Explore the vast range of titles available.

In this study, the positive matrix factorization (PMF) receptor model (version 5.0) was used to identify and quantify major sources contributing to particulate matter (PM) number concentrations, using PM number size distributions in the range of 13 nm to 10 µm combined with several auxiliary variables, including black carbon (BC), elemental and organic carbon (EC/OC), PM mass concentrations, gaseous pollutants, meteorological, and traffic counts data, collected for about 9 months between August 2014 and 2015 in central Los Angeles, CA. Several parameters, including particle number and volume size distribution profiles, profiles of auxiliary variables, contributions of different factors in different seasons to the total number concentrations, diurnal variations of each of the resolved factors in the cold and warm phases, weekday/weekend analysis for each of the resolved factors, and correlation between auxiliary variables and the relative contribution of each of the resolved factors, were used to identify PM sources. A six-factor solution was identified as the optimum for the aforementioned input data. The resolved factors comprised nucleation, traffic 1, traffic 2 (with a larger mode diameter than traffic 1 factor), urban background aerosol, secondary aerosol, and soil/road dust. Traffic sources (1 and 2) were the major contributor to PM number concentrations, collectively making up to above 60 % (60.8–68.4 %) of the total number concentrations during the study period. Their contribution was also significantly higher in the cold phase compared to the warm phase. Nucleation was another major factor significantly contributing to the total number concentrations (an overall contribution of 17 %, ranging from 11.7 to 24 %), with a larger contribution during the warm phase than in the cold phase. The other identified factors were urban background aerosol, secondary aerosol, and soil/road dust, with relative contributions of approximately 12 % (7.4–17.1), 2.1 % (1.5–2.5 %), and 1.1 % (0.2–6.3 %), respectively, overall accounting for about 15 % (15.2–19.8 %) of PM number concentrations. As expected, PM number concentrations were dominated by factors with smaller mode diameters, such as traffic and nucleation. On the other hand, PM volume and mass concentrations in the study area were mostly affected by sources with larger mode diameters, including secondary aerosols and soil/road dust. Results from the present study can be used as input parameters in future epidemiological studies to link PM sources to adverse health effects as well as by policymakers to set targeted and more protective emission standards for PM.

Elucidating the mechanisms that sustain asthmatic inflammation is critical for precision therapies. We found that interleukin-6- and STAT3 transcription factor-dependent upregulation of Notch4 receptor on lung tissue regulatory T (T reg ) cells is necessary for allergens and particulate matter pollutants to promote airway inflammation. Notch4 subverted T reg cells into the type 2 and type 17 helper (T H 2 and T H 17) effector T cells by Wnt and Hippo pathway-dependent mechanisms. Wnt activation induced growth and differentiation factor 15 expression in T reg cells, which activated group 2 innate lymphoid cells to provide a feed-forward mechanism for aggravated inflammation. Notch4, Wnt and Hippo were upregulated in circulating T reg cells of individuals with asthma as a function of disease severity, in association with reduced T reg cell-mediated suppression. Our studies thus identify Notch4-mediated immune tolerance subversion as a fundamental mechanism that licenses tissue inflammation in asthma. Dysregulation of lung T reg cell function contributes to asthma development. Chatila and colleagues find that allergens upregulate Notch4–Hippo–Wnt signaling in T reg cells, triggering their release of GDF15 growth factor, which drives type 2 innate lymphoid cell activity and asthma.

Recent research highlights that non-exhaust emissions from the abrasion of tires and other organic materials have emerged as a substantial source of airborne particulate matter and marine microplastics. Despite their growing impact, the underlying mechanisms driving these abrasion emissions have remained largely unexplored. In this study, we uncover that abrasion emissions from organic materials are fundamentally governed by a fatigue fracture process, wherein particles are progressively detached from the material surface under cyclic abrasion loads. Our findings demonstrate that these emissions increase significantly only when the applied abrasion loads surpass the material’s toughness threshold. We establish a scaling relationship between the concentration of emitted particulate matter and the measurable crack propagation rate of the organic material, offering a robust quantitative method to estimate abrasion emissions. This work not only introduces a novel mechanistic framework for understanding particulate matter pollution from organic material abrasion but also provides a scientific basis for developing strategies to mitigate emissions of airborne particulates and marine microplastics.

Numerous epidemiologic time-series studies have shown generally consistent associations of cardiovascular hospital admissions and mortality with outdoor air pollution, particularly mass concentrations of particulate matter (PM) ≤ 2.5 or ≤ 10 μm in diameter ( PM2.5, PM10). Panel studies with repeated measures have supported the time-series results showing associations between PM and risk of cardiac ischemia and arrhythmias, increased blood pressure, decreased heart rate variability, and increased circulating markers of inflammation and thrombosis. The causal components driving the PM associations remain to be identified. Epidemiologic data using pollutant gases and particle characteristics such as particle number concentration and elemental carbon have provided indirect evidence that products of fossil fuel combustion are important. Ultrafine particles < 0.1 μm (UFPs) dominate particle number concentrations and surface area and are therefore capable of carrying large concentrations of adsorbed or condensed toxic air pollutants. It is likely that redox-active components in UFPs from fossil fuel combustion reach cardiovascular target sites. High UFP exposures may lead to systemic inflammation through oxidative stress responses to reactive oxygen species and thereby promote the progression of atherosclerosis and precipitate acute cardiovascular responses ranging from increased blood pressure to myocardial infarction. The next steps in epidemiologic research are to identify more clearly the putative PM casual components and size fractions linked to their sources. To advance this, we discuss in a companion article (Sioutas C, Delfino RJ, Singh M. 2005. Environ Health Perspect 113:947-955) the need for and methods of UFP exposure assessment.

Background Exposure to traffic-related air pollution (TRAP) is associated with accelerated cognitive aging and higher dementia risk in human populations. Rodent brains respond to TRAP with activation of astrocytes and microglia, increased inflammatory cytokines, and neurite atrophy. A role for Toll-like receptor 4 (TLR4) was suggested in mouse TLR4-knockouts, which had attenuated lung macrophage responses to air pollution. Methods To further analyze these mechanisms, we examined mixed glial cultures (astrocytes and microglia) for RNA responses to nanoscale particulate matter (nPM; diameter <0.2 μm), a well-characterized nanoscale particulate matter subfraction of TRAP collected from a local freeway (Morgan et al. Environ Health Perspect 2011; 119,1003–1009, 2011). The nPM was compared with responses to the endotoxin lipopolysaccharide (LPS), a classic TLR4 ligand, using Affymetrix whole genome microarray in rats. Expression patterns were analyzed by significance analysis of microarrays (SAM) for fold change and by weighted gene co-expression network analysis (WGCNA) to identify modules of shared responses between nPM and LPS. Finally, we examined TLR4 activation in hippocampal tissue from mice chronically exposed to nPM. Results SAM and WGCNA analyses showed strong activation of TLR4 and NF-κB by both nPM and LPS. TLR4 siRNA attenuated TNFα and other inflammatory responses to nPM in vitro, via the MyD88-dependent pathway. In vivo, mice chronically exposed to nPM showed increased TLR4, MyD88, TNFα, and TNFR2 RNA, and decreased NF-κB and TRAF6 RNA TLR4 and NF-κB responses in the hippocampus. Conclusions These results show TLR4 activation is integral in brain inflammatory responses to air pollution, and warrant further study of TLR4 in accelerated cognitive aging by air pollution.

The neurotoxicity of air pollution is undefined for sex and APOE alleles. These major risk factors of Alzheimer’s disease (AD) were examined in mice given chronic exposure to nPM, a nano-sized subfraction of urban air pollution. In the cerebral cortex, female mice had two-fold more genes responding to nPM than males. Transcriptomic responses to nPM had sex-APOE interactions in AD-relevant pathways. Only APOE3 mice responded to nPM in genes related to Abeta deposition and clearance (Vav2, Vav3, S1009a). Other responding genes included axonal guidance, inflammation (AMPK, NFKB, APK/JNK signaling), and antioxidant signaling (NRF2, HIF1A). Genes downstream of NFKB and NRF2 responded in opposite directions to nPM. Nrf2 knockdown in microglia augmented NFKB responses to nPM, suggesting a critical role of NRF2 in air pollution neurotoxicity. These findings give a rationale for epidemiologic studies of air pollution to consider sex interactions with APOE alleles and other AD-risk genes.

This study examines long-term trends in fine particulate matter (PM2.5) composition and oxidative potential in Los Angeles based on data from the University of Southern California’s Particle Instrumentation Unit, with chemical composition retrieved from the EPA’s Air Quality System (AQS). While regulatory interventions have reduced PM2.5 mass concentration and primary combustion-related components, our findings reveal a more complex toxicity pattern. From 2001 to 2008, the PM2.5 oxidative potential, measured via the dithiothreitol (DTT) assay, declined from ~0.84 to ~0.16 nmol/min/m3 under stringent tailpipe controls. However, after this initial decline, PM2.5 DTT stabilized and gradually increased from ~0.35 in 2012 to ~0.97 nmol/min/m3 by 2024, reflecting the growing influence of non-tailpipe emissions such as brake/tire wear. Metals, such as iron (Fe, ~150 ng/m3) and zinc (Zn, ~10 ng/m3), remained relatively stable as organic and elemental carbon (OC and EC) declined, resulting in non-tailpipe contributions dominating PM2.5 toxicity. Although PM2.5 mass concentrations were effectively reduced, the growing contribution of non-tailpipe emissions (e.g., brake/tire wear and secondary organic aerosols) underscores the limitations of mass-based standards and tailpipe-focused strategies. Our findings emphasize the need to broaden regulatory strategies, targeting emerging sources that shape PM2.5 composition and toxicity and ensuring more improvements in public health outcomes.

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.

Exposure to ambient air pollution particulate matter (PM) is associated with increased risk of dementia and accelerated cognitive loss. Vascular contributions to cognitive impairment are well recognized. Chronic cerebral hypoperfusion (CCH) promotes neuroinflammation and blood-brain barrier weakening, which may augment neurotoxic effects of PM. This study examined interactions of nanoscale particulate matter (nPM; fine particulate matter with aerodynamic diameter ) and CCH secondary to bilateral carotid artery stenosis (BCAS) in a murine model to produce white matter injury. Based on other air pollution interactions, we predicted synergies of nPM with BCAS. nPM was collected using a particle sampler near a Los Angeles, California, freeway. Mice were exposed to 10 wk of reaerosolized nPM or filtered air (FA) for 150 h. CCH was induced by BCAS surgery. Mice (C57BL/6J males) were randomized to four exposure paradigms: ) FA, ) nPM, ) , and ) . Behavioral outcomes, white matter injury, glial cell activation, inflammation, and oxidative stress were assessed. The joint group exhibited synergistic effects on white matter injury (2.3× the additive nPM and scores) with greater loss of corpus callosum volume on T2 magnetic resonance imaging (MRI) (30% smaller than FA group). Histochemical analyses suggested potential microglial-specific inflammatory responses with synergistic effects on corpus callosum C5 immunofluorescent density and whole brain nitrate concentrations (2.1× and 3.9× the additive nPM and effects, respectively) in the joint exposure group. Transcriptomic responses (RNA-Seq) showed greater impact of than individual additive effects, consistent with changes in proinflammatory pathways. Although nPM exposure alone did not alter working memory, the cohort demonstrated impaired working memory when compared to the group. Our data suggest that nPM and CCH contribute to white matter injury in a synergistic manner in a mouse model. Adverse neurological effects may be aggravated in a susceptible population exposed to air pollution. https://doi.org/10.1289/EHP8792.

Background: Mechanisms involving oxidative stress and inflammation have been proposed to explain associations of ambient air pollution with cardiovascular morbidity and mortality. Experimental evidence suggests that organic components and ultrafine particles (UFP) are important. Methods: We conducted a panel study of 60 elderly subjects with coronary artery disease living in retirement communities within the Los Angeles, California, air basin. Weekly biomarkers of inflammation included plasma interleukin-6, tumor necrosis factorα soluble receptor II (sTNFRII), soluble platelet selectin (sP-selectin), and C-reactive protein (CRP). Biomarkers of erythrocyte antioxidant activity included glutathione peroxidase-1 and superoxide dismutase. Exposures included outdoor home daily particle mass [paniculate matter < 0.25, 0.25-2.5, and 2.5-10 ¼m in aerodynamic diameter (${\\rm{PM}}_{{\\rm{0}}{\\rm{.25}}} {\\rm{,}}\\,{\\rm{PM}}_{{\\rm{0}}{\\rm{.25 - 2}}{\\rm{.5}}} {\\rm{,}}\\,{\\rm{PM}}_{{\\rm{2}}{\\rm{.5 - 10}}} $], and hourly elemental and black carbon (EC-BC), estimated primary and secondary organic carbon (${\\rm{OC}}_{{\\rm{Pri}}} {\\rm{,}}\\,{\\rm{SOC}}$), particle number (PN), carbon monoxide (CO), and nitrogen oxides-nitrogen dioxide (NOₓ-NO₂). We analyzed the relation of biomarkers to exposures with mixed effects models adjusted for potential confounders. Results: Primary combustion markers (EC-BC,${\\rm{OC}}_{{\\rm{pri}}} $, CO, NOₓ-NO₂), but not SOC, were positively associated with inflammatory biomarkers and inversely associated with erythrocyte antioxidant enzymes (n = 578). PN and${\\rm{PM}}_{{\\rm{0}}{\\rm{.25}}} $were more strongly associated with biomarkers than${\\rm{PM}}_{{\\rm{0}}{\\rm{.25 - 2}}{\\rm{.5}}} $. Associations for all exposures were stronger during cooler periods when only${\\rm{OC}}_{{\\rm{pri}}} $, PN, and NOₓ were higher. We found weaker associations with statin (sTNF-RII, CRP) and clopidogrel use (sP-selectin). Conclusions: Traffic-related air pollutants are associated with increased systemic inflammation, increased platelet activation, and decreased erythrocyte antioxidant enzyme activity, which may be partly behind air pollutant-related increases in systemic inflammation. Differences in association by particle size, OC fraction, and seasonal period suggest components carried by UFP are important.