Abstract
Airborne ultrafine particles (UFP) mainly derive from combustion sources (e.g., diesel exhaust particles—DEP), abrasion sources (non-exhaust particles) or from the unintentional release of engineered nanoparticles (e.g., metal oxide nanoparticles—NPs), determining human exposure to UFP mixtures. The aim of the present study was to analyse the combined in vitro effects of DEP and metal oxide NPs (ZnO, CuO) on human lung A549 cells. The mixtures and the relative single NPs (DEP, ZnO, CuO) were characterized by transmission electron microscopy (TEM), dynamic light scattering (DLS) and inductively coupled plasma-optic emission spectroscopy (ICP-OES). Cells were exposed for different times (3–72 h) to mixtures of standard DEP at a subcytotoxic concentration and ZnO and CuO at increasing concentrations. At the end of the exposure, the cytotoxicity was assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) and clonogenic tests, the pro-inflammatory potential was evaluated by interleukin-8 (IL-8) release and the cell morphology was investigated by fluorescence and transmission electron microscopy. The obtained results suggest that the presence of DEP may introduce new physico-chemical interactions able to increase the cytotoxicity of ZnO and to reduce that of CuO NPs.
Highlights
Several epidemiological studies show an increase in respiratory and cardiac morbidity and mortality due to the exposure to particulate matter (PM), especially related to pulmonary and cardiovascular diseases [1]
ultrafine particles (UFP) are the fraction of inhalable particles that largely impact on human health, since they can deeply penetrate in the respiratory system, reaching the profound lungs, where they interact with the alveolar epithelium, potentially cross the respiratory barrier and eventually reach secondary target organs [2]
Diesel exhaust particles (DEP), which are composed of a carbonaceous core and adsorbed organic compounds, including polycyclic aromatic hydrocarbons (PAHs), metals, and other trace elements [4], are the emissions that mainly contribute to urban PM
Summary
Several epidemiological studies show an increase in respiratory and cardiac morbidity and mortality due to the exposure to particulate matter (PM), especially related to pulmonary and cardiovascular diseases [1]. Diesel exhaust particles (DEP), which are composed of a carbonaceous core and adsorbed organic compounds, including polycyclic aromatic hydrocarbons (PAHs), metals, and other trace elements [4], are the emissions that mainly contribute to urban PM. Another source of UFP are derived from non-exhaust sources, coming from tire and brake wearing [5] or from the unintentional release of engineered nanoparticles (NPs) in the environment. Non-exhaust particles derive from abrasive sources, which include tire and brake wear and abrasion of the road surface. NPs have been employed as engine fuel additives as an improvement in the abatement of greenhouse gases [15]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
