scholarly journals Particulate matter and the airway epithelium: the special case of the underground?

2019 ◽  
Vol 28 (153) ◽  
pp. 190066 ◽  
Author(s):  
Dawn M. Cooper ◽  
Matthew Loxham
Keyword(s):  
Particulate Matter ◽  
Epithelial Cells ◽  
Airway Epithelium ◽  
Inflammatory Responses ◽  
Current Knowledge ◽  
Airborne Particulate Matter ◽  
Initial Response ◽  
Mitigation Strategies ◽  
Chronic Obstructive ◽  
Potential Health

Airborne particulate matter (PM) is a leading driver of premature mortality and cardiopulmonary morbidity, associated with exacerbations of asthma and chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, and lung cancer. The airway epithelium, as the principal site of PM deposition, is critical to the effects of, and initial response to, PM. A key mechanism by which PM exerts its effects is the generation of reactive oxygen species (ROS), inducing antioxidant and inflammatory responses in exposed epithelial cells. However, much of what is known about the effects of PM is based on research using particulates from urban air. PM from underground railways is compositionally highly distinct from urban PM, being rich in metals associated with wheel, rail and brake wear and electrical arcing and component wear, which endows underground PM with potent ROS-generating capacity. In addition, underground PM appears to be more inflammogenic than urban PM in epithelial cells, but there is a lack of research into effects on exposed individuals, especially those with underlying health conditions. This review summarises current knowledge about the effects of PM on the airway epithelium, how the effects of underground PM may be different to urban PM and the potential health consequences and mitigation strategies for commuters and workers in underground railways.

scholarly journals Overproduction of growth differentiation factor 15 promotes human rhinovirus infection and virus-induced inflammation in the lung

2018 ◽  
Vol 314 (3) ◽  
pp. L514-L527 ◽  
Author(s):  
Qun Wu ◽  
Di Jiang ◽  
Niccolette R. Schaefer ◽  
Laura Harmacek ◽  
Brian P. O’Connor ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Responses ◽  
Airway Epithelial Cells ◽  
Human Rhinovirus ◽  
Chronic Obstructive ◽  
Airway Epithelial ◽  
Growth Differentiation Factor 15 ◽  
Human Airway ◽  
Differentiation Factor ◽  
Human Airway Epithelial Cells

Human rhinovirus (HRV) is the most common virus contributing to acute exacerbations of chronic obstructive pulmonary disease (COPD) nearly year round, but the mechanisms have not been well elucidated. Recent clinical studies suggest that high levels of growth differentiation factor 15 (GDF15) protein in the blood are associated with an increased yearly rate of all-cause COPD exacerbations. Therefore, in the current study, we investigated whether GDF15 promotes HRV infection and virus-induced lung inflammation. We first examined the role of GDF15 in regulating host defense and HRV-induced inflammation using human GDF15 transgenic mice and cultured human GDF15 transgenic mouse tracheal epithelial cells. Next, we determined the effect of GDF15 on viral replication, antiviral responses, and inflammation in human airway epithelial cells with GDF15 knockdown and HRV infection. Finally, we explored the signaling pathways involved in airway epithelial responses to HRV infection in the context of GDF15. Human GDF15 protein overexpression in mice led to exaggerated inflammatory responses to HRV, increased infectious particle release, and decreased IFN-λ2/3 (IL-28A/B) mRNA expression in the lung. Moreover, GDF15 facilitated HRV replication and inflammation via inhibiting IFN-λ1/IL-29 protein production in human airway epithelial cells. Lastly, Smad1 cooperated with interferon regulatory factor 7 (IRF7) to regulate airway epithelial responses to HRV infection partly via GDF15 signaling. Our results reveal a novel function of GDF15 in promoting lung HRV infection and virus-induced inflammation, which may be a new mechanism for the increased susceptibility and severity of respiratory viral (i.e., HRV) infection in cigarette smoke-exposed airways with GDF15 overproduction.

scholarly journals Can Plant Phenolic Compounds Protect the Skin from Airborne Particulate Matter?

Antioxidants ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 379 ◽  
Author(s):  
Yong Chool Boo
Keyword(s):  
Particulate Matter ◽  
Phenolic Compounds ◽  
Skin Diseases ◽  
Inflammatory Responses ◽  
Acne Vulgaris ◽  
Experimental Studies ◽  
Airborne Particulate Matter ◽  
Skin Aging ◽  
Atmospheric Environment ◽  
Airborne Particulate

The skin is directly exposed to the polluted atmospheric environment, and skin diseases, such as atopic dermatitis and acne vulgaris, can be induced or exacerbated by airborne particulate matter (PM). PM can also promote premature skin aging with its accompanying functional and morphological changes. PM-induced skin diseases and premature skin aging are largely mediated by reactive oxygen species (ROS), and the harmful effects of PM may be ameliorated by safe and effective natural antioxidants. Experimental studies have shown that the extracts and phenolic compounds derived from many plants, such as cocoa, green tea, grape, pomegranate, and some marine algae, have antioxidant and anti-inflammatory effects on PM-exposed cells. The phenolic compounds can decrease the levels of ROS in cells and/or enhance cellular antioxidant capacity and, thereby, can attenuate PM-induced oxidative damage to nucleic acids, proteins, and lipids. They also lower the levels of cytokines, chemokines, cell adhesion molecules, prostaglandins, and matrix metalloproteinases implicated in cellular inflammatory responses to PM. Although there is still much research to be done, current studies in this field suggest that plant-derived phenolic compounds may have a protective effect on skin exposed to high levels of air pollution.

Trans-Epithelial Exposure Model (TEEM) - Epithelial Cells and Fibroblasts

2020 ◽  
Author(s):  
Shaun D. McCullough
Keyword(s):  
Particulate Matter ◽  
Epithelial Cells ◽  
Cell Line ◽  
Environmental Protection Agency ◽  
Airway Epithelium ◽  
Exposure Model ◽  
Protection Agency ◽  
The Us ◽  
Trade Names

Abstract This exposure model is meant to serve as an in vitro representation of trans-epithelial effects of airway diesel and particulate matter exposures on fibroblasts in the stroma. The epithelial cells in the airway epithelium are represented by 16HBE cells and the fibroblasts are represented by either the IMR90 cell line or primary fibroblasts.Disclaimer: The contents of this article have been reviewed by the US Environmental Protection Agency and approved for publication and do not necessarily represent Agency policy. Mention of trade names or commercial products does not constitute endorsement or recommendations for use.

scholarly journals Large global variations in measured airborne metal concentrations driven by anthropogenic sources

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jacob McNeill ◽  
Graydon Snider ◽  
Crystal L. Weagle ◽  
Brenna Walsh ◽  
Paul Bissonnette ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Transport Model ◽  
Anthropogenic Activities ◽  
Ambient Air ◽  
Mitigation Strategies ◽  
Anthropogenic Sources ◽  
World Health ◽  
Risk Level ◽  
Potential Health ◽  
Metal Concentrations

AbstractGlobally consistent measurements of airborne metal concentrations in fine particulate matter (PM2.5) are important for understanding potential health impacts, prioritizing air pollution mitigation strategies, and enabling global chemical transport model development. PM2.5 filter samples (N ~ 800 from 19 locations) collected from a globally distributed surface particulate matter sampling network (SPARTAN) between January 2013 and April 2019 were analyzed for particulate mass and trace metals content. Metal concentrations exhibited pronounced spatial variation, primarily driven by anthropogenic activities. PM2.5 levels of lead, arsenic, chromium, and zinc were significantly enriched at some locations by factors of 100–3000 compared to crustal concentrations. Levels of metals in PM2.5 and PM10 exceeded health guidelines at multiple sites. For example, Dhaka and Kanpur sites exceeded the US National Ambient Air 3-month Quality Standard for lead (150 ng m−3). Kanpur, Hanoi, Beijing and Dhaka sites had annual mean arsenic concentrations that approached or exceeded the World Health Organization’s risk level for arsenic (6.6 ng m−3). The high concentrations of several potentially harmful metals in densely populated cites worldwide motivates expanded measurements and analyses.

scholarly journals Contribution of Lung Macrophages to the Inflammatory Responses Induced by Exposure to Air Pollutants

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Kunihiko Hiraiwa ◽  
Stephan F. van Eeden
Keyword(s):  
Bone Marrow ◽  
Particulate Matter ◽  
Epithelial Cells ◽  
Air Pollutants ◽  
Inflammatory Responses ◽  
Vascular System ◽  
Large Population ◽  
Lung Epithelial Cells ◽  
Lung Macrophages ◽  
Proinflammatory Mediators

Large population cohort studies have indicated an association between exposure to particulate matter and cardiopulmonary morbidity and mortality. The inhalation of toxic environmental particles and gases impacts the innate and adaptive defense systems of the lung. Lung macrophages play a critically important role in the recognition and processing of any inhaled foreign material such as pathogens or particulate matter. Alveolar macrophages and lung epithelial cells are the predominant cells that process and remove inhaled particulate matter from the lung. Cooperatively, they produce proinflammatory mediators when exposed to atmospheric particles. These mediators produce integrated local (lung, controlled predominantly by epithelial cells) and systemic (bone marrow and vascular system, controlled predominantly by macrophages) inflammatory responses. The systemic response results in an increase in the release of leukocytes from the bone marrow and an increased production of acute phase proteins from the liver, with both factors impacting blood vessels and leading to destabilization of existing atherosclerotic plaques. This review focuses on lung macrophages and their role in orchestrating the inflammatory responses induced by exposure to air pollutants.

scholarly journals Variations in Reactive Oxygen Species Generation by Urban Airborne Particulate Matter in Lung Epithelial Cells—Impact of Inorganic Fraction

2020 ◽  
Vol 8 ◽  
Author(s):  
Olga Mazuryk ◽  
Grazyna Stochel ◽  
Małgorzata Brindell
Keyword(s):  
Reactive Oxygen Species ◽  
Air Pollution ◽  
Particulate Matter ◽  
Epithelial Cells ◽  
A549 Cells ◽  
Reactive Oxygen ◽  
Airborne Particulate Matter ◽  
Oxygen Species ◽  
Airborne Particulate ◽  
Inorganic Fraction

Air pollution is associated with numerous negative effects on human health. The toxicity of organic components of air pollution is well-recognized, while the impact of their inorganic counterparts in the overall toxicity is still a matter of various discussions. The influence of airborne particulate matter (PM) and their inorganic components on biological function of human alveolar-like epithelial cells (A549) was investigated in vitro. A novel treatment protocol based on covering culture plates with PM allowed increasing the studied pollutant concentrations and prolonging their incubation time without cell exposure on physical suffocation and mechanical disturbance. PM decreased the viability of A549 cells and disrupted their mitochondrial membrane potential and calcium homeostasis. For the first time, the difference in the reactive oxygen species (ROS) profiles generated by organic and inorganic counterparts of PM was shown. Singlet oxygen generation was observed only after treatment of cells with inorganic fraction of PM, while hydrogen peroxide, hydroxyl radical, and superoxide anion radical were induced after exposure of A549 cells to both PM and their inorganic fraction.

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