction, peripheral arterial disease, prostate cancer, cervical cancer, pancreatic cancer, and various oral pathologies. Cadmium and zinc have a toxicologically inverse relationship. Zinc is an essential element and is reportedly antagonistic to some manifestations of Cadmium toxicity. This review summarizes associations between blood, urine, and tissue Cadmium concentrations with emphasis on Cadmium exposure due to tobacco use and several disease states. Available data about zinc and Cadmium/zinc ratios and tobacco-related diseases is summarized from studies reporting smoking status. Collectively, data suggest that blood, urine, and tissue Cadmium and Cadmium/zinc ratios are often significantly different between smokers and nonsmokers and they are also different in smokers for several diseases and cancers. Additional biomonitoring data such as blood or serum and urine zinc and Cadmium levels and Cadmium/zinc ratios in smokers may provide further insight into the development and progression of diseases of the lung, cardiovascular system, and possibly other organs.
Patricia Richter - One of the best experts on this subject based on the ideXlab platform.
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Cadmium and Cadmium/Zinc Ratios and Tobacco-Related Morbidities.
International Journal of Environmental Research and Public Health, 2017Co-Authors: Patricia Richter, Obaid Faroon, R. Steven PappasAbstract:Metals are one of five major categories of carcinogenic or toxic constituents in tobacco and tobacco smoke. Cadmium is highly volatile and a higher percentage of the total tobacco Cadmium content is efficiently transferred to mainstream tobacco smoke than many other toxic metals in tobacco. Inhaled Cadmium bioaccumulates in the lungs and is distributed beyond the lungs to other tissues, with a total body biological half-life of one to two decades. Chronic Cadmium exposure through tobacco use elevates blood and urine Cadmium concentrations. Cadmium is a carcinogen, and an inducer of proinflammatory immune responses. Elevated exposure to Cadmium is associated with reduced pulmonary function, obstructive lung disease, bronchogenic carcinoma, cardiovascular diseases including myocardial infarction, peripheral arterial disease, prostate cancer, cervical cancer, pancreatic cancer, and various oral pathologies. Cadmium and zinc have a toxicologically inverse relationship. Zinc is an essential element and is reportedly antagonistic to some manifestations of Cadmium toxicity. This review summarizes associations between blood, urine, and tissue Cadmium concentrations with emphasis on Cadmium exposure due to tobacco use and several disease states. Available data about zinc and Cadmium/zinc ratios and tobacco-related diseases is summarized from studies reporting smoking status. Collectively, data suggest that blood, urine, and tissue Cadmium and Cadmium/zinc ratios are often significantly different between smokers and nonsmokers and they are also different in smokers for several diseases and cancers. Additional biomonitoring data such as blood or serum and urine zinc and Cadmium levels and Cadmium/zinc ratios in smokers may provide further insight into the development and progression of diseases of the lung, cardiovascular system, and possibly other organs.
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Cadmium and Cadmium/zinc ratios and tobacco‐related morbidities
International Journal of Environmental Research and Public Health, 2017Co-Authors: Patricia Richter, Obaid Faroon, R. Steven PappasAbstract:Metals are one of five major categories of carcinogenic or toxic constituents in tobacco and tobacco smoke. Cadmium is highly volatile and a higher percentage of the total tobacco Cadmium content is efficiently transferred to mainstream tobacco smoke than many other toxic metals in tobacco. Inhaled Cadmium bioaccumulates in the lungs and is distributed beyond the lungs to other tissues, with a total body biological half-life of one to two decades. Chronic Cadmium exposure through tobacco use elevates blood and urine Cadmium concentrations. Cadmium is a carcinogen, and an inducer of proinflammatory immune responses. Elevated exposure to Cadmium is associated with reduced pulmonary function, obstructive lung disease, bronchogenic carcinoma, cardiovascular diseases including myocardial infarction, peripheral arterial disease, prostate cancer, cervical cancer, pancreatic cancer, and various oral pathologies. Cadmium and zinc have a toxicologically inverse relationship. Zinc is an essential element and is reportedly antagonistic to some manifestations of Cadmium toxicity. This review summarizes associations between blood, urine, and tissue Cadmium concentrations with emphasis on Cadmium exposure due to tobacco use and several disease states. Available data about zinc and Cadmium/zinc ratios and tobacco-related diseases is summarized from studies reporting smoking status. Collectively, data suggest that blood, urine, and tissue Cadmium and Cadmium/zinc ratios are often significantly different between smokers and nonsmokers and they are also different in smokers for several diseases and cancers. Additional biomonitoring data such as blood or serum and urine zinc and Cadmium levels and Cadmium/zinc ratios in smokers may provide further insight into the development and progression of diseases of the lung, cardiovascular system, and possibly other organs.
Obaid Faroon - One of the best experts on this subject based on the ideXlab platform.
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Cadmium and Cadmium/Zinc Ratios and Tobacco-Related Morbidities.
International Journal of Environmental Research and Public Health, 2017Co-Authors: Patricia Richter, Obaid Faroon, R. Steven PappasAbstract:Metals are one of five major categories of carcinogenic or toxic constituents in tobacco and tobacco smoke. Cadmium is highly volatile and a higher percentage of the total tobacco Cadmium content is efficiently transferred to mainstream tobacco smoke than many other toxic metals in tobacco. Inhaled Cadmium bioaccumulates in the lungs and is distributed beyond the lungs to other tissues, with a total body biological half-life of one to two decades. Chronic Cadmium exposure through tobacco use elevates blood and urine Cadmium concentrations. Cadmium is a carcinogen, and an inducer of proinflammatory immune responses. Elevated exposure to Cadmium is associated with reduced pulmonary function, obstructive lung disease, bronchogenic carcinoma, cardiovascular diseases including myocardial infarction, peripheral arterial disease, prostate cancer, cervical cancer, pancreatic cancer, and various oral pathologies. Cadmium and zinc have a toxicologically inverse relationship. Zinc is an essential element and is reportedly antagonistic to some manifestations of Cadmium toxicity. This review summarizes associations between blood, urine, and tissue Cadmium concentrations with emphasis on Cadmium exposure due to tobacco use and several disease states. Available data about zinc and Cadmium/zinc ratios and tobacco-related diseases is summarized from studies reporting smoking status. Collectively, data suggest that blood, urine, and tissue Cadmium and Cadmium/zinc ratios are often significantly different between smokers and nonsmokers and they are also different in smokers for several diseases and cancers. Additional biomonitoring data such as blood or serum and urine zinc and Cadmium levels and Cadmium/zinc ratios in smokers may provide further insight into the development and progression of diseases of the lung, cardiovascular system, and possibly other organs.
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Cadmium and Cadmium/zinc ratios and tobacco‐related morbidities
International Journal of Environmental Research and Public Health, 2017Co-Authors: Patricia Richter, Obaid Faroon, R. Steven PappasAbstract:Metals are one of five major categories of carcinogenic or toxic constituents in tobacco and tobacco smoke. Cadmium is highly volatile and a higher percentage of the total tobacco Cadmium content is efficiently transferred to mainstream tobacco smoke than many other toxic metals in tobacco. Inhaled Cadmium bioaccumulates in the lungs and is distributed beyond the lungs to other tissues, with a total body biological half-life of one to two decades. Chronic Cadmium exposure through tobacco use elevates blood and urine Cadmium concentrations. Cadmium is a carcinogen, and an inducer of proinflammatory immune responses. Elevated exposure to Cadmium is associated with reduced pulmonary function, obstructive lung disease, bronchogenic carcinoma, cardiovascular diseases including myocardial infarction, peripheral arterial disease, prostate cancer, cervical cancer, pancreatic cancer, and various oral pathologies. Cadmium and zinc have a toxicologically inverse relationship. Zinc is an essential element and is reportedly antagonistic to some manifestations of Cadmium toxicity. This review summarizes associations between blood, urine, and tissue Cadmium concentrations with emphasis on Cadmium exposure due to tobacco use and several disease states. Available data about zinc and Cadmium/zinc ratios and tobacco-related diseases is summarized from studies reporting smoking status. Collectively, data suggest that blood, urine, and tissue Cadmium and Cadmium/zinc ratios are often significantly different between smokers and nonsmokers and they are also different in smokers for several diseases and cancers. Additional biomonitoring data such as blood or serum and urine zinc and Cadmium levels and Cadmium/zinc ratios in smokers may provide further insight into the development and progression of diseases of the lung, cardiovascular system, and possibly other organs.
Carl Gustaf Elinder - One of the best experts on this subject based on the ideXlab platform.
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Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria
Environmental Health Perspectives, 2002Co-Authors: Tobias Alfven, Lars Jarup, Carl Gustaf ElinderAbstract:Long-term exposure to Cadmium may cause kidney and bone damage. Urinary Cadmium is commonly used as the dose estimate for the body burden of Cadmium. However, elevated levels of Cadmium in the urine may reflect not only high levels of Cadmium dose but also renal dysfunction. In this study we used blood Cadmium as the dose estimate. In addition, we analyzed blood lead. We examined 479 men and 542 women, ages 16-81 years, who were environmentally or occupationally exposed to Cadmium and lead. We used urinary protein alpha 1-microglobulin as a marker for tubular proteinuria and measured forearm bone mineral density using dual-energy X-ray absorptiometry. The relationship between blood Cadmium and tubular proteinuria was strong, even when we excluded occupationally exposed participants. The subgroup with the highest blood Cadmium levels had a 4-fold risk of tubular proteinuria compared to the subgroup with the lowest blood Cadmium levels. In the older age group (age > 60), the risk of low bone mineral density (z-score < -1) for the subgroup with the highest blood Cadmium levels was almost 3-fold compared to the group with lowest blood Cadmium levels. We found no similar associations for lead. The observed effects may be caused by higher Cadmium exposure in the past. This study strengthens previous evidence that Cadmium exposure may affect both bone mineral density and kidney function.
Michael P Waalkes - One of the best experts on this subject based on the ideXlab platform.
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Cadmium-induced cancers in animals and in humans
International Journal of Occupational and Environmental Health, 2007Co-Authors: James Huff, Ruth M. Lunn, Michael P Waalkes, Lorenzo Tomatis, Peter F. InfanteAbstract:Discovered in the early 1800s, the use of Cadmium and various Cadmium salts started to become industrially important near the close of the 19th century, rapidly thereafter began to flourish, yet has diminished more recently. Most Cadmium used in the United States is a byproduct from the smelting of zinc, lead, or copper ores, and is used to manufacture batteries. Carcinogenic activity of Cadmium was discovered first in animals and only subsequently in humans. Cadmium and Cadmium compounds have been classified as known human carcinogens by the International Agency for Research on Cancer and the National Toxicology Program based on epidemiologic studies showing a causal association with lung cancer, and possibly prostate cancer, and studies in experimental animals, demonstrating that Cadmium causes tumors at multiple tissue sites, by various routes of exposure, and in several species and strains. Epidemiologic studies published since these evaluations suggest that Cadmium is also associated with cancers of the breast, kidney, pancreas, and urinary bladder. The basic metal cationic portion of Cadmium is responsible for both toxic and carcinogenic activity, and the mechanism of carcinogenicity appears to be multifactorial. Available information about the carcinogenicity of Cadmium and Cadmium compounds is reviewed, evaluated, and discussed.
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Cadmium carcinogenesis
Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 2003Co-Authors: Michael P WaalkesAbstract:Cadmium is a heavy metal of considerable environmental and occupational concern. Cadmium compounds are classified as human carcinogens by several regulatory agencies. The most convincing data that Cadmium is carcinogenic in humans comes from studies indicating occupational Cadmium exposure is associated with lung cancer. Cadmium exposure has also been linked to human prostate and renal cancer, although this linkage is weaker than for lung cancer. Other target sites of Cadmium carcinogenesis in humans, such as liver, pancreas and stomach, are considered equivocal. In animals, Cadmium effectively induces cancers at multiple sites and by various routes. Cadmium inhalation in rats induces pulmonary adenocarcinomas, in accord with its role in human lung cancer. Cadmium can induce tumors and/or preneoplastic lesions within the rat prostate after ingestion or injection. At relatively high doses, Cadmium induces benign testicular tumors in rats, but these appear to be due to early toxic lesions and loss of testicular function, rather than from a specific carcinogenic effect of Cadmium. Like many other metals, Cadmium salts will induce mesenchymal tumors at the site of subcutaneous (s.c.) or intramuscular (i.m.) injections, but the human relevance of these is dubious. Other targets of Cadmium in rodents include the liver, adrenal, pancreas, pituitary, and hematopoietic system. With the exception of testicular tumors in rodents, the mechanisms of Cadmium carcinogenesis are poorly defined. Cadmium can cause any number of molecular lesions that would be relevant to oncogenesis in various cellular model systems. Most studies indicate Cadmium is poorly mutagenic and probably acts through indirect or epigenetic mechanisms, potentially including aberrant activation of oncogenes and suppression of apoptosis. © 2003 Elsevier B.V. All rights reserved.
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Cadmium carcinogenesis in review
Journal of Inorganic Biochemistry, 2000Co-Authors: Michael P WaalkesAbstract:Abstract Cadmium is an inorganic toxicant of great environmental and occupational concern which was classified as a human carcinogen in 1993. Occupational Cadmium exposure is associated with lung cancer in humans. Cadmium exposure has also, on occasion, been linked to human prostate cancer. The epidemiological data linking Cadmium and pulmonary cancer are much stronger than for prostatic cancer. Other target sites for Cadmium carcinogenesis in humans (liver, kidney, stomach) are considered equivocal. In rodents, Cadmium causes tumors at several sites and by various routes. Cadmium inhalation in rats results in pulmonary adenocarcinomas, supporting a role in human lung cancer. Prostate tumors and preneoplastic proliferative lesions can be induced in rats after Cadmium ingestion or injection. Prostatic carcinogenesis in rats occurs only at Cadmium doses below those that induce chronic degeneration and dysfunction of the testes, a well-known effect of Cadmium, confirming the androgen dependency of prostate tumors. Other targets of Cadmium in rodents include the testes, adrenals, injection sites, and hematopoietic system. Various treatments can modify Cadmium carcinogenesis including supplemental zinc, which prevents Cadmium-induced injection site and testicular tumors while facilitating prostatic tumors. Cadmium is poorly mutagenic and probably acts through indirect mechanisms, although the precise mechanisms remain unknown.
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Cadmium carcinogenesis in review
Journal of Inorganic Biochemistry, 2000Co-Authors: Michael P WaalkesAbstract:Cadmium is an inorganic toxicant of great environmental and occupational concern which was classified as a human carcinogen in 1993. Occupational Cadmium exposure is associated with lung cancer in humans. Cadmium exposure has also, on occasion, been linked to human prostate cancer. The epidemiological data linking Cadmium and pulmonary cancer are much stronger than for prostatic cancer. Other target sites for Cadmium carcinogenesis in humans (liver, kidney, stomach) are considered equivocal. In rodents, Cadmium causes tumors at several sites and by various routes. Cadmium inhalation in rats results in pulmonary adenocarcinomas, supporting a role in human lung cancer. Prostate tumors and preneoplastic proliferative lesions can be induced in rats after Cadmium ingestion or injection. Prostatic carcinogenesis in rats occurs only at Cadmium doses below those that induce chronic degeneration and dysfunction of the testes, a well-known effect of Cadmium, confirming the androgen dependency of prostate tumors. Other targets of Cadmium in rodents include the testes, adrenals, injection sites, and hematopoietic system. Various treatments can modify Cadmium carcinogenesis including supplemental zinc, which prevents Cadmium-induced injection site and testicular tumors while facilitating prostatic tumors. Cadmium is poorly mutagenic and probably acts through indirect mechanisms, although the precise mechanisms remain unknown. (C) 2000 Elsevier Science Inc.
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Toxicology of Cadmium
Handbook of experimental pharmacology, 1995Co-Authors: Peter L. Goering, Michael P Waalkes, Curtis D. KlaassenAbstract:Cadmium (Cd) is unique among metals because of its diverse toxic effects, extremely protracted biological half-life (approximately 20–30 years in humans), low rate of excretion from the body, and predominant storage in soft tissues (primarily liver and kidney) rather than bone. The health hazards associated with Cadmium exposure became known in the 1940s when FRiberg (1948) reported the occurrence of emphysema and proteinuria in workers exposed to Cadmium dust. In the 1960s, Cadmium was catapulted into the mainstream of metal toxicology research when Cadmium was identified as the major etiological factor in itai-itai disease, a condition that afflicted Japanese women exposed to Cadmium via their diet which contained Cadmium-contaminated rice and water. Cadmium is an extremely toxic element of continuing concern because environmental levels have risen steadily due to continued worldwide anthropogenic mobilization. The mobilization has derived from past and current industrial and agricultural practices.
