Special Issue "Molecular Basis of Air-Pollution-Induced Disease Risk"

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Toxicology".

Deadline for manuscript submissions: closed (30 June 2021).

Special Issue Editors

Prof. Dr. Andrij Holian
E-Mail Website
Guest Editor
University of Montana Missoula, Department of Biomedical and Pharmaceutical Sciences, Missoula, MT 59812, USA
Interests: nanoparticles; particulate matter; asbestos; silica; alveolar macrophages; innate immunity; NLRP3 inflammasome; macrophage receptors; lysosomes
Special Issues and Collections in MDPI journals
Dr. Luke Montrose
E-Mail
Guest Editor
Department of Community and Environmental Health, Boise State University, 950 Lusk Street, Boise, ID 83725-1835, USA
Interests: DNA methylation; epigenetics; toxicoepigenetics; pyrosequencing; wood smoke; wildland firefighters; asthma; COPD; air pollution; environmental toxicology

Special Issue Information

Dear Colleagues,

Air pollution is a nondiscriminatory toxicant capable of traveling from exhausts, stacks, and forest fires to communities both near and far from the original source. Made up of both gases and liquids, air pollutants exist as mixtures of hundreds of substances, including ozone, nitrogen dioxide, carbon monoxide, particulate matter, polycyclic aromatic hydrocarbons, and many different volatile organic compounds. The toxicity of an air pollution particle—a mixture of solid and liquid droplets—is dependent on its size, source, and interaction with the environment. Acute impacts of air pollution such as increased respiratory symptoms and decreased lung function are well documented, but increasingly, air pollution exposure has been associated with chronic disease risk. While the causal drivers of air pollution’s influence on diseases such as cancer, cardiovascular disease, respiratory disease, and dementias remain to be fully elucidated, mechanistic evidence points to a number of key players, including inflammation, oxidative stress, and epigenetics.

This Special Issue invites papers focusing on plausible molecular mechanisms, whereby air pollutants influence disease risk and progression. In vivo and in vitro studies will be considered, as well as studies that investigate single-source and mixtures of air pollutants. For the purposes of this Special Issue, we define epigenetic modifications as DNA methylation, posttranslational histone tail modifications, chromatin accessibility, and noncoding RNA. Submissions may include original research articles or comprehensive reviews.

Prof. Dr. Andrij Holian
Dr. Luke Montrose
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxics is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • wildfire smoke
  • cooker stove
  • diesel exhaust particulate
  • TRAP
  • ozone
  • immune response
  • DNA methylation
  • biomass combustion
  • histone modification

Published Papers (4 papers)

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Research

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Article
Comparative Cytotoxicity Study of PM2.5 and TSP Collected from Urban Areas
Toxics 2021, 9(7), 167; https://doi.org/10.3390/toxics9070167 - 14 Jul 2021
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Abstract
Ambient particulate matter 2.5 (PM2.5) and total suspended particles (TSPs) are common airborne pollutants that cause respiratory and cardiovascular diseases. We investigated the differences of cytotoxicity and mechanism between PM2.5 and TSP activity in human alveolar epithelial A549 cells. Atmospheric samples from the [...] Read more.
Ambient particulate matter 2.5 (PM2.5) and total suspended particles (TSPs) are common airborne pollutants that cause respiratory and cardiovascular diseases. We investigated the differences of cytotoxicity and mechanism between PM2.5 and TSP activity in human alveolar epithelial A549 cells. Atmospheric samples from the central district of Seoul were collected and their chemical compositions were analyzed by inductively-coupled plasma mass spectrometry and ion chromatography. PM2.5 and TSP contained high concentrations of heavy metals (Cu, Fe, Zn, and Pb). The most abundant ions in PM2.5 were SO42−, NH4+, and NO3. A549 cells were exposed to PM2.5 and TSP (25–200 µg/mL) for 24 h. TSP was more cytotoxic than PM2.5 per unit mass. PM2.5 induced oxidative stress, as evidenced by increased levels of a glutamate-cysteine ligase modifier, whereas low-concentration TSP increased hemeoxygenase-1 levels. PM2.5 and TSP did not affect c-Jun N-terminal kinase expression. The levels of nuclear factor erythroid 2-related factor 2 (Nrf2) in PM2.5- and TSP-treated cells decreased significantly in the cytosol and increased in the nucleus. Thus, Nrf2 may be a key transcription factor for detoxifying environmental airborne particles in A549 cells. TSP and PM2.5 could activate the protective Kelch-like ECH-associated protein 1/Nrf2 pathway in A549 cells. Full article
(This article belongs to the Special Issue Molecular Basis of Air-Pollution-Induced Disease Risk)
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Article
Eupatilin Inhibits Reactive Oxygen Species Generation via Akt/NF-κB/MAPK Signaling Pathways in Particulate Matter-Exposed Human Bronchial Epithelial Cells
Toxics 2021, 9(2), 38; https://doi.org/10.3390/toxics9020038 - 18 Feb 2021
Viewed by 836
Abstract
Background: Eupatilin is an active flavon extracted from the Artemisia species and has properties such as antioxidant, anti-inflammatory, and anti-cancer. We examined the effect of eupatilin using fine particulate matter (FPM) and human bronchial epithelial cell line (BEAS-2B) to confirm the potential of [...] Read more.
Background: Eupatilin is an active flavon extracted from the Artemisia species and has properties such as antioxidant, anti-inflammatory, and anti-cancer. We examined the effect of eupatilin using fine particulate matter (FPM) and human bronchial epithelial cell line (BEAS-2B) to confirm the potential of eupatilin as a therapeutic agent for respiratory diseases caused by FPM. Methods: Reactive oxygen species (ROS) levels were checked by flow cytometry to identify if FPM and eupatilin affect ROS production. Western blotting was performed to identify the mechanism of action of eupatilin in FPM-exposed BEAS-2B cells. Results: When cells were exposed to FPM above 12.5 μg/mL concentration for 24 h, ROS production increased significantly compared to the control. When eupatilin was added to cells exposed to FPM, the ROS level decreased proportionally with the eupatilin dose. The phosphorylation of Akt, NF-κB p65, and p38 MAPK induced by FPM was significantly reduced by eupatilin, respectively. Conclusion: FPM cause respiratory disease by producing ROS in bronchial epithelial cells. Eupatilin has been shown to inhibit ROS production through altering signaling pathways. The ROS inhibiting property of eupatilin can be exploited in FPM induced respiratory disorders. Full article
(This article belongs to the Special Issue Molecular Basis of Air-Pollution-Induced Disease Risk)
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Article
Sustained Effects on Lung Function in Community Members Following Exposure to Hazardous PM2.5 Levels from Wildfire Smoke
Toxics 2020, 8(3), 53; https://doi.org/10.3390/toxics8030053 - 05 Aug 2020
Cited by 4 | Viewed by 4095
Abstract
Extreme wildfire events are becoming more common and while the immediate risks of particulate exposures to susceptible populations (i.e., elderly, asthmatics) are appreciated, the long-term health effects are not known. In 2017, the Seeley Lake (SL), MT area experienced unprecedented levels of wildfire [...] Read more.
Extreme wildfire events are becoming more common and while the immediate risks of particulate exposures to susceptible populations (i.e., elderly, asthmatics) are appreciated, the long-term health effects are not known. In 2017, the Seeley Lake (SL), MT area experienced unprecedented levels of wildfire smoke from July 31 to September 18, with a daily average of 220.9 μg/m3. The aim of this study was to conduct health assessments in the community and evaluate potential adverse health effects. The study resulted in the recruitment of a cohort (n = 95, average age: 63 years), for a rapid response screening activity following the wildland fire event, and two follow-up visits in 2018 and 2019. Analysis of spirometry data found a significant decrease in lung function (FEV1/FVC ratio: forced expiratory volume in first second/forced vital capacity) and a more than doubling of participants that fell below the lower limit of normal (10.2% in 2017 to 45.9% in 2018) one year following the wildfire event, and remained decreased two years (33.9%) post exposure. In addition, observed FEV1 was significantly lower than predicted values. These findings suggest that wildfire smoke can have long-lasting effects on human health. As wildfires continue to increase both here and globally, understanding the health implications is vital to understanding the respiratory impacts of these events as well as developing public health strategies to mitigate the effects. Full article
(This article belongs to the Special Issue Molecular Basis of Air-Pollution-Induced Disease Risk)
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Review

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Review
Mechanistic Implications of Biomass-Derived Particulate Matter for Immunity and Immune Disorders
Toxics 2021, 9(2), 18; https://doi.org/10.3390/toxics9020018 - 20 Jan 2021
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Abstract
Particulate matter (PM) is a major and the most harmful component of urban air pollution, which may adversely affect human health. PM exposure has been associated with several human diseases, notably respiratory and cardiovascular diseases. In particular, recent evidence suggests that exposure to [...] Read more.
Particulate matter (PM) is a major and the most harmful component of urban air pollution, which may adversely affect human health. PM exposure has been associated with several human diseases, notably respiratory and cardiovascular diseases. In particular, recent evidence suggests that exposure to biomass-derived PM associates with airway inflammation and can aggravate asthma and other allergic diseases. Defective or excess responsiveness in the immune system regulates distinct pathologies, such as infections, hypersensitivity, and malignancies. Therefore, PM-induced modulation of the immune system is crucial for understanding how it causes these diseases and highlighting key molecular mechanisms that can mitigate the underlying pathologies. Emerging evidence has revealed that immune responses to biomass-derived PM exposure are closely associated with the risk of diverse hypersensitivity disorders, including asthma, allergic rhinitis, atopic dermatitis, and allergen sensitization. Moreover, immunological alteration by PM accounts for increased susceptibility to infectious diseases, such as tuberculosis and coronavirus disease-2019 (COVID-19). Evidence-based understanding of the immunological effects of PM and the molecular machinery would provide novel insights into clinical interventions or prevention against acute and chronic environmental disorders induced by biomass-derived PM. Full article
(This article belongs to the Special Issue Molecular Basis of Air-Pollution-Induced Disease Risk)
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