Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter

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...

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Main Authors: Hussein Traboulsi, Necola Guerrina, Matthew Iu, Dusica Maysinger, Parisa Ariya, Carolyn J. Baglole
Format: Article
Language:English
Published: MDPI AG 2017-01-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:http://www.mdpi.com/1422-0067/18/2/243
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author Hussein Traboulsi
Necola Guerrina
Matthew Iu
Dusica Maysinger
Parisa Ariya
Carolyn J. Baglole
author_facet Hussein Traboulsi
Necola Guerrina
Matthew Iu
Dusica Maysinger
Parisa Ariya
Carolyn J. Baglole
author_sort Hussein Traboulsi
collection DOAJ
description 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.
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spelling doaj.art-1e1453a0329c46b59b4063fd5091f1ab2022-12-22T03:32:50ZengMDPI AGInternational Journal of Molecular Sciences1422-00672017-01-0118224310.3390/ijms18020243ijms18020243Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate MatterHussein Traboulsi0Necola Guerrina1Matthew Iu2Dusica Maysinger3Parisa Ariya4Carolyn J. Baglole5Department of Medicine, McGill University, Montreal, QC H4A 3J1, CanadaDepartment of Pathology, McGill University, Montreal, QC H4A 3J1, CanadaDepartment of Medicine, McGill University, Montreal, QC H4A 3J1, CanadaDepartment of Pharmacology & Therapeutics, McGill University, Montreal, QC H3G 1Y6, CanadaDepartment of Chemistry, McGill University, Montreal, QC H3A 2K6, CanadaDepartment of Medicine, McGill University, Montreal, QC H4A 3J1, CanadaAir 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.http://www.mdpi.com/1422-0067/18/2/243air pollutionepigeneticschronic obstructive pulmonary diseaseparticulate matteraryl hydrocarbon receptornuclear factor-κB
spellingShingle Hussein Traboulsi
Necola Guerrina
Matthew Iu
Dusica Maysinger
Parisa Ariya
Carolyn J. Baglole
Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter
International Journal of Molecular Sciences
air pollution
epigenetics
chronic obstructive pulmonary disease
particulate matter
aryl hydrocarbon receptor
nuclear factor-κB
title Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter
title_full Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter
title_fullStr Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter
title_full_unstemmed Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter
title_short Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter
title_sort inhaled pollutants the molecular scene behind respiratory and systemic diseases associated with ultrafine particulate matter
topic air pollution
epigenetics
chronic obstructive pulmonary disease
particulate matter
aryl hydrocarbon receptor
nuclear factor-κB
url http://www.mdpi.com/1422-0067/18/2/243
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