Log in

Relevant bibliographies by topics / ENVIRONMENTAL EXPOSURE PATHWAY / Books

To see the other types of publications on this topic, follow the link: ENVIRONMENTAL EXPOSURE PATHWAY.

Books on the topic 'ENVIRONMENTAL EXPOSURE PATHWAY'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 18 books for your research on the topic 'ENVIRONMENTAL EXPOSURE PATHWAY.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse books on a wide variety of disciplines and organise your bibliography correctly.

1

Jensen, Per Hedemann. Atmospheric dispersion and environmental consequences: Exposure from radioactive plume pathways. Roskilde: Risø National Laboratory, 1992.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

2

Meeker, John D. Occupational and Environmental Hygiene. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190662677.003.0008.

Full text

Abstract:

This chapter covers occupational and environmental hygiene principles and their application. This information is vital to understanding and preventing hazardous exposures and associated adverse health effects, among workers and the general population. The chapter addresses anticipation, recognition, evaluation, and control of hazards, including toxic materials, noise, ionizing and non-ionizing radiation, air pollution, water contamination, and related topics. Illustrative examples of these topics are described, such as common industrial processes that may result in exposure to hazardous agents, important exposure pathways, strategies to characterize exposure, the hierarchy of exposure control strategies, and known sources of environmental contaminants of concern. The chapter also includes lists of resources that provide additional information on relevant topics of interest.

APA, Harvard, Vancouver, ISO, and other styles

3

1962-, Harrad Stuart, ed. Persistent organic pollutants: Environmental behaviour and pathways of human exposure. Boston, Mass: Kluwer Academic Publishers, 2001.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

4

Persistent Organic Pollutants: Environmental Behaviour and Pathways of Human Exposure. Springer, 2011.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

5

Weil, Andrew. Integrative Environmental Medicine. Edited by Aly Cohen and Frederick S. vom Saal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190490911.001.0001.

Full text

Abstract:

Integrative Environmental Medicine looks at the history and changing landscape of environmental issues in the United States, including water supply, air quality, extensive plastic pollution, harmful chemicals in cleaning and personal care products, radiofrequency radiation, food additives, pesticides, and medications. The unique properties of compounds such as endocrine-disrupting chemicals are explored along with their ability to disturb the body’s normal signaling pathways, genetic profile, and gut microbiome. Resulting molecular derangements promote thyroid and other autoimmune diseases, diabetes, cardiovascular disease, cancer, and influence developmental problems in children. Analysis of current research identifies ways to reduce exposures and health risks, improve regulations and appropriate testing for chemicals, remediate environmental pollution, and design healthier products for the future. Best practices are considered for clinicians to ascertain exposure history, test for toxins, and teach patients how to avoid harmful exposures. Patients will be prepared and empowered with information about healthier food choices and cooking practices, appropriate supplement use, water filtration, cleaning and personal care product selection, improved sleep, stress reduction, sauna, fasting, chelation, safe cell phone use, and other means of reducing harmful environmental exposures. Solutions at every level require interdisciplinary collaboration to advance assessment, design, stewardship, and regulation of chemicals to promote environmental and human health.

APA, Harvard, Vancouver, ISO, and other styles

6

Lewis, Myles, and Tim Vyse. Genetics of connective tissue diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0042.

Full text

Abstract:

The advent of genome-wide association studies (GWAS) has been an exciting breakthrough in our understanding of the genetic aetiology of autoimmune diseases. Substantial overlap has been found in susceptibility genes across multiple diseases, from connective tissue diseases and rheumatoid arthritis (RA) to inflammatory bowel disease, coeliac disease, and psoriasis. Major technological advances now permit genotyping of millions of single nucleotide polymorphisms (SNPs). Group analysis of SNPs by haplotypes, aided by completion of the Hapmap project, has improved our ability to pinpoint causal genetic variants. International collaboration to pool large-scale cohorts of patients has enabled GWAS in systemic lupus erythematosus (SLE), systemic sclerosis and Behçet's disease, with studies in progress for ANCA-associated vasculitis. These 'hypothesis-free' studies have revealed many novel disease-associated genes. In both SLE and systemic sclerosis, identified genes map to known pathways including antigen presentation (MHC, TNFSF4), autoreactivity of B and T lymphocytes (BLK, BANK1), type I interferon production (STAT4, IRF5) and the NFκ‎B pathway (TNIP1). In SLE alone, additional genes appear to be involved in dysregulated apoptotic cell clearance (ITGAM, TREX1, C1q, C4) and recognition of immune complexes (FCGR2A, FCGR3B). Future developments include whole-genome sequencing to identify rare variants, and efforts to understand functional consequences of susceptibility genes. Putative environmental triggers for connective tissue diseases include infectious agents, especially Epstein-Barr virus; cigarette smoking; occupational exposure to toxins including silica; and low vitamin D, due to its immunomodulatory effects. Despite numerous studies looking at toxin exposure and connective tissue diseases, conclusive evidence is lacking, due to either rarity of exposure or rarity of disease.

APA, Harvard, Vancouver, ISO, and other styles

7

Cohen, Aly. Proactive Approaches to Reduce Environmental Exposures. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190490911.003.0014.

Full text

Abstract:

This chapter gives healthcare providers recommendations and tools to help patients mitigate exposure to harmful environmental chemicals, radiation, and other stressors; limiting contact and maximizing innate biological detoxification pathways through the safe use of exercise, diet, and appropriate supplements. Of particular concern are the vulnerable periods of biological development, when harmful chemicals can have the most deleterious effects. Therefore, particular attention is paid to the care of young children and pregnant women. Whether chemical exposure comes from food additives and food packaging, water, personal care and cleaning products, air contamination, or radiation, this chapter gives clear, practical, and safe recommendations for chemical reduction and embraces the precautionary principle when there is evidence of harm, but proof of causality, a very high standard, has not been established. The current approach of only regulating products after there is certainty of human harm has failed to protect the public health.

APA, Harvard, Vancouver, ISO, and other styles

8

Laumbach, Robert, and Michael Gochfeld. Toxicology. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190662677.003.0007.

Full text

Abstract:

This chapter describes the basic principles of toxicology and their application to occupational and environmental health. Topics covered include pathways that toxic substances may take from sources in the environment to molecular targets in the cells of the body where toxic effects occur. These pathways include routes of exposure, absorption into the body, distribution to organs and tissues, metabolism, storage, and excretion. The various types of toxicological endpoints are discussed, along with the concepts of dose-response relationships, threshold doses, and the basis of interindividual differences and interspecies differences in response to exposure to toxic substances. The diversity of cellular and molecular mechanisms of toxicity, including enzyme induction and inhibition, oxidative stress, mutagenesis, carcinogenesis, and teratogenesis, are discussed and the chapter concludes with examples of practical applications in clinical evaluation and in toxicity testing.

APA, Harvard, Vancouver, ISO, and other styles

9

United States. Environmental Protection Agency. Office of Pesticide Programs, ed. ANALYSIS OF PATHWAYS OF RESIDENTIAL LEAD EXPOSURE IN CHILDREN... U.S. ENVIRONMENTAL PROTECTION AGENCY... DECEMBER 2000. [S.l: s.n., 2001.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

10

Lippmann, Morton, and Richard B. Schlesinger. Effects of Contaminants on Human Health. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190688622.003.0006.

Full text

Abstract:

This chapter describes the methodology used for evaluating potential human health effects resulting from exposure to environmental chemicals. It discusses the concept of the dose-response relationship, and reviews the processes by which chemicals may be delivered to and absorbed by the body. Concepts of the metabolic transformation of absorbed chemical are provided, as are the potential for storage and excretion. It explores the biological mechanisms and pathways underlying specific responses to chemical contaminants, which range from disruption of physiology to alteration of biochemical pathways and hereditary material. A discussion of responses due to exposure to mixtures of chemicals is provided.

APA, Harvard, Vancouver, ISO, and other styles

11

R, Berry Maurice, National Exposure Research Laboratory (U.S.). Microbiological and Chemical Exposure Assessment Research Division., and National Exposure Research Laboratory (U.S.). Human Exposure and Atmospheric Sciences Division., eds. Draft protocol for measuring children's non-occupational exposure to pesticides by all relevant pathways. Research Triangle Park, NC: National Exposure Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, 2001.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

12

Draft protocol for measuring children's non-occupational exposure to pesticides by all relevant pathways. Research Triangle Park, NC: National Exposure Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, 2001.

Find full text

APA, Harvard, Vancouver, ISO, and other styles

13

Naidu, Ravi, Euan Smith, Gary Owens, Prosun Bhattacharya, and Peter Nadebaum. Managing Arsenic in the Environment. CSIRO Publishing, 2006. http://dx.doi.org/10.1071/9780643093515.

Full text

Abstract:

Arsenic is one of the most toxic and carcinogenic elements in the environment. This book brings together the current knowledge on arsenic contamination worldwide, reviewing the field, highlighting common themes and pointing to key areas needing future research. Contributions discuss methods for accurate identification and quantification of individual arsenic species in a range of environmental and biological matrices and give an overview of the environmental chemistry of arsenic. Next, chapters deal with the dynamics of arsenic in groundwater and aspects of arsenic in soils and plants, including plant uptake studies, effects on crop quality and yield, and the corresponding food chain and human health issues associated with these exposure pathways. These concerns are coupled with the challenge to develop efficient, cost effective risk management and remediation strategies: recent technological advances are described and assessed, including the use of adsorbants, photo-oxidation, bioremediation and electrokinetic remediation. The book concludes with eleven detailed regional perspectives of the extent and severity of arsenic contamination from around the world. It will be invaluable for arsenic researchers as well as environmental scientists and environmental chemists, toxicologists, medical scientists, and statutory authorities seeking an in-depth view of the issues surrounding this toxin.

APA, Harvard, Vancouver, ISO, and other styles

14

Barr, Christina S. Gene-by-Environment Interactions in Primates. Edited by Turhan Canli. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.006.

Full text

Abstract:

Because of their complex social structures, behaviors, and genetic similarities to humans, nonhuman primates are useful for studying how genetic factors influence alcohol consumption. The neurobiological systems that influence addiction vulnerability may do so by acting on alcohol response, reward pathways, behavioral dyscontrol, and vulnerability to stress and anxiety. Rhesus macaques show individual differences in alcohol response and temperament, and such differences are influenced by genetic variants that are similar functionally to those present in humans. Genes in which variation moderates these phenotypes provide opportunities for modeling how genetic and environmental factors (i.e., stress exposure, individual’s sex, or alcohol response) interact to influence alcohol consumption. Studies in primates may also reveal selective factors that have driven maintenance or fixation of alleles that increase risk for alcohol use disorders in modern humans.

APA, Harvard, Vancouver, ISO, and other styles

15

Huang, Ruili, and Menghang Xia, eds. Tox21 Challenge to Build Predictive Models of Nuclear Receptor and Stress Response Pathways as Mediated by Exposure to Environmental Toxicants and Drugs. Frontiers Media SA, 2017. http://dx.doi.org/10.3389/978-2-88945-197-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Merriman, Tony R. The genetic basis of gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0040.

Full text

Abstract:

An individual’s risk of gout is determined by a complex relationship between inherited genetic variants and environmental exposures. Genetic variants that control hyperuricaemia and subsequent progression to clinical gout specify pathogenic pathways that could be therapeutically targeted. Genome-wide association studies (GWAS) have provided novel insights into the pathways leading to hyperuricaemia. GWAS have identified the renal uric acid transporter SLC2A9/GLUT9 and the gut excretory molecule ABCG2, which each have very strong genetic effects in the control of urate levels and risk of gout. Histone deacetylase inhibitors are able to correct the genetically-determined ABCG2 dysfunction. Other renal uric acid transporters, such as SLC22A11/OAT4 and SLC22A12/URAT1 have been confirmed to be genetically associated with urate and the risk of gout. Genes that generate urate during glycolysis (e.g. GCKR) are also implicated. In contrast very little is known about genetic variants that control the progression from hyperuricaemia to gout with the toll-like receptor 4 gene being the only gene with replicated evidence of association.

APA, Harvard, Vancouver, ISO, and other styles

17

Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.

Full text

Abstract:

The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.

APA, Harvard, Vancouver, ISO, and other styles

18

Tillema, Jan-Mendelt, J. Graves, L. A. Benson, G. S. Aaen, A. Belman, J. Parrish, B. Weinstock-Guttman, L. Krupp, T. Chitnis, and E. Wauban. Pediatric Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0022.

Full text

Abstract:

Increased interest in pediatric-onset multiple sclerosis (MS) has contributed to improved knowledge of the presentation and evolution of central nervous system demyelinating diseases in childhood. This chapter reviews the unique features and challenges related to pediatric MS. The close proximity of pediatric MS to the biological onset of the disease provides a unique window into disease pathogenesis at stages of life when innate and adaptive immune pathways are still maturing. It is expected that the interplay between genetics, epigenetics, environmental exposures, and the maturing central nervous system in children with MS will provide important insights into the earliest phases of the disease. This chapter reviews the unique features that distinguish pediatric patients with MS from their adult counterparts. Specific emphasis is placed on the work-up and management of these patients in the context of current knowledge.

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!