The Impact of Russia-Ukraine geopolitical conflict on the air quality and toxicological properties of ambient PM2.5 in Milan, Italy.

The geopolitical conflict between Russia and Ukraine has disrupted Europe's natural gas supplies, driving up gas prices and leading to a shift towards biomass for residential heating during colder months. This study assessed the consequent air quality and toxicological impacts in Milan, Italy, focusing on fine particulate matter (PM2.5, dp < 2.5 µm) emissions. PM2.5 samples were analyzed for their chemical composition and assessed for their oxidative potential using the dithiothreitol (DTT) assay across three periods reflecting residential heating deployment (RHD): pre-RHD, intra-RHD, and post-RHD periods. During the intra-RHD period, PM2.5 levels were significantly higher than those in other periods, with concentrations reaching 57.94 ± 7.57 µg/m3, indicating a deterioration in air quality. Moreover, levoglucosan was 9.2 times higher during the intra-RHD period compared to the pre-RHD period, correlating with elevated levels of elemental carbon (EC) and polycyclic aromatic hydrocarbons (PAHs). These findings were compared with previous local studies before the conflict, underscoring a significant rise in biomass-related emissions. DTT assay levels during the intra-RHD were 2.1 times higher than those observed during the same period in 2022, strongly correlating with biomass burning emissions. Our findings highlight the necessity for policies to mitigate the indirect health effects of increased biomass burning emissions due to the energy crisis triggered by the geopolitical conflict.

Microglial TLR4 Mediates White Matter Injury in a Combined Model of Diesel Exhaust Exposure and Cerebral Hypoperfusion.

BACKGROUND: Air pollution particulate matter exposure and chronic cerebral hypoperfusion (CCH) contribute to white matter toxicity through shared mechanisms of neuroinflammation, oxidative stress, and myelin breakdown. Prior studies showed that exposure of mice to joint particulate matter and CCH caused supra-additive injury to corpus callosum white matter. This study examines the role of TLR4 (toll-like receptor 4) signaling in mediating neurotoxicity and myelin damage observed in joint particulate matter and CCH exposures. METHODS: Experiments utilized a novel murine model of inducible monocyte/microglia-specific TLR4 knockout (i-mTLR4-ko). Bilateral carotid artery stenosis (BCAS) was induced surgically to model CCH. TLR4-intact (control) and i-mTLR4-ko mice were exposed to 8 weeks of either aerosolized diesel exhaust particulate (DEP) or filtered air (FA) in 8 experimental groups: (1) control/FA (n=10), (2) control/DEP (n=10), (3) control/FA+BCAS (n=9), (4) control/DEP+BCAS (n=10), (5) i-mTLR4-ko/FA (n=9), (6) i-mTLR4-ko/DEP (n=8), (7) i-mTLR4-ko/FA+BCAS (n=8), and (8) i-mTLR4-ko/DEP+BCAS (n=10). Corpus callosum levels of 4-hydroxynonenal, 8-Oxo-2'-deoxyguanosine, Iba-1 (ionized calcium-binding adapter molecule 1), and dMBP (degraded myelin basic protein) were assayed via immunofluorescence to measure oxidative stress, neuroinflammation, and myelin breakdown, respectively. RESULTS: Compared with control/FA mice, control/DEP+BCAS mice exhibited increased dMBP (41%; P<0.01), Iba-1 (51%; P<0.0001), 4-hydroxynonenal (100%; P<0.0001), and 8-Oxo-2'-deoxyguanosine (65%; P<0.05). I-mTLR4 knockout attenuated responses to DEP/BCAS for all markers. CONCLUSIONS: i-mTLR4-ko markedly reduced neuroinflammation and oxidative stress and attenuated white matter degradation following DEP and CCH exposures. This suggests a potential role for targeting TLR4 signaling in individuals with vascular cognitive impairment, particularly those exposed to substantial ambient air pollution.

Development and performance evaluation of online monitors for near real-time measurement of total and water-soluble organic carbon in fine and coarse ambient PM.

In this study, we developed two online monitors for total organic carbon (TOC) and water-soluble organic carbon (WSOC) measurements in fine (dp < 2.5µm) and coarse (2.5µm < dp < 10µm) particulate matter (PM), respectively. Their performance has been evaluated in laboratory and field tests to demonstrate the feasibility of using these monitors to measure near real-time concentrations, with consideration of their potential for being employed in long-term measurements. The fine PM collection setup was equipped with a versatile aerosol concentration enrichment system (VACES) connected to an aerosol-into-liquid-sampler (AILS), whereas two virtual impactors (VIs) in tandem with a modified BioSampler were used to collect coarse PM. These particle collection setups were in tandem with a Sievers M9 TOC analyzer to read TOC and WSOC concentrations in aqueous samples hourly. The average hourly TOC concentration measured by our developed monitors in fine and coarse PM were 5.17 ± 2.41 and 0.92 ± 0.29 µg/m3, respectively. In addition, our TOC readings showed good agreement and were comparable with those quantified using Sunset Lab EC/OC analyzer operating in parallel as a reference. Furthermore, we conducted field tests to produce diurnal profiles of fine PM-bound WSOC, which can show the effects of ambient temperature on maximum values in the nighttime chemistry of the winter, as well as on increased photochemical activities in afternoon peaks during the summer. According to our experimental campaign, WSOC mean values during the study period (3.07 µg/m3 for the winter and 2.7 µg/m3 for the summer) were in a comparable range with those of earlier studies in Los Angeles. Overall, our results corroborate the performance of our developed monitors in near real-time measurements of TOC and WSOC, which can be employed for future source apportionment studies in Los Angeles and other areas, aiding in understanding the health impacts of different pollution sources.

Subchronic inhalation exposure to ultrafine particulate matter alters the intestinal microbiome in various mouse models.

Exposure to ultrafine particles (UFPs) has been associated with multiple adverse health effects. Inhaled UFPs could reach the gastrointestinal tract and influence the composition of the gut microbiome. We have previously shown that oral ingestion of UFPs alters the gut microbiome and promotes intestinal inflammation in hyperlipidemic Ldlr-/- mice. Particulate matter (PM)2.5 inhalation studies have also demonstrated microbiome shifts in normolipidemic C57BL/6 mice. However, it is not known whether changes in microbiome precede or follow inflammatory effects in the intestinal mucosa. We hypothesized that inhaled UFPs modulate the gut microbiome prior to the development of intestinal inflammation. We studied the effects of UFP inhalation on the gut microbiome and intestinal mucosa in two hyperlipidemic mouse models (ApoE-/- mice and Ldlr-/- mice) and normolipidemic C57BL/6 mice. Mice were exposed to PM in the ultrafine-size range by inhalation for 6 h a day, 3 times a week for 10 weeks at a concentration of 300-350 µg/m3.16S rRNA gene sequencing was performed to characterize sequential changes in the fecal microbiome during exposures, and changes in the intestinal microbiome at the end. PM exposure led to progressive differentiation of the microbiota over time, associated with increased fecal microbial richness and evenness, altered microbial composition, and differentially abundant microbes by week 10 depending on the mouse model. Cross-sectional analysis of the small intestinal microbiome at week 10 showed significant changes in α-diversity, ß-diversity, and abundances of individual microbial taxa in the two hyperlipidemic models. These alterations of the intestinal microbiome were not accompanied, and therefore could not be caused, by increased intestinal inflammation as determined by histological analysis of small and large intestine, cytokine gene expression, and levels of fecal lipocalin. In conclusion, 10-week inhalation exposures to UFPs induced taxonomic changes in the microbiome of various animal models in the absence of intestinal inflammation.

Los Angeles Basin's air quality transformation: a long-term investigation on the impacts of PM regulations on the trends of ultrafine particles and co-pollutants.

This study investigates the long-term trends of ambient ultrafine particles (UFPs) and associated airborne pollutants in the Los Angeles Basin from 2007 to 2022, focusing on the indirect effects of regulations on UFP levels. The particle number concentration (PNC) of UFPs was compiled from previous studies in the area, and associated co-pollutant data, including nitrogen oxides (NOx), carbon monoxide (CO), elemental carbon (EC), organic carbon (OC), and ozone (O3), were obtained from the chemical speciation network (CSN) database. Over the study period, a general decrease was noted in the PNC of UFPs, NOx, EC, and OC, except for CO, the concentration trends of which did not exhibit a consistent pattern. UFPs, NOx, EC, and OC were positively correlated, while O3 had a negative correlation, especially with NOx. Our analysis discerned two distinct subperiods in pollutant trends: 2007-2015 and 2016-2022. For example, there was an overall decrease in the PNC of UFPs at an annual rate of -850.09 particles/cm3/year. This rate was more pronounced during the first sub-period (2007-2015) at -1814.9 particles/cm3/year and then slowed to -227.21 particles/cm3/year in the second sub-period (2016-2023). The first sub-period (2007-2015) significantly influenced pollutant level changes, exhibiting more pronounced and statistically significant changes than the second sub-period (2016-2022). Since 2016, almost all primary pollutants have stabilized, indicating a reduced impact of current regulations, and emphasizing the need for stricter standards. In addition, the study included an analysis of Vehicle Miles Traveled (VMT) trends from 2007 to 2022 within the Los Angeles Basin. Despite the general increase in VMT, current regulations and cleaner technologies seem to have successfully mitigated the potential increase in increase in PNC. Overall, while a decline in UFPs and co-pollutant levels was observed, the apparent stabilization of these levels underscores the need for more stringent regulatory measures and advanced emission standards.

Outdoor Ultrafine Particulate Matter and Risk of Lung Cancer in Southern California.

Rationale: Particulate matter ⩽2.5 µm in aerodynamic diameter (PM2.5) is an established cause of lung cancer, but the association with ultrafine particulate matter (UFP; aerodynamic diameter < 0.1 µm) is unclear. Objectives: To investigate the association between UFP and lung cancer overall and by histologic subtype. Methods: The Los Angeles Ultrafines Study includes 45,012 participants aged ⩾50 years in southern California at enrollment (1995-1996) followed through 2017 for incident lung cancer (n = 1,770). We estimated historical residential ambient UFP number concentrations via land use regression and back extrapolation using PM2.5. In Cox proportional hazards models adjusted for smoking and other confounders, we estimated associations between 10-year lagged UFP (per 10,000 particles/cm3 and quartiles) and lung cancer overall and by major histologic subtype (adenocarcinoma, squamous cell carcinoma, and small cell carcinoma). We also evaluated relationships by smoking status, birth cohort, and historical duration at the residence. Measurements and Main Results: UFP was modestly associated with lung cancer risk overall (hazard ratio [HR], 1.03 [95% confidence interval (CI), 0.99-1.08]). For adenocarcinoma, we observed a positive trend among men; risk was increased in the highest exposure quartile versus the lowest (HR, 1.39 [95% CI, 1.05-1.85]; P for trend = 0.01) and was also increased in continuous models (HR per 10,000 particles/cm3, 1.09 [95% CI, 1.00-1.18]), but no increased risk was apparent among women (P for interaction = 0.03). Adenocarcinoma risk was elevated among men born between 1925 and 1930 (HR, 1.13 [95% CI, 1.02-1.26] per 10,000) but not for other birth cohorts, and was suggestive for men with ⩾10 years of residential duration (HR, 1.11 [95% CI, 0.98-1.26]). We found no consistent associations for women or other histologic subtypes. Conclusions: UFP exposure was modestly associated with lung cancer overall, with stronger associations observed for adenocarcinoma of the lung.

Identifying urban emission sources and their contribution to the oxidative potential of fine particulate matter (PM2.5) in Kuwait.

In this study, we investigated the seasonal variations, chemical composition, sources, and oxidative potential of ambient PM2.5 (particles with a diameter of less than 2.5 µm) in Kuwait City. The sampling campaign was conducted within the premises of Kuwait Institute for Scientific Research from June 2022 to May 2023, covering different seasons throughout the year. The personal cascade impactor sampler (PCIS) operated at flow rate of 9 L/min was employed to collect weekly PM2.5 samples on PTFE and quarts filters. These collected samples were analyzed for carbonaceous species (i.e., elemental and organic carbon), metals and transition elements, inorganic ions, and DTT (dithiothreitol) redox activity. Furthermore, principal component analysis (PCA) and multi-linear regression (MLR) were used to identify the predominant emission sources and their percentage contribution to the redox activity of PM2.5 in Kuwait. The results of this study highlighted that the annual-averaged ambient PM2.5 mass concentrations in Kuwait (59.9 µg/m3) substantially exceeded the World Health Organization (WHO) guideline of 10 µg/m3. Additionally, the summer season displayed the highest PM2.5 mass concentration (75.2 µg/m3) compared to other seasons, primarily due to frequent dust events exacerbated by high-speed winds. The PCA identified four primary PM2.5 sources: mineral dust, fossil fuel combustion, road traffic, and secondary aerosols. The mineral dust was found to be the predominant source, contributing 36.1% to the PM2.5 mass, followed by fossil fuel combustion and traffic emissions with contributions of 23.7% and 20.3%, respectively. The findings of MLR revealed that road traffic was the most significant contributor to PM2.5 oxidative potential, accounting for 47% of the total DTT activity. In conclusion, this comprehensive investigation provides essential insights into the sources and health implications of PM2.5 in Kuwait, underscoring the critical need for effective air quality management strategies to mitigate the impacts of particulate pollution in the region.

Size-segregated source identification of water-soluble and water-insoluble metals and trace elements of coarse and fine PM in central Los Angeles.

In this study, the water-solubility and sources of metals and trace elements in both fine and coarse particulate matter (PM) were investigated in Central Los Angeles. Sampling was performed in the winter, spring, and summer of 2022 at the Particle Instrumentation Unit (PIU) of the University of Southern California located in the proximity of I-110 freeway. Both fine and coarse PM samples were collected using Personal Cascade Impactors (PCIS) and chemically analyzed to determine their water-soluble and water-insoluble metal content. Principal Component Analysis (PCA) and Multiple Linear Regression (MLR) were used to determine the sources of soluble and insoluble metals and obtain their contributions to total metal concentration. Our results indicate that the water-solubility of most of the metals is higher in the fine size fraction compared to the coarse fraction. Seasonal variations in the water solubility of selected metals for both coarse and fine fractions were observed, with higher water-soluble metal concentrations in summer for several species (e.g., Fe, S, Pb, Cu, La, Ni, and Al), possibly due to higher photochemical processing, while in winter, almost all species exhibited higher insoluble fraction concentrations. The PCA and MLR analyses results showed that tire and brake wear was the most significant contributor to the total metals for both fine soluble and insoluble portions, accounting for 35% and 75% of the total metals, respectively. Combustion sources also contributed substantially to water-soluble metals for fine and coarse size ranges, representing 40% and 32% of the total metal mass, respectively. In addition, mineral dust and soil and re-suspended dust were identified as the highest contributors to coarse metals. The MLR analysis also revealed that secondary aerosols contributed 11% to the fine water-soluble metals. Our results suggest that non-tailpipe emissions significantly contribute to both coarse and fine PM metals in the Central Los Angeles region.

Assessing Lifetime Cancer Risk Associated with Population Exposure to PM-Bound PAHs and Carcinogenic Metals in Three Mid-Latitude Metropolitan Cities.

Lifetime cancer risk characterization of ambient PM-bound carcinogenic metals and polycyclic aromatic hydrocarbons (PAHs) were examined in the cities of Los Angeles (USA), Thessaloniki (Greece) and Milan (Italy), which share similar Mediterranean climates but are different in their urban emission sources and governing air quality regulations. The samples in Milan and Thessaloniki were mostly dominated by biomass burning activities whereas the particles collected in Los Angeles were primary impacted by traffic emissions. We analyzed the ambient PM2.5 mass concentration of Cadmium (Cd), Hexavalent Chromium (Cr(VI)), Nickel (Ni), Lead (Pb), as well as 13 PAH compounds in the PM samples, collected during both cold and warm periods at each location. Pb exhibited the highest annual average concentration in all three cities, followed by Ni, As, Cr(VI), Cd and PAHs, respectively. The cancer risk assessment based on outdoor pollutants was performed based on three different scenarios, with each scenario corresponding to a different level of infiltration of outdoor pollutants into the indoor environment. Thessaloniki exhibited a high risk associated with lifetime inhalation of As, Cr(VI), and PAHs, with values in the range of (0.97-1.57) × 10-6, (1.80-2.91) × 10-6, and (0.77-1.25) × 10-6, respectively. The highest cancer risk values were calculated in Milan, exceeding the US EPA standard by a considerable margin, where the lifetime risk values of exposure to As, Cr(VI), and PAHs were in the range of (1.29-2.08) × 10-6, (6.08-9.82) × 10-6, and (1.10-1.77) × 10-6, respectively. In contrast, the estimated risks associated with PAHs and metals, except Cr(VI), in Los Angeles were extremely lower than the guideline value, even when the infiltration factor was assumed to be at peak. The lifetime cancer risk values associated with As, Cd, Ni, Pb, and PAHs in Los Angeles were in the range of (0.04-0.33) × 10-6. This observation highlights the impact of local air quality measures in improving the air quality and lowering the cancer risks in Los Angeles compared to the other two cities.

Kinetics of autophagic activity in nanoparticle-exposed lung adenocarcinoma (A549) cells.

Autophagy, a homeostatic mechanism, is crucial in maintaining normal cellular function. Although dysregulation of autophagic processes is recognized in certain diseases, it is unknown how maintenance of cellular homeostasis might be affected by the kinetics of autophagic activity in response to various stimuli. In this study, we assessed those kinetics in lung adenocarcinoma (A549) cells in response to exposure to nanoparticles (NP) and/or Rapamycin. Since NP are known to induce autophagy, we wished to determine if this phenomenon could be a driver of the harmful effects seen in lung tissues exposed to air pollution. A549 cells were loaded with a fluorescent marker (DAPRed) that labels autophagosomes and autolysosomes. Autophagic activity was assessed based on the fluorescence intensity of DAPRed measured over the entire cell volume of live single cells using confocal laser scanning microscopy (CLSM). Autophagic activity over time was determined during exposure of A549 cells to single agents (50 nM Rapamycin; 80 µg/mL, 20 nm carboxylated polystyrene NP (PNP); or, 1 µg/mL ambient ultrafine particles (UFP) (<180 nm)), or double agents (Rapamycin + PNP or Rapamycin + UFP; concomitant and sequential), known to stimulate autophagy. Autophagic activity increased in all experimental modalities, including both single agent and double agent exposures, and reached a steady state in all cases ~2 times control from ~8 to 24 hrs, suggesting the presence of an upper limit to autophagic capacity. These results are consistent with the hypothesis that environmental stressors might exert their harmful effects, at least in part, by limiting available autophagic response to additional stimulation, thereby making nanoparticle-exposed cells more susceptible to secondary injury due to autophagic overload.

Magnetic resonance imaging of white matter response to diesel exhaust particles.

Air pollution is associated with risks of dementia and accelerated cognitive decline. Rodent air pollution models have shown white matter vulnerability. This study uses diffusion tensor imaging (DTI) to quantify changes to white matter microstructure and tractography in multiple myelinated regions after exposure to diesel exhaust particulate (DEP). Adult C57BL/6 male mice were exposed to re-aerosolized DEP (NIST SRM 2975) at a concentration of 100 ug/m3 for 200 hours. Ex-vivo MRI analysis and fractional anisotropy (FA)-aided white matter tractography were conducted to study the effect of DEP exposure on the brain white matter tracts. Immunohistochemistry was used to assess myelin and axonal structure. DEP exposure for 8 weeks altered myelin composition in multiple regions. Diffusion tensor imaging (DTI) showed decreased FA in the corpus callosum (30%), external capsule (15%), internal capsule (15%), and cingulum (31 %). Separate immunohistochemistry analyses confirmed prior findings. Myelin basic protein (MBP) was decreased (corpus callosum: 28%, external capsule: 29%), and degraded MPB increased (corpus callosum: 32%, external capsule: 53%) in the DEP group. White matter is highly susceptible to chronic DEP exposure. This study demonstrates the utility of DTI as a neuroanatomical tool in the context of air pollution and white matter myelin vulnerability.

Design, optimization, and evaluation of a wet electrostatic precipitator (ESP) for aerosol collection.

In this study, we developed, optimized, and evaluated in lab and field experiments a wet electrostatic precipitator (ESP) for the collection of ambient PM2.5 (particulate matter with aerodynamic diameter < 2.5 µm) into ultrapure water by applying an electrostatic charge to the particles. We operated the wet ESP at different flow rates and voltages to identify the optimal operating conditions. According to our experimental measurements, a flow rate of 125 lpm and an applied positive voltage of 11 kV resulted in a lower ozone generation of 133 ppb and a particle collection efficiency exceeding 80-90% in all size ranges. For the field tests, the wet ESP was compared with the versatile aerosol concentration enrichment system (VACES) connected to a BioSampler, a PTFE filter sampler, and an OC/EC analyzer (Sunset Laboratory Inc., USA) as a reference. The chemical analysis results indicated the wet ESP concentrations of metal and trace elements were in very good agreement with those measured by the VACES/BioSampler and PTFE filter sampler. Moreover, our results showed comparable total organic carbon (TOC) concentrations measured by the wet ESP, BioSampler, and OC/EC analyzer, while somewhat lower TOC concentrations were measured by the PTFE filter sampler, possibly due to the limitations of extracting water-insoluble organic carbon (WIOC) from a dry substrate in the latter sampler. The comparable TOC content in the wet ESP and BioSampler samples differs from previous findings that showed higher TOC content in BioSampler samples compared to those collected by dry ESP. The results of the Dithiothreitol (DTT) assay showed comparable DTT activity in the VACES/BioSampler and wet ESP PM samples while slightly lower in the PTFE filter samples. Overall, our results suggest that the wet ESP could be a promising alternative to other conventional sampling methods.

Air pollution nanoparticle and alpha-synuclein fibrils synergistically decrease glutamate receptor A1, depending upon nPM batch activity.

Background: Epidemiological studies have variably linked air pollution to increased risk of Parkinson's disease (PD). However, there is little experimental evidence for this association. Alpha-synuclein (α-syn) propagation plays central roles in PD and glutamate receptor A1 (GluA1) is involved in memory and olfaction function. Methods: Each mouse was exposed to one of three different batches of nano-particulate matter (nPM) (300 µg/m3, 5 h/d, 3 d/week), collected at different dates, 2017-2019, in the same urban site. After these experiments, these nPM batches were found to vary in activity. C57BL/6 female mice (3 mo) were injected with pre-formed murine α-synuclein fibrils (PFFs) (0.4 µg), which act as seeds for α-syn aggregation. Two exposure paradigms were used: in Paradigm 1, PFFs were injected into olfactory bulb (OB) prior to 4-week nPM (Batch 5b) exposure and in Paradigm 2, PFFs were injected at 4th week during 10-week nPM exposure (Batches 7 and 9). α-syn pSer129, microglia Iba1, inflammatory cytokines, and Gria1 expression were measured by immunohistochemistry or qPCR assays. Results: As expected, α-syn pSer129 was detected in ipsilateral OB, anterior olfactory nucleus, amygdala and piriform cortex. One of the three batches of nPM caused a trend for elevated α-syn pSer129 in Paradigm 1, but two other batches showed no effect in Paradigm 2. However, the combination of nPM and PFF significantly decreased Gria1 mRNA in both the ipsi- and contra-lateral OB and frontal cortex for the most active two nPM batches. Neither nPM nor PFFs alone induced responses of microglia Iba1 and expression of Gria1 in the OB and cortex. Conclusion: Exposures to ambient nPM had weak effect on α-syn propagation in the brain in current experimental paradigms; however, nPM and α-syn synergistically downregulated the expression of Gria1 in both OB and cortex.

Development and performance evaluation of a two-stage cascade impactor equipped with gelatin filter substrates for the collection of multi-sized particulate matter.

This study presents the development and evaluation of a high flow rate gelatin cascade impactor (GCI) to collect different PM particle sizes on water-soluble gelatin substrates. The GCI operates at a flow rate of 100 lpm, and consists of two impaction stages, followed by a filter holder to separate particles in the following diameter ranges: >2.5 µm, 0.2-2.5 µm, and <0.2 µm. Laboratory characterization of the GCI performance was conducted using monodisperse polystyrene latex (PSL) particles as well as polydisperse ammonium sulfate, sodium chloride, and ammonium nitrate aerosols to obtain the particle collection efficiency curves for both impaction stages. In addition to the laboratory characterization, we performed concurrent field experiments to collect PM2.5 employing both GCI equipped with gelatin filter and personal cascade impactor sampler (PCIS) equipped with PTFE filter for further toxicological analysis using macrophage-based reactive oxygen species (ROS) and dithiothreitol consumption (DTT) assays. Our results showed that the experimentally determined cut-point diameters for the first and second impaction stages were 2.4 µm and 0.21 µm, respectively, which agreed with the theoretical predictions. Although the GCI has been developed primarily to collect particles on gelatin filters, the use of a different type of substrate (i.e., quartz) led to similar particle separation characteristics. The findings of the field tests demonstrated the advantage of using the GCI in toxicological studies due to its ability to collect considerable PM-toxic constituents, as corroborated by the DTT and ROS values for the GCI-collected particles which were 26.44 nmoles/min/mg PM and 8813.2 µg Zymosan Units/mg PM, respectively. These redox activity values were more than twice those of particles collected concurrently on PTFE filter using the PCIS. This high-flow-rate impactor can collect considerable amounts of size-fractionated PM on water-soluble filters (i.e., gelatin), which can completely dissolve in water allowing for the extraction of soluble and insoluble PM species for further toxicological analysis.

Particulate matter exposure and chronic cerebral hypoperfusion promote oxidative stress and induce neuronal and oligodendrocyte apoptosis in male mice.

Chronic cerebral hypoperfusion (CCH) may amplify the neurotoxicity of nanoscale particulate matter (nPM), resulting in white matter injury. This study characterized the joint effects of nPM (diameter ≤ 200 nm) and CCH secondary to bilateral carotid artery stenosis (BCAS) exposure on neuronal and white matter injury in a murine model. nPM was collected near a highway and re-aerosolized for exposure. Ten-week-old C57BL/6 male mice were randomized into four groups: filtered air (FA), nPM, FA + BCAS, and nPM + BCAS. Mice were exposed to FA or nPM for 10 weeks. BCAS surgeries were performed. Markers of inflammation, oxidative stress, and apoptosis were examined. nPM + BCAS exposure increased brain hemisphere TNFα protein compared to FA. iNOS and HNE immunofluorescence were increased in the corpus callosum and cerebral cortex of nPM + BCAS mice compared to FA. While nPM exposure alone did not decrease cortical neuronal cell count, nPM decreased corpus callosum oligodendrocyte cell count. nPM exposure decreased mature oligodendrocyte cell count and increased oligodendrocyte precursor cell count in the corpus callosum. nPM + BCAS mice exhibited a 200% increase in cortical neuronal TUNEL staining and a 700% increase in corpus callosum oligodendrocyte TUNEL staining compared to FA. There was a supra-additive interaction between nPM and BCAS on cortical neuronal TUNEL staining (2.6× the additive effects of nPM + BCAS). nPM + BCAS exposure increased apoptosis, neuroinflammation, and oxidative stress in the cerebral cortex and corpus callosum. nPM + BCAS exposure increased neuronal apoptosis above the separate responses to each exposure. However, oligodendrocytes in the corpus callosum demonstrated a greater susceptibility to the combined neurotoxic effects of nPM + BCAS exposure.

The Role of Portable Air Purifiers and Effective Ventilation in Improving Indoor Air Quality in University Classrooms.

In this study we investigated the effectiveness of air purifiers and in-line filters in ventilation systems working simultaneously inside various classrooms at the University of Southern California (USC) main campus. We conducted real-time measurements of particle mass (PM), particle number (PN), and carbon dioxide (CO2) concentrations in nine classrooms from September 2021 to January 2022. The measurement campaign was carried out with different configurations of the purifier (i.e., different flow rates) while the ventilation system was continuously working. Our results showed that the ventilation systems in the classrooms were adequate in providing sufficient outdoor air to dilute indoor CO2 concentrations due to the high air exchange rates (2.63-8.63 h-1). The particle penetration coefficients (P) of the investigated classrooms were very low for PM (<0.2) and PN (<0.1), with the exception of one classroom, corroborating the effectiveness of in-line filters in the ventilation systems. Additionally, the results showed that the efficiency of the air purifier exceeded 95% in capturing ultrafine and coarse particles and ranged between 82-88% for particles in the accumulation range (0.3-2 µm). The findings of this study underline the effectiveness of air purifiers and ventilation systems equipped with efficient in-line filters in substantially reducing indoor air pollution.

The oxidative potential of particulate matter (PM) in different regions around the world and its relation to air pollution sources.

In this study, we investigated the impact of urban emission sources on the chemical composition of ambient particulate matter (PM) as well as the associated oxidative potential. We collected six sets of PM samples in five urban location sites around the world over long time periods varying from weeks to months, intentionally selected for their PM to be dominated by unique emission sources: (1) PM2.5 produced mainly by traffic emissions in central Los Angeles, United States (US); (2) PM2.5 dominated by biomass burning in Milan, Italy; (3) PM2.5 formed by secondary photochemical reactions thus dominated by secondary aerosols in Athens, Greece; (4) PM10 emitted by refinery and dust resuspension in Riyadh, Saudi Arabia (SA); (5) PM10 generated by dust storms in Riyadh, SA, and (6) PM2.5 produced mainly by industrial and traffic emissions in Beirut, Lebanon. The PM samples were chemically analyzed and their oxidative potential were quantified by employing the dithiothreitol (DTT) assay. Our results revealed that the Milan samples were rich in water soluble organic carbon (WSOC) and PAHs, even exceeding the levels measured on Los Angeles (LA) freeways. The PM in Athens was characterized by high concentrations of inorganic ions, specifically sulfate which was the highest of all PM samples. The ambient PM in LA was impacted by the traffic-emitted primary organic and elemental carbon. Furthermore, the contribution of metals and elements per mass of PM in Riyadh and Beirut samples were more pronounced relative to other sampling areas. The highest intrinsic PM redox activity was observed for PM with the highest WSOC fraction, including Milan (biomass burning) and Athens (secondary organic aerosols, SOA). PM in areas characterized by high metal emissions including dust events, refinery and industry, such as Riyadh and Beirut, had the lowest oxidative potential as assessed by the DTT assay. The results of this study illustrate the impact of major emission sources in urban areas on the redox activity and oxidative potential of ambient PM, providing useful information for developing efficient air pollution control and mitigation policies in polluted areas around the globe.

Investigation of organic carbon profiles and sources of coarse PM in Los Angeles.

Source apportionment analyses are essential tools to determine sources of ambient coarse particles (2.5

Neurotoxicity of Diesel Exhaust Particles.

BACKGROUND: Air pollution particulate matter (PM) is strongly associated with risks of accelerated cognitive decline, dementia and Alzheimer's disease. Ambient PM batches have variable neurotoxicity by collection site and season, which limits replicability of findings within and between research groups for analysis of mechanisms and interventions. Diesel exhaust particles (DEP) offer a replicable model that we define in further detail. OBJECTIVE: Define dose- and time course neurotoxic responses of mice to DEP from the National Institute of Science and Technology (NIST) for neurotoxic responses shared by DEP and ambient PM. METHODS: For dose-response, adult C57BL/6 male mice were exposed to 0, 25, 50, and 100µg/m3 of re-aerosolized DEP (NIST SRM 2975) for 5 h. Then, mice were exposed to 100µg/m3 DEP for 5, 100, and 200 h and assayed for amyloid-ß peptides, inflammation, oxidative damage, and microglial activity and morphology. RESULTS: DEP exposure at 100µg/m3 for 5 h, but not lower doses, caused oxidative damage, complement and microglia activation in cerebral cortex and corpus callosum. Longer DEP exposure for 8 weeks/200 h caused further oxidative damage, increased soluble Aß, white matter injury, and microglial soma enlargement that differed by cortical layer. CONCLUSION: Exposure to 100µg/m3 DEP NIST SRM 2975 caused robust neurotoxic responses that are shared with prior studies using DEP or ambient PM0.2. DEP provides a replicable model to study neurotoxic mechanisms of ambient PM and interventions relevant to cognitive decline and dementia.