11 research outputs found
Chemical characterisation of primary emissions and secondary aerosol formation from a gasoline vehicle compliant with EURO6 emission standard
On the Complementarity and Informative Value of Different Electron Ionization Mass Spectrometric Techniques for the Chemical Analysis of Secondary Organic Aerosols
Chemical Fingerprinting of Biomass Burning Organic Aerosols from Sugar Cane Combustion: Complementary Findings from Field and Laboratory Studies
Agricultural fires are a major source of biomass-burning
organic
aerosols (BBOAs) with impacts on health, the environment, and climate.
In this study, globally relevant BBOA emissions from the combustion
of sugar cane in both field and laboratory experiments were analyzed
using comprehensive two-dimensional gas chromatography time-of-flight
mass spectrometry. The derived chemical fingerprints of fresh emissions
were evaluated using targeted and nontargeted evaluation approaches.
The open-field sugar cane burning experiments revealed the high chemical
complexity of combustion emissions, including compounds derived from
the pyrolysis of (hemi)cellulose, lignin, and further biomass, such
as pyridine and oxime derivatives, methoxyphenols, and methoxybenzenes,
as well as triterpenoids. In comparison, laboratory experiments could
only partially model the complexity of real combustion events. Our
results showed high variability between the conducted field and laboratory
experiments, which we, among others, discuss in terms of differences
in combustion conditions, fuel composition, and atmospheric processing.
We conclude that both field and laboratory studies have their merits
and should be applied complementarily. While field studies under real-world
conditions are essential to assess the general impact on air quality,
climate, and environment, laboratory studies are better suited to
investigate specific emissions of different biomass types under controlled
conditions
Are reactive oxygen species (ROS) a suitable metric to predict toxicity of carbonaceous aerosol particles?
Abstract. It is being suggested that particle-bound or particle-induced reactive oxygen species (ROS), which significantly contribute to the oxidative potential (OP) of aerosol particles, are a promising metric linking aerosol compositions to toxicity and adverse health effects. However, accurate ROS quantification remains challenging due to the reactive and short-lived nature of many ROS components and the lack of appropriate analytical methods for a reliable quantification. Consequently, it remains difficult to gauge their impact on human health, especially to identify how aerosol particle sources and atmospheric processes drive particle-bound ROS formation in a real-world urban environment. In this study, using a novel online particle-bound ROS instrument (OPROSI), we comprehensively characterized and compared the formation of ROS in secondary organic aerosols (SOA) generated from organic compounds that represent anthropogenic (naphthalene, SOANAP) and biogenic (β-pinene, SOAβPIN) precursors. The SOA mass was condensed onto soot particles (SP) under varied atmospherically relevant conditions (photochemical aging and humidity). We systematically analysed the ability of the aqueous extracts of the two aerosol types (SOANAP-SP and SOAβPIN-SP) to induce ROS production and OP. We further investigated cytotoxicity and cellular ROS production after exposing human lung epithelial cell cultures (A549) to extracts of the two aerosols. A significant finding of this study is that more than 90 % of all ROS components in both SOA types have a short lifetime, highlighting the need to develop online instruments for a meaningful quantification of ROS. Our results also show that photochemical aging promotes particle-bound ROS production and enhances the OP of the aerosols. Compared to SOAβPIN-SP, SOANAP-SP elicited a higher acellular and cellular ROS production, a higher OP and a lower cell viability. These consistent results between chemical-based and biological-based analyses indicate that particle-bound ROS quantification could be a feasible metric to predict aerosol particle toxicity and adverse human effects. Moreover, the cellular ROS production caused by SOA exposure not only depends on aerosol type, but is also affected by exposure dose, highlighting a need to mimic the process of particle deposition onto lung cells and their interactions as realistically as possible to avoid unknown biases
Atmospheric aging increases the cytotoxicity of bare soot particles in BEAS-2B lung cells
Soot particles (SP) are ubiquitous components of atmospheric particulate matter and have been shown to cause various adverse health effects. In the atmosphere, freshly emitted SP can be coated by condensed low-volatility secondary organic and inorganic species. In addition, gas-phase oxidants may react with the surface of SP. Due to the chemical and physical resemblance of SP carbon backbone with polyaromatic hydrocarbon species and their potent oxidation products, we investigated the biological responses of BEAS-2B lung epithelial cells following exposure to fresh- and photochemically aged-SP at the air–liquid interface. A comprehensive physical and chemical aerosol characterization was performed to depict the atmospheric transformations of SP, showing that photochemical aging increased the organic carbon fraction and the oxidation state of the SP. RNA-sequencing and qPCR analysis showed varying gene expression profiles for fresh- and aged-SP. Exposure to aged-SP increased DNA damage, oxidative damage, and upregulation of NRF2-mediated oxidative stress response genes compared to fresh-SP. Furthermore, aged-SP augmented inflammatory cytokine secretion and activated AhR-response, as evidenced by increased expression of AhR-responsive genes. These results indicate that oxidative stress, inflammation, and DNA damage play a key role in the cytotoxicity of SP in BEAS-2B cells, where aging leads to higher toxic responses. Collectively, our results suggest that photochemical aging may increase SP toxicity through surface modifications that lead to an increased toxic response by activating different molecular pathways