Relevant bibliographies by topics / Toxicity

Academic literature on the topic 'Toxicity'

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Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Toxicity"

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Hutchings, Matt, Ian Johnson, Elaine Hayes, Andrew E. Girling, John Thain, Kevin Thomas, Rachel Benstead, et al. "Toxicity Reduction Evaluation, Toxicity Identification Evaluation and Toxicity Tracking in Direct Toxicity Assessment." Ecotoxicology 13, no. 5 (July 2004): 475–84. http://dx.doi.org/10.1023/b:ectx.0000035297.90620.73.

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Paulíková, I., G. Kováč, J. Bíreš, Š. Paulík, H. Seidel, and O. Nagy. "Iodine toxicity in ruminants." Veterinární Medicína 47, No. 12 (March 30, 2012): 343–50. http://dx.doi.org/10.17221/5845-vetmed.

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The inadequate intake of iodine is still a topical problem, because it contributes to a reduction in performance through the disturbed health of adult animals and their offspring. The necessity of iodine is frequently described in association with hypothyroidal state. In our work we want to assign the hidden risk of prolonged iodine feeding in ruminants. We discuss the possible sources of iodine intoxication, the clinical signs of the intoxication, its effects on production, reproduction, and thyroid functions; animal susceptibility to intoxication; laboratory and necropsy findings; diagnostic, and therapeutic possibilities.
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A, Semwal. "Phytotherapy Toxicity in Aquaculture." Advances in Pharmacology and Clinical Trials 8, no. 3 (July 6, 2023): 1–4. http://dx.doi.org/10.23880/apct-16000219.

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The fish disease significantly affects the aquaculture industry and causes economic harm. Antibiotics, chemotherapeutics and other synthetic pharmaceuticals are continuously used by farmers to mitigate infectious diseases. Phytotherapy without side effects is an eco-friendly, socio-economic and modern approach to mitigate disease. Toxicological and pharmacological studies are prerequisites for phytotherapy-related research and help to decide a safe dose for the main experiment and commercial aqua products. In toxicity studies, LD50 and LC50 are reliable and widely used acute toxicity parameters.
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HALL, Stephen. "Toxicity." Nephrology 3, s2 (September 1997): s788. http://dx.doi.org/10.1111/j.1440-1797.1997.tb00310.x.

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Enara, Mohamed. "Case Report (Acute Iron Toxicity)." Advances in Clinical Toxicology 5, no. 2 (2020): 1–2. http://dx.doi.org/10.23880/act-16000185.

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Hussain, Sadique. "Nanotoxicology: Nano Toxicity in Humans." Pharmaceutics and Pharmacology Research 5, no. 1 (January 4, 2022): 01–03. http://dx.doi.org/10.31579/2693-7247/059.

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Nanoparticles (NPs) have attracted a lot of attention in the fields of electronics, biology, and astronautics because of their unique physicochemical and electrical characteristics. NPs are materials with at least one dimension of fewer than 100 nanometres that are commercially manufactured (Bahadar et al., 2016; Vishwakarma et al., 2010). In the medical field, drugs, proteins, DNA, and monoclonal antibodies are all being delivered via NPs(Hussain et al., 2021).
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Quimby, Alexandra Elizabeth, and Rajeev Sachdeva. "Lithium Toxicity at Therapeutic Blood Levels: A Case Report." University of Ottawa Journal of Medicine 5, no. 2 (November 2, 2015): 26–28. http://dx.doi.org/10.18192/uojm.v5i2.1368.

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ABSTRACT:This report describes a case of lithium toxicity occurring at therapeutic blood levels in a 47-year-old man with bipolar disorder and a history of alcohol abuse. We discuss the clinical presentation of lithium toxicity, as well as factors that may contribute to a reduction in the blood levels required for the precipitation of toxic effects. In addition, we review the literature on cases of lithium toxicity occurring at therapeutic blood levels, including diagnosis and management thereof.RÉSUMÉ:Ce rapport décrit un cas de toxicité au lithium se produisant à des niveaux sanguins thérapeutiques chez un homme de 47 ans avec un trouble bipolaire et une histoire d’abus d’alcool. Nous discutons la présentation clinique de toxicité au lithium, ainsi que les facteurs pouvant contribuer à une réduction des niveaux sanguins nécessaires à la précipitation des effets toxiques. En outre, nous passons en revue la littérature sur les cas de toxicité au lithium se produisant à des niveaux sanguins thérapeutiques, y compris son diagnostic et sa gestion.
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Usman, A., M. U. Kawu, M. Shittu, N. B. Ibrahim, and A. A. Yahaya. "Synergistic ameliorative effect of ascorbic acid and Moringa oleifera in lead-induced toxicity: a review." Nigerian Journal of Animal Production 50, no. 3 (May 14, 2024): 86–97. http://dx.doi.org/10.51791/njap.v50i3.4031.

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This review is aimed at discussing the synergism between Moringa oleifera and ascorbic acid in lead poisoning. Lead is one of the heavy metals that is ubiquitous in nature and has various industrial applications. This is because of its advantageous physical properties. Although its use has been phased out in some industrial applications such as paints in developed countries, it remains a widely used heavy metal in the developing world. Lead toxicity accounts for thousands of deaths annually. Children are mostly affected by serious outcomes such as permanent neurocognitive damage. A literature search was conducted using ScienceDirect, PubMed, MDPI, Wiley, and Springer. Keywords used for search include “Moringa oleifera” “Ascorbic acid” “Lead toxicity” “Medicinal preparations” “Nutraceuticals” and “Chinese herbal medicine”. Oxidative stress was the major mechanism underlying Pb toxicity. Oxidative stress causes the depletion of endogenous antioxidant systems. Both Moringa oleifera and ascorbic acid have antioxidant properties. This has made it possible for these two agents to be used for treating various ailments, including Pb toxicity. Previous findings have shown a probable synergism between Moringa oleifera and ascorbic acid in ameliorating Pb-induced toxicity. This study indicates that a combined treatment approach comprising of Moringa oleifera and ascorbic acid could provide the best solution for managing Pb-induced toxicity. The classical management for Pb toxicity is chelation therapy, which is usually accompanied by serious side effects. Hence, there is a need for the deployment of nutraceuticals and other plant-derived substances for the better management of Pb toxicity Cette revue vise à discuter de la synergie entre le Moringa oleifera et l'acide ascorbique dans le saturnisme. Le plomb est l'un des métaux lourds omniprésent dans la nature et qui a diverses applications industrielles. Cela est dû à ses propriétés physiques avantageuses. Bien que son utilisation ait été progressivement abandonnée dans certaines applications industrielles telles que les peintures dans les pays développés, il reste un métal lourd largement utilisé dans les pays en développement. La toxicité du plomb est responsable de milliers de décès chaque année. Les enfants sont principalement touchés par des conséquences graves telles que des dommages neurocognitifs permanents. Une recherche documentaire a été menée à l'aide de ScienceDirect, PubMed, MDPI, Wiley et Springer. Les mots clés utilisés pour la recherche incluent « Moringa oleifera », « Acide ascorbique », « Toxicité au plomb », « Préparations médicinales », « Produits nutraceutiques » et « Plantes médicinales chinoises ». Le stress oxydatif était le principal mécanisme sous-jacent à la toxicité du plomb. Le stress oxydatif entraîne l'épuisement des systèmes antioxydants endogènes. Le Moringa oleifera et l'acide ascorbique ont tous deux des propriétés antioxydantes. Cela a permis à ces deux agents d'être utilisés pour traiter diverses affections, notamment la toxicité du plomb. Des découvertes antérieures ont montré une synergie probable entre le Moringa oleifera et l'acide ascorbique pour améliorer la toxicité induite par le Pb. Cette étude indique qu'une approche thérapeutique combinée comprenant du Moringa oleifera et de l'acide ascorbique pourrait constituer la meilleure solution pour gérer la toxicité induite par le Pb. La prise en charge classique de la toxicité du Pb est la thérapie par chélation, qui s'accompagne généralement d'effets secondaires graves. Il est donc nécessaire de déployer des nutraceutiques et d'autres substances d'origine végétale pour une meilleure gestion de la toxicité du plomb.
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Messinger, Horst, and Albert Bär. "Subchronic toxicity, toxicity to reproduction and prenatal developmental toxicity of vinyl laurate." Regulatory Toxicology and Pharmacology 70, no. 1 (October 2014): 80–86. http://dx.doi.org/10.1016/j.yrtph.2014.06.015.

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Pumpaisalchai, W., S. Kaewvichit, S. Siriaunkgul, T. Taesothikul, W. Niwatananun, and K. Sanichwankul. "TOXICITY OF BARAKOL: HEPATOTOXICITY AND SUBACUTE TOXICITY." Acta Horticulturae, no. 679 (February 2005): 157–63. http://dx.doi.org/10.17660/actahortic.2005.679.19.

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Dissertations / Theses on the topic "Toxicity"

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Marcelová, Štěpánka. "Toxicita nitroderivátů toluenu a produktů jejich transformací." Master's thesis, Vysoké učení technické v Brně. Fakulta chemická, 2010. http://www.nusl.cz/ntk/nusl-216647.

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This work is focused on verification of p-Nitrotoluenu toxicity and compounds resulting from the aerobic transformation, and methyl group oxidation and reduction of nitro. Some of these products are not commercially available and had to be made soon. Toxicity of the substances was determined by toxicity tests. Were tested root growth inhibition Sinapis alba, which resulted in an inhibitory concentration IC50; test inhibition duckweed Lemna minor , which was also the determination of IC50 inhibitory concentration, and acute toxicity test Artemia salina, which was observed in mortality and immobility organisms and the test result was an efficient concentration EC50 value. Results of tests are compared in the conclusion of the work and is made evaluation of the toxicity of individual substances.
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Anderson, James Ainslie. "Interleukin-2 toxicity." Thesis, University of Southampton, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245045.

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El-Daher, Marie-Thérèse. "Huntingtin proteolysis and toxicity." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T029/document.

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La maladie de Huntington (MH) est une maladie neurodégénérative héréditaire autosomique dominante. Elle est due à l’expansion anormale de polyglutamine dans la partie N-terminal de la protéine huntingtine (HTT). Une des étapes clés de la pathologie est le clivage de la HTT pleine longueur en fragments N-terminaux plus petits, contenant l’expansion de polyglutamine, et qui sont toxiques pour les neurones. En effet, les clivages de la HTT mutée génère des fragments N-terminaux (N-ter) de tailles comprises entre les acides aminés 1-105 et 1-586 observés dans des extraits de cerveaux de patients MH post-mortem et dont l’implication dans la mort neuronal est bien caractérisée. Mes travaux de thèse ont visé à modéliser le clivage de la HTT et à évaluer les conséquences sur la survie neuronale.Au cours de ma thèse, j’ai développé un outil permettant de contrôler le clivage de la HTT dans le temps et à des sites spécifiques. J’ai étudié le clivage de la HTT à deux sites stratégiques : les positions clivées par la caspase-6 et par la bléomycine hydrolase/cathepsine Z. A l’aide de cet outil, j’ai montré que le clivage de la HTT confère une toxicité cellulaire qui dépend du profil du clivage. Plus précisément, J’ai décrit une interaction intramoléculaire au sein des domaines de la HTT. Mes résultats indiquent que cette interaction protège les cellules de la toxicité induite par le clivage de la HTT mutée. En effet, les clivages successifs de la HTT annulent cette interaction, ce qui induit la libération des fragments N-ter mutants et provoque la mort cellulaire à l’issue de leur translocation nucléaire. Pour conclure, au cours de ma thèse, j’ai montré que la protéolyse successive de la HTT induit des processus cytotoxiques différents
Huntington’s disease (HD) is an autosomal dominant inherited neurodegenerative disorder caused by an abnormal polyglutamine (polyQ) expansion in the N-terminus of the protein huntingtin (HTT). A crucial step in HD pathogenesis is the cleavage of full-length HTT into smaller N-terminal (N-ter) fragments that contain the polyQ stretch and that are toxic to neurons. HTT cleavage generates short N-ter fragments whose amino-acid positions range from 1-105 to 1-586. These fragments are observed in HD post mortem brain samples and their participation in neuronal death in HD is well characterized. During my PhD research, I investigated the consequences of full-length mutant HTT proteolysis by developing a time and site-specific controlled system for HTT proteolysis. I have assessed HTT cleavage on two sites caspase-6 and cathepsin Z. My results show that HTT cleavage induces neurotoxicity in vitro as well as in vivo, toxicity which depends on HTT proteolysis pattern. Briefly, we described an intramolecular interaction within the HTT domains which is impaired upon successive proteolysis of HTT. We found that HTT intramolecular interaction buffer mutant N-ter HTT-induced toxicity. Moreover, specific cleavages of the mutant HTT generated toxic N-ter fragments as they translocate into the nucleus. To conclude, my PhD work has shown that additional cleavage of mutant HTT induces cytotoxicity by different mechanisms
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Kratchman, Jessica. "Predicting Chronic Non-Cancer Toxicity Levels from Short-Term Toxicity Data." Thesis, The George Washington University, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10263969.

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This dissertation includes three separate but related studies performed in partial fulfillment of the requirements for the degree of Doctor of Public Health in Environmental and Occupational Health. The main goal this dissertation was to develop and assess quantitative relationships for predicting doses associated with chronic non-cancer toxicity levels in situations where there is an absence of chronic toxicity data, and to consider the applications of these findings to chemical substitution decisions. Data from National Toxicology Program (NTP) Technical Reports (TRs) (and where applicable Toxicity Reports), which detail the results of both short-term and chronic rodent toxicity tests, have been extracted and modeled using the Environmental Protection Agency’s (EPA’s) Benchmark Dose Software (BMDS). Best-fit minimum benchmark doses (BMDs) and benchmark dose lower limits (BMDL) were determined. Endpoints of interest included non-neoplastic lesions, final mean body weights and mean organ weights. All endpoints were identified by NTP Pathologists in the abstract of the TRs as either statistically or biologically significant. A total of 41 chemicals tested between 2000 and 2012 were included with over 1700 endpoints for short-term (13 week) and chronic (2 year) exposures.

Non-cancer endpoints were the focus of this research. Chronic rodent bioassays have been used by many methodologies in predicting the carcinogenic potential of chemicals in humans (1). However, there appears to be less emphasis on non-cancer endpoints. Further, it has been shown in the literature that there is little concordance in cancerous endpoints between humans and rodents (2). The first study, Quantitative Relationship of Non-Cancer Benchmark Doses in Short-Term and Chronic Rodent Bioassays (Chapter 2), investigated quantitative relationships between non-cancer chronic and short-term toxicity levels using best-fit modeling results and orthogonal regression techniques. The findings indicate that short-term toxicity studies reasonably provide a quantitative estimate of minimum (and median) chronic non-cancer BMDs and BMDLs.

The next study, Assessing Implicit Assumptions in Toxicity Testing Guidelines (Chapter 3) assessed the most sensitive species and species-sex combinations associated with the best-fit minimum BMDL10 for the 41 chemicals. The findings indicate that species and species-sex sensitivity for this group of chemicals is not uniform and that rats are significantly more sensitive than mice for non-cancerous outcomes. There are also indications that male rats may be more than the other species sex groups in certain instances.

The third and final study, Comparing Human Health Toxicity of Alternative Chemicals (Chapter 4), considered two pairs of target and alternative chemicals. A target is the chemical of concern and the alternative is the suggested substitution. The alternative chemical lacked chronic toxicity data, whereas the target had well studied non-cancer health effects. Using the quantitative relationships established in Chapter 2, Quantitative Relationship of Non-Cancer Benchmark Doses in Short-Term and Chronic Rodent Bioassays, chronic health effect levels were predicted for the alternative chemicals and compared to known points of departure (PODs) for the targets. The findings indicate some alternatives can lead to chemical exposures potentially more toxic than the target chemical.

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Lampi, Mark. "Environmental Photoinduced Toxicity of Polycyclic Aromatic Hydrocarbons: Occurrence and Toxicity of Photomodified PAHs and Predictive Modeling of Photoinduced Toxicity." Thesis, University of Waterloo, 2005. http://hdl.handle.net/10012/1248.

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Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental contaminants known for their photoinduced toxicity. There are two mechanisms through which this may occur: photosensitization and photomodification. Photosensitization generally leads to the production of singlet oxygen, a reactive oxygen species (ROS), which is highly damaging to biological molecules. Photomodification of PAHs, usually via oxygenation, results in the formation of new compounds (oxyPAHs), and can occur under environmentally relevant levels of actinic radiation.

PAHs and oxyPAHs readily adsorb to the organic phase of particulate matter in the environment such as sediments. It is logical to conclude that sediment transport will also facilitate the transport of these contaminants, and it has been shown that in the course of transport, degradative processes evoke a change in the profile of the PAHs present. Sediment samples taken along a transect from Hamilton Harbour were fractionated, and analyzed using a 2D HPLC method. All sediments contained intact and modified PAHs, although a marked change was noted in the profile of compounds present in the samples, which differ in distance from shore. Fractions of sediment extract were tested for toxicity using a bacterial respiration assay. Toxicity was observed in fractions containing modified PAHs, and was similar to that of intact PAH-containing fractions.

Subsequently, the toxicities of 16 intact PAHs were assessed to Daphnia magna under two ultraviolet radiation (UV) conditions. The toxicity of intact PAHs generally increased in the presence of full spectrum simulated solar radiation (SSR), relative to visible light plus UVA only. To expand the existing data on the effects of PAH photoproducts to animals, fourteen oxyPAHs were also assayed with D. magna, most of which were highly toxic without further photomodification. The data presented highlight the effects of UV radiation on mediating PAH toxicity. The importance of the role of photomodification is also stressed, as several oxyPAHs were highly toxic to D. magna, a key bioindicator species in aquatic ecosystems.

A QSAR model previously developed for Lemna gibba showed that a photosensitization factor (PSF) and a photomodification factor (PMF) could be combined to describe toxicity. To determine whether it was predictive for D. magna, toxicity was assessed as both EC50 and ET50. As with L. gibba and Vibrio fischeri, neither the PSF nor the PMF alone correlated to D. magna toxicity. However, a PSF modified for D. magna did in fact exhibit correlation with toxicity, which was further improved when summed with a modified PMF. The greatest correlation was observed with EC50 toxicity data. This research provides further evidence that models that include factors for photosensitization and photomodification will likely be applicable across a broad range of species. To gain further knowledge of the roles that the variables contributing to the photosensitization and photomodification, a structural equation model was constructed based on the D. magna QSAR. This model accounted for a high amount of variance in six sets of toxicity data, as well as insight into the mechanisms of phototoxicity affecting different aquatic organisms.
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Mazzatorta, Paolo. "Evaluation of pesticide toxicity : a hierarchical QSAR approach to model the acute aquatic toxicity and avian oral toxicity of pesticides." Thesis, Open University, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424819.

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The thesis aimed to extract information relevant to the hazard and risk assessment of pesticides. In particular, quantitative structure-activity relationship (QSAR) approaches have been used to build up a mathematical model able to predict the aquatic acute toxicity, Leso, and the avian oral toxicity, LDso, for pesticides. Ecotoxicological values were collected from several databases, and screened according to quality criteria. A hierarchical QSAR approach was applied for the prediction of acute aquatic toxicity. Chemical structures were encoded into molecular descriptors by an automated, seamless procedure available within the OpenMolGRID system. Different linear and non-linear regression techniques were used to obtain reliable and thoroughly validated QSARs. The final model was developed by a counter-propagation neural network coupled with genetic algorithms for variable selection. The proposed QSAR is consistent with McFarland's principle for biological activity and makes use of seven molecular descriptors. The model was assessed thoroughly in test (R2 = 0.8) and validation sets (R2 = 0.72), the y-scrambling test and a sensitivity/stability test. The second endpoint considered in this thesis was avian oral toxicity. As previously, the chemical description of chemicals was generated automatically by the OpenMolGRID system. The best classification model was chosen on the basis of the performances on a validation set of 19 data points, and was obtained from a support vector machine using 94 data points and nine variables selected by genetic algorithms (Error Ratetraining = 0.021, Error Ratevaiidalion = 0.158). The model allowed for a mechanistic estimation of the toxicological action. In fact, several descriptors selected for the final classification model encode for the interaction of the pesticides with other molecules. The presence of hetero-atoms, e.g. sulphur atoms, is correlated with the toxicity, and the pool of descriptor selected is generally dependent from the 3D conformation of the structures. These suggest that, in the case of avian oral toxicity, pesticides probably exert their toxic action through the interaction with some macromolecule and/or protein of the biological system.
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Travers, Sarah. "Toxicity of Lake Sediments." Thesis, Ulster University, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487669.

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The profundal sediment of many lakes is contaminated by heavy metals and persistent organic pollutants (POPs) deposited from the atmosphere, yet there has been little assessment of the biological effects of these toxicants. A Tier I sediment ecological risk assessment of profundal lake sediment that covers the range of contamination in the UK and Ireland was completed. Three laboratory sediment bioassays were used, Daphnia magna 7-day survival and reproduction, Gammarus pulex 14-day survival and growth and Chironomus riparius 10-day survival and growth/reproduction, and the concentrations of seven heavy metals and four groups of POPs (polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls, organochlorine pesticides and polybrominated diphenyl ethers) were determined.
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Al-Mustafa, Z. H. "Methotrexate pharmacokinetics and toxicity." Thesis, University of Newcastle Upon Tyne, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383988.

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Aljebab, Fahad. "Corticosteroid toxicity in children." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/43388/.

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Corticosteroid medicines have anti-inflammatory and immunosuppressant effects. Corticosteroids are prescribed for a wide range of conditions in children. The duration of treatment ranges from a few days (short course) to long term. They are usually given orally in the different dosage form of tablets, syrup or soluble tablets. There are a wide range of adverse drug reactions (ADRs) associated with corticosteroids. This thesis initially evaluates the incidence of each individual ADR in children using systematic reviews. Prospective studies of palatability and pharmacoepidemiology using different methods are also used to evaluate aspects of using corticosteroids in children in Saudi Arabia and the UK. A systematic review of the toxicity of short-course oral corticosteroids in children was conducted. Six electronic databases were searched for articles that evaluated the toxicity of oral corticosteroids in children for up to and including 14 days of treatment. Thirty eight articles including 22 randomised controlled trials (RCTs). The review found that the three most frequent ADRs were vomiting, behavioural changes and sleep disturbance, with incidence rates of 4.3 – 5.4% of patients. Infection was one of the most serious ADRs. A systematic review of the toxicity of long-course oral corticosteroids in children was conducted. One hundred studies including 33 prospective cohort studies and 21 RCTs met the inclusion criteria. The review found that the three most frequent ADRs were weight gain, growth retardation and Cushingoid features, with incidence rates of 18.1 – 21.1% of patients. Infection was one of the most serious ADRs, with twenty one deaths. Hypothalamic-pituitary-adrenal (HPA) axis suppression was detected in 249 of 429 patients in whom it was measured. Based on the findings that were highlighted from the systematic review, a prospective observational/interview study was performed. This study evaluated the tolerability and palatability of oral prednisolone and dexamethasone in children in Saudi Arabia and the UK. Palatability was evaluated by asking patient/parent’s opinions of the taste and acceptability of the medication. Tolerability in particular nausea, vomiting and abdominal pain was evaluated by direct questioning of the patient/parents after each administration. Dexamethasone sodium phosphate solution was the most palatable preparation. Prednisolone base tablets were rated the least palatable and were also the least well tolerated. Palatability scores seemed to improve with second doses. A prospective pharmacoepidemiological study of corticosteroids use in Saudi Arabian children was conducted. This study aimed to evaluate the prescribing pattern of corticosteroids for children in the Emergency, outpatient clinics and paediatric wards in the Gurayat General Hospital (GGH) in Saudi Arabia. A total of 1000 patients were approached for the study. Most of whom were asthmatic, eczema, bronchiolitis, and croup patients. A total of 1209 prescriptions were prescribed from different departments. The three most frequently prescribed corticosteroids medications were hydrocortisone ampoules (24.4%), prednisolone tablets (16.4%) and mometasone furoate ointment (9%). This research has contributed to the field of corticosteroids in children by providing more information about the most common and serious ADRs and determining their relative risk levels.
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Jacox, Laura (Laura A. ). "Molecular toxicity of lead." Thesis, Massachusetts Institute of Technology, 2008. http://hdl.handle.net/1721.1/114343.

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Thesis: S.B., Massachusetts Institute of Technology, Department of Earth, Atmospheric, and Planetary Sciences, 2008.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 23-28).
Introduction - Lead is a heavy metal that has been in use for over 8000 years (White, 2007). It was first smelted it 4000BC as a byproduct of silver processing. Since then, Pb has played a dynamic role in history, possibly contributing to the fall of the Roman Empire (Nraigu, 1983). Pb is a highly malleable and ductile Group IVa metal. It has been utilized in a variety of products including makeup, water pipes, cooking vessels, wine bottle seals, glass, batteries, solder, electronic components, paint, and antiknock fuel additives (White, 2007). Its prevalent, long-term use has distributed anthropogenic Pb across the planet in soil, air-borne dust, and water (White, 2007). As a result, human exposure can occur via inhaled air, dust, food, and drinking water. Pb has no known biological functions, yet it has numerous detrimental effects on the body, several of which have been recognized for millennia.
by Laura Jacox.
S.B.
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Books on the topic "Toxicity"

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Hellmann, Libby Fischer. Toxicity. Chicago: Red Herrings Press, 2011.

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Albert, Adrien, ed. Selective Toxicity. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4846-4.

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Himeno, Seiichiro, and Keiko Aoshima, eds. Cadmium Toxicity. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-3630-0.

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Palmeira, Carlos Manuel Marques, Danielle Palma de Oliveira, and Daniel Junqueira Dorta, eds. Toxicity Assessment. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1091-6.

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Logan, David. Gasoline toxicity. Atlanta, GA: U.S. Dept. of Health & Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry, 1993.

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Kosnett, Michael. Arsenic toxicity. Atlanta, GA: U.S. Dept. of Health & Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry, 1990.

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William, Daniell, Brodkin Carl A, United States. Agency for Toxic Substances and Disease Registry, and DeLima Associates, eds. Tetrachloroethylene toxicity. Atlanta, GA: U.S. Dept. of Health & Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry, 1990.

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Wayne, Snodgrass, United States. Agency for Toxic Substances and Disease Registry, and DeLima Associates, eds. Chlordane toxicity. Atlanta, GA: U.S. Dept. of Health & Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry, 1992.

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1834-1870, Keogh James, United States. Agency for Toxic Substances and Disease Registry., and DeLima Associates, eds. Chromium toxicity. Atlanta, GA: U.S. Dept. of Health & Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry, 1990.

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Frank, Arthur L. Benzene toxicity. Atlanta, Ga: U.S. Dept. of Health & Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry, 2000.

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Book chapters on the topic "Toxicity"

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O’Hara, James E., Igor UsUpensky, N. J. Bostanian, John L. Capinera, Reg Chapman, Carl S. Barfield, Marilyn E. Swisher, et al. "Toxicity." In Encyclopedia of Entomology, 3833. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_2495.

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Radatz, Matthias, and Heinz Nau. "Toxicity." In Valproate, 91–128. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8759-5_5.

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Penteado Schmidt, Carolina Witchmichen. "Toxicity." In Chemotherapy in Neonates and Infants, 137–46. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-70591-0_7.

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Gooch, Jan W. "Toxicity." In Encyclopedic Dictionary of Polymers, 757. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_11986.

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Pala, Nezih, Ahmad Nabil Abbas, Carsten Rockstuhl, Christoph Menzel, Stefan Mühlig, Falk Lederer, Joseph J. Brown, et al. "Toxicity." In Encyclopedia of Nanotechnology, 2763. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-90-481-9751-4_100865.

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Samanta, Indranil, and Samiran Bandyopadhyay. "Toxicity." In Pet bird diseases and care, 253–62. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3674-3_4.

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Singh, Visakha, Rabhya Asthana, M. Kiranmai Reddy, Hari Sharan Misra, M. Pradeep, and Saladi Sri Kala Venkata Butchi Raju. "Application and Development Strategies of Nano-Adsorbents on Mercury Remediation." In Mercury Toxicity, 271–95. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-7719-2_11.

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Uddin, Shihab, Sumona Khanom, and Md Rafiqul Islam. "Mercury Contamination in Food—An Overview." In Mercury Toxicity, 33–70. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-7719-2_2.

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Pant, Rakesh, Umangjit Kaur, Sunidhi Shreya, Nirmal Patrick, and Amit Gupta. "Removal of Mercury from Wastewater by Different Natural Biomasses." In Mercury Toxicity, 187–200. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-7719-2_7.

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Acosta, Ismael, Adriana Rodríguez, Juan Fernando Cárdenas, and Víctor Manuel Martínez. "Biosorption of Mercury from Aqueous Solutions by Biosorbents." In Mercury Toxicity, 357–74. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-7719-2_14.

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Conference papers on the topic "Toxicity"

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Ilia, Gheorghe, Ana Borota, and Simona Funar-Timofei. "Interspecies Quantitative Structure-Toxicity-Toxicity Relationships for Predicting the Acute Toxicity of Organophosphorous Compounds." In ECSOC-25. Basel Switzerland: MDPI, 2021. http://dx.doi.org/10.3390/ecsoc-25-11672.

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Makki, I., and P. Kidambi. "Bleomycin Toxicity Controlled." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2158.

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Zhou, Zhi-Xiang, Meng-Nan Qin, Yang-Hua Liu, Xiao-Long Zhang, and Han-Dong Li. "Quantitative Structure-Toxicity Relationship for Predicting Acute Toxicity of Phenols." In The International Conference on Biological Sciences and Technology. Paris, France: Atlantis Press, 2016. http://dx.doi.org/10.2991/bst-16.2016.2.

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Mishra, Meenakshi, Hongliang Fei, and Jun Huan. "Computational prediction of toxicity." In 2010 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2010. http://dx.doi.org/10.1109/bibm.2010.5706653.

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Mody, M., J. Onwochei, C. Migliore, P. S. Patel, and T. Anandarangam. "Amiodarone Induced Pulmonary Toxicity." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5512.

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Broess, J., D. Guerrero Vinsard, and D. Datta. "Flavocoxid-Induced Pulmonary Toxicity." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6266.

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Panchal, Amar M., Harish Seethamraju, and Abida Haque. "Dronaderone Induced Pulmonary Toxicity." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5672.

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Tišler, T., and J. Zagorc-Končan. "Toxicity assessment of effluents." In ENVIRONMENTAL TOXICOLOGY 2008. Southampton, UK: WIT Press, 2008. http://dx.doi.org/10.2495/etox080091.

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Jahan, K., S. Balzer, and P. Mosto. "Toxicity of nonionic surfactants." In ENVIRONMENTAL TOXICOLOGY 2008. Southampton, UK: WIT Press, 2008. http://dx.doi.org/10.2495/etox080301.

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Sabata, R. W., and E. L. Dewailly. "Toxicity Testing With Bioluminescence." In Offshore Technology Conference. Offshore Technology Conference, 1990. http://dx.doi.org/10.4043/6301-ms.

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Reports on the topic "Toxicity"

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Braun, Emil, Barbara C. Levin, Maya Paabo, Joshua Gurman, Trudi Holt, and J. Samuel Steel. Fire toxicity scaling. Gaithersburg, MD: National Bureau of Standards, 1987. http://dx.doi.org/10.6028/nbs.ir.87-3510.

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Specht, Winona L. Update On Aquatic Toxicity/Whole Effluent Toxicity (WET) Issues, 2005. Office of Scientific and Technical Information (OSTI), July 2005. http://dx.doi.org/10.2172/881434.

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Park, Jiyeon, Robert T. Jeters, Gary A. Gill, Li-Jung Kuo, and George T. Bonheyo. Toxicity of Uranium Adsorbent Materials using the Microtox Toxicity Test. Office of Scientific and Technical Information (OSTI), October 2015. http://dx.doi.org/10.2172/1179520.

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Vann, Richard D. Oxygen Toxicity Risk Assessment. Fort Belvoir, VA: Defense Technical Information Center, May 1988. http://dx.doi.org/10.21236/ada299552.

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Holland, J. M. Chronic Dermal Toxicity of Epoxy Resins I. Skin Carcinogenic Potency and General Toxicity. Office of Scientific and Technical Information (OSTI), January 2001. http://dx.doi.org/10.2172/777676.

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LaHann, T. Borocaptate sodium (BSH) toxicity issues. Office of Scientific and Technical Information (OSTI), November 1995. http://dx.doi.org/10.2172/421329.

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Lahnert, Bruce E. Evaluation of NOX-Induced Toxicity. Fort Belvoir, VA: Defense Technical Information Center, December 1992. http://dx.doi.org/10.21236/ada261034.

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Haley, Mark V., Dennis W. Johnson, William T. Muse, and Wayne G. Landis. Aquatic Toxicity of Pinacolyl Alcohol. Fort Belvoir, VA: Defense Technical Information Center, September 1986. http://dx.doi.org/10.21236/ada173604.

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Schowen, Richard L., and Ildiko M. Kovach. Molecular Origins of Selective Toxicity. Fort Belvoir, VA: Defense Technical Information Center, November 1987. http://dx.doi.org/10.21236/ada219667.

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Rabalais, Lauren, Jennifer Laird, Alan Kennedy, John Farrar, Guilherme Lotufo, and James Biedenbach. Acute Toxicity Testing and Culture Methods for Calanoid Copepods in Water Column (Elutriate) Toxicity Evaluations. Environmental Laboratory (U.S.), July 2018. http://dx.doi.org/10.21079/11681/27968.

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