The current study aims to integrate a methodology to quantify the translocation of UFPs from the nose to the olfactory (OLF) region and estimate the OLF deposition combined with an analysis of using different metrics for particles with an aerodynamic diameter smaller than 0.1 μm: mass (PM_0.1), number (PN_0.1), and surface concentration (PS_0.1). Simulations examined the source-specific impact from exposure to four distinct common urban sources: nucleation event, heating emissions, traffic emissions, and background levels. The estimation of the regional dose, clearance, and retention of UFPs in the HRT was also evaluated whilst the number of deposited particles per surface area/cell was estimated.

This study presents a novel methodology for measuring aerosol inhalation dose in enclosed environments using human participants while ensuring safety. Magnesium aerosols serve as tracers, collected via inhaler filters and analyzed with ICP-MS to quantify inhaled dose. Experiments were conducted under three airflow conditions: no ventilation, forced ventilation, and forced ventilation with air filtration. Results showed that inhalation dose decreased with distance and was significantly reduced under forced ventilation. Protection factors indicated that air filtration was most effective at short distances. This approach provides a practical and accurate means to assess aerosol exposure,.

The inhalation of virus-laden microdroplets, emitted through breathing or talking, is a mode of transmission of airborne diseases that is difficult to control, especially since the mechanisms of virus persistence in aerosols are not yet fully understood. The aim of this research is to study the evaporation dynamics of virus-laden respiratory microdroplets, with a particular focus on the impact of their composition on this process. We present initial results on the study of real saliva aerosols, highlighting the need to investigate pathogen survival in biological matrices rather than in synthetic media, which have traditionally been used in the literature.

The present study aims to assess how the OP of traffic-originated UPFs is linked to adverse effects in vitro and in vivo. In vitro, assessment includes cell exposures utilising a thermophoresis-based air-liquid interface (ALI) system and submerged exposures with traffic exhaust emissions. For in vivo assessment C57BL/6 mice were exposed to fresh and atmospheric aged traffic emissions from gasoline and diesel vehicles. The present study provides new, important insights into the cellular mechanisms induced by different air pollutants and how the OP of the UFPs is connected to those.

We measured the OP of aerosols derived from laboratory-generated air masses using various acellular methods after sampling on filters. These experiments were conducted on the PolluRisk platform, which enables preclinical models to be exposed for several days to simulated urban atmospheres. This platform includes an atmospheric chamber capable of generating realistic air masses, which are then transferred to exposure systems housing preclinical models. Additionally, a suite of analytical instruments is connected to these systems to characterize the physicochemical properties of the simulated air masses (gases and particles).

This study found that 6PPD was not cytotoxic at concentrations up to 10 μg/mL but was able to cause oxidative stress by glutathione (GSH) depletion (P<0.05) and cause DNA damage (P<0.05) after 24 hours exposure. The presence of N-acetyl-L-cysteine (NAC), a GSH precursor, mitigated both GSH depletion and DNA damage.