Outdoor Air Pollution and Childhood Respiratory Disease: The Role of Oxidative Stress (original) (raw)

Oxidative Stress and Air Pollution: Its Impact on Chronic Respiratory Diseases

International Journal of Molecular Sciences

Redox regulation participates in the control of various aspects of metabolism. Reactive oxygen and nitrogen species participate in many reactions under physiological conditions. When these species overcome the antioxidant defense system, a distressed status emerges, increasing biomolecular damage and leading to functional alterations. Air pollution is one of the exogenous sources of reactive oxygen and nitrogen species. Ambient airborne particulate matter (PM) is important because of its complex composition, which includes transition metals and organic compounds. Once in contact with the lungs’ epithelium, PM components initiate the synthesis of inflammatory mediators, macrophage activation, modulation of gene expression, and the activation of transcription factors, which are all related to the physiopathology of chronic respiratory diseases, including cancer. Even though the pathophysiological pathways that give rise to the development of distress and biological damage are not full...

Air Pollution and Child Respiratory Health

American Journal of Respiratory and Critical Care Medicine, 2005

Rationale. The strength of the association between outdoor air pollution and hospital admissions in children has not yet been well defined.

Role of air pollutants mediated oxidative stress in respiratory diseases

Pediatric Allergy and Immunology, 2022

Airborne particulate (PM) components, especially those deriving from anthropogenic activities such as the combustion of fossil fuels, can induce oxidative stress triggered by reactive oxygen species (ROS). The reported associations between asthma morbidity and exposure to air pollutants, mainly PM 2.5, could be related to the oxidative potential of PM capable of inducing oxidative stress and airways inflammation, which are the hallmarks of asthma disease. 1 However, the oxidative potential of PM may be, in part, independent of the PM mass. Therefore, a potentially small fraction of chemical components can even produce the same effects. Many aerosol components have redox activities (e.g., polycyclic aromatic hydrocarbons (IPA), transition metals), and epidemiological associations can be influenced if the analyzes are based only on mass concentrations and not on the chemical characterization of PM2.5 and/or of PM10. Few studies have addressed this possibility by characterizing the overall oxidative potential of PM2.5 and correlating it with daily changes in fractional exhaled nitric oxide (FENO), which is a pivotal biomarker of airway inflammation in children with asthma. 2 One of the most used methods to evaluate the oxidative potential of PM components in acellular mode is the dithiothreitol (DTT) assay. DTT assay is used to demonstrate the ability of PM to transfer electrons from the DTT to oxygen, resulting in the generation of superoxide. DTT is an indicator of redox activity, positively correlated to the content of IPA, organic carbon (OC), metals, and partially inhibited by metal chelators. 3 DTT consumption is highest in ultrafine PM (<0.15 µm) and combustion sources of organic chemicals and transition metals, which have a high oxidative potential. The intracellular response to exposure to PMs with high OP (oxidative potential) consists in the production of ROS, with the parallel activation of signals for the synthesis of pro-inflammatory cytokines, determining an

Airway inflammation and oxidative potential of air pollutant particles in a pediatric asthma panel

Journal of Exposure Science and Environmental Epidemiology, 2013

Airborne particulate matter (PM) components from fossil fuel combustion can induce oxidative stress initiated by reactive oxygen species (ROS). Reported associations between worsening asthma and PM 2.5 mass could be related to PM oxidative potential to induce airway oxidative stress and inflammation (hallmarks of asthma pathology). We followed 45 schoolchildren with persistent asthma in their southern California homes daily over 10 days with offline fractional exhaled nitric oxide (FE NO), a biomarker of airway inflammation. Ambient exposures included daily average PM 2.5 , PM 2.5 elemental and organic carbon (EC, OC), NO 2 , O 3 , and endotoxin. We assessed PM 2.5 oxidative potential using both an abiotic and an in vitro bioassay on aqueous extracts of daily particle filters: (1) dithiothreitol (DTT) assay (abiotic), representing chemically produced ROS; and (2) ROS generated intracellularly in a rat alveolar macrophage model using the fluorescent probe 2 0 7 0-dicholorohidroflourescin diacetate. We analyzed relations of FE NO to air pollutants in mixed linear regression models. FE NO was significantly positively associated with lag 1-day and 2-day averages of traffic-related markers (EC, OC, and NO 2), DTT and macrophage ROS, but not PM 2.5 mass. DTT associations were nearly twice as strong as other exposures per interquartile range: median FE NO increased 8.7-9.9% per 0.43 nmole/min/m 3 DTT. Findings suggest that future research in oxidative stress-related illnesses such as asthma and PM exposure would benefit from assessments of PM oxidative potential and composition.

Air pollution and childhood asthma: recent advances and future directions

Current Opinion in Pediatrics, 2009

Purpose of review-Current levels of air pollution are consistently associated with asthma development and morbidity among children, suggesting that current regulatory policies may be insufficient. This review will describe recent studies that have examined specific emission sources or components of pollutants that may be associated with pediatric asthma and identify subpopulations that may be particularly susceptible to the effects of air pollution exposure.

What impact of air pollution in pediatric respiratory allergic diseases

Pediatric Allergy and Immunology, 2020

The problem of respiratory allergies concerns about 40% of the world population, with a significant impact on the quality of life for those who suffer from it. The most common clinical manifestations are allergic rhinoconjunctivitis and asthma, determined by genetic and environmental factors that can alter lung development in children and adolescents. Air pollution has a significant responsibility in this. 1 Among the main pollutants are certainly PM10 (particulate matter) with an aerodynamic diameter of 10 µm and <2.5 µm (PM2.5) and ultrafine particulate matter (UFP), which are particles <0.1 µm. 2 European legislation has set the "recommended" maximum concentration levels at 50 and 25 µg/ m 3 for the annual average, respectively, for PM10 and PM2.5. The particulates are produced from anthropogenic sources such as traffic, combustion processes, and industrial gas activities, and from natural sources, such as marine spray, crustal minerals, and forest fires. It also has a secondary component that is formed in the atmosphere and which, especially in the urban area, constitutes a significant fraction. Dimensions, surface, and composition of the polluting particle determine the potential risk for a patient who is exposed regularly. 3-5 Early exposure, in gestational or neonatal times, for example, can trigger epigenetic mechanisms, such as DNA methylation and oxidative stress, which increase the risk of adverse outcomes at birth and the subsequent development of asthma and allergic rhinitis. 6 Another powerful

EXPOSURE TO AIR POLLUTION AND RESPIRATORY DISORDERS: AN OVERVIEW

Air pollution continues to pose a significant threat to health worldwide. According to a WHO assessment of the burden of disease due to air pollution, more than two million premature deaths each year can be attributed to the effects of urban outdoor air pollution and indoor air pollution ( from the burning of solid fuels). More than half of this disease burden is borne by the populations of developing countries.Scientific studies conducted during last sixty years have provided sufficient evidence to establish a correlation between exposure to air pollutants and the developing of severe respiratory disorders. When we breathe in dirty air, we bring air pollutants deep into our lungs, thus air pollution causes serious damage to the respiratory tract. Air pollution exposure can trigger new cases of asthma, exacerbate (worsen) a previously existing respiratory illness, and provoke development or progression of chronic illnesses including lung cancer, chronic bronchitis, chronic obstructive pulmonary disease, and emphysema. Air pollution is a complex mix of gases and particles. It has been seen that five pollutants generally account for 98 percent of air pollution which are carbon monoxide (CO), sulfur oxides, hydrocarbons, particulate matter , nitrogen oxides. Air pollutants enter the body predominantly through the lungs. Some of these chemicals are absorbed into the blood and some that are not absorbed are eliminated by the lungs and some are retained. Gaseous pollutants disseminate deeply into the alveoli, allowing its diffusion through the blood-air barrier to several organs. The site of deposition of aerosols in the respiratory tract depends on the size of the particle. Many particles are irregular in shape. There are a number of ways to delineate particle size or behavior like aerodynamic diameter, mass mean etc. Particulate matter ( PM ) is a mix of solid or liquid particles suspended in the air. Particulate matter is deposited at different levels of the respiratory tract, depending on its size: coarse particles (PM ) in upper airways and fine particles 10 (PM ) can be accumulated in the lung parenchyma, inducing several respiratory diseases.

Immunopathological features of air pollution and its impact on inflammatory airway diseases (IAD)

World Allergy Organization Journal, 2020

Air pollution causes significant morbidity and mortality in patients with inflammatory airway diseases (IAD) such as allergic rhinitis (AR), chronic rhinosinusitis (CRS), asthma, and chronic obstructive pulmonary disease (COPD). Oxidative stress in patients with IAD can induce eosinophilic inflammation in the airways, augment atopic allergic sensitization, and increase susceptibility to infection. We reviewed emerging data depicting the involvement of oxidative stress in IAD patients. We evaluated biomarkers, outcome measures and immunopathological alterations across the airway mucosal barrier following exposure, particularly when accentuated by an infectious insult.