Radionuclides in water *
Jamie Bartram, Rachel Baum, Peter A. Coclanis, David M. Gute, David Kay, Stéphanie McFadyen, Katherine Pond, William Robertson, Michael J. Rouse in Routledge Handbook of Water and Health, 2015
Radon that is dissolved in groundwater supplies off-gasses as the water is used in the home for showering, bathing, dishwashing, etc. The U.S. National Academy of Science (NAS, 1999) estimates the transfer coefficient of radon between water and air in homes in North America is 1.0 x 10-4 (i.e., 10:000 to 1 transfer ratio). However, the transfer factor can vary significantly and does not represent short term ratios in specific rooms where the water is utilized (e.g., bathroom) (Nazaroff et al., 1987; Vinson et al., 2008). While ingestion of waterborne radon was estimated to cause approximately 20 deaths from stomach cancer in the United States in 1999 (NAS, 1999), the greatest health risk from waterborne radon is from the off-gassing of radon into the air of a building. As radon gas undergoes further decay in the air, it produces a series of solid radioactive decay products that can be inhaled (WHO, 2009). Two of the α-particle emitting decay products, polonium-218 and polonium-214, deliver the majority of the radiation dose to the lining of the lung (i.e., respiratory epithelium). The α-particles can cause changes in the cells of the lining of the lung (e.g., double strand DNA breaks, etc.) that have the potential to lead to lung cancer.
Histopathology of the Nasal Cavity in Laboratory Animals Exposed to Cigarette Smoke and Other Irritants
D. V. M. Gerd Reznik, Sherman F. Stinson in Nasal Tumors in Animals and Man, 2017
Pathogenesis identifies cigarette smoke as an irritant. Its target tissue in the nasal region is the lining respiratory epithelium. The peracute effect is a rapid degeneration of epithelium which provokes an acute inflammatory, usually suppurative, reaction. This is followed by epithelial regeneration which then progresses to hyperplasia or squamous metaplasia. This proliferative change usually resolves after removal of the insult. The two descriptions of this sequence in the nasal region, referred to above,3,53 are entirely consistent with the observations of Lam58 on the ventral epithelium of the rat larynx. The findings, after 60 min of exposure to cigarette smoke, were necrosis and inflammatory reaction followed by regeneration within 20 hr and hyperplasia between 30 and 70 hr before a return to the normal state.
Bronchus-associated lymphoid tissue and immune-mediated respiratory diseases
Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald in Principles of Mucosal Immunology, 2020
Although the respiratory epithelium has been traditionally thought to be primarily a physical barrier and a base for ciliary activity, it is now clear that respiratory epithelial epithelium has a major role in sensing the environment, maintaining homeostasis, and repairing injury. Airway epithelial cells respond to microbial challenge and environmental insults by rapidly producing an array of cytokines and growth factors that initiate innate immunity, prime adaptive immunity, and establish homeostasis. For example, airway epithelial cells respond to PAMPs associated with antigens or microbes that enter the airways, through toll-like receptors (TLRs), nucleotide-binding oligomerization domain (NOD)-like receptors, and C-type lectin receptors. Signals generated by these receptors or due to direct injury of epithelial cells induce lung epithelial cells to produce cytokines such as interleukin (IL)-1, IL-25, IL-33, thymic stromal lymphopoietin (TSLP), granulocyte-macrophage colony-stimulating factor (GM-CSF), and transforming growth factor (TGF)-β, as well as chemokines (CCL20 [MIP-3α; ligand of CCR6], CCL17 [TARC; ligand of CCR4], and CCL22 [MDC; ligand of CCR4]) and antimicrobial peptides such as defensins. Epithelial cells are also a copious source of endogenous danger signals like adenosine triphosphate (ATP), uric acid, and high mobility group box 1 (HMGB1) that can alert immune cells. Thus, epithelial cells can initiate innate immunity that can later affect adaptive mucosal immunity.
Nose to brain transport pathways an overview: potential of nanostructured lipid carriers in nose to brain targeting
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Kousalya Selvaraj, Kuppusamy Gowthamarajan, Veera Venkata Satyanarayana Reddy Karri
The nose is a complex structure. The nasal cavity is divided into three regions namely vestibule, respiratory and olfactory region. Vestibule region is not involved in the absorption functions and it is the anterior external region opening to the nasal cavity. The respiratory epithelium consists of ciliated and non-ciliated columnar cells, mucus secreting goblet cells and basal cells. The respiratory region is mainly involved in the drug absorption and the surface area of respiratory region is approximately 160 cm2 in humans. The third region is olfactory region consists of olfactory receptor cells, basal and sustentacular cells. The olfactory region has a surface area of 10 cm2. Olfactory receptor neurons are bipolar neurons involves in the transduction of information from epithelium to olfactory bulb [13]. The olfactory pathway is explained in the following section.
Biomarkers and their potential functions in idiopathic pulmonary fibrosis
Published in Expert Review of Respiratory Medicine, 2020
Shanshan Ni, Min Song, Wei Guo, Ting Guo, Qinxue Shen, Hong Peng
The respiratory epithelium is lined by mucus, a gel consisting of water, ions, proteins, and macromolecules [101]. Mucin glycoproteins, the major macromolecular components of mucus, are vital to local defense of the airway [101]. MUC5B is one of mucins in the airways, and its deficiency leads to accumulation of substances in the upper and lower airways [101,102]. The gene MUC5B plays an important role in lung host defense, an immune process influenced by oxidative signaling [103]. Locating in the promoter region of the MUC5B gene, the most widely replicated variant (rs35705950), is the strongest (at least 30% of the total) risk factor for the development of IPF [104,105,106]. MUC5B polymorphism rs35705950 might participate in IPF by increasing MUC5B expression in terminal bronchi and honeycombed cysts, and it could interfere with physiological mucosal host defense, reduce the clearance of microorganisms or inorganic harmful substances or induce endoplasmic reticulum stress, and finally, increase the risk of IPF severity, and reduce the overall survival [107,108,109].
Epithelial cell dysfunction in chronic rhinosinusitis: the epithelial–mesenchymal transition
Published in Expert Review of Clinical Immunology, 2023
Jing Yuan, Ming Wang, Chengshuo Wang, Luo Zhang
The nasal respiratory epithelium is a ciliated pseudostratified columnar epithelium, consisting of ciliated cells, goblet cells, basal cells, and non-ciliated columnar cells [7,8]. Nasal epithelial cells form the first mechanical barrier, preventing harmful substances from entering the submucosa. When the epithelium is damaged, the basal cells, which act as stem cells, proliferate and migrate to the damaged area, where they differentiate into ciliated cells or goblet cells to reconstruct epithelium to restore the barrier function [9]. In addition to the epithelial barrier, ciliated cells and goblet cells also form another effective defensive barrier known as mucociliary clearance, which traps and removes particles and gases dissolved in the mucus. Goblet cells and the submucosal plasma-secreting glands secrete large amounts of fluid to form a mucus blanket that adheres to the epithelial surface and traps pathogens and inhaled particles, whereas ciliated cells beat in metachronal waves to propel the pathogens and inhaled particles that are trapped in the mucous layer out of the airways [10,11].
Related Knowledge Centers
- Basement Membrane
- Epithelium
- Mucociliary Clearance
- Mucus
- Pharynx
- Pseudostratified Columnar Epithelium
- Respiratory Tract
- Stratified Squamous Epithelium
- Vocal Cords
- Larynx