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Toxics
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Air Pollutant Exposure and Respiratory Diseases
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Air Pollutant Exposure and Respiratory Diseases

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Air Pollution and Health".

Deadline for manuscript submissions: closed (15 May 2024) | Viewed by 8609

Special Issue Editors

Prof. Dr. Miao He

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Guest Editor
Environmental Health, School of Public Health, China Medical University, Shenyang 110122, China
Interests: environmental exposure and health hazard; inhalable particle and respiratory inflammation
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Wenjun Ding

E-Mail Website
Guest Editor
College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China
Interests: environment and health; diabetes mellitus; obesity; oxidative stress
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Kefang Lai

E-Mail Website
Guest Editor
State Key Laboratory of Respiratory Diseases, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China
Interests: pathogenesis of bronchial asthma and chronic cough
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Exposure to air pollution is a major contributor to the pathogenesis of respiratory diseases worldwide. The Special Issue on “Air Pollutants Exposure and Respiratory Diseases” will aim to highlight the latest advances in clinical and experimental work relating to all aspects of adult and paediatric respiratory medicine induced by gaseous and particulate components of air pollution, including but not limited to: COPD, asthma, cystic fibrosis, IPF, pneumonia, influenza, tuberculosis, sarcoidosis, pulmonary hypertension, sleep medicine, respiratory infections, pulmonary vascular disease, and lung cancer. Emphasis is placed on findings that identify novel hazards and that can be extrapolated to environmental exposures and human respiratory risk. Topics are defined on both the macro (e.g., cell biology, epidemiology, immunology, oncology, pathophysiology, imaging and occupational medicine, etc.) and molecular (genomic, transcriptomic, metabolic, etc.) scale. Authors are invited to submit original research papers, reviews, and short communications.

Prof. Dr. Miao He
Prof. Dr. Wenjun Ding
Prof. Dr. Kefang Lai
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 submissions that pass pre-check are 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 2600 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

  • epidemiology
  • allergy
  • allergic airway inflammation
  • endoplasmic reticulum homeostasis
  • mitochodrial dysfunction
  • oxdiative stress
  • cell metabolism reprogramming/epigenetics

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Related Special Issue

Published Papers (6 papers)

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Research

14 pages, 3155 KiB  
Article
TBHQ Alleviates Particulate Matter-Induced Pyroptosis in Human Nasal Epithelial Cells
by Ji-Sun Kim, Hyunsu Choi, Jeong-Min Oh, Sung Won Kim, Soo Whan Kim, Byung Guk Kim, Jin Hee Cho, Joohyung Lee and Dong Chang Lee
Toxics 2024, 12(6), 407; https://doi.org/10.3390/toxics12060407 - 3 Jun 2024
Viewed by 705
Abstract
Pyroptosis represents a type of cell death mechanism notable for its cell membrane disruption and the subsequent release of proinflammatory cytokines. The Nod-like receptor family pyrin domain containing inflammasome 3 (NLRP3) plays a critical role in the pyroptosis mechanism associated with various diseases [...] Read more.
Pyroptosis represents a type of cell death mechanism notable for its cell membrane disruption and the subsequent release of proinflammatory cytokines. The Nod-like receptor family pyrin domain containing inflammasome 3 (NLRP3) plays a critical role in the pyroptosis mechanism associated with various diseases resulting from particulate matter (PM) exposure. Tert-butylhydroquinone (tBHQ) is a synthetic antioxidant commonly used in a variety of foods and products. The aim of this study is to examine the potential of tBHQ as a therapeutic agent for managing sinonasal diseases induced by PM exposure. The occurrence of NLRP3 inflammasome-dependent pyroptosis in RPMI 2650 cells treated with PM < 4 µm in size was confirmed using Western blot analysis and enzyme-linked immunosorbent assay results for the pyroptosis metabolites IL-1β and IL-18. In addition, the inhibitory effect of tBHQ on PM-induced pyroptosis was confirmed using Western blot and immunofluorescence techniques. The inhibition of tBHQ-mediated pyroptosis was abolished upon nuclear factor erythroid 2-related factor 2 (Nrf2) knockdown, indicating its involvement in the antioxidant mechanism. tBHQ showed potential as a therapeutic agent for sinonasal diseases induced by PM because NLRP3 inflammasome activation was effectively suppressed via the Nrf2 pathway. Full article
(This article belongs to the Special Issue Air Pollutant Exposure and Respiratory Diseases)
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15 pages, 2016 KiB  
Article
Associations of Insecticide Exposure with Childhood Asthma and Wheezing: A Population-Based Cross-Sectional Study in Sanya, China
by Yabin Hu, Guiyan Yang, Dan Wang, Wangyang Gu, Dan Xie, Tingyue Huang, Peng Xue, Jingyi Tang, Hui Wei, Shenghui Li, Shilu Tong and Shijian Liu
Toxics 2024, 12(6), 392; https://doi.org/10.3390/toxics12060392 - 27 May 2024
Viewed by 775
Abstract
Insecticide exposure may affect childhood asthma/wheezing, but evidence is scarce in low- and middle-income countries. We conducted a population-based cross-sectional study in Sanya, China. Generalized linear models were adopted to assess the associations of insecticide exposure with childhood asthma/wheezing, reported as odds ratios [...] Read more.
Insecticide exposure may affect childhood asthma/wheezing, but evidence is scarce in low- and middle-income countries. We conducted a population-based cross-sectional study in Sanya, China. Generalized linear models were adopted to assess the associations of insecticide exposure with childhood asthma/wheezing, reported as odds ratios (ORs) and 95% confidence intervals (CIs). A subgroup analysis was performed to explore the possible effects of sociodemographic and environmental factors on these associations. The median age of the 9754 children was 6.7 years, and 5345 (54.8%) were boys. The prevalences of ever asthma (EA), ever wheezing (EW), and current wheezing (CW) were 7.4%, 5.3%, and 2.9%, respectively. We found a greater prevalence of childhood EA with insecticide exposure (OR = 1.18, 95% CI: 1.00, 1.38). Outdoor insecticide exposure was associated with elevated ORs for EA (1.24, 95% CI: 1.03, 1.50), EW (1.27, 95% CI: 1.03, 1.57), and CW (1.38, 95% CI: 1.04, 1.81). The p for the trend in insecticide exposure frequency was significant for EA (p = 0.001) and CW (p = 0.034). These adverse impacts were pronounced in girls who were exposed to low temperatures. Our findings suggest adverse effects of insecticide use, especially outdoors, on childhood asthma/wheezing. Further studies are warranted to verify this association and develop tailored prevention measures. Full article
(This article belongs to the Special Issue Air Pollutant Exposure and Respiratory Diseases)
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12 pages, 4217 KiB  
Article
Decadal Trends in Ambient Air Pollutants and Their Association with COPD and Lung Cancer in Upper Northern Thailand: 2013–2022
by Pachara Sapbamrer, Pheerasak Assavanopakun and Jinjuta Panumasvivat
Toxics 2024, 12(5), 321; https://doi.org/10.3390/toxics12050321 - 28 Apr 2024
Viewed by 1764
Abstract
Air pollution in upper northern Thailand raises health concerns. This study examined trends and associations between air pollutants and respiratory diseases, focusing on COPD and lung cancer during haze (December–May) and non-haze (June–November) seasons in upper northern Thailand from 2013 to 2022. This [...] Read more.
Air pollution in upper northern Thailand raises health concerns. This study examined trends and associations between air pollutants and respiratory diseases, focusing on COPD and lung cancer during haze (December–May) and non-haze (June–November) seasons in upper northern Thailand from 2013 to 2022. This study utilized data from the Pollution Control Department and Chiang Mai Provincial Public Health. The key air pollutants included PM10, PM2.5, SO2, NO2, CO, and O3. Respiratory disease data included fatality rates for lung cancer and COPD and the re-admission rate for COPD. Results indicated peak air pollutant levels and COPD re-admission rates in March, with PM2.5 concentrations exceeding air quality standards from January to April. During haze periods, COPD fatality and re-admission rates significantly increased (mean difference: 0.43 and 4.23 per 1000-case population, respectively; p < 0.001), while lung cancer fatality rates were higher without statistical significance. Pearson correlation analysis found positive correlations between PM10, PM2.5, O3, and NO2 concentrations and COPD re-admission and fatality rates at 0–1 month lag times, with a declining trend observed at subsequent lag intervals of 2 to 3 months. Overall, this study highlights the predictable pattern of air pollution in the region, correlating with higher COPD fatality and re-admission rates. Full article
(This article belongs to the Special Issue Air Pollutant Exposure and Respiratory Diseases)
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16 pages, 4828 KiB  
Article
Mechanism of Interaction between hsa_circ_0002854 and MAPK1 Protein in PM2.5-Induced Apoptosis of Human Bronchial Epithelial Cells
by Jinchang Hong, Yi Tan, Yuyu Wang, Hongjie Wang, Caixia Li, Wenjia Jin, Yi Wu, Dechun Ni and Xiaowu Peng
Toxics 2023, 11(11), 906; https://doi.org/10.3390/toxics11110906 - 6 Nov 2023
Viewed by 1477
Abstract
Fine particulate matter (PM2.5) pollution increases the risk of respiratory diseases and death, and apoptosis is an important factor in the occurrence of respiratory diseases caused by PM2.5 exposure. In addition, circular RNAs (circRNAs) can interact with proteins [...] Read more.
Fine particulate matter (PM2.5) pollution increases the risk of respiratory diseases and death, and apoptosis is an important factor in the occurrence of respiratory diseases caused by PM2.5 exposure. In addition, circular RNAs (circRNAs) can interact with proteins and widely participate in physiological and pathological processes in the body. The aim of this study was to investigate the mechanism of circRNA and protein interaction on PM2.5-induced apoptosis of human bronchial epithelial cells (16HBE) in vitro. In this study, we exposed human bronchial epithelial cells to a PM2.5 suspension with different concentration gradients for 24 h. The results showed that apoptosis of 16HBE cells after PM2.5 treatment was accompanied by cell proliferation. After exposure of PM2.5 to 16HBE cells, circRNAs related to apoptosis were abnormally expressed. We further found that the expression of hsa_circ_0002854 increased with the increase in exposure concentration. Functional analysis showed that knocking down the expression of hsa_circ_0002854 could inhibit apoptosis induced by PM2.5 exposure. We then found that hsa_circ_0002854 could interact with MAPK1 protein and inhibit MAPK1 phosphorylation, thus promoting apoptosis. Our results suggest that hsa_circ_0002854 can promote 16HBE apoptosis due to PM2.5 exposure, which may provide a gene therapy target and scientific basis for PM2.5-induced respiratory diseases. Full article
(This article belongs to the Special Issue Air Pollutant Exposure and Respiratory Diseases)
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15 pages, 1627 KiB  
Article
Effects of Ambient O3 on Respiratory Mortality, Especially the Combined Effects of PM2.5 and O3
by Ye Deng, Junlong Wang, Li Sun, Yue Wang, Jiaoyang Chen, Zhixin Zhao, Tianyun Wang, Yuting Xiang, Yuting Wang, Jiamei Chen and Miao He
Toxics 2023, 11(11), 892; https://doi.org/10.3390/toxics11110892 - 30 Oct 2023
Cited by 4 | Viewed by 1628
Abstract
Background: In China, the increasing concentration of ozone (O3) has emerged as a significant air pollution issue, leading to adverse effects on public health, particularly the respiratory system. Despite the progress made in managing air pollution in China, it is crucial [...] Read more.
Background: In China, the increasing concentration of ozone (O3) has emerged as a significant air pollution issue, leading to adverse effects on public health, particularly the respiratory system. Despite the progress made in managing air pollution in China, it is crucial to address the problem of environmental O3 pollution at present. Methods: The connection between O3 exposure and respiratory mortality in Shenyang, China, from 2014 to 2018 was analyzed by a time-series generalized additive regression model (GAM) with quasi-Poisson regression. Additionally, the potential combined effects of fine particulate matter (PM2.5) and O3 were investigated using the synergy index (SI). Results: Our findings indicate that each 10 μg/m3 increase in O3 at lag 2 days was associated with a maximum relative risk (RR) of 1.0150 (95% CI: 1.0098–1.0202) for respiratory mortality in the total population. For individuals aged ≥55 years, unmarried individuals, those engaged in indoor occupations, and those with low educational attainment, each 10 μg/m3 increase in O3 at lag 07 days was linked to RR values of 1.0301 (95% CI: 1.0187–1.0417), 1.0437 (95% CI: 1.0266–1.0610), 1.0317 (95% CI: 1.0186–1.0450), and 1.0346 (95% CI: 1.0222–1.0471), respectively. Importantly, we discovered a synergistic effect of PM2.5 and O3, resulting in an SI of 2.372 on the occurrence of respiratory mortality. Conclusions: This study confirmed a positive association between O3 exposure and respiratory mortality. Furthermore, it highlighted the interaction between O3 and PM2.5 in exacerbating respiratory deaths. Full article
(This article belongs to the Special Issue Air Pollutant Exposure and Respiratory Diseases)
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19 pages, 2466 KiB  
Article
Job Exposure Matrix, a Solution for Retrospective Assessment of Particle Exposure in a Subway Network and Their Long-Term Effects
by Tesnim Ben Rayana, Pascal Wild, Amélie Debatisse, Valérie Jouannique, Kirushanthi Sakthithasan, Guillaume Suarez and Irina Guseva Canu
Toxics 2023, 11(10), 836; https://doi.org/10.3390/toxics11100836 - 2 Oct 2023
Cited by 3 | Viewed by 1664
Abstract
Introduction: Health effects after long-term exposure to subway particulate matter (PM) remain unknown due to the lack of individual PM exposure data. This study aimed to apply the job exposure matrix (JEM) approach to retrospectively assess occupational exposure to PM in the Parisian [...] Read more.
Introduction: Health effects after long-term exposure to subway particulate matter (PM) remain unknown due to the lack of individual PM exposure data. This study aimed to apply the job exposure matrix (JEM) approach to retrospectively assess occupational exposure to PM in the Parisian subway. Methods: Job, the line and sector of the transport network, as well as calendar period were four JEM dimensions. For each combination of these dimensions, we generated statistical models to estimate the annual average PM10 concentration using data from an exhaustive inventory of the PM measurement campaigns conducted between 2004 and 2020 in the Parisian subway and historical data from the Parisian air pollution monitoring network. The resulting JEM and its exposure estimates were critically examined by experts using the uncertainty analysis framework. Results: The resulting JEM allows for the assignment of the estimated annual PM10 concentration to three types of professionals working in the subway: locomotive operators, station agents, and security guards. The estimates’ precision and validity depend on the amount and quality of PM10 measurement data used in the job-, line-, and sector-specific models. Models using large amounts of personal exposure measurement data produced rather robust exposure estimates compared to models with lacunary data (i.e., in security guards). The analysis of uncertainty around the exposure estimates allows for the identification of the sources of uncertainty and parameters to be addressed in the future in order to refine and/or improve the JEM. Conclusions: The JEM approach seems relevant for the retrospective exposure assessment of subway workers. When applied to available data on PM10, it allows for the estimation of this exposure in locomotive operators and station agents with an acceptable validity. Conversely, for security guards, the current estimates have insufficient validity to recommend their use in an epidemiological study. Therefore, the current JEM should be considered as a valid prototype, which shall be further improved using more robust measurements for some jobs. This JEM can also be further refined by considering additional exposure determinants. Full article
(This article belongs to the Special Issue Air Pollutant Exposure and Respiratory Diseases)
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