Pub Date : 2020-05-04DOI: 10.5772/intechopen.92141
O. Bansal
Groundwater which fulfills globally 50–80% need of drinking water, due to Anthropogenic and geologic activities, has been continuously contaminated by potentially toxic metals, causing a range of effects to animals and citizenry. In the developing countries, about 80% of diseases are waterborne diseases. Bio accumulation of these metals in citizenry due to intake of contaminated vegetables, fruits, fishes, seafood and drinking water and beverages causes a serious threat to citizenry. Toxicity of these metals is due to metabolic interference and mutagenesis, interference in the normal functioning of structural proteins, enzymes, and nucleic acids by binding them, adversely affecting the immune and hematopoietic systems in citizenry and animals. The toxic metals also enrich antibiotic resistant microbes particularly bacteria by Co-selection (occurring by Co-resistance and cross-resistance) as it promotes antibiotic resistance in bacteria even in absence of antibiotics. These metals in living cells cause cytotoxicity, oxidative stress resulting in the damages of antioxidants, enzyme inhibition, loss of DNA repair mechanism, protein dysfunction and damage to lipid per oxidase. Endocrine disruption, neuro-developmental toxicity, biosynthesis of hemoglobin, metabolism of vitamin D, renal toxicity, damage to central nervous system, hearing speech and visual disorders, hypertension, anemia, dementia, hematemesis, bladder, lung, nose, larynx, prostate cancer, and bone diseases are some other health’s risks to human.
{"title":"Health Risks of Potentially Toxic Metals Contaminated Water","authors":"O. Bansal","doi":"10.5772/intechopen.92141","DOIUrl":"https://doi.org/10.5772/intechopen.92141","url":null,"abstract":"Groundwater which fulfills globally 50–80% need of drinking water, due to Anthropogenic and geologic activities, has been continuously contaminated by potentially toxic metals, causing a range of effects to animals and citizenry. In the developing countries, about 80% of diseases are waterborne diseases. Bio accumulation of these metals in citizenry due to intake of contaminated vegetables, fruits, fishes, seafood and drinking water and beverages causes a serious threat to citizenry. Toxicity of these metals is due to metabolic interference and mutagenesis, interference in the normal functioning of structural proteins, enzymes, and nucleic acids by binding them, adversely affecting the immune and hematopoietic systems in citizenry and animals. The toxic metals also enrich antibiotic resistant microbes particularly bacteria by Co-selection (occurring by Co-resistance and cross-resistance) as it promotes antibiotic resistance in bacteria even in absence of antibiotics. These metals in living cells cause cytotoxicity, oxidative stress resulting in the damages of antioxidants, enzyme inhibition, loss of DNA repair mechanism, protein dysfunction and damage to lipid per oxidase. Endocrine disruption, neuro-developmental toxicity, biosynthesis of hemoglobin, metabolism of vitamin D, renal toxicity, damage to central nervous system, hearing speech and visual disorders, hypertension, anemia, dementia, hematemesis, bladder, lung, nose, larynx, prostate cancer, and bone diseases are some other health’s risks to human.","PeriodicalId":424083,"journal":{"name":"Heavy Metal Toxicity in Public Health","volume":"120 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123214536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-01-21DOI: 10.5772/intechopen.90060
Mustafa Ertan Akün
Some of the heavy metals, (arsenic, cadmium, chromium and nickel) tend to endanger public health, when found above critical limits in soil and water, becom-ing carcinogenic. The heavy metals are taken by humans through the food chain. As shown by numerous researchers all over the world, the heavy metal contamination mostly come from sewage waters and pesticides, as well as naturally. The natural resources come from the composition of the rock formations present at the area of study. One or all of the above mentioned sources of heavy metal contamination may be present. The study concentrates on the internationally accepted critical limits for soil and water, explains scientific methods of entering into vegetables and fruit, and also tries to shed light on the transfer factors of heavy metals imposing dangers on public health. Remediation of the contaminated soil and water is also discussed, and phytoremediation methods are brought forward, as compared with chemical methods. Details of different phytoremediation (phyto-accumulation, phyto-stabilization, phyto-degradation, phyto-volatilization, and hydraulic control) are also discussed. Actual case studies from North Cyprus are also provided, with real contamination levels observed. Different areas and soil/water/plant species were assessed in detail, displaying concentrations, critical limits, transfer factors, and recommendations.
{"title":"Heavy Metal Contamination and Remediation of Water and Soil with Case Studies From Cyprus","authors":"Mustafa Ertan Akün","doi":"10.5772/intechopen.90060","DOIUrl":"https://doi.org/10.5772/intechopen.90060","url":null,"abstract":"Some of the heavy metals, (arsenic, cadmium, chromium and nickel) tend to endanger public health, when found above critical limits in soil and water, becom-ing carcinogenic. The heavy metals are taken by humans through the food chain. As shown by numerous researchers all over the world, the heavy metal contamination mostly come from sewage waters and pesticides, as well as naturally. The natural resources come from the composition of the rock formations present at the area of study. One or all of the above mentioned sources of heavy metal contamination may be present. The study concentrates on the internationally accepted critical limits for soil and water, explains scientific methods of entering into vegetables and fruit, and also tries to shed light on the transfer factors of heavy metals imposing dangers on public health. Remediation of the contaminated soil and water is also discussed, and phytoremediation methods are brought forward, as compared with chemical methods. Details of different phytoremediation (phyto-accumulation, phyto-stabilization, phyto-degradation, phyto-volatilization, and hydraulic control) are also discussed. Actual case studies from North Cyprus are also provided, with real contamination levels observed. Different areas and soil/water/plant species were assessed in detail, displaying concentrations, critical limits, transfer factors, and recommendations.","PeriodicalId":424083,"journal":{"name":"Heavy Metal Toxicity in Public Health","volume":"179 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123734840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-01-16DOI: 10.5772/intechopen.90333
N. R. Jyothi, Nainar Abdulkhader Mohamed Farook
Mercury was the name of the Roman messenger of god who can move really fast. It is also called as quicksilver due to its fast movement and silvery tinge. Liquid metal state mercury (Hg) has little to no solubility and is not poisonous. But the liquid mercury can vaporize, and gaseous mercury becomes poisonous due to its nature of being absorbed into the blood. Mercury in +2 state is more poisonous due to high solubility. Mercury is the only metal that exists in liquid state at normal temperature and pressure. Mercury poisoning occurs by exposure to mercury, i.e., acute and chronic exposures. Symptoms of mercury poisoning depend on the type, dose, method, and duration of exposure. Mercury poisoning effects on the human body are not limited to reddishness of hands and feet; renal failures; cardiovascular, liver, brain, and hormonal issues; and intestinal ulceration. The present chapter describes the mercury sources, types of exposures, types of poisoning, treatments, and preventive measures of mercury poisoning.
{"title":"Mercury Toxicity in Public Health","authors":"N. R. Jyothi, Nainar Abdulkhader Mohamed Farook","doi":"10.5772/intechopen.90333","DOIUrl":"https://doi.org/10.5772/intechopen.90333","url":null,"abstract":"Mercury was the name of the Roman messenger of god who can move really fast. It is also called as quicksilver due to its fast movement and silvery tinge. Liquid metal state mercury (Hg) has little to no solubility and is not poisonous. But the liquid mercury can vaporize, and gaseous mercury becomes poisonous due to its nature of being absorbed into the blood. Mercury in +2 state is more poisonous due to high solubility. Mercury is the only metal that exists in liquid state at normal temperature and pressure. Mercury poisoning occurs by exposure to mercury, i.e., acute and chronic exposures. Symptoms of mercury poisoning depend on the type, dose, method, and duration of exposure. Mercury poisoning effects on the human body are not limited to reddishness of hands and feet; renal failures; cardiovascular, liver, brain, and hormonal issues; and intestinal ulceration. The present chapter describes the mercury sources, types of exposures, types of poisoning, treatments, and preventive measures of mercury poisoning.","PeriodicalId":424083,"journal":{"name":"Heavy Metal Toxicity in Public Health","volume":"71 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124621323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-11-11DOI: 10.5772/intechopen.90092
C. Siddoo-Atwal
Cigarette smoke and air pollution have been associated with lung cancer and naso pharyngeal and laryngeal cancer, respectively. Significant concentrations of select heavy metals including lead and cadmium have been isolated in popular cigarette brands, and these heavy metals can be inhaled via smoking. Lead is able to mimic the activity of calcium in the human body, thereby leading to toxic effects in a variety of target organs. Lead perturbs and alters the release of intracellular calcium stores from organelles like the endoplasmic reticulum (ER) and mitochondria. A rise in mitochondrial calcium stimulates the generation of reactive oxygen species (ROS) and free fatty acids which can further promote calcium release and, ultimately, result in cell death. In the case of cadmium, the renal proximal tubule of the kidney accumulates freely filtered and metallothionein-bound metal, which is degraded in endosomes and lysosomes. This results in the release of free cadmium into the cytosol where it can generate reactive oxygen species and activate cell death pathways. In developing countries, indoor air pollution due to the domestic use of unprocessed biomass fuels such as wood, dung, and coal is another cause of respiratory tract cancers in humans. In some developed countries such as Australia and Canada, the alarming increase in forest fire frequency due to climate change and the associated smoke released into the environment is also likely to pose a future human health risk. Polycyclic organic particles in biomass and forest fire smoke can include carcinogens such as benzo[a]pyrene, which is also found in cigarette smoke. Benzo[a]pyrene can induce apoptosis in mammalian cells by initiating mitochondrial dysfunction, activating the intrinsic caspase pathway (caspase-3 and caspase-9), and via p53 activation. The constitutive activation of apoptotic pathways has been linked to carcinogenesis in a number of cancer models.
{"title":"A Role for Heavy Metal Toxicity and Air Pollution in Respiratory Tract Cancers","authors":"C. Siddoo-Atwal","doi":"10.5772/intechopen.90092","DOIUrl":"https://doi.org/10.5772/intechopen.90092","url":null,"abstract":"Cigarette smoke and air pollution have been associated with lung cancer and naso pharyngeal and laryngeal cancer, respectively. Significant concentrations of select heavy metals including lead and cadmium have been isolated in popular cigarette brands, and these heavy metals can be inhaled via smoking. Lead is able to mimic the activity of calcium in the human body, thereby leading to toxic effects in a variety of target organs. Lead perturbs and alters the release of intracellular calcium stores from organelles like the endoplasmic reticulum (ER) and mitochondria. A rise in mitochondrial calcium stimulates the generation of reactive oxygen species (ROS) and free fatty acids which can further promote calcium release and, ultimately, result in cell death. In the case of cadmium, the renal proximal tubule of the kidney accumulates freely filtered and metallothionein-bound metal, which is degraded in endosomes and lysosomes. This results in the release of free cadmium into the cytosol where it can generate reactive oxygen species and activate cell death pathways. In developing countries, indoor air pollution due to the domestic use of unprocessed biomass fuels such as wood, dung, and coal is another cause of respiratory tract cancers in humans. In some developed countries such as Australia and Canada, the alarming increase in forest fire frequency due to climate change and the associated smoke released into the environment is also likely to pose a future human health risk. Polycyclic organic particles in biomass and forest fire smoke can include carcinogens such as benzo[a]pyrene, which is also found in cigarette smoke. Benzo[a]pyrene can induce apoptosis in mammalian cells by initiating mitochondrial dysfunction, activating the intrinsic caspase pathway (caspase-3 and caspase-9), and via p53 activation. The constitutive activation of apoptotic pathways has been linked to carcinogenesis in a number of cancer models.","PeriodicalId":424083,"journal":{"name":"Heavy Metal Toxicity in Public Health","volume":"6 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130462048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-02DOI: 10.5772/INTECHOPEN.86399
P. Seligman, G. Siriwardana
Iron is essential for numerous cellular reactions that require oxygen transfer. Iron deficiency is a common problem in humans and is the most common nutritional disease worldwide. However, excess cellular iron can be toxic. Maintenance of iron hemostasis utilizes specialized pathways responsible for iron transport, iron uptake by cells, and appropriate cellular distribution of iron for utilization or storage. This chapter reviews how iron depletion is associated with inhibition of cellular proliferation and cell cycle arrest at different parts of the cell cycle. These effects are based on the effective chelation of iron, and more importantly on differences in various tissue responses to both iron depletion and iron toxicity. These differences may explain why in some tissues, particularly rapidly growing cancer cells, iron depletion causes cell cycle arrest and apoptosis, a form of programed cell death. Other neoplastic tissues are more prone to the toxic effects of iron, which can induce autophagic cell death (termed ferroptosis) via reactive oxygen species resulting in lysosomal degradation of cellular constituents. An appreciation of these differences can be utilized by novel pharmaceutical agents discussed below designed to treat specific cancers.
{"title":"Intracellular Iron Concentration and Distribution Have Multiple Effects on Cell Cycle Events","authors":"P. Seligman, G. Siriwardana","doi":"10.5772/INTECHOPEN.86399","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.86399","url":null,"abstract":"Iron is essential for numerous cellular reactions that require oxygen transfer. Iron deficiency is a common problem in humans and is the most common nutritional disease worldwide. However, excess cellular iron can be toxic. Maintenance of iron hemostasis utilizes specialized pathways responsible for iron transport, iron uptake by cells, and appropriate cellular distribution of iron for utilization or storage. This chapter reviews how iron depletion is associated with inhibition of cellular proliferation and cell cycle arrest at different parts of the cell cycle. These effects are based on the effective chelation of iron, and more importantly on differences in various tissue responses to both iron depletion and iron toxicity. These differences may explain why in some tissues, particularly rapidly growing cancer cells, iron depletion causes cell cycle arrest and apoptosis, a form of programed cell death. Other neoplastic tissues are more prone to the toxic effects of iron, which can induce autophagic cell death (termed ferroptosis) via reactive oxygen species resulting in lysosomal degradation of cellular constituents. An appreciation of these differences can be utilized by novel pharmaceutical agents discussed below designed to treat specific cancers.","PeriodicalId":424083,"journal":{"name":"Heavy Metal Toxicity in Public Health","volume":"47 11 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128594965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nanosized manganese oxide has excellent prospects. Some data imply that its particles can be toxic when introduced in various ways, and it requires further examination of this nanomaterial. The authors conducted research of nanodisperse MnO 2 water suspension at intragastric, inhalation, and skin-resorptive introduction into small rodents and obtained profound characteristics of its toxic effects, determined target organs and revealed dose-dependent effects. The substance was characterized with acute toxicity, and its bioaccumulation under long-term exposure caused morphofunctional disorders in brain, lipid peroxidation activation, and lower antioxidant system activity. The authors detected vessel hyperemia, subarachnoid hemorrhages, brain edema with perivascular and pericellular spaces dilatation, nerve fiber demyelinization, and focal dystrophic changes in vessels endothelium. After a long-term introduction in doses from 0.25 to 2.5 mg/kg, oxidizing-antioxidant imbalance occurred, neurotransmitters and electrolytes balance was violated, and there was also brush border epithelium insufficiency. Nanodisperse MnO 2 water suspension in doses equal to 2.5 and 0.25 mg/kg at intragastric introduction into Wistar rats did not have embryotoxic or teratogenic effects. It did not have any mutagenic effects in doses equal to 10.3 and 5.15 mg/kg or gonadotoxic effects either when introduced into Wistar male rats in doses equal to 10.3–5.15 mg/kg via gastric tube.
{"title":"Toxicologic Characteristics of Nanodisperse Manganese Oxide: Physical-Chemical Properties, Biological Accumulation, and Morphological-Functional Properties at Various Exposure Types","authors":"Nina Vladimirovna Zaitseva, Marina Alexandrovna Zemlyanova","doi":"10.5772/INTECHOPEN.83499","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.83499","url":null,"abstract":"Nanosized manganese oxide has excellent prospects. Some data imply that its particles can be toxic when introduced in various ways, and it requires further examination of this nanomaterial. The authors conducted research of nanodisperse MnO 2 water suspension at intragastric, inhalation, and skin-resorptive introduction into small rodents and obtained profound characteristics of its toxic effects, determined target organs and revealed dose-dependent effects. The substance was characterized with acute toxicity, and its bioaccumulation under long-term exposure caused morphofunctional disorders in brain, lipid peroxidation activation, and lower antioxidant system activity. The authors detected vessel hyperemia, subarachnoid hemorrhages, brain edema with perivascular and pericellular spaces dilatation, nerve fiber demyelinization, and focal dystrophic changes in vessels endothelium. After a long-term introduction in doses from 0.25 to 2.5 mg/kg, oxidizing-antioxidant imbalance occurred, neurotransmitters and electrolytes balance was violated, and there was also brush border epithelium insufficiency. Nanodisperse MnO 2 water suspension in doses equal to 2.5 and 0.25 mg/kg at intragastric introduction into Wistar rats did not have embryotoxic or teratogenic effects. It did not have any mutagenic effects in doses equal to 10.3 and 5.15 mg/kg or gonadotoxic effects either when introduced into Wistar male rats in doses equal to 10.3–5.15 mg/kg via gastric tube.","PeriodicalId":424083,"journal":{"name":"Heavy Metal Toxicity in Public Health","volume":"85 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129680030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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