Michal Pardo

Vehicular emissions are an important source of urban air pollution that can age through atmospheric processes, but how their health effects change during atmospheric aging remains poorly understood. To simulate realistic urban emissions, we sampled air in a parking garage where cold-start and urban emissions coexist. Following aging in an oxidation flow reactor (OFR), we studied the cellular and acellular effects of the fresh and aged aerosols. Photochemical aging in the OFR increased secondary organic aerosol (SOA) mass by up to 6.9-fold, the oxygen-to-carbon (O:C) ratio from 0.26 to 0.79, and both the intrinsic oxidative potential (OPm) and the volume-normalized oxidative potential (OPv). In contrast, the peroxide-sensitive DCF activity decreased following aging. Cellular exposure to aged aerosol extracts increased cellular reactive oxygen species (ROS) formation in lung (A549) and liver (HepG2) cells, whereas fresh extracts strongly reduced cellular respiration, particularly in HepG2 cells. Cell painting analysis showed distinct morphological profiles. Exposure to aged extracts showed greater oxidative stress and DNA damage responses than those of exposure to fresh extracts. These findings suggest that atmospheric aging shifts the toxicity of fresh emissions from suppression of mitochondrial respiration toward oxygenated organics that can drive intracellular oxidative stress and DNA damage phenotypes. In conclusion, atmospheric aging of cold-start and urban vehicular emissions contributes to enhanced SOA formation and leads to distinct biological outcomes that depend on the degree of oxidative aging.

In this study, the acellular dithiothreitol (DTT) assay, the in vitro cellular DCFH-DA assay on human lung epithelial cells, and gene expression measurements were used to assess the toxicity of water-soluble (WS) PM₁₀ relating to reactive oxygen species (ROS) in summer at an Eastern Mediterranean urban site. Large influences from anthropogenic sources on health risks were observed with acellular and cellular assays. Anthropogenic biomass burning (BB) and natural dust events increased human pulmonary exposure to the oxidative potential (OP_dose,T) of WS-PM₁₀ by 209 and 47%, respectively, compared to regular periods. OP_v ^DTT and ROS_v results were positively correlated in anthropogenic-dominant samples, while showed no significant correlation in the remaining samples. As a result, the BB and dust event had higher and lower levels of cellular ROS_v compared with the nonevent period, respectively. Source apportionment results suggest that specific organic contents (e.g., PAHs) had relatively low contents in samples less influenced by anthropogenic sources, possibly explaining the divergence in acellular and cellular results. Heavy metals were dominant contributors of OP_v ^DTT throughout the campaign, and a Chelex method is recommended over a EDTA method for quantification of their summed OP_v ^DTT.

Tailpipe emissions from road traffic contribute substantially to the burden of fine inhalable particulate matter (PM _2.5 ) and deteriorate air quality. Exhaust emission standards, forcing improvements in combustion and exhaust after-treatment technology, considerably decreases combustion-related PM _2.5 emitted by modern cars. A549 cancerous alveolar and BEAS-2B normal bronchial epithelial cells were exposed at the air-liquid interface to the total aerosol or gas phase of either fresh or photochemically aged tailpipe emissions from a gasoline EURO 6d car equipped with a gasoline particulate filter. Diluted fresh emissions contained particle number concentrations comparable to low ambient air levels and induced no detectable cytotoxicity. Photochemical aging led to the formation of secondary aerosols and caused significant cytotoxicity. While the aged aerosol induced significant DNA damage, oxidative stress was more associated with volatile secondary species. Our results call for the consideration of the exhaust emission atmospheric transformation processes in future emission standards toward health effect-driven emission regulations.

Exposure to airborne particulate matter (PM) has been attributed to millions of deaths annually. However, the PM components responsible for observed health effects remain unclear. Oxidative potential (OP) has gained increasing attention as a key property that may explain PM toxicity. Using online measurement methods that impinge particles for OP quantification within seconds, we reveal that 60 to 99% of reactive oxygen species (ROS) and OP in secondary organic aerosol and combustion-generated PM have a lifetime of minutes to hours and that the ROS activity of ambient PM decays substantially before offline analysis. This implies that current offline measurement methods substantially underestimate the true OP of PM. We demonstrate that short-lived OP components activate different toxicity pathways upon direct deposition onto reconstituted human bronchial epithelia. Therefore, we suggest that future air pollution and health studies should include online OP quantification, allowing more accurate assessments of links between OP and health effects.

Decades of research have established the toxicity of soot particles resulting from incomplete combustion. However, the unique chemical compounds responsible for adverse health effects have remained uncertain. This study utilized mass spectrometry to analyze the chemical composition of extracted soot organics at three oxidation states, aiming to establish quantitative relationships between potentially toxic chemicals and their impact on human alveolar basal epithelial cells (A549) through metabolomics-based evaluations. Targeted analysis using MS/MS indicated that particles with a medium oxidation state contained the highest total abundance of compounds, particularly oxygen-containing polycyclic aromatic hydrocarbons (OPAHs) composed of fused benzene rings and unsaturated carbonyls, which may cause oxidative stress, characterized by the upregulation of three specific metabolites. Further investigation focused on three specific OPAH standards: 1,4-naphthoquinone, 9-fluorenone, and anthranone. Pathway analysis indicated that exposure to these compounds affected transcriptional functions, the tricarboxylic acid cycle, cell proliferation, and the oxidative stress response. Biodiesel combustion emissions had higher concentrations of PAHs, OPAHs, and nitrogen-containing PAHs (NPAHs) compared with other fuels. Quinones and 9,10-anthraquinone were identified as the dominant compounds within the OPAH category. This knowledge enhances our understanding of the compounds contributing to adverse health effects observed in epidemiological studies and highlights the role of aerosol composition in toxicity.