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Continuous exposure of human skin to air pollution can result in a range of undesirable skin conditions. In our recent study, UV and visible light were found to increase cytotoxicity of fine particulate matter (PM 2.5 ) against human keratinocytes. Since it is impossible to avoid exposure of human skin to PM 2.5 , effective strategies are needed to reduce their damaging effects. l-ascorbic acid and resveratrol were tested as potential topical agents against pollution-related skin impairment. Although these agents were previously found to ameliorate PM-dependent damage, the effect of light and seasonal variation of particles were not previously studied. EPR spin-trapping, DPPH assay, and singlet oxygen phosphorescence were used to determine the scavenging activities of the antioxidants. MTT, JC-10 and iodometric assays were used to analyze the effect on PM 2.5 -induced cytotoxicity, mitochondrial damage and oxidation of lipids. Live-cell imaging was employed to examine wound-healing properties of cells. Light-induced, PM 2.5 -mediated oxidative damage was examined by immunofluorescent staining. Both antioxidants effectively scavenged free radicals and singlet oxygen produced by PM 2.5 , reduced cell death and prevented oxidative damage to HaCaT cells. l-ascorbic acid and resveratrol, especially when applied in combination, can protect HaCaT cells against the dark and light induced toxicity of PM 2.5 ., (© 2023 American Society for Photobiology.)

Hydroxyl radicals were generated from an aqueous suspension of ambient PM2.5 and detected utilizing 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) as a spin trap coupled with electron paramagnetic resonance (EPR) spectroscopy. Results from this study suggested the importance of environmentally persistent free radicals (EPFRs) in PM2.5 to generate significant levels of ·OH without the addition of H2O2. Particles for which the EPFRs were allowed to decay over time induced less hydroxyl radical. Additionally, higher particle concentrations produced more hydroxyl radical. Some samples did not alter hydroxyl radical generation when the solution was purged by air. This is ascribed to internal, rather than external surface associated EPFRs.

Environmentally persistent free radicals (EPFRs) are formed by the chemisorption of substituted aromatics on metal oxide surfaces in both combustion sources and superfund sites. The current study reports the dependency of EPFR yields and their persistency on metal loading in particles (0.25, 0.5, 0.75, 1, 2, and 5% CuO/silica). The EPFRs were generated through exposure of particles to three adsorbate vapors at 230 °C: phenol, 2-monochlorophenol (2-MCP), and dichlorobenzene (DCBz). Adsorption resulted in the formation of surface-bound phenoxyl- and semiquinoine-type radicals with characteristic EPR spectra displaying a g value ranging from ∼ 2.0037 to 2.006. The highest EPFR yield was observed for CuO concentrations between 1 and 3% in relation to MCP and phenol adsorption. However, radical density, which is expressed as the number of radicals per copper atom, was highest at 0.75-1% CuO loading. For 1,2-dichlorobenzene adsorption, radical concentration increased linearly with decreasing copper content. At the same time, a qualitative change in the radicals formed was observed--from semiquinone to chlorophenoxyl radicals. The two longest lifetimes, 25 and 23 h, were observed for phenoxyl-type radicals on 0.5% CuO and chlorophenoxyl-type radicals on 0.75% CuO, respectively.

The health risks brought by particles cannot be present via a sole parameter. Instead, the particulate matter oxidative potential (PM OP), which expresses combined redox properties of particles, is used as an integrated metric to assess associated hazards and particle-induced health effects. OP definition provides the capacity of PM toward target oxidation. The latest technologies of a cellular OP measurement has been growing in relevant studies. In this review, OP measurement techniques are focused on discussing along with PM characterization because of many related studies via OP measurements investigating relationship with human health. Many OP measurement methods, such as dithiothreitol (DTT), ascorbic acid (AA), glutathione (GSH) assay and other a cellular assays, are used to study the association between PM toxicity and PM characterization that make different responses, including PM components, size and sources. Briefly, AA and DTT assays are sensitive to metals (such as copper, manganese and iron etc.) and organics (quinones, VOCs and PAH). Measured OP have significant association with certain PM-related end points, for example, lung cancer, COPD and asthma. Literature has found that exposure to measured OP has higher risk ratios than sole PM mass, which may be containing the PM health-relevant fraction. PM characterization effect on health via OP measurement display a promising method., (© 2020 Walter de Gruyter GmbH, Berlin/Boston.)

Studies on particulate air pollution indicate that a new type of pollutant should be considered from mainly fossil fuel combustion and automobile exhaust emissions, i.e., environmentally persistent free radicals. These radicals, ubiquitous in the environment, have a long life span and are capable of producing harmful reactive oxygen species. Samples of dandelion were collected in 2020 and 2021 in spring and late summer. Roots, leaves, flower stalks, and inflorescences of Taraxacum sp. were collected from six sites with three plants each, along with monitoring of particulate matter air pollution. Four sites were located at streets with heavy traffic and two were control sites in the rural part of the city. The free radical content in each part of the plant was measured by electron paramagnetic resonance. The leaf was selected as the most appropriate part of the plant for the measurement of carbon-derived free radicals. The geff value and the total number of spins were calculated. Relationships were found between location, season, and measurements. The electron paramagnetic resonance spectrum consists of at least two components, which can be attributed to C-type radicals and mixed C + O radicals. Their increase in numbers in the fall seasons, compared to the spring seasons, is also noticeable. It has also been observed that leaves collected in autumn have a higher geff value, which is probably related to the higher amount of oxygen- and carbon-derived free radicals. [ABSTRACT FROM AUTHOR]

Environmentally persistent free radicals (EPFRs) represent a novel class of hazardous substances, posing risks to human health and the environment. In this study, we investigated the EPFRs in ambient fine, coarse, and total suspended particles (PM2.5 , PM10 , and TSPs) in the rural North China Plain, where local primary emissions of EPFRs were limited. We observed that the majority of EPFRs occurred in PM2.5. Moreover, distinct seasonal patterns and higher g factors of EPFRs were found compared to those in urban environments, suggesting unique characteristics of EPFRs in rural areas. The source apportionment analyses revealed atmospheric oxidation as the largest contributor (33.6 %) to EPFRs. A large water-soluble fraction (35.2 %) of EPFRs was determined, potentially resulting from the formation of more oxidized EPFRs through atmospheric oxidation processes during long-range or regional transport. Additionally, significant positive correlations were observed between EPFRs and the oxidative potential of water-soluble PM2.5 measured by dithiothreitol-depletion and hydroxyl-generation assays, likely attributable to the water-soluble fractions of EPFRs. Overall, our findings reveal the prevalence of water-soluble EPFRs in rural areas and underscore the fact that atmospheric oxidation processes can modify their properties, such as increasing their water solubility. This evolution may alter their roles in contributing to the oxidative potential of PM2.5 and potentially also influence their impact on climate-related cloud chemistry. [ABSTRACT FROM AUTHOR]

The formation of environmentally persistent free radicals (EPFRs) is mediated by the particulate matter's surface, especially transition metal oxide surfaces. In the context of current atmospheric complex pollution, various atmospheric components, such as key atmospheric oxidants ·OH and O3, are often absorbed on particulate matter surfaces, forming particulate matter surfaces containing ·OH and O3. This, in turn, influences EPFRs formation. Here, density functional theory (DFT) calculations were used to explore the formation mechanism of EPFRs by C6H5OH on α-Fe2O3(0001) surface containing the ·OH and O3, and compare it with that on clean surface. The results show that, compared to EPFRs formation with an energy barrier on a clean surface, EPFRs can be rapidly formed through a barrierless process on these surfaces. Moreover, during the hydrogen abstraction mechanism leading to EPFRs formation, the hydrogen acceptor shifts from a surface O atom on a clean surface to an O atom of ·OH or O₃ on these surfaces. However, the detailed hydrogen abstraction process differs on surfaces containing oxidants: on surfaces containing ·OH, it occurs directly through a one-step mechanism, while, on surfaces containing O3, it occurs through a two-step mechanism. But, in both types of surfaces, the essence of this promotional effect mainly lies in increasing the electron transfer amounts during the reaction process. This research provides new insights into EPFRs formation on particle surfaces within the context of atmospheric composite pollution. [ABSTRACT FROM AUTHOR]

Environmental persistent free radicals (EPFRs) are receiving growing concerns owing to their potentially adverse impacts on human health. Road dust is one important source of air pollution in most cities and may pose significant health risks. Characteristics of EPFRs in urban road dusts and its formation mechanism(s) are still rarely studied. Here, we evaluated occurrence and size distributions of EPFRs in road dusts from different functional areas of an urban city, and assessed relationship between EPFRs and some transition metals. Strong electron paramagnetic resonance signals of 6.01 × 1016 − 1.3 × 1019 spins/g with the mean g value of 2.0029 ± 0.0019 were observed, indicating that EPFRs consisted of a mixture of C-centered radicals, and C-centered radicals with an adjacent oxygen atom in the urban road dust. Much more EPFRs enriched in finer dust particles. EPFRs significantly correlated with the total Fe, but not water-soluble Fe, suggesting different impacts of water-soluble and insoluble metals in the formation of EFPRs. Health risk assessment results indicated high risk potentials via the ingestion and dermal exposure to EPFRs in road dusts. Future studies are calling to look into formation mechanisms of EPFRs in urban road dusts and to quantitatively evaluate its potential risks on human health. [ABSTRACT FROM AUTHOR]

This study was conducted to confirm the effects of Korean red ginseng on lung and brain dysfunction in a BALB/c mice model exposed to particulate matter (PM)2.5 for 12 weeks. Learning and cognitive abilities were assessed with Y-maze, passive avoidance, and Morris water maze tests. To evaluate the ameliorating effect of red ginseng extract (RGE), the antioxidant system and mitochondrial function were investigated. The administration of RGE protected lung and brain impairment by regulating the antioxidant system and mitochondrial functions damaged by PM2.5-induced toxicity. Moreover, RGE prevented pulmonary fibrosis by regulating the transforming growth factor beta 1 (TGF-β1) pathway. RGE attenuated PM2.5-induced pulmonary and cognitive dysfunction by regulating systemic inflammation and apoptosis via the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)/c-Jun N-terminal kinases (JNK) pathway. In conclusion, RGE might be a potential material that can regulate chronic PM2.5-induced lung and brain cognitive dysfunction. [ABSTRACT FROM AUTHOR]

Environmentally persistent free radicals (EPFRs) are a pollutant found on fine atmospheric particulate matter (PM 2.5) , particularly on PM 2.5 formed from combustion processes. EPFRs are organic radicals that can endure in the environment for days to years. Interest in the toxicity of EPFRs has increased significantly in recent years, as it has been shown to have substantial ability to form reactive oxygen species (ROS), but little is known about how its characteristics change as PM 2.5 ages in the atmosphere. Here, we exposed newly produced hexane-generated soot to simulated sunlight for 24 h. Changes to the EPFR characteristics of the particles were measured by electron paramagnetic resonance (EPR) spectroscopy. The soot was then added to water, and a second exposure to light was used to measure hydroxyl radical (OH) formation from both photoaged and dark-aged soot. There were no changes to EPFR characteristics (spin concentration, g factor, peak width, or lineshape) due to the exposure to simulated sunlight; however, the soot's ability to form OH was greatly reduced by photoaging. Photoaged soot resulted in an almost 60 % reduction in OH formation over soot which had been aged in the dark for the same amount of time. [ABSTRACT FROM AUTHOR]

Environmentally persistent free radicals (EPFRs) are a kind of hazardous substance that exist stably in the atmosphere for a long time. EPFRs combined with fine particulate matter (PM2.5) can enter the human respiratory tract through respiration, causing oxidative stress and DNA damage, and they are also closely related to lung cancer. In this study, the inhalation risk for EPFRs in PM2.5 and factors influencing this risk were assessed using the equivalent number of cigarette tar EPFRs. The daily inhalation exposure for EPFRs in PM2.5 was estimated to be equivalent to 0.66–8.40 cigarette tar EPFRs per day. The concentration level and species characteristics were investigated using electron paramagnetic resonance spectroscopy. The concentration of EPFRs in the study ranged from 1.353–4.653 × 1013 spins/g, and the types of EPFRs were mainly oxygen- or carbon-centered semiquinone-type radicals. Our study showed that there is a strong correlation between the concentrations of EPFRs and conventional pollutants, except for sulfur dioxide. The major factors influencing EPFR concentration in the atmosphere were temperature and wind speed; the higher the temperature and wind speed, the lower the concentration of EPFRs. The findings of this study provide an important basis for further research on the formation mechanism and health effects of EPFRs. [ABSTRACT FROM AUTHOR]

Nanomaterials for air filtration have been studied by researchers for decades. Owing to the advantages of high porosity, small pore size, and good connectivity, nanofiber membranes prepared by electrospinning technology have been considered as an outstanding air-filter candidate. To satisfy the requirements of material functionalization, electrospinning can provide a simple and efficient one-step process to fabricate the complex structures of functional nanofibers such as core–sheath structures, Janus structures, and other multilayered structures. Additionally, as a nanoparticle carrier, electrospun nanofibers can easily achieve antibacterial properties, flame-retardant properties, and the adsorption properties of volatile gases, etc. These simple and effective approaches have benefited from the significate development of electrospun nanofibers for air-filtration applications. In this review, the research progress on electrospun nanofibers as air filters in recent years is summarized. The fabrication methods, filtration performances, advantages, and disadvantages of single-polymer nanofibers, multipolymer composite nanofibers, and nanoparticle-doped hybrid nanofibers are investigated. Finally, the basic principles of air filtration are concluded upon and prospects for the application of complex-structured nanofibers in the field of air filtration are proposed. [ABSTRACT FROM AUTHOR]

Background: Epidemiological data associate high levels of combustion-derived particulate matter (PM) with deleterious respiratory outcomes, but the mechanism underlying those outcomes remains elusive. It has been acknowledged by the World Health Organization that PM exposure contributes to more than 4.2 million all-cause mortalities worldwide each year. Current literature demonstrates that PM exacerbates respiratory diseases, impairs lung function, results in chronic respiratory illnesses, and is associated with increased mortality. The proposed mechanisms revolve around oxidative stress and inflammation promoting pulmonary physiological remodeling. However, our previous data found that PM is capable of inducing T helper cell 17 (Th17) immune responses via aryl hydrocarbon receptor (Ahr) activation, which was associated with neutrophilic invasion characteristic of steroid insensitive asthma.Methods: In the present study, we utilized a combination of microarray and single cell RNA sequencing data to analyze the immunological landscape in mouse lungs following acute exposure to combustion derived particulate matter.Results: We present data that suggest epithelial cells produce specific cytokines in the aryl hydrocarbon receptor (Ahr) pathway that inform dendritic cells to initiate the production of pathogenic T helper (eTh17) cells. Using single-cell RNA sequencing analysis, we observed that upon exposure epithelial cells acquire a transcriptomic profile indicative of increased Il-17 signaling, Ahr activation, Egfr signaling, and T cell receptor and co-stimulatory signaling pathways. Epithelial cells further showed, Ahr activation is brought on by Ahr/ARNT nuclear translocation and activation of tyrosine kinase c-src, Egfr, and subsequently Erk1/2 pathways.Conclusions: Collectively, our data corroborates that PM initiates an eTh17 specific inflammatory response causing neutrophilic asthma through pathways in epithelial, dendritic, and T cells that promote eTh17 differentiation during initial PM exposure. [ABSTRACT FROM AUTHOR]

Ambient air particulate matter (PM) and PM-associated environmentally persistent free radicals (EPFRs) have been documented to contribute to pollution-related health effects. Studies of ambient air PM potentially bear artifacts stemming from the collection methods. We have investigated the applicability of PM phytosampling (PHS) as a supplementary tool to a classic PM sampler in respect of achieving better PM chemical composition assessment (primarily organic fraction). Phytosampling is a static PM collection method relying on the particle entrapment by the plant's leaf through electrostatic forces and surface trichomes. We have investigated the differences in the EPFR and polycyclic aromatic hydrocarbon (PAH) speciation and concentration on ambient air PM for PHS and high-volume PM sampler (HVS). The advantages of PHS are easy particle recovery from the matrix, collection under natural environmental conditions, and the ability to apply a dense collection network to accurately represent spatial pollutant distribution. The experimental results show that the PHS can provide valuable speciation information, sometimes different from that observed for HVS. For PM collected by PHS, we detected the larger contribution of oxygen-centered EPFRs, different decay behavior, and more consistent PAH distribution between different PM sizes compared to the PM from HVS. These results indicate that the isolation of samples from the ambient during HVS sampling and exposure to high-volume airflow may alter the chemical composition of the samples, while the PHS method could provide details on the original speciation and concentration and be more representative of the PM surface. However, PHS cannot evaluate an absolute air concentration of PM, so it serves as an excellent supplementary tool to work in conjunction with the standard PM collection method. [ABSTRACT FROM AUTHOR]

Background: Particulate matter (PM), a major component of ambient air pollution, accounts for a substantial burden of diseases and fatality worldwide. Maternal exposure to PM during pregnancy is particularly harmful to children's health since this is a phase of rapid human growth and development. Method: In this review, we synthesize the scientific evidence on adverse health outcomes in children following prenatal exposure to the smallest toxic components, fine (PM2.5) and ultrafine (PM0.1) PM. We highlight the established and emerging findings from epidemiologic studies and experimental models. Results: Maternal exposure to fine and ultrafine PM directly and indirectly yields numerous adverse birth outcomes and impacts on children's respiratory systems, immune status, brain development, and cardiometabolic health. The biological mechanisms underlying adverse effects include direct placental translocation of ultrafine particles, placental and systemic maternal oxidative stress and inflammation elicited by both fine and ultrafine PM, epigenetic changes, and potential endocrine effects that influence long-term health. Conclusion: Policies to reduce maternal exposure and health consequences in children should be a high priority. PM2.5 levels are regulated, yet it is recognized that minority and low socioeconomic status groups experience disproportionate exposures. Moreover, PM0.1 levels are not routinely measured or currently regulated. Consequently, preventive strategies that inform neighborhood/regional planning and clinical/nutritional recommendations are needed to mitigate maternal exposure and ultimately protect children's health. [ABSTRACT FROM AUTHOR]

In the aqueous phase, fine particulate matter can form reactive species (RS) that influence the aging, properties, and health effects of atmospheric aerosols. In this study, we explore the RS yields of aerosol samples from a remote forest (Hyytiälä, Finland) and polluted urban locations (Mainz, Germany; Beijing, China), and we relate the RS yields to different chemical constituents and reaction mechanisms. Ultra-high-resolution mass spectrometry was used to characterize organic aerosol composition, electron paramagnetic resonance (EPR) spectroscopy with a spin-trapping technique was applied to determine the concentrations of ⚫ OH, O 2⚫- , and carbon- or oxygen-centered organic radicals, and a fluorometric assay was used to quantify H 2 O 2. The aqueous H 2 O 2 -forming potential per mass unit of ambient PM 2.5 (particle diameter < 2.5 µm) was roughly the same for all investigated samples, whereas the mass-specific yields of radicals were lower for sampling sites with higher concentrations of PM 2.5. The abundances of water-soluble transition metals and aromatics in ambient PM 2.5 were positively correlated with the relative fraction of ⚫ OH and negatively correlated with the relative fraction of carbon-centered radicals. In contrast, highly oxygenated organic molecules (HOM) were positively correlated with the relative fraction of carbon-centered radicals and negatively correlated with the relative fraction of ⚫ OH. Moreover, we found that the relative fractions of different types of radicals formed by ambient PM 2.5 were comparable to surrogate mixtures comprising transition metal ions, organic hydroperoxide, H 2 O 2 , and humic or fulvic acids. The interplay of transition metal ions (e.g., iron and copper ions), highly oxidized organic molecules (e.g., hydroperoxides), and complexing or scavenging agents (e.g., humic or fulvic acids) leads to nonlinear concentration dependencies in aqueous-phase RS production. A strong dependence on chemical composition was also observed for the aqueous-phase radical yields of laboratory-generated secondary organic aerosols (SOA) from precursor mixtures of naphthalene and β -pinene. Our findings show how the composition of PM 2.5 can influence the amount and nature of aqueous-phase RS, which may explain differences in the chemical reactivity and health effects of particulate matter in clean and polluted air. [ABSTRACT FROM AUTHOR]

Environmentally persistent free radicals (EPFRs) are a new type of substance with potential health risks. EPFRs are widely present in atmospheric particulates, but there is a limited understanding of the size-resolved health risks of these radicals. This study reports the exposure risks and source of EPFRs in atmospheric particulate matter (PM) of different particle sizes (<10 µm) in Linfen, a typical coal-burning city in China. The type of EPFRs in fine particles (< 2.1 µm) is different from that in coarse particles (2.1–10 µm) in both winter and summer. However, the EPFR concentration is higher in coarse particles than in fine particles in summer, and the opposite trend is found in winter. In both seasons, combustion sources are the main sources of EPFRs, with coal combustion as the major contributor in winter, while other fuels are the major source in summer. Dust contributes part of the EPFRs, and it is mainly present in coarse particles in winter and the opposite in summer. The upper respiratory tract was found to be the area with the highest risk of exposure to EPFRs of the studied aerosols, with an exposure equivalent to that of approximately 21 cigarettes per person per day. Alveolar exposure to EPFRs is equivalent to 8 cigarettes per person per day, with combustion sources contributing the most to EPFRs in the alveoli. This study helps us to better understand the potential health risks of atmospheric PM with different particle sizes. [ABSTRACT FROM AUTHOR]

The capability of ambient particles to generate in vivo reactive oxygen species (ROS), called oxidative potential (OP), is a potential metric for evaluating the health effects of particulate matter (PM) and is supported by several recent epidemiological investigations. Studies using various types of OP assays differ in their sensitivities to varying PM chemical components. In this study, we systematically compared two health-relevant acellular OP assays that track the depletion of antioxidants or reductant surrogates: (i) the synthetic respiratory-tract lining fluid (RTLF) assay that tracks the depletion of ascorbic acid (AA) and glutathione (GSH) and (ii) the dithiothreitol (DTT) assay that tracks the depletion of DTT. Yearlong daily samples were collected at an urban site in Atlanta, GA (Jefferson Street), during 2017, and both DTT and RTLF assays were performed to measure the OP of water-soluble PM2.5 components. PM2.5 mass and major chemical components, including metals, ions, and organic and elemental carbon were also analyzed. Correlation analysis found that OP as measured by the DTT and AA depletion (OP DTT and OP AA , respectively) were correlated with both organics and some water-soluble metal species, whereas that from the GSH depletion (OP GSH) was exclusively sensitive to water-soluble Cu. These OP assays were moderately correlated with each other due to the common contribution from metal ions. OP DTT and OP AA were moderately correlated with PM2.5 mass with Pearson's r=0.55 and 0.56, respectively, whereas OP GSH exhibited a lower correlation (r=0.24). There was little seasonal variation in the OP levels for all assays due to the weak seasonality of OP-associated species. Multivariate linear regression models were developed to predict OP measures from the particle composition data. Variability in OP DTT and OP AA were not only attributed to the concentrations of metal ions (mainly Fe and Cu) and organic compounds but also to antagonistic metal–organic and metal–metal interactions. OP GSH was sensitive to the change in water-soluble Cu and brown carbon (BrC), a proxy for ambient humic-like substances. [ABSTRACT FROM AUTHOR]

Particulate matter (PM) is emitted during the combustion of fuels and wastes. PM exposure exacerbates pulmonary diseases, and the mechanism may involve oxidative stress. At lower combustion temperatures such as occurs in the cool zone of a flame, aromatic compounds chemisorb to the surface of metal-oxide-containing PM, resulting in the formation of surface-stabilized environmentally persistent free radicals (EPFR). Prior studies showed that PM-containing EPFR redox cycle to produce reactive oxygen species (ROS), and after inhalation, EPFR induce pulmonary inflammation and oxidative stress. Our objective was to elucidate mechanisms linking EPFR-induced oxidant injury with increased cytokine production by pulmonary epithelial cells. We thus treated human bronchial epithelial cells with EPFR at sub-toxic doses and measured ROS and cytokine production. To assess aryl hydrocarbon receptor (AhR) activity, cells were transfected with a luciferase reporter for xenobiotic response element activation. To test whether cytokine production was dependent upon AhR activation or oxidative stress, some cells were co-treated with an antioxidant or an AhR antagonist. EPFR increased IL-6 release in an ROS and AhR- and oxidant-dependent manner. Moreover, EPFR induced an AhR activation that was dependent upon oxidant production, since antioxidant co-treatment blocked AhR activation. On the other hand, EPFR treatment increased a cellular ROS production that was at least partially attenuated by AhR knockdown using siRNA. While AhR activation was correlated with an increased expression of oxidant-producing enzymes like cytochrome P450 CYP1A1, it is possible that AhR activation is both a cause and effect of EPFR-induced ROS. Finally, lipid oxidation products also induced AhR activation. ROS-dependent AhR activation may be a mechanism for altered epithelial cell responses after EPFR exposure, potentially via formation of bioactive lipid or protein oxidation products. [ABSTRACT FROM AUTHOR]

Pyrolysis of biodiesel at high temperatures may result in the formation of transient and stable free radicals immobilized on particulate emissions. Consequently, free radicals adsorbed on particulates are believed to be precursors for health-related illnesses such as cancer, cardiac arrest, and oxidative stress. This study explores the nature of free radicals and particulate emissions generated when Croton megalocarpus biodiesel is pyrolyzed at 600 °C in an inert environment of flowing nitrogen at a residence time of 0.5 s at 1 atm. The surface morphology of thermal emissions were imaged using a field emission gun scanning electron microscope (FEG SEM) while the radical characteristics were investigated using an electron paramagnetic resonance spectrometer (EPR). A g-value of 2.0024 associated with a narrow ∆Hp-p of 3.65 G was determined. The decay rate constant for the radicals was low (1.86 × 10−8 s−1) while the half-life was long ≈ 431 days. The observed EPR characterization of Croton megalocarpus thermal particulates revealed the existence of free radicals typical of those found in coal. The low g-value and low decay rate constant suggests that the free radicals in particulates are possibly carbon-centered. The mechanistic channel for the formation of croton char from model biodiesel component (9-dodecenoic acid, methyl ester) has been proposed in this study. [ABSTRACT FROM AUTHOR]

Background: Tobacco smoke is a toxic gas-phase cocktail consisting of a broad range of organics, and free radical intermediates. The formation of smoke from a burning cigarette depends on a series of mechanisms, including generation of products by pyrolysis and combustion, aerosol formation, and physical mass transfer processes. Methods: The current study simulates the deposition of particulate matter on the human lung surface by trapping the tobacco smoke particulates in situ on silica gel. To mimic this phenomenon, the cigarette was smoked directly on siliga gel. The surface morphology of smoke condensate trapped on silica gel, and pure silica gel (control) was investigated using a scanning electron microscope (SEM). Electron paramagnetic resonance (EPR) was used to explore the presence of free radicals on the particulate matter trapped on silica. Standard procedures for cigarette smoking (ISO 3402:1999) were adopted. The char yields of tobacco cigarette in the temperature range 200-700 °C was also investigated in an inert atmosphere using a quartz reactor. Results: SEM images showed the surface morphology of pure silica gel was smooth while silica gel on which cigarette smoke was smoked on contained particulates of various sizes. Generally, the particulate size of cigarette smoke adsorbed on silica was found to be 2.47 ± 0.0043 µm (~PM). Electron paramagnetic resonance (EPR) results showed a g-value of 2.0037 typically that of a carbon-centred radical. Conclusions: It is therefore evident from this investigation that cigarette smoke contains surface bound radicals considered harmful to the health of cigarette smokers. The particulate size of tobacco smoke (PM) can impact severely on the lives of the cigarette smoking community because of its near ultrafine nature. This significantly small particulate size in cigarette smoke can be inhaled deeper into the lungs thus causing serious cell injury and possible tumour growth in addition to other grave diseases. [ABSTRACT FROM AUTHOR]

The current study describes a method for assessing the oxidative potential of common environmental stressors (ambient air particulate matter), using a plasmid relaxation assay where the extract caused single-strand breaks, easily visualised through electrophoresis. This assay utilises a miniscule amount (11 µg) of particulate matter (PM) extract compared to other, cell-based methods (~3,000 µg). The negative impact of air pollution on human health has been extensively recognised. Among the air pollutants, PM plays an eminent role, as reflected in the broad scientific interest. PM toxicity highly depends on its composition (metals and organic compounds), which in turn has been linked to multiple health effects (such as cardiorespiratory diseases and cancer) through multiple toxicity mechanisms; the induction of oxidative stress is considered a major mechanism among these. In this study, the PM levels, oxidative potential, cytotoxicity and genotoxicity of PM in the region of Larissa, Greece were examined using the plasmid relaxation assay. Finally, coffee extracts from different varieties, derived from both green and roasted seeds, were examined for their ability to inhibit PM-induced DNA damage. These extracts also exerted an inhibitory effect on xanthine oxidase and catalase, but had no effect against superoxide dismutase. Overall, this study highlights the importance of assays for assessing the oxidative potential of widespread environmental stressors (PM), as well as the antioxidant capacity of beverages and food items, with the highlight being the development of a plasmid relaxation assay to assess the genotoxicity caused by PM using only a miniscule amount. [ABSTRACT FROM AUTHOR]

In the present study, metal-facilitated free radical generation in particulate matter (PM) and its association with deoxyribonucleic acid (DNA) damage were studied. The examined data showed that the concentration of fine PM in Pune exhibited seasonal variations. Inductively coupled plasma-atomic emission spectrometry (ICP-AES) was used to examine the metal composition, which showed the presence of metals such as Cu, Zn, Mn, Fe, Co, Cr, Pb, Cd, and Ni. Fe metal was present in the highest concentrations in both the seasons, followed by Zn. The scanning electron microscopy-energy-dispersive spectrometer (SEM-EDS) results also demonstrated that the fine PM particles deposited in summer samples were less than those of winter samples, suggesting that the PM load in winter was higher as compared to that in summer. Elemental mapping of these particles substantiates deposition of metals as Fe, Zn, etc. on particles. The electron paramagnetic species (EPR) technique was utilized for free radical detection, and plasmid DNA assay was utilized to study the genotoxicity of ambient fine PM. Obtained g values show the presence of radicals in PM samples of Pune. PM contains the C-centered radical with a vicinal oxygen atom ( g = 2.003). In addition to this, the g value for Fe was also observed. Therefore, we intend that the radicals related with fine PM comprise metal-mediated radicals and produce DNA damage. The plasmid DNA assay results indicated that the TM values (toxic mass of PM causing 50 % of plasmid DNA damage) of PM exhibited seasonal variations with higher TM values for summer and lower TM values during winter. [ABSTRACT FROM AUTHOR]

Fine particulate matter plays a central role in the adverse health effects of air pollution. Inhalation and deposition of aerosol particles in the respiratory tract can lead to the release of reactive oxygen species (ROS), which may cause oxidative stress. In this study, we have detected and quantified a wide range of particle-associated radicals using electron paramagnetic resonance (EPR) spectroscopy. Ambient particle samples were collected using a cascade impactor at a semi-urban site in central Europe, Mainz, Germany, in May-June 2015. Concentrations of environmentally persistent free radicals (EPFR), most likely semiquinone radicals, were found to be in the range of (1-7) x 1011 spins µg-1 for particles in the accumulation mode, whereas coarse particles with a diameter larger than 1 µm did not contain substantial amounts of EPFR. Using a spin trapping technique followed by deconvolution of EPR spectra, we have also characterized and quantified ROS, including OH, superoxide (O2-) and carbon- and oxygen-centered organic radicals, which were formed upon extraction of the particle samples in water. Total ROS amounts of (0.1-3) x 1011 spins µg-1 were released by submicron particle samples and the relative contributions of OH, O2-, C-centered and O-centered organic radicals were ~11-31, ~2-8, ~41-72 and ~0-25 %, respectively, depending on particle sizes. OH was the dominant species for coarse particles. Based on comparisons of the EPR spectra of ambient particulate matter with those of mixtures of organic hydroperoxides, quinones and iron ions followed by chemical analysis using liquid chromatography mass spectrometry (LC-MS), we suggest that the particle-associated ROS were formed by decomposition of organic hydroperoxides interacting with transition metal ions and quinones contained in atmospheric humic-like substances (HULIS). [ABSTRACT FROM AUTHOR]

Since air pollution has been linked to a plethora of human health problems, strategies to improve air quality are indispensable. Despite the complexity in composition of air pollution, phytoremediation was shown to be effective in cleaning air. Plants are known to scavenge significant amounts of air pollutants on their aboveground plant parts. Leaf fall and runoff lead to transfer of (part of) the adsorbed pollutants to the soil and rhizosphere below. After uptake in the roots and leaves, plants can metabolize, sequestrate and/or excrete air pollutants. In addition, plant-associated microorganisms play an important role by degrading, detoxifying or sequestrating the pollutants and by promoting plant growth. In this review, an overview of the available knowledge about the role and potential of plant-microbe interactions to improve indoor and outdoor air quality is provided. Most importantly, common air pollutants (particulate matter, volatile organic compounds and inorganic air pollutants) and their toxicity are described. For each of these pollutant types, a concise overview of the specific contributions of the plant and its microbiome is presented. To conclude, the state of the art and its related future challenges are presented. [ABSTRACT FROM AUTHOR]

Increases in airborne particulate matter (PM) are linked to increased mortality from myocardial ischemia. PM contains environmentally persistent free radicals (EPFRs) that form as halogenated hydrocarbons chemisorb to transition metal oxide-coated particles, and are capable of sustained redox cycling. We hypothesized that exposure to the EPFR DCB230 would increase cardiac vulnerability to subsequent myocardial ischemia-reperfusion (MI/R) injury. Rats were exposed to DCB230 or vehicle via nose-only inhalation (230 μg max/day) over 30 min/day for 7 days. MI/R or sham MI/R (sham) was initiated 24 h after the final exposure. Following 1 or 7 days of reperfusion, left ventricular (LV) function was assessed and infarct size measured. In vehicle-exposed rats, MI/R injury did not significantly reduce cardiac output (CO), stroke volume (SV), stroke work (SW), end-diastolic volume (EDV), or end-systolic volume (ESV) after 1 day of reperfusion, despite significant reductions in end-systolic pressure (ESP). Preload-recruitable SW (PRSW; contractility) was elevated, presumably to maintain LV function. MI/R 1-day rats exposed to DCB230 also had similarly reduced ESP. Compared with vehicle controls, CO, SV, and SW were significantly reduced in DCB230-exposed MI/R 1-day rats; moreover, PRSW did not increase. DCB230's effects on LV function dissipated within 8 days of exposure. These data show that inhalation of EPFRs can exacerbate the deficits in LV function produced by subsequent MI/R injury. Infarct size was not different between the MI/R groups. We conclude that inhalation of EPFRs can compromise cardiac function during MI/R injury and may help to explain the link between PM and MI/R-related mortality. [ABSTRACT FROM AUTHOR]

Epidemiologic studies have suggested that particulate matter (PM)-associated adverse health effects are related to particle composition. To study the toxicological characteristics of dust storm, airborne PM was collected at two sites in Beijing from March to May 2012. The production of reactive oxygen species (ROS), quantified by dithiothreitol (DTT), was used to measure the PM-induced oxidative potential. Two dust storm (DS) samples were monitored during the sampling period: one happened on March 28th (DS1) and the other one was on April 28th (DS2). The backward trajectory results showed that both events originated from Inner Mongolia and Mongolia, respectively. The increased trends of ROS activities during the dust storm episode in PM were observed for all the dust storms owing to a higher concentration of water-soluble components for all the PM samples compared to nondust storm ones. Interestingly, the correlations between DTT consumption with water-soluble species yield interesting results about the spatial variability of redox activity between sites. In particular, a tracer of soil suspension, namely Fe, contributed the most fraction to ROS variability in the urban background site. Water-soluble organic carbon (WSOC) made the highest contribution to ROS variability, suggesting that vehicle emission might be important driving factors of the PM-induced oxidative stress in the urban site. [ABSTRACT FROM AUTHOR]

Human exposure to particulate matter (PM) air pollution is associated with human morbidity and mortality. The mechanisms by which PM impacts human health are unresolved, but evidence suggests that PM intake leads to cellular oxidative stress through the generation of reactive oxygen species (ROS). Therefore, reliable tools are needed for estimating the oxidant generating capacity, or oxidative load, of PM at high temporal resolution (minutes to hours). One of the most widely reported methods for assessing PM oxidative load is the dithiothreitol (DTT) assay. The traditional DTT assay utilizes filter-based PM collection in conjunction with chemical analysis to determine the oxidation rate of reduced DTT in solution with PM. However, the traditional DTT assay suffers from poor time resolution, loss of reactive species during sampling, and high limit of detection. Recently, a new DTT assay was developed that couples a particle-into-liquid-sampler with microfluidic-electrochemical detection. This “on-line” system allows high temporal resolution monitoring of PM reactivity with improved detection limits. This study reports on a laboratory comparison of the traditional and on-line DTT approaches. An urban dust sample was aerosolized in a laboratory test chamber at three atmospherically relevant concentrations. The on-line system gave a stronger correlation between DTT consumption rate and PM mass (R2= 0.69) than the traditional method (R2= 0.40) and increased precision at high temporal resolution, compared to the traditional method. Copyright 2014 American Association for Aerosol Research [ABSTRACT FROM AUTHOR]

ABSTRACT The health impacts of airborne particulate matter (PM) are of global concern, and the direct implications to the development/exacerbation of lung disease are immediately obvious. Most studies to date have sought to understand mechanisms associated with PM exposure in adults/adult animal models; however, infants are also at significant risk for exposure. Infants are affected differently than adults due to drastic immaturities, both physiologically and immunologically, and it is becoming apparent that they represent a critically understudied population. Highlighting our work funded by the ONES award, in this review we argue the understated importance of utilizing infant models to truly understand the etiology of PM-induced predisposition to severe, persistent lung disease. We also touch upon various mechanisms of PM-mediated respiratory damage, with a focus on the emerging importance of environmentally persistent free radicals (EPFRs) ubiquitously present in combustion-derived PM. In conclusion, we briefly comment on strengths/challenges facing current PM research, while giving perspective on how we may address these challenges in the future. © 2012 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:56-68, 2013; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.21465 [ABSTRACT FROM AUTHOR]

BACKGROUND: Inhalation of airborne particulate matter (PM) derived from urban traffic is associated with pathology in the arteries, heart, and lung; effects on brain are also indicated but are less documented. OBJECTIVE: We evaluated rodent brain responses to urban nanoscale (< 200 nm) PM (nPM). METHODS: Ambient nPM collected near an urban freeway was transferred to aqueous suspension and reaerosolized for 10-week inhalation exposure of mice or directly applied to rat brain cell cultures. RESULTS: Free radicals were detected by electron paramagnetic resonance in the nPM 30 days after initial collection. Chronic inhalation of reaerosolized nPM altered selected neuronal and glial activities in mice. The neuronal glutamate receptor subunit (GluA1) was decreased in hippocampus, whereas glia were activated and inflammatory cytokines were induced [interleukin-1α (IL.1α), tumor necrosis factor-α (TNFα)] in cerebral cortex. Two in vitro models showed effects of nPM suspensions within 24-48 hr of exposure that involved glutamatergic functions. In hippocampal slice cultures, nPM increased the neurotoxicity of NMDA (N-methyl-d-aspartic acid), a glutamatergic agonist, which was in turn blocked by the NMDA antagonist AP5 [(2R)-amino-5-phosphonopentanoate]. In embryonic neuron cultures, nPM impaired neurite outgrowth, also blocked by AP5. Induction of IL-1α and TNFα in mixed glia cultures required higher nPM concentrations than did neuronal effects. Because conditioned media from nPM-exposed glia also impaired outgrowth of embryonic neurites, nPM can act indirectly, as well as directly, on neurons in vitro. CONCLUSIONS: nPM can affect embryonic and adult neurons through glutamatergic mechanisms. The interactions of nPM with glutamatergic neuronal functions suggest that cerebral ischemia, which involves glutamatergic excitotoxicity, could be exacerbated by nPM. [ABSTRACT FROM AUTHOR]

Environmentally persistent free radicals (EPFRs) were previously considered an unrecognized composition of air pollutants and might help explain the long-standing medical mystery of why non-smokers develop tobacco-related diseases such as lung cancer. However, there is no investigated on EPFRs in Xuanwei rural areas, especially in high prevalence of lung cancer areas. In this study, we selected six types of coal and three types of biomass in Xuanwei, then conducted simulated combustion, and six group of atmospheric particulate matters (APMs) to explore the content and particle size distribution pattern of EPFRs and a new health risk assessment method to evaluate the risk of EPFRs in PM for adults and children. Our results show that the contribution of EPFRs for biomass combustion, coal combustion and APMs were mainly distributed in the size range of <1.1 μm, which accounted for 76.15 ± 4.14%, 74.85 ± 10.76%, and 75.23 ± 8.18% of PM3.3. The mean g factors and ΔHp-p indicated that the EPFRs were mainly oxygen-centered radicals in PM in Xuanwei. The results suggest that the health risk of EPFRs is significantly increased when the particle size distribution of EPFRs is taken into account, and coal combustion particulate matter (174.70 ± 37.86 cigarettes for an adult, 66.39 ± 14.39 cigarettes per person per year for a child) is more hazardous to humans than biomass combustion particulate matter (69.41 ± 4.83 cigarettes for an adult, 26.37 ± 1.84 cigarettes per person per year for), followed by APMs (102.88 ± 39.99 cigarettes for an adult, 39.10 ±15.20 cigarettes per person per year for) in PM3.3. Our results provides a new perspective and evidence for revealing the reason for the high incidence of lung cancer in Xuanwei, China. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The article focuses on a study regarding environmentally persistent free radicals (EPFRs) and links between exposure to air pollution (both indoor and outdoor) and adverse respiratory outcomes. It mentions EPFRs participate in the redox cycle in biological systems through the Fenton reaction and produce reactive oxygen species. It also mentions EPFRs induce oxidative stress (OS) in animal models and in human cells that can be mitigated with antioxidants such as resveratrol.

Background: The atmosphere has become a major transport corridor for free radicals and particulate matter from combustion events. The motivation behind this study was to determine the nature of particulate emissions and surface bound radicals formed during the thermal degradation of diesel blends in order to assess the health and environmental hazards of binary transport fuels.Methodology: Accordingly, this contribution explored the interactions that occur when Croton megalocarpus biodiesel and fossil diesel in the ratio of 1:1 by weight were co-pyrolyzed in a quartz reactor at a residence time of 0.5 s under an inert flow of nitrogen at 600 °C. The surface morphology of the thermal char formed were imaged using a Feld emission gun scanning electron microscope (FEG SEM) while Electron paramagnetic resonance spectrometer (EPR) was used to explore the presence of free radicals on the surface of thermal char. Molecular functional groups adsorbed on the surface of thermal char were explored using Fourier transform infrared spectroscopy (FTIR).Results: FTIR spectrum showed that the major functional groups on the surface of the char were basically aromatic and some methylene groups. The particulate emissions detected in this work were ultrafine (~ 32 nm). The particulates are consistent with the SEM images observed in this study. Electron paramagnetic resonance results gave a g-value of 2.0027 characteristic of carbon-based radicals of aromatic nature. Spectral peak-to-peak width (∆Hp-p) obtained was narrow (4.42 G).Conclusions: The free radicals identified as carbon-based are medically notorious and may be transported by various sizes of particulate matter on to the surface of the human lung which may trigger cancer and pulmonary diseases. The nanoparticulates determined in this work can precipitate severe biological health problems among humans and other natural ecosystems. [ABSTRACT FROM AUTHOR]

Background: Pollutant particles containing environmentally persistent free radicals (EPFRs) are formed during many combustion processes (e.g. thermal remediation of hazardous wastes, diesel/gasoline combustion, wood smoke, cigarette smoke, etc.). Our previous studies demonstrated that acute exposure to EPFRs results in dendritic cell maturation and Th17-biased pulmonary immune responses. Further, in a mouse model of asthma, these responses were enhanced suggesting exposure to EPFRs as a risk factor for the development and/or exacerbation of asthma. The aryl hydrocarbon receptor (AHR) has been shown to play a role in the differentiation of Th17 cells. In the current study, we determined whether exposure to EPFRs results in Th17 polarization in an AHR dependent manner. Results: Exposure to EPFRs resulted in Th17 and IL17A dependent pulmonary immune responses including airway neutrophilia. EPFR exposure caused a significant increase in pulmonary Th17 cytokines such as IL6, IL17A, IL22, IL1β, KC, MCP-1, IL31 and IL33. To understand the role of AHR activation in EPFR-induced Th17 inflammation, A549 epithelial cells and mouse bone marrow-derived dendritic cells (BMDCs) were exposed to EPFRs and expression of Cyp1a1 and Cyp1b1, markers for AHR activation, was measured. A significant increase in Cyp1a1 and Cyp1b1 gene expression was observed in pulmonary epithelial cells and BMDCs in an oxidative stress and AHR dependent manner. Further, in vivo exposure of mice to EPFRs resulted in oxidative stress and increased Cyp1a1 and Cyp1b1 pulmonary gene expression. To further confirm the role of AHR activation in pulmonary Th17 immune responses, mice were exposed to EPFRs in the presence or absence of AHR antagonist. EPFR exposure resulted in a significant increase in pulmonary Th17 cells and neutrophilic inflammation, whereas a significant decrease in the percentage of Th17 cells and neutrophilic inflammation was observed in mice treated with AHR antagonist. Conclusion: Exposure to EPFRs results in AHR activation and induction of Cyp1a1 and in vitro this is dependent on oxidative stress. Further, our in vivo studies demonstrated a role for AHR in EPFR-induced pulmonary Th17 responses including neutrophilic inflammation. [ABSTRACT FROM AUTHOR]