1,721,031 research outputs found
Controlling PM by proxy? International regulation of sulphur and PM emissions from shipping
Ships are major contributors to global emissions of air pollutants, with their health and environmental effects being of particular concern in port cities and heavily populated coastal areas adjacent to major shipping lanes. This paper outlines the international regulations tackling two such ship pollutants, being sulphur dioxide (SOx) and particulate matter (PM). In order to understand the current regulatory strategy, it reviews the health and environmental impact of these emissions. The paper then addresses the 2020 sulphur cap on marine fuel imposed by MARPOL and its potential efficacy in reducing the health and environmental effects of shipping emissions. Examples of differing regional and national regulation of sulphur and PM are presented and discussed. The paper questions whether the current international regulatory framework directed at reducing sulphur emissions from ships is an appropriate means to reduce PM emissions
Particulate matter and the airway epithelium – the special case of the underground?
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. Underground PM also 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
The potential health effects of transition metals in particulate air pollution
Background: Inhaled air contains myriad potential toxicants, which vary by source and site. These may include particulate matter (PM) containing transition metals, polyaromatic hydrocarbons and soot, aeroallergens, and pathogens. Different toxicants exert their deleterious effects via a variety of mechanisms, and may also differentially affect individuals depending on other factors such as the presence of disease.Methods: Size-fractionated airborne particulate matter (10-2.5 µm, <2.5 µm, <0.18 µm) was collected at a busy mainline underground railway station. PM composition was analysed by inductively-coupled plasma mass spectrometry alongside comparator PM samples from a woodstove, roadwear simulator, and road tunnel. Underground railway PM-mediated generation of reactive oxygen species (ROS) was measured using dichlorofluorescein. Primary bronchial epithelial cells (PBECs) were cultured as monolayers and differentiated air-liquid interface (ALI) cultures before exposure to underground railway PM for 24 h. IL-8 release, barrier integrity, and antioxidant gene expression were assayed. Intracellular PM was studied by transmission EM. As a separate PM type, the effects of the allergenic fungus Alternaria alternata on PBECs were similarly examined, and interactions with underground railway PM were studied.Results: Underground PM was metal-rich, especially iron, and generated ROS in a concentration-, size-, and iron-dependent manner. PBEC monolayer cultures showed a moderate PM concentration-dependent increase in IL-8 release without LDH release, but this was absent in ALI cultures. There was observable intracellular PM 24 h post-challenge in ALI cultures, and an upregulation of antioxidant genes (HO-1, NQO1) which could be diminished by DFX and NAC. Alternaria extract induced a significant and marked concentration-dependent increase in IL-8 release and a drop in transepithelial electrical resistance (TER), predominantly due to a heat-labile serine protease. Alternaria extract appeared to have more pronounced effects on cells pre-treated with underground railway PM, but this was independent of a heat-labile component.Conclusion: Metal-rich underground railway PM potently generates ROS, with modest pro-inflammatory effects and a marked induction of antioxidant defences. The potential effects of PM entry into cells merits further study. The novel metal-rich nature of such an environmental ultrafine PM warrants further work in light of its high surface area/volume ratio and potential ability to penetrate into the alveoli and possibly the systemic circulation Additionally, the ability of underground railway PM to generate ROS potently suggests that individuals with defective antioxidant defences, such as seen in asthmatic airways, may be at heightened risk of the effects of metal-rich PM, as may those concomitantly exposed to airborne fungi
The health effects of fine particulate air pollution: The harder we look, the more we find
Phenotypic and genetic aspects of epithelial barrier function in asthmatic patients
The bronchial epithelium is continuously exposed to a multitude of noxious challenges in inhaled air. Cellular contact with most damaging agents is reduced by the action of the mucociliary apparatus and by formation of a physical barrier that controls passage of ions and macromolecules. In conjunction with these defensive barrier functions, immunomodulatory cross-talk between the bronchial epithelium and tissue-resident immune cells controls the tissue microenvironment and barrier homeostasis. This is achieved by expression of an array of sensors that detect a wide variety of viral, bacterial, and nonmicrobial (toxins and irritants) agents, resulting in production of many different soluble and cell-surface molecules that signal to cells of the immune system. The ability of the bronchial epithelium to control the balance of inhibitory and activating signals is essential for orchestrating appropriate inflammatory and immune responses and for temporally modulating these responses to limit tissue injury and control the resolution of inflammation during tissue repair. In asthmatic patients abnormalities in many aspects of epithelial barrier function have been identified. We postulate that such abnormalities play a causal role in immune dysregulation in the airways by translating gene-environment interactions that underpin disease pathogenesis and exacerbation
Health effects of particulate matter air pollution in underground railway systems – A critical review of the evidence
BackgroundExposure to ambient airborne particulate matter is a major risk factor for mortality and morbidity, associated with asthma, lung cancer, heart disease, myocardial infarction, and stroke, and more recently type 2 diabetes, dementia and loss of cognitive function. Less is understood about differential effects of particulate matter from different sources. Underground railways are used by millions of people on a daily basis in many cities. Poor air exchange with the outside environment means that underground railways often have an unusually high concentration of airborne particulate matter, while a high degree of railway-associated mechanical activity produces particulate matter which is physicochemically highly distinct from ambient particulate matter. The implications of this for the health of exposed commuters and employees is unclear.Main bodyA literature search found 27 publications directly assessing the potential health effects of underground particulate matter, including in vivo exposure studies, in vitro toxicology studies, and studies of particulate matter which might be similar to that found in underground railways. The methodology, findings, and conclusions of these studies were reviewed in depth, along with further publications directly relevant to the initial search results. In vitro studies suggest that underground particulate matter may be more toxic than exposure to ambient/urban particulate matter, especially in terms of endpoints related to reactive oxygen species generation and oxidative stress. This appears to be predominantly a result of the metal-rich nature of underground particulate matter, which is suggestive of increased health risks. However, while there are measureable effects on a variety of endpoints following exposure in vivo, there is a lack of evidence for these effects being clinically significant as may be implied by the in vitro evidenceConclusionThere is little direct evidence that underground railway PM exposure is more harmful than ambient PM exposure. This may be due to disparities between in vivo exposures and in vitro models, and differences in exposure doses, as well as statistical underpowering of in vivo studies of chronic exposure. Future research should focus on outcomes of chronic in vivo exposure, as well as further work to understand mechanisms and potential biomarkers of exposure
Simulation of outdoor air pollution in Southampton
The city of Southampton is committed to monitoring and reducing outdoor air pollution, in particular, Nitrogen Dioxide (NO2) and Particulate Matters (PM2.5/PM10), which have been linked with adverse health effects under short- or long-term exposure. This project investigates the air pollution contributed mainly by road sources, which consist of major and minor roads in Southampton, by using Atmospheric Dispersion Modelling Software (ADMSRoads), and provides further understanding on the air pollution contributions based on qualitative and quantitative analysis. The model was validated by comparing the modelled concentration with the observed data from the Southampton AURN pollution monitoring station. This study has found out that although the simulation exhibits a tendency to underpredict pollution concentrations, the dynamics of the model were relatively promising as it managed to capture the trends over time of the concentration of air pollutants relatively consistently. Therefore, future improvements to the model may be made by applying correction factors to overcome the bias offset to obtain more realistic predictions of air quality. The simulation has also correctly predicted poorer air quality within the Air Quality Management Areas (AQMA) declared by Southampton City Council (SCC), which implies that road sources have a notable contribution towards the air pollution. The advantages of this model are that it can be quickly altered to predict response to future policy actions and that it has sufficient resolution to be used for epidemiological studies linking air pollution with the prevalence of health conditions in the city. The findings so far indicate that further pollution control measures are still warranted as most of the pollutant concentrations from road sources exceed the latest (2021) WHO air quality guidelines developed to protect public health from effects of exposure to air pollutants
Epithelial function and dysfunction in asthma
Asthma was previously defined as an allergic Th2‐mediated inflammatory immune disorder. Recently, this paradigm has been challenged because not all pathological changes observed in the asthmatic airways are adequately explained simply as a result of Th2‐mediated processes. Contemporary thought holds that asthma is a complex immune disorder involving innate as well as adaptive immune responses, with the clinical heterogeneity of asthma perhaps a result of the different relative contribution of these two systems to the disease. Epidemiological studies show that exposure to certain environmental substances is strongly associated with the risk of developing asthma. The airway epithelium is first barrier to interact with, and respond to, environmental agents (pollution, viral infection, allergens), suggesting that it is a key player in the pathology of asthma. Epithelial cells play a key role in the regulation of tissue homeostasis by the modulation of numerous molecules, from antioxidants and lipid mediators to growth factors, cytokines, and chemokines. Additionally, the epithelium is also able to suppress mechanisms involved in, for example, inflammation in order to maintain homeostasis. An intrinsic alteration or defect in these regulation mechanisms compromises the epithelial barrier, and therefore, the barrier may be more prone to environmental substances and thus more likely to exhibit an asthmatic phenotype. In support of this, polymorphisms in a number of genes that are expressed in the bronchial epithelium have been linked to asthma susceptibility, while environmental factors may affect epigenetic mechanisms that can alter epithelial function and response to environmental insults. A detailed understanding of the regulatory role of the airway epithelium is required to develop new therapeutic strategies for asthma that not only address the symptoms but also the underlining pathogenic mechanism(s) and prevent airway remodelling.<br/
Particulate air pollution on London Underground: health effects
COMEAP statement on the evidence of health effects on the travelling public from exposure to particulate matter in the London Underground
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