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.
Highlights
Air pollutants are released into the atmosphere and can cause significant harm to humans
This study demonstrated that mice with impaired autophagy had significantly reduced airway inflammation and mucus hyper-production in response to the PM0.1, suggesting that autophagy contributes to particulate matter (PM)-induced airway epithelial injury and inflammation [50]
We have shown that the Aryl Hydrocarbon Receptor (AhR) protects against cigarette smoke-induced pulmonary oxidative stress, apoptosis and inflammation [11,70,71,72], and that cigarette smoke contains large amounts of PM0.1 [73], we cannot ascribe a protective function regarding protection against PM0.1 in smoke
Summary
Air pollutants are released into the atmosphere and can cause significant harm to humans. Studies in healthy human volunteers using Technegas, an ultrafine dispersion of Technetium-labelled carbon (99 mTc) particles approximately 4–20 nm in diameter, revealed that the PM0.1 remained in the lung up to 6 h after installation some were detected in the blood immediately after inhalation [6]. These particles have a very large effective surface area where chemical interactions can occur and may be important biologically, as PM0.1 cross cell membranes and directly interact with cellular structures. FigFuigreur1e. 1T.hTehme moloelceuclualrarmmecehchaannisismmssaassssoocciiaatted wiitthh iinnffllaammmmaatotorryyaannddooxixdidataivtievestrsetrsessisnirnesrpesopnosense to ctohrcohnroicneicxepxopsousruerteotoPMPM0.10..1.PPMM,,ppaarrttiiccuulate mattteerr;; RROOSS,,ggeenneerraatitoionnoof freraecatcivtieveoxoyxgyegne;nJN; JKN,Kc-,Jcu-nJun kinkainsea;seA; hARh,RA, Aryrlylhyhdyrdorcoacrabrboonnrreecceeppttoorr;; Nrf, nuucclleeaarr ffaaccttoorr(e(eryryththroriodid-d-edreivrievded2)-2l)ik-leik2e; 2A; RAER, E, antainotxioidxaidnatnrtersepsopnosneseeleelmemenent;t;XXRREE,,xxeennoobbiiootic respoonnsseeeelleemmeennt;t;AAPP-1--1R-RE,EA, AP-P1-1rersepsopnosneseeleemleemnte;nt; NFN-κFB-κ-RB-ER,EN, FN-Fκ-BκBrersepsopnosneseeleelmemeennt;t;RReellAA,,vv--rreell aavian reticcuullooeennddooththeeliloiosissisvviriarlaol nocnocgoegneenheohmoomlooglog A oAr opr65p;6R5;eRlBe,lBr,etriectuicluoleonednodtohtheleiloiossisisvviriraalloonnccooggene hommoolloogguueeBB;;NNAADDPPHH, ,nnicioctointianmamidiedaedaedneinneine dinduinculecoletiodtiedephpohsopshpahtaet-eo-oxxididaassee;; AArrnntt,, aarryl hhydrocaarrbboonn rreecceepptotorrnnuuclcelaerartrtarnasnlsolcoactaotro. rS. oSliodlildinlei:ne: actaivctaivtiaotnio;nd; adsahshededlilninee:: trraannssllooccaatitoionn; ;rerdedlinlein: ein: flianmflmamatmorayt/oorxyid/aonxtidpanthtwpaayt;hrwedayd;asrhededdlainseh:eadntlii-ne: antiin-filnaflmammamtoartyo/rayn/tia-onxtii-doaxnitdpaantthpwaathy.way
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