Search

In the framework of the 2017 “carbonaceous aerosol in Rome and Environs” (CARE) experiment, particle number size distributions have been continuously measured on February 2017 in downtown Rome. These data have been used to estimate, through MPPD model, size and time resolved particle mass, surface area and number doses deposited into the respiratory system. Dosimetry estimates are presented for PM10, PM2.5, PM1 and Ultrafine Particles (UFPs), in relation to the aerosol sources peculiar to the Mediterranean basin and to the atmospheric conditions. Particular emphasis is focused on UFPs and their fraction deposited on the olfactory bulb, in view of their possible translocation to the brain. The site of PM10 deposition within the respiratory system considerably changes, depending on the aerosol sources and then on its different size distributions. On making associations between health endpoints and aerosol mass concentrations, the relevant coarse and fine fractions would be more properly adopted, because they have different sources, different capability of penetrating deep into the respiratory system and different toxicological implications. The separation between them should be set at 1 µm, rather than at 2.5 µm, because the fine fraction is considerably less affected by the contribution of the natural sources. Mass dose is a suitable metric to describe coarse aerosol events but gives a poor representation of combustion aerosol. This fraction of particles, made of UFPs and of accumulation mode particles (mainly with size below 0.2 µm), is of high health relevance. It elicited the highest oxidative activity in the CARE experiment and is properly described by the particle surface area and by the number metrics. Such metrics are even more relevant for the UFP doses deposited on the olfactory bulb, in consideration of the role recognized to oxidative stress in the progression of neurodegenerative diseases. Such metrics would be more appropriate, rather than PMx mass conce

The “Carbonaceous Aerosol in Rome and Environs” (CARE) experiment took place at a Mediterranean urban background site in Rome (Italy) deploying a variety of instrumentation to assess aerosol physical-chemical and optical properties with high-time resolution (from 1 min to 2 h). In this study, aerosol optical properties, chemical composition, and size distribution data were examined with a focus on the analysis of several intensive optical properties obtained from multi-wavelength measurements of aerosol scattering and absorption coefficients. The spectral behaviour of several quantities related to both aerosol composition and size was explored, analysing their high-time resolved temporal patterns and combining them in order to extract the maximum information from all the available data. A methodology to separate aerosol types using optical data only is here proposed and applied to an urban area characterised by a complex mixture of particles. A key is given to correctly disentangle cases that could not be distinguished observing only one or few parameters, but that can be clearly separated using a suitable ensemble of optical properties. The SSCAAE, i.e. the wavelength dependence of the Single Scattering co-albedo 1-SSA (where SSA is the Single Scattering Albedo) - that efficiently responds to both aerosol size and chemical composition – resulted to be the best optical intensive parameter to look at for the discrimination between episodes characterised by specific aerosol types (e.g. sea salt, Saharan dust) and more mixed conditions dominated by local emissions. However, this study also highlighted that it is necessary to combine temporal patterns of different optical parameters to robustly associate SSCAAE features to specific aerosol types. In addition, the complete chemical speciation and the high-time resolved size distribution were used to confirm the aerosol types identified via a combination of aerosol optical properties. Look-up tables with most suitable ran

The causal link between ambient PM2.5 and adverse health effects is still not clear enough, nor it is clear what factors (physical and/or chemical) contribute to PM2.5 toxicity and by what mechanism(s). With a view on this, we launched the CARE experiment, during which we performed a comprehensive characterisation of the physicochemical properties of fine and ultrafine particles under exposure levels dominated by the urban combustion aerosol, and their toxicological assessment through in-vitro tests (lung epithelia cells cultured at the ALI) directly under ambient conditions, oxidative potential (determined through 2′,7′-dichlorouorescin, OPDCFH), and human biomonitoring. We already reported about aerosol characterisation, and in-vitro model results during CARE. Building upon these, in this work we assess the combustion aerosol oxidative response through the analysis of consistency between the three independent aerosol oxidative responses obtained, and the exploration of any causality link with the combustion aerosol. This is the first time to our knowledge that combustion related PM2.5 physicochemical properties and its OPDCFH are compared to the cellular-oxidative response (C-OR) obtained through the PM in-vitro test carried out (for the first time) directly under atmospheric ambient conditions, and to certain biomarkers of oxidative damage to DNA/RNA (8-oxo-7,8-dihydroguanine, 8-oxo-7,8-dihydro-2′-deoxyguanosine and 8-oxo-7,8 - dihydroguanosine). Our results provide a first evidence of a combustion-dependent association between the in vitro C-OR, the PM2.5 OPDCFH, and the urinary excretion of the 8-Oxo-7,8-dihydroguanosine. Yet this is not a substantial basis for drawing any cause-effect relationship. However, our findings support previous literature suggesting a link between combustion and oxidative response of PM2.5. Moreover, we add a consistency across completely independent oxidative response measurements with a possible dependence on the combustion traffic

Air pollution and particulate matter are recognised cause of increased disease incidence in exposed population. The toxicological processes underlying air pollution associated effects have been investigated by in vivo and/or in vitro experimentation. The latter is usually performed by exposing cells cultured under submerged condition to particulate matter concentration quite far from environmental exposure expected in humans. Here we report for the first time the feasibility of a direct exposure of air liquid interface cultured cells to environmental concentration of particulate matter. Inflammatory proteins release was analysed in cell medium while differential expression of selected genes was analysed in cells. Significant association of anti-oxidant genes was observed with secondary and aged aerosol, while cytochrome activation with primary and PAHs enriched ultrafine particles. The results obtained clearly show the opportunity to move from the lab bench to the field for properly understanding the toxicological effects also of ultrafine particles on selected in vitro models.