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Special Issue "Inhaled Pollutants Modulate Respiratory and Systemic Diseases"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 September 2017)

Special Issue Editors

Guest Editor
Dr. Paul R. Reynolds

Associate Professor, Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA
Website | E-Mail
Interests: mechanisms of pulmonary injury and disease related to oxidative stress
Guest Editor
Dr. Benjamin T. Bikman

Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA
Website | E-Mail
Interests: effects of insulin and ketones on cellular metabolism and mitochondrial function

Special Issue Information

Dear Colleagues,

Given its intimate apposition with the environment, the respiratory system provides a robust gateway through which particulates gain access to pulmonary and non-pulmonary tissues. The remarkable worldwide incidence of lung disease and diffuse systemic inflammatory diseases has given rise to novel perspectives that explore etiological overlap in an effort to slow current trends. Accordingly, recent research indicates a growing appreciation for inhaled pollutants that impact organismal health.

Of the myriad of molecules that are regularly inhaled, two broad classifications that appear to exacerbate physiological functions are those that stem from both vehicular traffic and cigarettes. Whether it is a result of the size or the shape of the molecule, various inhaled substances appear to effectively penetrate delicate lung structures and pulmonary inflammatory foci translate noxious stimuli into a systemic insult.

We invite authors to contribute original research articles, as well as review articles, that will illustrate and stimulate the blossoming effort to understand the role of inhaled personal (i.e., secondhand smoke) or environmental pollution in diverse disease settings. The accepted papers will highlight to readers the importance of environmental exposures and, thus, potentially provide a new paradigm on the treatment and prevention of related disorders.

Dr. Paul R. Reynolds
Dr. Benjamin T. Bikman
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. International Journal of Molecular Sciences 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 1800 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

  • environmental tobacco
  • oxidative stress
  • lung disease
  • systemic diseases
  • respiratory system
  • diffuse systemic inflammatory diseases
  • inhaled pollutants
  • environmental pollution

Published Papers (10 papers)

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Research

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Open AccessArticle Cigarette Smoke Regulates the Competitive Interactions between NRF2 and BACH1 for Heme Oxygenase-1 Induction
Int. J. Mol. Sci. 2017, 18(11), 2386; https://doi.org/10.3390/ijms18112386
Received: 5 October 2017 / Revised: 31 October 2017 / Accepted: 8 November 2017 / Published: 10 November 2017
Cited by 1 | PDF Full-text (3118 KB) | HTML Full-text | XML Full-text
Abstract
Cigarette smoke has been shown to trigger aberrant signaling pathways and pathophysiological processes; however, the regulatory mechanisms underlying smoke-induced gene expression remain to be established. Herein, we observed that two smoke-responsive genes, HO-1 and CYP1A1, are robustly induced upon smoke by different
[...] Read more.
Cigarette smoke has been shown to trigger aberrant signaling pathways and pathophysiological processes; however, the regulatory mechanisms underlying smoke-induced gene expression remain to be established. Herein, we observed that two smoke-responsive genes, HO-1 and CYP1A1, are robustly induced upon smoke by different mechanisms in human bronchial epithelia. CYP1A1 is mediated by aryl hydrocarbon receptor signaling, while induction of HO-1 is regulated by oxidative stress, and suppressed by N-acetylcysteine treatment. In light of a pivotal role of NRF2 and BACH1 in response to oxidative stress and regulation of HO-1, we examined if smoke-induced HO-1 expression is modulated through the NRF2/BACH1 axis. We demonstrated that smoke causes significant nuclear translocation of NRF2, but only a slight decrease in nuclear BACH1. Knockdown of NRF2 attenuated smoke-induced HO-1 expression while down-regulation of BACH1 had stimulatory effects on both basal and smoke-induced HO-1 with trivial influence on NRF2 nuclear translocation. Chromatin immunoprecipitation assays showed that smoke augments promoter-specific DNA binding of NRF2 but suppresses BACH1 binding to the HO-1 promoter ARE sites, two of which at −1.0 kb and −2.6 kb are newly identified. These results suggest that the regulation of NRF2 activator and BACH1 repressor binding to the ARE sites are critical for smoke-mediated HO-1 induction. Full article
(This article belongs to the Special Issue Inhaled Pollutants Modulate Respiratory and Systemic Diseases)
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Open AccessArticle Association of Smoking with Metabolic Volatile Organic Compounds in Exhaled Breath
Int. J. Mol. Sci. 2017, 18(11), 2235; https://doi.org/10.3390/ijms18112235
Received: 25 September 2017 / Revised: 16 October 2017 / Accepted: 20 October 2017 / Published: 25 October 2017
Cited by 1 | PDF Full-text (4546 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Lung cancer (LC) screening will be more efficient if it is applied to a well-defined high-risk population. Characteristics including metabolic byproducts may be taken into account to access LC risk more precisely. Breath examination provides a non-invasive method to monitor metabolic byproducts. However,
[...] Read more.
Lung cancer (LC) screening will be more efficient if it is applied to a well-defined high-risk population. Characteristics including metabolic byproducts may be taken into account to access LC risk more precisely. Breath examination provides a non-invasive method to monitor metabolic byproducts. However, the association between volatile organic compounds (VOCs) in exhaled breath and LC risk or LC risk factors is not studied. Exhaled breath samples from 122 healthy persons, who were given routine annual exam from December 2015 to December 2016, were analyzed using thermal desorption coupled with gas chromatography mass spectrometry (TD-GC-MS). Smoking characteristics, air quality, and other risk factors for lung cancer were collected. Univariate and multivariate analyses were used to evaluate the relationship between VOCs and LC risk factors. 7, 7, 11, and 27 VOCs were correlated with smoking status, smoking intensity, years of smoking, and depth of inhalation, respectively. Exhaled VOCs are related to smoking and might have a potential to evaluate LC risk more precisely. Both an assessment of temporal stability and testing in a prospective study are needed to establish the performance of VOCs such as 2,5-dimethylfuranm and 4-methyloctane as lung cancer risk biomarkers. Full article
(This article belongs to the Special Issue Inhaled Pollutants Modulate Respiratory and Systemic Diseases)
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Open AccessArticle High-Mobility Group Box 1 Disrupts Metabolic Function with Cigarette Smoke Exposure in a Ceramide-Dependent Manner
Int. J. Mol. Sci. 2017, 18(5), 1099; https://doi.org/10.3390/ijms18051099
Received: 17 April 2017 / Revised: 16 May 2017 / Accepted: 18 May 2017 / Published: 20 May 2017
Cited by 3 | PDF Full-text (2017 KB) | HTML Full-text | XML Full-text
Abstract
We have previously found that cigarette smoke disrupts metabolic function, in part, by increasing muscle ceramide accrual. To further our understanding of this, we sought to determine the role of the cytokine high-mobility group box 1 (HMGB1), which is increased with smoke exposure,
[...] Read more.
We have previously found that cigarette smoke disrupts metabolic function, in part, by increasing muscle ceramide accrual. To further our understanding of this, we sought to determine the role of the cytokine high-mobility group box 1 (HMGB1), which is increased with smoke exposure, in smoke-induced muscle metabolic perturbations. To test this theory, we determined HMGB1 from lungs of human smokers, as well as from lung cells from mice exposed to cigarette smoke. We also treated cells and mice directly with HMGB1, in the presence or absence of myriocin, an inhibitor of serine palmitoyltransferase, the rate-limiting enzyme in ceramide biosynthesis. Outcomes included assessments of insulin resistance and muscle mitochondrial function. HMGB1 was significantly increased in both human lungs and rodent alveolar macrophages. Further testing revealed that HMGB1 treatment elicited a widespread increase in ceramide species and reduction in myotube mitochondrial respiration, an increase in reactive oxygen species, and reduced insulin-stimulated Akt phosphorylation. Inhibition of ceramide biosynthesis with myriocin was protective. In mice, by comparing treatments of HMGB1 injections with or without myriocin, we found that HMGB1 injections resulted in increased muscle ceramides, especially C16 and C24, which were necessary for reduced muscle mitochondrial respiration and compromised insulin and glucose tolerance. In conclusion, HMGB1 may be a necessary intermediate in the ceramide-dependent metabolic consequences of cigarette smoke exposure. Full article
(This article belongs to the Special Issue Inhaled Pollutants Modulate Respiratory and Systemic Diseases)
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Open AccessArticle The Dose–Response Association between Nitrogen Dioxide Exposure and Serum Interleukin-6 Concentrations
Int. J. Mol. Sci. 2017, 18(5), 1015; https://doi.org/10.3390/ijms18051015
Received: 31 March 2017 / Revised: 26 April 2017 / Accepted: 28 April 2017 / Published: 8 May 2017
Cited by 1 | PDF Full-text (800 KB) | HTML Full-text | XML Full-text
Abstract
Systemic inflammation is an integral part of chronic obstructive pulmonary disease (COPD), and air pollution is associated with cardiorespiratory mortality, yet the interrelationships are not fully defined. We examined associations between nitrogen dioxide (NO2) exposure (as a marker of traffic-related air
[...] Read more.
Systemic inflammation is an integral part of chronic obstructive pulmonary disease (COPD), and air pollution is associated with cardiorespiratory mortality, yet the interrelationships are not fully defined. We examined associations between nitrogen dioxide (NO2) exposure (as a marker of traffic-related air pollution) and pro-inflammatory cytokines, and investigated effect modification and mediation by post-bronchodilator airflow obstruction (post-BD-AO) and cardiovascular risk. Data from middle-aged participants in the Tasmanian Longitudinal Health Study (TAHS, n = 1389) were analyzed by multivariable logistic regression, using serum interleukin (IL)-6, IL-8 and tumor necrosis factor-α (TNF-α) as the outcome. Mean annual NO2 exposure was estimated at residential addresses using a validated satellite-based land-use regression model. Post-BD-AO was defined by post-BD forced expiratory ratio (FEV1/FVC) < lower limit of normal, and cardiovascular risk by a history of either cerebrovascular or ischaemic heart disease. We found a positive association with increasing serum IL-6 concentration (geometric mean 1.20 (95% CI: 1.1 to 1.3, p = 0.001) per quartile increase in NO2). This was predominantly a direct relationship, with little evidence for either effect modification or mediation via post-BD-AO, or for the small subgroup who reported cardiovascular events. However, there was some evidence consistent with serum IL-6 being on the causal pathway between NO2 and cardiovascular risk. These findings raise the possibility that the interplay between air pollution and systemic inflammation may differ between post-BD airflow obstruction and cardiovascular diseases. Full article
(This article belongs to the Special Issue Inhaled Pollutants Modulate Respiratory and Systemic Diseases)
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Open AccessArticle Nrf2 Regulates the Risk of a Diesel Exhaust Inhalation-Induced Immune Response during Bleomycin Lung Injury and Fibrosis in Mice
Int. J. Mol. Sci. 2017, 18(3), 649; https://doi.org/10.3390/ijms18030649
Received: 28 January 2017 / Revised: 3 March 2017 / Accepted: 9 March 2017 / Published: 17 March 2017
PDF Full-text (3749 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
The present study investigated the effects of diesel exhaust (DE) on an experimental model of bleomycin (BLM)-induced lung injury and fibrosis in mice. BLM was intravenously administered to both Nrf2+/+ and Nrf2−/− C57BL/6J mice on day 0. The mice were exposed
[...] Read more.
The present study investigated the effects of diesel exhaust (DE) on an experimental model of bleomycin (BLM)-induced lung injury and fibrosis in mice. BLM was intravenously administered to both Nrf2+/+ and Nrf2−/− C57BL/6J mice on day 0. The mice were exposed to DE for 56 days from 28 days before the BLM injection to 28 days after the BLM injection. Inhalation of DE induced significant inhibition of airway clearance function and the proinflammatory cytokine secretion in macrophages, an increase in neutrophils, and severe lung inflammatory injury, which were greater in Nrf2−/− mice than in Nrf2+/+ mice. In contrast, inhalation of DE was observed to induce a greater increase of hydroxyproline content in the lung tissues and significantly higher pulmonary antioxidant enzyme mRNA expression in the Nrf2+/+ mice than in Nrf2−/− mice. DE is an important risk factor, and Nrf2 regulates the risk of a DE inhalation induced immune response during BLM lung injury and fibrosis in mice. Full article
(This article belongs to the Special Issue Inhaled Pollutants Modulate Respiratory and Systemic Diseases)
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Open AccessArticle Dectin-1-Mediated Pathway Contributes to Fusarium proliferatum-Induced CXCL-8 Release from Human Respiratory Epithelial Cells
Int. J. Mol. Sci. 2017, 18(3), 624; https://doi.org/10.3390/ijms18030624
Received: 12 January 2017 / Revised: 7 March 2017 / Accepted: 10 March 2017 / Published: 13 March 2017
Cited by 2 | PDF Full-text (1229 KB) | HTML Full-text | XML Full-text
Abstract
Fusarium species are causative agents of human respiratory disorders and are distributed widely in our environment. Little is known of their interaction with human respiratory epithelial cells, which may contribute to allergic airway responses. In this study, we report on the release of
[...] Read more.
Fusarium species are causative agents of human respiratory disorders and are distributed widely in our environment. Little is known of their interaction with human respiratory epithelial cells, which may contribute to allergic airway responses. In this study, we report on the release of C–X–C motif chemokine ligand 8 (CXCL-8) from human bronchial epithelial BEAS-2B cells upon stimulation with Fusarium proliferatum extracts. F. proliferatum-induced cytokine release from BEAS-2B cells was determined by cytokine array and CXCL-8 enzyme-linked immunosorbent assay (ELISA) kits. Blocking antibodies and signaling pathway inhibitors were employed to delineate cell surface receptors and signaling pathways participating in CXCL-8 release. F. proliferatum extracts induced the release of CXCL-8 in a time-dependent manner. The dectin-1 receptor ligands, curdlan and laminarin, reduced CXCL-8 release. Cells pre-treated with anti-Dectin-1 antibodies (2 µg/mL) decreased CXCL-8 release by 24%. Furthermore, F. proliferatum-stimulated CXCL-8 release was reduced by 32%, 53%–81%, 40% and 26% after BEAS-2B cells were pretreated with activation inhibitors of spleen tyrosine kinase (Syk)—piceatannol—, mitogen-activated protein kinases (MAPKs)—PD98059, U0126, SB202190, SP600125—, phosphatidylinositol-3-kinase (PI3K)—LY294002—and nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB)—BAY117082—, respectively. These results suggest that Dectin-1-mediated activation of the Syk, MAPKs, PI3K and NF-κB signaling pathways contributes to F. proliferatum-stimulated CXCL-8 release from BEAS-2B cells and provides an important basis for developing novel therapeutic strategies in clinical allergy. Full article
(This article belongs to the Special Issue Inhaled Pollutants Modulate Respiratory and Systemic Diseases)
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Open AccessArticle Biomass Smoke Exposure Enhances Rhinovirus-Induced Inflammation in Primary Lung Fibroblasts
Int. J. Mol. Sci. 2016, 17(9), 1403; https://doi.org/10.3390/ijms17091403
Received: 1 July 2016 / Revised: 18 August 2016 / Accepted: 22 August 2016 / Published: 25 August 2016
Cited by 2 | PDF Full-text (1686 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Biomass smoke is one of the major air pollutants and contributors of household air pollution worldwide. More than 3 billion people use biomass fuels for cooking and heating, while other sources of exposure are from the occurrence of bushfires and occupational conditions. Persistent
[...] Read more.
Biomass smoke is one of the major air pollutants and contributors of household air pollution worldwide. More than 3 billion people use biomass fuels for cooking and heating, while other sources of exposure are from the occurrence of bushfires and occupational conditions. Persistent biomass smoke exposure has been associated with acute lower respiratory infection (ALRI) as a major environmental risk factor. Children under the age of five years are the most susceptible in developing severe ALRI, which accounts for 940,000 deaths globally. Around 90% of cases are attributed to viral infections, such as influenza, adenovirus, and rhinovirus. Although several epidemiological studies have generated substantial evidence of the association of biomass smoke and respiratory infections, the underlying mechanism is still unknown. Using an in vitro model, primary human lung fibroblasts were stimulated with biomass smoke extract (BME), specifically investigating hardwood and softwood types, and human rhinovirus-16 for 24 h. Production of pro-inflammatory mediators, such as IL-6 and IL-8, were measured via ELISA. Firstly, we found that hardwood and softwood smoke extract (1%) up-regulate IL-6 and IL-8 release (p ≤ 0.05). In addition, human rhinovirus-16 further increased biomass smoke-induced IL-8 in fibroblasts, in comparison to the two stimulatory agents alone. We also investigated the effect of biomass smoke on viral susceptibility by measuring viral load, and found no significant changes between BME exposed and non-exposed infected fibroblasts. Activated signaling pathways for IL-6 and IL-8 production by BME stimulation were examined using signaling pathway inhibitors. p38 MAPK inhibitor SB239063 significantly attenuated IL-6 and IL-8 release the most (p ≤ 0.05). This study demonstrated that biomass smoke can modulate rhinovirus-induced inflammation during infection, which can alter the severity of the disease. The mechanism by which biomass smoke exposure increases inflammation in the lungs can be targeted and inhibited via p38 MAP kinase pathway. Full article
(This article belongs to the Special Issue Inhaled Pollutants Modulate Respiratory and Systemic Diseases)
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Review

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Open AccessReview Adverse Health Effects of Thirdhand Smoke: From Cell to Animal Models
Int. J. Mol. Sci. 2017, 18(5), 932; https://doi.org/10.3390/ijms18050932
Received: 13 March 2017 / Revised: 18 April 2017 / Accepted: 24 April 2017 / Published: 28 April 2017
Cited by 5 | PDF Full-text (827 KB) | HTML Full-text | XML Full-text
Abstract
The newly identified smoke hazard, thirdhand smoke (THS), has gained public attention in recent years but its health impact and biological effects are largely unknown. THS may be defined by “the four Rs”: tobacco chemicals that remain, react, re-emit, and/or are resuspended long
[...] Read more.
The newly identified smoke hazard, thirdhand smoke (THS), has gained public attention in recent years but its health impact and biological effects are largely unknown. THS may be defined by “the four Rs”: tobacco chemicals that remain, react, re-emit, and/or are resuspended long after active smoking has ceased. This review summarizes recent research progress in the effects of THS on genotoxicity, metabolism and early life development using cellular and animal models. We first reported that THS generated in laboratory systems caused significant DNA damage in human cell lines. Our finding that THS significantly induces oxidative base lesions has been confirmed in skin wounds of mice models exposed to THS. THS also induced metabolomic changes in human reproductive cell lines. Furthermore, we demonstrated that early exposure to THS not only negatively impacts body weight in both male and female mice, but also induces persistent changes to immunological parameters in peripheral blood in these mice. These results indicate that THS is genotoxic at realistic experimental doses and that there may be a window of susceptibility for some forms of cellular damage induced by THS. Full article
(This article belongs to the Special Issue Inhaled Pollutants Modulate Respiratory and Systemic Diseases)
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Open AccessReview Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure
Int. J. Mol. Sci. 2017, 18(3), 652; https://doi.org/10.3390/ijms18030652
Received: 30 January 2017 / Revised: 7 March 2017 / Accepted: 14 March 2017 / Published: 17 March 2017
Cited by 4 | PDF Full-text (289 KB) | HTML Full-text | XML Full-text
Abstract
Approximately 1 billion people smoke worldwide, and the burden placed on society by primary and secondhand smokers is expected to increase. Smoking is the leading risk factor for myriad health complications stemming from diverse pathogenic programs. First- and second-hand cigarette smoke contains thousands
[...] Read more.
Approximately 1 billion people smoke worldwide, and the burden placed on society by primary and secondhand smokers is expected to increase. Smoking is the leading risk factor for myriad health complications stemming from diverse pathogenic programs. First- and second-hand cigarette smoke contains thousands of constituents, including several carcinogens and cytotoxic chemicals that orchestrate chronic inflammatory responses and destructive remodeling events. In the current review, we outline details related to compromised pulmonary and systemic conditions related to smoke exposure. Specifically, data are discussed relative to impaired lung physiology, cancer mechanisms, maternal-fetal complications, cardiometabolic, and joint disorders in the context of smoke exposure exacerbations. As a general unifying mechanism, the receptor for advanced glycation end-products (RAGE) and its signaling axis is increasingly considered central to smoke-related pathogenesis. RAGE is a multi-ligand cell surface receptor whose expression increases following cigarette smoke exposure. RAGE signaling participates in the underpinning of inflammatory mechanisms mediated by requisite cytokines, chemokines, and remodeling enzymes. Understanding the biological contributions of RAGE during cigarette smoke-induced inflammation may provide critically important insight into the pathology of lung disease and systemic complications that combine during the demise of those exposed. Full article
(This article belongs to the Special Issue Inhaled Pollutants Modulate Respiratory and Systemic Diseases)
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Open AccessReview Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter
Int. J. Mol. Sci. 2017, 18(2), 243; https://doi.org/10.3390/ijms18020243
Received: 21 November 2016 / Revised: 9 January 2017 / Accepted: 13 January 2017 / Published: 24 January 2017
Cited by 16 | PDF Full-text (1685 KB) | HTML Full-text | XML Full-text
Abstract
Air pollution of anthropogenic origin is largely from the combustion of biomass (e.g., wood), fossil fuels (e.g., cars and trucks), incinerators, landfills, agricultural activities and tobacco smoke. Air pollution is a complex mixture that varies in space and time, and contains hundreds of
[...] Read more.
Air pollution of anthropogenic origin is largely from the combustion of biomass (e.g., wood), fossil fuels (e.g., cars and trucks), incinerators, landfills, agricultural activities and tobacco smoke. Air pollution is a complex mixture that varies in space and time, and contains hundreds of compounds including volatile organic compounds (e.g., benzene), metals, sulphur and nitrogen oxides, ozone and particulate matter (PM). PM0.1 (ultrafine particles (UFP)), those particles with a diameter less than 100 nm (includes nanoparticles (NP)) are considered especially dangerous to human health and may contribute significantly to the development of numerous respiratory and cardiovascular diseases such as chronic obstructive pulmonary disease (COPD) and atherosclerosis. Some of the pathogenic mechanisms through which PM0.1 may contribute to chronic disease is their ability to induce inflammation, oxidative stress and cell death by molecular mechanisms that include transcription factors such as nuclear factor κB (NF-κB) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Epigenetic mechanisms including non-coding RNA (ncRNA) may also contribute towards the development of chronic disease associated with exposure to PM0.1. This paper highlights emerging molecular concepts associated with inhalational exposure to PM0.1 and their ability to contribute to chronic respiratory and systemic disease. Full article
(This article belongs to the Special Issue Inhaled Pollutants Modulate Respiratory and Systemic Diseases)
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