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Int. J. Mol. Sci. 2017, 18(2), 243; doi:10.3390/ijms18020243

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

1
Department of Medicine, McGill University, Montreal, QC H4A 3J1, Canada
2
Department of Pathology, McGill University, Montreal, QC H4A 3J1, Canada
3
Department of Pharmacology & Therapeutics, McGill University, Montreal, QC H3G 1Y6, Canada
4
Department of Chemistry, McGill University, Montreal, QC H3A 2K6, Canada
*
Author to whom correspondence should be addressed.
Academic Editors: Paul R. Reynolds and Benjamin T. Bikman
Received: 21 November 2016 / Revised: 9 January 2017 / Accepted: 13 January 2017 / Published: 24 January 2017
(This article belongs to the Special Issue Inhaled Pollutants Modulate Respiratory and Systemic Diseases)
View Full-Text   |   Download PDF [1685 KB, uploaded 24 January 2017]   |  

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 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. View Full-Text
Keywords: air pollution; epigenetics; chronic obstructive pulmonary disease; particulate matter; aryl hydrocarbon receptor; nuclear factor-κB air pollution; epigenetics; chronic obstructive pulmonary disease; particulate matter; aryl hydrocarbon receptor; nuclear factor-κB
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Traboulsi, H.; Guerrina, N.; Iu, M.; Maysinger, D.; Ariya, P.; Baglole, C.J. Inhaled Pollutants: The Molecular Scene behind Respiratory and Systemic Diseases Associated with Ultrafine Particulate Matter. Int. J. Mol. Sci. 2017, 18, 243.

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