Effect of Biomass Burning, Diwali Fireworks, and Polluted Fog Events on the Oxidative Potential of Fine Ambient Particulate Matter in Delhi, India.

We investigated the influence of biomass burning (BURN), Diwali fireworks, and fog events on the ambient fine particulate matter (PM2.5) oxidative potential (OP) during the postmonsoon (PMON) and winter season in Delhi, India. The real-time hourly averaged OP (based on a dithiothreitol assay) and PM2.5 chemical composition were measured intermittently from October 2019 to January 2020. The peak extrinsic OP (OPv: normalized by the volume of air) was observed during the winter fog (WFOG) (5.23 ± 4.6 nmol·min-1·m-3), whereas the intrinsic OP (OPm; normalized by the PM2.5 mass) was the highest during the Diwali firework-influenced period (29.4 ± 18.48 pmol·min-1·µg-1). Source apportionment analysis using positive matrix factorization revealed that traffic + resuspended dust-related emissions (39%) and secondary sulfate + oxidized organic aerosols (38%) were driving the OPv during the PMON period, whereas BURN aerosols dominated (37%) the OPv during the WFOG period. Firework-related emissions became a significant contributor (∼32%) to the OPv during the Diwali period (4 day period from October 26 to 29), and its contribution peaked (72%) on the night of Diwali. Discerning the influence of seasonal and episodic sources on health-relevant properties of PM2.5, such as OP, could help better understand the causal relationships between PM2.5 and health effects in India.

Review of in vitro studies evaluating respiratory toxicity of aerosols: impact of cell types, chemical composition, and atmospheric processing.

In recent decades, several cell-based and acellular methods have been developed to evaluate ambient particulate matter (PM) toxicity. Although cell-based methods provide a more comprehensive assessment of PM toxicity, their results are difficult to comprehend due to the diversity in cellular endpoints, cell types, and assays and the interference of PM chemical components with some of the assays' techniques. In this review, we attempt to clarify some of these issues. We first discuss the morphological and immunological differences among various macrophage and epithelial cells, belonging to the respiratory systems of human and murine species, used in the in vitro studies evaluating PM toxicity. Then, we review the current state of knowledge on the role of different PM chemical components and the relevance of atmospheric processing and aging of aerosols in the respiratory toxicity of PM. Our review demonstrates the need to adopt more physiologically relevant cellular models such as epithelial (or endothelial) cells instead of macrophages for oxidative stress measurement. We suggest limiting macrophages for investigating other cellular responses (e.g., phagocytosis, inflammation, and DNA damage). Unlike monocultures (of macrophages and epithelial cells), which are generally used to study the direct effects of PM on a given cell type, the use of co-culture systems should be encouraged to investigate a more comprehensive effect of PM in the presence of other cells. Our review has identified two major groups of toxic PM chemical species from the existing literature, i.e., metals (Fe, Cu, Mn, Cr, Ni, and Zn) and organic compounds (PAHs, ketones, aliphatic and chlorinated hydrocarbons, and quinones). However, the relative toxicities of these species are still a matter of debate. Finally, the results of the existing studies investigating the effect of aging on PM toxicity are ambiguous, with varying results due to different cell types, different aging conditions, and the presence/absence of specific oxidants. More systematic studies are necessary to understand the role of different SOA precursors, interactions between different PM components, and aging conditions in the overall toxicity of PM. We anticipate that our review will guide future investigations by helping researchers choose appropriate cell models, resulting in a more meaningful interpretation of cell-based assays and thus ultimately leading to a better understanding of the health effects of PM exposure.

Inter-continental variability in the relationship of oxidative potential and cytotoxicity with PM2.5 mass.

Most fine ambient particulate matter (PM2.5)-based epidemiological models use globalized concentration-response (CR) functions assuming that the toxicity of PM2.5 is solely mass-dependent without considering its chemical composition. Although oxidative potential (OP) has emerged as an alternate metric of PM2.5 toxicity, the association between PM2.5 mass and OP on a large spatial extent has not been investigated. In this study, we evaluate this relationship using 385 PM2.5 samples collected from 14 different sites across 4 different continents and using 5 different OP (and cytotoxicity) endpoints. Our results show that the relationship between PM2.5 mass vs. OP (and cytotoxicity) is largely non-linear due to significant differences in the intrinsic toxicity, resulting from a spatially heterogeneous chemical composition of PM2.5. These results emphasize the need to develop localized CR functions incorporating other measures of PM2.5 properties (e.g., OP) to better predict the PM2.5-attributed health burdens.

Sources of cellular oxidative potential of water-soluble fine ambient particulate matter in the Midwestern United States.

We investigated the spatiotemporal distribution and sources of cellular oxidative potential (OP) in the Midwest US. Weekly samples were collected from three urban [Chicago (IL), Indianapolis (IN), and St. Louis (MO)], one rural [Bondville (IL], and one roadside site [Champaign (IL)] for a year (May 2018 to May 2019), and analyzed for water-soluble cellular OP using a macrophage reactive oxygen species (ROS) assay. Chemical composition of the samples including several carbonaceous components, inorganic ions, and water-soluble elementals, were also analyzed. The emission sources contributing to water-soluble cellular OP and PM2.5 mass were analyzed using positive matrix factorization. The secondary organic aerosols contributed substantially (≥54%) to PM2.5 cellular OP at urban sites, while the roadside and rural OP were dominated by road dust (54%) and agricultural activities (62%), respectively. However, none of these sources contributed substantially to the PM2.5 mass (≤21%). Other sources contributing significantly to the PM2.5 mass, i.e., secondary sulfate and nitrate, biomass burning and coal combustion (14-26%) contributed minimally to the cellular OP (≤13%). Such divergent profiles of the emission sources contributing to cellular OP vs. PM2.5 mass demonstrate the need of considering more health-relevant metrics such as OP in the design of air pollution control strategies.