High levels of ambient air pollution are associated with exacerbation of asthma and respiratory morbidity, yet little is known concerning the mechanisms of inflammation and toxicity by components of inhaled particulate matter (PM). Brief inhalation of PM(2.5) (particles of an aerodynamic diameter of < 2.5 microns) (300 microg/m(3) air for 6 h followed by a period of 24 h in clean air) by either C3H/HeJ or C57/BL6 mice caused significant (P

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BackgroundShip engine emissions are important with regard to lung and cardiovascular diseases especially in coastal regions worldwide. Known cellular responses to combustion particles include oxidative stress and inflammatory signalling.ObjectivesTo provide a molecular link between the chemical and physical characteristics of ship emission particles and the cellular responses they elicit and to identify potentially harmful fractions in shipping emission aerosols.MethodsThrough an air-liquid interface exposure system, we exposed human lung cells under realistic in vitro conditions to exhaust fumes from a ship engine running on either common heavy fuel oil (HFO) or cleaner-burning diesel fuel (DF). Advanced chemical analyses of the exhaust aerosols were combined with transcriptional, proteomic and metabolomic profiling including isotope labelling methods to characterise the lung cell responses.ResultsThe HFO emissions contained high concentrations of toxic compounds such as metals and polycyclic aromatic hydrocarbon, and were higher in particle mass. These compounds were lower in DF emissions, which in turn had higher concentrations of elemental carbon (“soot”). Common cellular reactions included cellular stress responses and endocytosis. Reactions to HFO emissions were dominated by oxidative stress and inflammatory responses, whereas DF emissions induced generally a broader biological response than HFO emissions and affected essential cellular pathways such as energy metabolism, protein synthesis, and chromatin modification.ConclusionsDespite a lower content of known toxic compounds, combustion particles from the clean shipping fuel DF influenced several essential pathways of lung cell metabolism more strongly than particles from the unrefined fuel HFO. This might be attributable to a higher soot content in DF. Thus the role of diesel soot, which is a known carcinogen in acute air pollution-induced health effects should be further investigated. For the use of HFO and DF we recommend a reduction of carbonaceous soot in the ship emissions by implementation of filtration devices.

Coronavirus disease 2019 (COVID-19), an acute respiratory disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has rapidly developed into a pandemic throughout the world. This disease is a highly infectious novel coronavirus and can affect people of all ages. Previous reports observed that particulate matter (PM) provided a platform for intermixing with viruses (i.e., influenza). However, the role of PM in SARS-CoV-2 transmission remains unclear. In this paper, we propose that PM plays a direct role as a “carrier” of SARS-CoV-2. SARS-CoV-2 is reported to have a high affinity for the angiotensin-converting enzyme 2 (ACE2) receptor. Indirectly, exposure to PM increases ACE2 expression in the lungs which facilitates SARS-CoV-2 viral adhesion. Thus, the high risk of SARS-CoV-2 in heavily polluted regions can be explained by upregulation of ACE2 caused by PM. PM could be both a direct and indirect transmission model for SARS-CoV-2 infection.

Most particles breathed on rail subway platforms are highly ferruginous (FePM) and extremely small (nanometric to a few microns in size). High magnification observations of particle texture and chemistry on airborne PM₁₀ samples collected from the Barcelona Metro, combined with published experimental work on particle generation by frictional sliding, allow us to propose a general model to explain the origin of most subway FePM. Particle generation occurs by mechanical wear at the brake-wheel and wheel-rail interfaces, where magnetic metallic flakes and splinters are released and undergo progressive atmospheric oxidation from metallic iron to magnetite and maghemite. Flakes of magnetite typically comprise mottled mosaics of octahedral nanocrystals (10-20 nm) that become pseudomorphed by maghemite. Continued oxidation results in extensive alteration of the magnetic nanostructure to more rounded aggregates of non-magnetic hematite nanocrystals, with magnetic precursors (including iron metal) still preserved in some particle cores. Particles derived from steel wheel and rails contain a characteristic trace element chemistry, typically with Mn/Fe=0.01. Flakes released from brakes are chemically very distinctive, depending on the pad composition, being always carbonaceous, commonly barium-rich, and texturally inhomogeneous, with trace elements present in nanominerals incorporated within the crystalline structure. In the studied subway lines of Barcelona at least there appears to be only a minimal aerosol contribution from high temperature processes such as sparking. To date there is no strong evidence that these chemically and texturally complex inhalable metallic materials are any more or less toxic than street-level urban particles, and as with outdoor air, the priority in subway air quality should be to reduce high mass concentrations of aerosol present in some stations.

The respiratory tract is the primary site of exposure to airborne compounds, with the bronchial epithelium providing one of the first lines of defence. A growing need exists for an accurate in vitro model of the bronchial epithelium. Here, normal human bronchial epithelial (NHBE) cells cultured at an air/liquid interface create a fully differentiated, in-vivo-like model of the human bronchial epithelium. Developmental characterisation includes (i) trans-epithelial electrical resistance, (ii) morphology and (iii) bronchial cell specific stains/markers. It is concluded that the basal/progenitor cells create a pseudo-stratified, mucociliary NHBE model containing basal, serous, Clara, goblet and ciliated cells, reflective of the normal human bronchial epithelium (days 24-33 ALI culture).

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