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New health index derived from oxidative potential and cell toxicity of fine particulate matter to assess its potential health effect.

ABSTRACT: Toxicological data and exposure levels of fine particulate matters (PM_2.5) are necessary to better understand their health effects. Simultaneous measurements of PM_2.5 oxidative potential (OP) and cell toxicity in urban areas (Beijing, China and Gwangju, Korea) reveal their dependence on chemical composition. Notably, acids (Polar), benzocarboxylic acids, and Pb were the chemical components that affected both OP and cell toxicity. OP varied more significantly among different locations and seasons (winter and summer) than cell toxicity. Using the measured OP, cell toxicity, and PM_2.5 concentration, a health index was developed to better assess the potential health effects of PM_2.5. The health index was related to the sources of PM_2.5 derived from the measured chemical components. The contributions of secondary organic aerosols and dust to the proposed health index were more significant than their contributions to PM_2.5 mass. The developed regression equation was used to predict the health effect of PM_2.5 without further toxicity measurements. This new index could be a valuable health metric that provides information beyond just the PM_2.5 concentration level.

SUBMITTER: Park M

PROVIDER: S-EPMC10864913 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature

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New health index derived from oxidative potential and cell toxicity of fine particulate matter to assess its potential health effect.

Park Minhan M Lee Seunghye S Lee Haebum H Denna Ma Cristine Faye J MCFJ Jang Jiho J Oh Dahye D Bae Min-Suk MS Jang Kyoung-Soon KS Park Kihong K

Heliyon 20240202 3

Toxicological data and exposure levels of fine particulate matters (PM<sub>2.5</sub>) are necessary to better understand their health effects. Simultaneous measurements of PM<sub>2.5</sub> oxidative potential (OP) and cell toxicity in urban areas (Beijing, China and Gwangju, Korea) reveal their dependence on chemical composition. Notably, acids (Polar), benzocarboxylic acids, and Pb were the chemical components that affected both OP and cell toxicity. OP varied more significantly among different ...[more]

PMID: 38356560

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Project description:BackgroundAlthough many studies have linked prenatal exposure to PM2.5 to adverse birth outcomes, little is known about the effects of exposure to specific constituents of PM2.5 or mechanisms that contribute to these outcomes.ObjectivesOur objective was to investigate effects of oxidative potential and PM2.5 metal components from non-exhaust traffic emissions, such as brake and tire wear, on the risk of preterm birth (PTB) and term low birth weight (TLBW).MethodsFor a birth cohort of 285,614 singletons born in Los Angeles County, California, in the period 2017-2019, we estimated speciated PM2.5 exposures modeled from land use regression with cokriging, including brake and tire wear related metals (barium and zinc), black carbon, and three markers of oxidative potential (OP), including modeled reactive oxygen species based on measured iron and copper (ROS), OH formation (OPOH), and dithiothreitol (DTT) loss (OPDTT). Using logistic regression, we estimated odds ratios (OR) and 95% confidence intervals (CI) for PTB and TLBW with speciated PM2.5 exposures and PM2.5 mass as continuous variables scaled by their interquartile range (IQR).ResultsFor both metals and oxidative potential metrics, we estimated increased risks for PTB (ORs ranging from 1.01 to 1.03) and TLBW (ORs ranging from 1.02 to 1.05) per IQR exposure increment that were robust to adjustment for PM2.5 mass. Associations for PM2.5 mass, black carbon, metal components, and oxidative potential (especially ROS and OPOH) with adverse birth outcomes were stronger in Hispanic, Black, and mixed-race or Native American women.DiscussionOur results indicate that exposure to PM2.5 metals from brake and tire wear and particle components that contribute to oxidative potential were associated with an increased risk of PTB and TLBW in Los Angeles County, particularly among Hispanic, Black, and mixed-race or Native American women. Thus, reduction of PM2.5 mass only may not be sufficient to protect the most vulnerable pregnant women and children from adverse effects due to traffic source exposures. https://doi.org/10.1289/EHP12196.

Project description:The main objective of this study was chemical characterization and source apportionment of the oxidative potential of ambient PM2.5 samples collected in an urban background area in Athens, Greece. Ambient PM2.5 samples were collected during the summer (June-September) of 2017 and winter (February-March) of 2018 at a residential, urban background site in the outlying neighborhood of the Demokritos National Laboratory in Athens, Greece. The collected PM samples were analyzed for their chemical constituents including metals and trace elements, water-soluble organic carbon (WSOC), elemental and organic carbon (EC/OC), and marker of biomass burning (i.e., levoglucosan). In addition, the DCFH in vitro assay was performed to determine the oxidative potential of the PM2.5 samples. We performed a series of statistical analyses, including Spearman rank-order correlation analysis, principal component analysis (PCA), and multi linear regression (MLR) to determine the most significant species (as source tracers) contributing to the oxidative potential of PM2.5. Our findings revealed that the intrinsic (per PM mass) and extrinsic (per m3 of air volume) oxidative potentials of the collected ambient PM2.5 samples were significantly higher than those measured in many urban areas around the world. The results of the MLR analyses indicated that the major pollution sources contributing to the oxidative potential of ambient PM2.5 were vehicular emissions (characterized by EC) (44%), followed by secondary organic aerosol (SOA) formation (characterized by WSOC) (16%), and biomass burning (characterized by levoglucosan) (9%). The oxidative potential of the collected ambient PM2.5 samples was also higher in summer compared to the winter, mainly due to higher concentrations of EC and WSOC during this season. Results from this study corroborate the impact of traffic and SOA on the oxidative potential of ambient PM2.5 in greater Athens area, and can be helpful in adopting appropriate public health policies regarding detrimental outcomes of exposure to PM2.5.

Project description:Using particulate matter (PM) mass as exposure metric does not reveal the intrinsic PM chemical characteristics or toxic potential, which is crucial for monitoring the sources of emission causing adverse health effects and developing risk mitigating strategies. Oxidative stress and ensuing lipid peroxidation (LPO) in the lung are crucial underlying mechanisms of action by which PM drives cardiorespiratory disease. In the current study, we have postulated and demonstrated that the intrinsic potential of PM to elicit LPO, defined as "LPO index" as a novel approach for characterizing oxidative potential of PM (PMOP) and predicting biological toxicity. First, we exposed unsaturated phosphatidylcholine (PC), an abundant phospholipid in the cell membrane, pulmonary surfactant, and lipoproteins to PM and analyzed the total burden of LPO byproducts generated as a measure of LPO index using a LPO reporter dye, BODIPY-C11. PM exposure resulted in a concentration-dependent increase in LPO. Second, we developed a novel method to expose the captured serum apoB100 lipoprotein particles to PM or its constituents and assessed the levels of specific oxidized-phospholipid on apoB100 particles by immunoassay using E06 monoclonal antibody (mab) that recognizes only PC containing oxidized-phospholipids (Ox-PCs). The immunoassay was highly sensitive to evaluate the PM LPO index and was modifiable by metal quenchers and exogenous antioxidant and radical quenchers. Third, to prove the pathophysiological relevance of Ox-PCs, we found that PM exposure generates Ox-PCs in mice lungs, pulmonary surfactant and lung cells. Fourth, we observed that treatment of macrophages with BAL fluid from PM exposed mice or PM-exposed pulmonary surfactant stimulated IL-6 production, which was abrogated by neutralization of Ox-PCs by mab E06 suggesting that Ox-PCs in lungs are proinflammatory. Overall, our study suggests that Ox-PCs as a probe of PM LPO index is a biologically relevant pathogenic biomarker and has a high value for evaluating PMOP.

Project description:The human skin is exposed to various environmental factors including solar radiation and ambient air pollutants. Although, due to its physical and biological properties, the skin efficiently protects the body against the harm of environmental factors, their excessive levels and possible synergistic action may lead to harmful effects. Among particulate matter present in ambient air pollutants, PM2.5 is of particular importance for it can penetrate both disrupted and intact skin, causing adverse effects to skin tissue. Although certain components of PM2.5 can exhibit photochemical activity, only a limited amount of data regarding the interaction of PM2.5 with light and its effect on skin tissue are available. This study focused on light-induced toxicity in cultured human keratinocytes, which was mediated by PM2.5 obtained in different seasons. Dynamic Light Scattering (DLS) and Atomic Force Microscopy (AFM) were employed to determine sizes of the particles. The ability of PM2.5 to photogenerate free radicals and singlet oxygen was studied using EPR spin-trapping and time-resolved singlet oxygen phosphorescence, respectively. Solar simulator with selected filters was used as light source for cell treatment to model environmental lightning conditions. Cytotoxicity of photoexcited PM2.5 was analyzed using MTT assay, PI staining and flow cytometry, and the apoptotic pathway was further examined using Caspase-3/7 assay and RT-PCR. Iodometric assay and JC-10 assay were used to investigate damage to cell lipids and mitochondria. Light-excited PM2.5 were found to generate free radicals and singlet oxygen in season-dependent manner. HaCaT cells containing PM2.5 and irradiated with UV-Vis exhibited oxidative stress features-increased peroxidation of intracellular lipids, decrease of mitochondrial membrane potential, enhanced expression of oxidative stress related genes and apoptotic cell death. The data indicate that sunlight can significantly increase PM2.5-mediated toxicity in skin cells.

Dataset Information

New health index derived from oxidative potential and cell toxicity of fine particulate matter to assess its potential health effect.

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New health index derived from oxidative potential and cell toxicity of fine particulate matter to assess its potential health effect.

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