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Atmospheric waters – including fog/cloud drops and aerosol liquid water – are important sites for the transformations of atmospheric species, largely through reactions with photoformed oxidants such as hydroxyl radical (●OH), singlet molecular oxygen (1O2*), and oxidizing triplet excited states of organic matter (3C*). Despite this, there are few measurements of these photooxidants, especially in extracts of ambient particles, and very little information about how oxidant levels vary with season or particle type. To address this gap, we collected ambient PM2.5 from Davis, California over the course of a year and measured photooxidant concentrations in dilute aqueous extracts of the particles. We categorized samples into four groups: Winter & Spring (Win-Spr), Summer & Fall (Sum-Fall) without wildfire influence, fresh biomass burning (FBB), and aged biomass burning (ABB). FBB contains significant amounts of brown carbon (BrC) from wildfires, and the highest mass absorption coefficients (MAC) normalized by dissolved organic carbon, with an average (± 1 σ) value of 3.3 (± 0.4) m2 (g C)−1 at 300 nm. Win-Spr and ABB have similar MAC averages, 1.9 (± 0.4) and 1.5 (± 0.3) m2 (g C)−1, respectively, while Sum-Fall has the lowest MACDOC (0.65 (± 0.19) m2 (g C)−1). ●OH concentrations in extracts range from (0.2–4.7) × 10−15 M and generally increase with concentration of dissolved organic carbon (DOC), although this might be because DOC is a proxy for extract concentration. The average quantum yield for ●OH formation (ΦOH) across all sample types is 3.7 (± 2.4) %, with no statistical difference among sample types. 1O2* concentrations have a range of (0.7−45) × 10−13 M, exhibiting a good linearity with DOC that is independent of sample type (R2 = 0.93). Fresh BB samples have the highest [1O2*] but the lowest average Φ1O2*, while Sum-Fall samples are the opposite. Φ1O2* is negatively correlated with MACDOC, indicating that less light-absorbing samples form 1O2* more efficiently. We quantified 3C* concentrations with two triplet probes: syringol (SYR), which captures both strongly and weakly oxidizing triplets, and (phenylthio)acetic acid (PTA), which is only sensitive to strongly oxidizing triplets. Concentrations of 3C* are in the range of (0.03–7.9) × 10−13 M and linearly increase with DOC (R2 = 0.85 for SYR and R2 = 0.80 for PTA); this relationship for [3C*]SYR is independent of sample type. The average ratio of [3C*]PTA/[3C*]SYR is 0.58 (± 0.38), indicating that roughly 60 % of oxidizing triplets are strongly oxidizing. Win-Spr samples have the highest fraction of strongly oxidizing 3C*, with an average of 86 (± 43) %. Φ3C*,SYR is in the range of (0.6–8.8) %, with an average value, 3.3 (± 1.9) %, two times higher than Φ3C*,PTA. FBB has the lowest average Φ3C*, while the aging process tends to enhance Φ3C*, as well as Φ1O2*. To estimate photooxidant concentrations in particle water, we extrapolate the photooxidant kinetics in our dilute particle extracts to aerosol liquid water (ALW) conditions of 1 µg PM/µg H2O for each sample type. The estimated ALW ●OH concentration is 7 × 10−15 M when including mass transport of gas-phase ●OH to the particles. 1O2* and 3C* concentrations in ALW have ranges of (0.6–7) × 10−12 M and (0.08–1) × 10−12 M, respectively. In the Win-Spr and Sum-Fall samples, photooxidant concentrations increase significantly from lab particle extracts to ALW, while the changes for the FBB and ABB samples are minor. The small increases in 1O2* and 3C* from extract to ALW for the biomass burning particles are likely due to the high amounts of organic compounds in the extracts, which lead to strong quenching of these oxidants even under our dilute conditions. Compared to the photooxidant concentration estimates in Kaur et al. (2019), our updated ALW estimates show higher ●OH (by roughly a factor of 10), higher 3C* (by factors of 1–5) and lower 1O2* concentrations (by factors of 20–100). Our results indicate that 3C* and 1O2* in ALW dominate the processing of organic compounds that react quickly with these oxidants (such as phenols and furans, respectively), while ●OH is more important for less reactive organics.

Aerosol liquid water (ALW) is a unique reaction medium, but its chemistry is poorly understood. For example, little is known of photooxidant concentrations – including hydroxyl radical (●OH), singlet molecular oxygen (1O2*), and oxidizing triplet excited states of organic matter (3C*) – even though they likely drive much of ALW chemistry. Due to the very limited water content of particles, it is difficult to quantify oxidant concentrations in ALW directly. To predict these values, we measured photooxidant concentrations in illuminated aqueous particle extracts as a function of dilution and used the resulting oxidant kinetics to extrapolate to ALW conditions. We prepared dilution series from two sets of particles collected in Davis, California: one from winter (WIN) and one from summer (SUM). Both periods are influenced by biomass burning, with dissolved organic carbon (DOC) in the extracts ranging from 10 to 495 mg C L−1. In the winter sample, the ●OH concentration is independent of particle mass concentration, with an average value of 5.0 (± 2.2) × 10−15 M, while in summer ●OH increases with DOC in the range (0.4 − 7.7) × 10−15 M. In both winter and summer samples, 3C* concentrations increase rapidly with particle mass concentrations in the extracts, and then plateau under more concentrated conditions, with a range of (0.2 − 7) × 10−13 M. WIN and SUM have the same range of 1O2* concentrations, (0.2 − 8.5) × 10−12 M, but in WIN the 1O2* concentration increases linearly with DOC, while in SUM 1O2* approaches a plateau. We next extrapolated the relationships of oxidant formation rates and sinks as a function of particle mass concentration from our dilute extracts to the much more concentrated condition of aerosol liquid water. Predicted ●OH concentrations in ALW (including mass transport of ●OH from the gas phase) are (5 − 8) × 10−15 M, similar to those in fog/cloud waters. In contrast, predicted concentrations of 3C* and 1O2* in ALW are approximately 10 to 100 times higher than in cloud/fogs, with values of (4 – 9) × 10−13 M and (1 – 5) × 10−12 M, respectively. Although ●OH is often considered the main sink for organic compounds in the atmospheric aqueous phase, the much higher concentrations of 3C* and 1O2* in aerosol liquid water suggest these photooxidants will be more important sinks for many organics in particle water.

Chronic exposure to traffic-related air pollution (TRAP) is known to promote systemic inflammation, which is thought to underlie respiratory, cardiovascular, metabolic and neurological disorders. It is not known whether chronic TRAP exposure dampens inflammation resolution, the homeostatic process for stopping inflammation and repairing damaged cells. In vivo, inflammation resolution is facilitated by bioactive lipid mediators known as oxylipins, which are derived from the oxidation of polyunsaturated fatty acids. To understand the effects of chronic TRAP exposure on lipid-mediated inflammation resolution pathways, we measured total (i.e. free+bound) pro-inflammatory and pro-resolving lipid mediators in serum of female rats exposed to TRAP or filtered air (FA) for 14 months. Compared to rats exposed to FA, TRAP-exposed rats showed a significant 36-48% reduction in fatty acid alcohols, specifically, 9-hydroxyoctadecadienoic acid (9-HODE), 11,12-dihydroxyeicosatetraenoic acid (11,12-DiHETE) and 16,17-dihydroxydocosapentaenoic acid (16, 17-DiHDPA). The decrease in fatty acid diols (11,12-DiHETE and 16, 17-DiHDPA) corresponded to a significant 34-39% reduction in the diol to epoxide ratio, a marker of soluble epoxide hydrolase activity; this enzyme is typically upregulated during inflammation. The findings demonstrate that 14 months exposure to TRAP reduced pro-inflammatory 9-HODE concentration and dampened soluble epoxide hydrolase activation, suggesting adaptive immune changes in lipid mediator pathways involved in inflammation resolution.

Ambient PM2.5 was collected during the winter season from Taiyuan, Shanxi, China; Jinan, Shandong, China; and Sacramento, California, USA, and used to create PMSX, PMSD, and PMCA extracts, respectively. Time-lag experiments were performed to explore the in vivo and in vitro toxicity of the PM extracts. In vivo inflammatory lung responses were assessed in BALB/c mice using a single oropharyngeal aspiration (OPA) of PM extract or vehicle (CTRL) on Day 0. Necropsies were performed on Days 1, 2, and 4 post-OPA, and pulmonary effects were determined using bronchoalveolar lavage (BAL) and histopathology. On Day 1, BAL neutrophils were significantly elevated in all PM- versus CTRL-exposed mice, with PMCA producing the strongest response. However, histopathological scoring showed greater alveolar and perivascular effects in PMSX-exposed mice compared to all three other groups. By Day 4, BAL neutrophilia and tissue inflammation were resolved, similar across all groups. In vitro effects were examined in human HepG2 hepatocytes, and U937 cells following 6, 24, or 48 h of exposure to PM extract or DMSO (control). Luciferase reporter and quantitative polymerase chain reaction assays were used to determine in vitro effects on aryl hydrocarbon receptor (AhR) activation and gene transcription, respectively. Though all three PM extracts activated AhR, PMSX produced the greatest increases in AhR activation, and mRNA levels of cyclooxygenase-2, cytochrome P450, interleukin (IL)-8, and interleukin (IL)-1β. These effects were assumed to result from a greater abundance of polycyclic aromatic hydrocarbons (PAHs) in PMSX compared to PMSD and PMCA.

Epidemiological and toxicological studies continue to demonstrate correlative and causal relationships between exposure to traffic-related air pollution and various metrics of adverse pulmonary, cardiovascular, and neurological health effects. The key challenge for in vivo studies is replicating real-world, near-roadway exposure dynamics in laboratory animal models that mimic true human exposures. The advantage of animal models is the accelerated time scales to show statistically significant physiological and/or behavioral response. This work describes a novel exposure facility adjacent to a major freeway tunnel system that provides a platform for real-time chronic exposure studies. The primary conclusion is that particulate matter (PM) concentrations at this facility are routinely well below the National Ambient Air Quality Standards (NAAQS), but studies completed to date still demonstrate significant neurological and cardiovascular effects. Internal combustion engines produce large numbers of ultrafine particles that contribute negligible mass to the atmosphere relative to NAAQS regulated PM2.5 but have high surface area and mobility in the body. It is posited here that current federal and state air quality standards are thus insufficient to fully protect human health, most notably the developing and aging brain, due to regulatory gaps for ultrafine particles.

Traffic-related air pollution (TRAP) is a risk factor for Alzheimer’s disease (AD) where neuroinflammation underlies disease progression and pathogenesis. Unresolved inflammation in AD is known to be exacerbated by brain deficits in unesterified pro-resolving lipid mediators enzymatically synthesized from polyunsaturated fatty acids. Recently, we reported that in the brain, unesterified pro-resolving lipid mediators which are bioactive, can also be supplied from less bioactive esterified lipid pools such as neutral lipids (NLs) and phospholipids (PLs). It is not known whether esterified pro-resolving lipid mediators are affected by AD pathology and exacerbated by TRAP exposure. In the present study we addressed this data gap using TgF344-AD male and female rats that express human AD risk genes and their wildtype littermates exposed to filtered air (FA) or TRAP from 1 to 15 months of age. Esterified lipid mediators within NLs and PLs were quantified by mass-spectrometry. We observed a significant reduction in pro-resolving lipid mediators in both NLs and PLs of female TgF344-AD rats compared to wildtype controls. TRAP exposure also reduced pro-resolving lipids in the female brain, mainly in PL pools, but did not exacerbate changes observed in TgF344-AD rats. Minimal changes were observed in males. Our findings indicate that AD genotype and chronic TRAP exposure result in sex-specific deficits in brain esterified pro-resolving lipid mediators, the pool that supplies free and bioactive lipid mediators. These data provide new information on lipid-mediated mechanisms regulating impaired inflammation resolution in AD, and show for the first time that chronic TRAP exposure targets the same lipid network implicated in AD.

Epidemiological studies show strong associations between fine particulate matter (PM2.5) air pollution and adverse pulmonary effects. In the present study, wintertime PM2.5 samples were collected from three geographically similar regions—Sacramento, California, USA; Jinan, Shandong, China; and Taiyuan, Shanxi, China—and extracted to form PMCA, PMSD, and PMSX, respectively, for comparison in a BALB/c mouse model. Each of four groups was oropharyngeally administered Milli-Q water vehicle control (50 μ L) or one type of PM extract (20 μg/50 μL) five times over two weeks. Mice were necropsied on post-exposure days 1, 2, and 4 and examined using bronchoalveolar lavage (BAL), histopathology, and assessments of cytokine/chemokine mRNA and protein expression. Chemical analysis demonstrated all three extracts contained black carbon, but PMSX contained more sulfates and polycyclic aromatic hydrocarbons (PAHs) associated with significantly greater neutrophil numbers and greater alveolar/bronchiolar inflammation on post-exposure days 1 and 4. On day 4, PMSX-exposed mice also exhibited significant increases in interleukin-1 beta, tumor necrosis factor-alpha, and chemokine C-X-C motif ligands-3 and −5 mRNA, and monocyte chemoattractant protein-1 protein. These combined findings suggest greater sulfate and PAH content contributed to a more intense and progressive inflammatory response with repeated PMSX compared to PMCA or PMSD exposure., GRAPHICAL ABSTRACT

Background: Epidemiological data link traffic-related air pollution (TRAP) to increased risk of Alzheimer’s disease (AD). Preclinical data corroborating this association are largely from studies of male animals exposed acutely or subchronically to high levels of isolated fractions of TRAP. What remains unclear is whether chronic exposure to ambient TRAP modifies AD risk and the influence of sex on this interaction. Objectives: This study sought to assess effects of chronic exposure to ambient TRAP on the time to onset and severity of AD phenotypes in a preclinical model and to determine whether sex or genetic susceptibility influences outcomes. Methods: Male and female TgF344-AD rats that express human AD risk genes and wildtype littermates were housed in a vivarium adjacent to a heavily trafficked tunnel in Northern California and exposed for up to 14 months to filtered air (FA) or TRAP drawn from the tunnel and delivered to animals unchanged in real time. Refractive particles in the brain and AD phenotypes were quantified in 3-, 6-, 10-, and 15-month-old animals using hyperspectral imaging, behavioral testing, and neuropathologic measures. Results: Particulate matter (PM) concentrations in TRAP exposure chambers fluctuated with traffic flow but remained below 24-h PM with aerodynamic diameter less than or equal to 2.5 micrometers (PM2.5) U.S. National Ambient Air Quality Standards limits. Ultrafine PM was a predominant component of TRAP. Nano-sized refractive particles were detected in the hippocampus of TRAP animals. TRAP-exposed animals had more amyloid plaque deposition, higher hyperphosphorylated tau levels, more neuronal cell loss, and greater cognitive deficits in an age-, genotype-, and sex-dependent manner. TRAP-exposed animals also had more microglial cell activation, but not astrogliosis. Discussion: These data demonstrate that chronic exposure to ambient TRAP promoted AD phenotypes in wildtype and genetically susceptible rats. TRAP effects varied according to age, sex, and genotype, suggesting that AD progression depends on complex interactions between environment and genetics. These findings suggest current PM2.5 regulations are insufficient to protect the aging brain. https://doi.org/10.1289/EHP8905

Interleukin 22 (IL-22) is critically involved in gut immunity and host defense and primarily produced by activated T cells. In different circumstances IL-22 may contribute to pathological conditions or act as a cancer promoting cytokine secreted by infiltrating immune cells. Here we show that bone marrow-derived macrophages (BMM) express and produce IL-22 after activation of the aryl hydrocarbon receptor (AhR) when cells are activated through the Toll-like receptor (TLR) family. The additional activation of AhR triggered a significant induction of IL-22 in TLR-activated BMM. Deletion and mutation constructs of the IL-22 promoter revealed that a consensus DRE and RelBAhRE binding element are necessary to mediate the synergistic effects of AhR and TLR ligands. Inhibitor studies and analysis of BMM derived from knockout mice confirmed that the synergistic induction of IL-22 by AhR and TLR ligands depend on the expression of AhR and Nuclear Factor-kappa B (NF-κB) member RelB. The exposure to particulate matter (PM) collected from traffic related air pollution (TRAP) and wildfires activated AhR as well as NF-κB signaling and significantly induced the expression of IL-22. In summary this study shows that simultaneous activation of the AhR and NF-κB signaling pathways leads to synergistic and prolonged induction of IL-22 by integrating signals of the canonical and non-canonical AhR pathway.

Background: Traffic-related air pollution (TRAP) is made up of complex mixtures of particulate matter, gases and volatile compounds. However, the effects of TRAP on the cardiopulmonary system in mo...

Epidemiological studies consistently implicate traffic-related air pollution (TRAP) and/or proximity to heavily trafficked roads as risk factors for developmental delays and neurodevelopmental disorders (NDDs); however, there are limited preclinical data demonstrating a causal relationship. To test the effects of TRAP, pregnant rat dams were transported to a vivarium adjacent to a major freeway tunnel system in northern California where they were exposed to TRAP drawn directly from the face of the tunnel or filtered air (FA). Offspring remained housed under the exposure condition into which they were born and were tested in a variety of behavioral assays between postnatal day 4 and 50. To assess the effects of near roadway exposure, offspring of dams housed in a standard research vivarium were tested at the laboratory. An additional group of dams was transported halfway to the facility and then back to the laboratory to control for the effect of potential transport stress. Near roadway exposure delayed growth and development of psychomotor reflexes and elicited abnormal activity in open field locomotion. Near roadway exposure also reduced isolation-induced 40-kHz pup ultrasonic vocalizations, with the TRAP group having the lowest number of call emissions. TRAP affected some components of social communication, evidenced by reduced neonatal pup ultrasonic calling and altered juvenile reciprocal social interactions. These findings confirm that living in close proximity to highly trafficked roadways during early life alters neurodevelopment.

The objective of this study was to explore the role of the aryl hydrocarbon receptor (AhR) in ambient particulate matter (PM)-mediated activation of dendritic cells (DCs) and Th17-immune responses in vitro. To assess the potential role of the AhR in PM-mediated activation of DCs, co-stimulation, and cytokine expression, bone marrow (BM)-derived macrophages and DCs from C57BL6 wildtype or AhR knockout (AhR(−/−)) mice were treated with PM. Th17 differentiation was assessed via co-cultures of wildtype or AhR(−/−) BMDCs with autologous naive T cells. PM(2.5) significantly induced AhR DNA binding activity to dioxin responsive elements (DRE) and expression of the AhR repressor (AhRR), cytochrome P450 (CYP) 1A1, and CYP1B1, indicating activation of the AhR. In activated (OVA sensitized) BMDCs, PM(2.5) induced interleukin (IL)-1β, CD80, CD86, and MHC class II, suggesting enhanced DC activation, co-stimulation, and antigen presentation; responses that were abolished in AhR deficient DCs. DC-T cell co-cultures treated with PM and lipopolysaccharide (LPS) led to elevated IL-17A and IL-22 expression at the mRNA level, which is mediated by the AhR. PM-treated DCs were essential in endowing T cells with a Th17-phenotype, which was associated with enhanced expression of MHC class II and cyclooxygenase (COX)-2. In conclusion, PM enhances DC activation that primes naive T cell differentiation towards a Th17-like phenotype in an AhR-dependent manner.

Author(s): Silverman, Jill L; Berg, Elizabeth L; Patten, Kelley T; Valenzuela, Anthony E; Wallis, Christopher; LaSalle, Janine M; Ciernia, Annie Vogel; Bein, Keith J; Wexler, Anthony S; Lein, Pamela J

Background: Epidemiological studies show a strong association between fine particulate matter (PM 2.5 ) air pollution and adverse pulmonary effects. While PM concentration can vary by time and location, PM toxicity has been most recently linked to both physicochemical composition and exposure scenario. To study the relevance of particle characteristics to toxicity, winter PM 2.5 samples were obtained from three geographically similar regions (Sacramento, California, USA; Jinan, Shandong, China; and Taiyuan, Shanxi, China), with typically high atmospheric PM 2.5 emissions. PM extract samples (PM CA , PM SD , and PM SX , respectively) were administered by oropharyngeal aspiration (OPA) to different groups of BALB/C mice, at equal mass concentrations [0 (water vehicle control only) or 20 µg/50 µL], on five different occasions over a two-week period, for a cumulative PM dose of 0 or 100 µg/mouse. Mice were necropsied on Days 1, 2 and 4 after the final exposure, and pulmonary effects were evaluated by bronchoalveolar lavage (BAL), histopathology, quantitative polymerase chain reaction tests, and enzyme-linked immunosorbent assays. Results: Unique differences were noted in the chemical composition for each geographic region with PM SX containing the highest concentration of sulfates (organic and inorganic). A systematic examination of the time lag effects of repeated PM exposure demonstrated unique differences. In mice administered PM SX versus the control, BAL neutrophilia, alveolitis, and bronchiolitis were observed on Days 1 and 4. By Day 4, PM SX -exposed mice also exhibited increased gene expression for multiple inflammatory cytokines/chemokines (interleukin 1 beta, tumor necrosis factor alpha, chemokine C-X-C motif ligands-3 and -5), and increased levels of monocyte chemoattractant protein-1 relative to control-, PM CA -, or PM SD -exposed mice . Conclusions: Direct comparison of the toxic effects of three geographically different PM samples on an equal mass basis demonstrate unique pathobiology with increasing lag time post-exposure. Higher sulfate levels in PM SX versus PM CA and PM SD may contribute to the greater inflammatory responses noted that progressed over time.

Ambient PM(2.5) was collected during the winter season from Taiyuan, Shanxi, China; Jinan, Shandong, China; and Sacramento, California, USA, and used to create PM(SX), PM(SD), and PM(CA) extracts, respectively. Time-lag experiments were performed to explore the in vivo and in vitro toxicity of the PM extracts. In vivo inflammatory lung responses were assessed in BALB/C mice using a single oropharyngeal aspiration (OPA) of PM extract or vehicle (CTRL) on Day 0. Necropsies were performed on Days 1, 2, and 4 post-OPA, and pulmonary effects were determined using bronchoalveolar lavage (BAL) and histopathology. On Day 1, BAL neutrophils were significantly elevated in all PM- versus CTRL-exposed mice, with PM(CA) producing the strongest response. However, histopathological scoring showed greater alveolar and perivascular effects in PM(SX)-exposed mice compared to all three other groups. By Day 4, BAL neutrophilia and tissue inflammation were resolved, similar across all groups. In vitro effects were examined in human HepG2 hepatocytes, and U937 cells following 6, 24, or 48 hours of exposure to PM extract or DMSO (control). Luciferase reporter and quantitative polymerase chain reaction assays were used to determine in vitro effects on aryl hydrocarbon receptor (AhR) activation and gene transcription, respectively. Though all three PM extracts activated AhR, PM(SX) produced the greatest increases in AhR activation, and mRNA levels of cyclooxygenase-2, cytochrome P450, interleukin (IL)-8, and IL-1β. These effects were assumed to result from a greater abundance of polycyclic aromatic hydrocarbons (PAHs) in PM(SX) compared to PM(SD) and PM(CA).

While photooxidants are important in atmospheric condensed phases, there are very few measurements in particulate matter (PM). Here we measure light absorption and the concentrations of three photooxidants – hydroxyl radical (⚫OH), singlet molecular oxygen (1O2*), and oxidizing triplet excited states of organic matter (3C*) – in illuminated aqueous extracts of wintertime particles from Davis, California. 1O2* and 3C*, which are formed from photoexcitation of brown carbon (BrC), have not been previously measured in PM. In the extracts, mass absorption coefficients for dissolved organic compounds (MACDOC) at 300 nm range between 13 000 and 30 000 cm2 (g C)−1 are approximately twice as high as previous values in Davis fogs. The average (±1σ)⚫OH steady-state concentration in particle extracts is 4.4(±2.3)×10-16 M, which is very similar to previous values in fog, cloud, and rain: although our particle extracts are more concentrated, the resulting enhancement in the rate of ⚫OH photoproduction is essentially canceled out by a corresponding enhancement in concentrations of natural sinks for ⚫OH. In contrast, concentrations of the two oxidants formed primarily from brown carbon (i.e., 1O2* and 3C*) are both enhanced in the particle extracts compared to Davis fogs, a result of higher concentrations of dissolved organic carbon and faster rates of light absorption in the extracts. The average 1O2* concentration in the PM extracts is 1.6(±0.5)×10-12 M, 7 times higher than past fog measurements, while the average concentration of oxidizing triplets is 1.0(±0.4)×10-13 M, nearly double the average Davis fog value. Additionally, the rates of 1O2* and 3C* photoproduction are both well correlated with the rate of sunlight absorption. Since we cannot experimentally measure photooxidants under ambient particle water conditions, we measured the effect of PM dilution on oxidant concentrations and then extrapolated to ambient particle conditions. As the particle mass concentration in the extracts increases, measured concentrations of ⚫OH remain relatively unchanged, 1O2* increases linearly, and 3C* concentrations increase less than linearly, likely due to quenching by dissolved organics. Based on our measurements, and accounting for additional sources and sinks that should be important under PM conditions, we estimate that [⚫OH] in particles is somewhat lower than in dilute cloud/fog drops, while [3C*] is 30 to 2000 times higher in PM than in drops, and [1O2*] is enhanced by a factor of roughly 2400 in PM compared to drops. Because of these enhancements in 1O2* and 3C* concentrations, the lifetimes of some highly soluble organics appear to be much shorter in particle liquid water than under foggy/cloudy conditions. Based on extrapolating our measured rates of formation in PM extracts, BrC-derived singlet molecular oxygen and triplet excited states are overall the dominant sinks for organic compounds in particle liquid water, with an aggregate rate of reaction for each oxidant that is approximately 200–300 times higher than the aggregate rate of reactions for organics with ⚫OH. For individual, highly soluble reactive organic compounds it appears that 1O2* is often the major sink in particle water, which is a new finding. Triplet excited states are likely also important in the fate of individual particulate organics, but assessing this requires additional measurements of triplet interactions with dissolved organic carbon in natural samples.

Ambient particulate matter (PM), a component of air pollution, exacerbates airway inflammation and hyperreactivity in asthmatic patients. Studies showed that PM possesses adjuvant-like properties that enhance the allergic inflammatory response; however, the mechanism (or mechanisms) by which PM enhances the allergic response remains to be determined. The aim of this study was to assess how exposure to fine PM collected from Sacramento, CA, shapes the allergic airway immune response in BALB/c mice undergoing sensitization and challenge with ovalbumin (OVA). Eight-week-old BALB/c male mice were sensitized/challenged with phosphate-buffered saline (PBS/PBS; n = 6), PM/PBS (n = 6), OVA/OVA (n = 6), or OVA + PM/OVA (n = 6). Lung tissue, bronchoalveolar lavage fluid (BALF), and plasma were analyzed for cellular inflammation, cytokines, immunoglobulin E, and heme oxygenase-1 (HO-1) expression. Mice in the OVA + PM/OVA group displayed significantly increased airway inflammation compared to OVA/OVA animals. Total cells, macrophages, and eosinophils recovered in BALF were significantly elevated in the OVA + PM/OVA compared to OVA/OVA group. Histopathological grading indicated that OVA + PM/OVA treatment induced significant inflammation compared to OVA/OVA. Both immunoglobulin (Ig) E and tumor necrosis factor (TNF) α levels were significantly increased in OVA/OVA and OVA + PM /OVA groups compared to PBS/PBS control. The number of HO-1 positive alveolar macrophages was significantly elevated in lungs of mice treated with OVA + PM /OVA compared to OVA/OVA. Our findings suggest that fine PM enhances allergic inflammatory response in pulmonary tissue through mechanisms involving increased oxidative stress.

Particulate matter (PM) in Imperial Valley originates from a variety of sources such as agriculture, traffic at the border crossing, emissions from the cross-border city of Mexicali, and the drying lakebed of the Salton Sea. Dust storms in Imperial Valley, California regularly lead to exceedances of the federal air quality standards for PM(10) (diameter less than 10 microns). To determine if there are differences in the composition and biological response to Imperial County PM by size, ambient PM samples were collected from a sampling unit stationed in the northern-most part of the valley, South of the Salton Sea. Ultrafine, fine, and coarse PM samples were collected and extracted separately. Chemical composition of each size fraction was obtained after extraction by using several analytical techniques, and biological response was measured by exposing a cell line of macrophages to particles and quantifying subsequent gene expression. Biological measurements demonstrated coarse PM induced an inflammatory response in macrophages measured in increases of inflammatory markers IL-1β, IL-6, IL-8 and CXCL2 expression, whereas ultrafine and fine PM only demonstrated significant increases in expression of CYP1a1. These differential responses were due not only to particle size, but to the distinct chemical profiles of each size faction as well. Community groups in Imperial Valley have already completed several projects to learn more about local air quality, giving residents access to data that provides real-time levels of PM(2.5) and PM(10) as well as recommendations on health-based practices dependent on the current AQI (air quality index). However, to date there is no information on the composition or toxicity of ambient PM from the region. The data presented here could provide more definitive information on the toxicity of PM by size, and further inform the community on local air quality.

There is strong evidence that exposure to fine particulate matter (PM2.5) and a high-fat diet (HFD) increase the risk of mortality from atherosclerotic cardiovascular diseases. Recent studies indicate that PM2.5 generated by combustion activates the Aryl Hydrocarbon Receptor (AHR) and inflammatory cytokines contributing to PM2.5-mediated atherogenesis. Here we investigate the effects of components of a HFD on PM-mediated activation of AHR in macrophages. Cells were treated with components of a HFD and AHR-activating PM and the expression of biomarkers of vascular inflammation was analyzed. The results show that glucose and triglyceride increase AHR-activity and PM2.5-mediated induction of cytochrome P450 (CYP)1A1 mRNA in macrophages. Cholesterol, fructose, and palmitic acid increased the PM- and AHR-mediated induction of proinflammatory cytokines in macrophages. Treatment with palmitic acid significantly increased the expression of inflammatory cytokines and markers of vascular injury in human aortic endothelial cells (HAEC) after treatment with PM2.5. The PM2.5-mediated activation of the atherogenic markers C-reactive protein (CRP) and S100A9, a damage-associated molecular pattern molecule, was found to be AHR-dependent and involved protein kinase A (PKA) and a CCAAT/enhancer-binding protein (C/EBP) binding element. This study identified nutritional factors interacting with AHR signaling and contributing to PM2.5-induced markers of atherogenesis and future cardiovascular risk.

Ambient particulate matter (PM) exacerbates airway inflammation and hyper-reactivity in asthmatic patients. Studies show that PM has adjuvant-like properties that enhance the allergic inflammatory response; however, the mechanisms through which PM enhances these processes remain elusive. The objective of the study was to examine how ambient PM enhances the allergic immune response. Eight-week-old BALB/c mice were sensitized with house dust mite (HDM) or HDM and ambient particulate matter (PM, 2.5μm; Sacramento, CA) to assess how PM modulates the development of adaptive immune responses against allergens. Both groups were challenged with HDM only. Bronchoalveolar lavage (BAL) was analyzed for extent of airway inflammation. Lung tissue was used for histological analysis, mucosubstance quantification, and heme oxygenase-1 (HO-1) localization/quantification. Gene expression was analyzed in whole lung to characterize immune markers of inflammation: cytokines, chemokines, antioxidant enzymes, and transcription factors. Cytokine and chemokine protein levels were quantified in whole lung to confirm gene expression patterns. Compared to HDM-only sensitization, exposure to PM during HDM sensitization led to significant immune cell recruitment into the airway subepithelium, IgE gene expression, mucosubstance production, and Th2-associated cytokine expression. HO-1 levels were not significantly different between the treatment groups. Gene expression profiles suggest that polycyclic aromatic hydrocarbon (PAH) content in PM activated the aryl hydrocarbon receptor (AhR) and enhanced Th17-responses in the mice that received HDM and PM compared to mice that received HDM-only. The findings suggest that PM enhances allergic sensitization via enhancement of Th2-mediated inflammation and that AhR activation by PAHs in PM promotes Th17-immune responses.

Asthma is a global and increasingly prevalent disease. According to the World Health Organization, approximately 235 million people suffer from asthma. Studies suggest that fine particulate matter (PM(2.5)) can induce innate immune responses, promote allergic sensitization, and exacerbate asthmatic symptoms and airway hyper-responsiveness. Recently, severe asthma and allergic sensitization have been associated with T-helper cell type 17 (T(H)17) activation. Few studies have investigated the links between PM(2.5) exposure, allergic sensitization, asthma, and T(H)17 activation. This study aimed to determine whether (1) low-dose extracts of PM(2.5) from California (PM(CA)) or China (PM(CH)) enhance allergic sensitization in mice following exposure to house dust mite (HDM) allergen; (2) eosinophilic or neutrophilic inflammatory responses result from PM and HDM exposure; and (3) T(H)17-associated cytokines are increased in the lung following exposure to PM and/or HDM. Ten-week-old male BALB/c mice (n = 6–10/group) were intranasally instilled with phosphate-buffered saline (PBS), PM+PBS, HDM, or PM+HDM, on days 1, 3, and 5 (sensitization experiments), and PBS or HDM on days 12–14 (challenge experiments). Pulmonary function, bronchoalveolar lavage cell differentials, plasma immunoglobulin (Ig) protein levels, and lung tissue pathology, cyto-/chemo-kine proteins, and gene expression were assessed on day 15. Results indicated low-dose PM(2.5) extracts can enhance allergic sensitization and T(H)17-associated responses. Although PM(CA)+HDM significantly decreased pulmonary function, and significantly increased neutrophils, Igs, and T(H)17-related protein and gene levels compared with HDM, there were no significant differences between HDM and PM(CH)+HDM treatments. This may result from greater copper and oxidized organic content in PM(CA) versus PM(CH).

© 2015 Elsevier Ltd. Previous work successfully implemented a novel system that uses a single particle mass spectrometer to conditionally sample size-segregated, source-oriented particles from the ambient atmosphere in real-time. The underlying hypothesis is that the composition of individual particles is a metric of particle source and thus sampling particles based on composition should be synonymous with sampling based on source. System operation relies on real-time pattern recognition to control the actuation of different ChemVol samplers, where each ChemVol is associated with a unique composition signature. In the current work, a synthesis of data collected during these studies is used in retrospect to reconcile the actual source combinations contributing to the particles collected by each ChemVol. Source attribution is based on correlations between ChemVol sampling periods and coincident wind direction and temporal emissions patterns, coupled to knowledge of single particle composition and surrounding sources. Residential and commercial cooking, vehicular emissions, residential heating and highly processed regional background PM were identified as the major sources. Results show that real-time patterns in single particle mixing state correctly identified specific sources and that these sources were successfully separated into different ChemVols for both summer and winter seasons.

Airborne particulate matter (PM) is associated with adverse cardiorespiratory effects. To better understand source-orientated PM toxicity, a comparative study of the biological effects of fine PM (diameter≤2.5μm, PM2.5) collected during the winter season from Shanxi Province, China, and the Central Valley, California, United States, was conducted. The overarching hypothesis for this study was to test whether the chemical composition of PM on an equal mass basis from two urban areas, one in China and one in California, can lead to significantly different effects of acute toxicity and inflammation in the lungs of healthy young mice. Male, 8-week old BALB/C mice received a single 50μg dose of vehicle, Taiyuan PM or Sacramento PM by oropharyngeal aspiration and were sacrificed 24h later. Bronchoalveolar lavage, ELISA and histopathology were performed along with chemical analysis of PM composition. Sacramento PM had a greater proportion of oxidized organic material, significantly increased neutrophil numbers and elevated CXCL-1 and TNF-α protein levels compared to the Taiyuan PM. The findings suggest that Sacramento PM2.5 was associated with a greater inflammatory response compared to that of Taiyuan PM2.5 that may be due to a higher oxidice. Male, 8-week old BALB/C mice received a single 50μg dose of vehicle, Taiyuan PM or Sacramento PM by oropharyngeal aspiration and were sacrificed 24h later. Bronchoalveolar lavage, ELISA and histopathology were performed along with chemical analysis of PM composition. Sacramento PM had a greater proportion of oxidized organic material, significantly increased neutrophil numbers and elevated CXCL-1 and TNF-α protein levels compared to the Taiyuan PM. The findings suggest that Sacramento PM2.5 was associated with a greater inflammatory response compared to that of Taiyuan PM2.5 that may be due to a higher oxidized state of organic carbon and copper content.

Ambient particulate matter (PM), a component of air pollution, exacerbates airway inflammation and hyperreactivity in asthmatic patients. Studies showed that PM possesses adjuvant-like properties that enhance the allergic inflammatory response; however, the mechanism (or mechanisms) by which PM enhances the allergic response remains to be determined. The aim of this study was to assess how exposure to fine PM collected from Sacramento, CA, shapes the allergic airway immune response in BALB/c mice undergoing sensitization and challenge with ovalbumin (OVA). Eight-week-old BALB/c male mice were sensitized/challenged with phosphate-buffered saline (PBS/PBS; n = 6), PM/PBS (n = 6), OVA/OVA (n = 6), or OVA + PM/OVA (n = 6). Lung tissue, bronchoalveolar lavage fluid (BALF), and plasma were analyzed for cellular inflammation, cytokines, immunoglobulin E, and heme oxygenase-1 (HO-1) expression. Mice in the OVA + PM/OVA group displayed significantly increased airway inflammation compared to OVA/OVA animals. Total cells, macrophages, and eosinophils recovered in BALF were significantly elevated in the OVA + PM/OVA compared to OVA/OVA group. Histopathological grading indicated that OVA + PM/OVA treatment induced significant inflammation compared to OVA/OVA. Both immunoglobulin (Ig) E and tumor necrosis factor (TNF) α levels were significantly increased in OVA/OVA and OVA + PM /OVA groups compared to PBS/PBS control. The number of HO-1 positive alveolar macrophages was significantly elevated in lungs of mice treated with OVA + PM /OVA compared to OVA/OVA. Our findings suggest that fine PM enhances allergic inflammatory response in pulmonary tissue through mechanisms involving increased oxidative stress.

Particulate matter (PM) exposure contributes to respiratory diseases and cardiopulmonary mortality. PM toxicity is related to sources and composition, such as abundance of polycyclic aromatic hydrocarbons (PAHs). We exposed adult male BALB/c mice, via oropharyngeal aspiration, to a range of doses of PM2.5 collected during the winter in downtown Sacramento near a major freeway interchange (SacPM). Two preparation methods (spin-down and multi-solvent extraction) were tested to remove particles from collection filters. Three doses were analyzed 24 h after treatment for (1) leukocytes and total protein in bronchoalveolar lavage fluid (BALF), (2) airway-specific and whole lobe expression of PAH-sensitive genes (CYP1B1 and CYP1A1) and IL-1 b, (3) lung histology, and (4) platelet function. Both extraction methods stimulated biological responses, but the spin-down method was more robust at producing IL-1 b and CYP1B1 gene responses and the multi-solvent extraction induced whole lung CYP1A1. Neutrophils in the BALF were increased 5- to 10-fold at the mid and high dose for both preparations. Histopathology scores indicated dose-dependent responses and increased pathology associated with spin-down-derived PM exposure. In microdissected airways, spin-down PM increased CYP1B1 gene expression significantly, but multi-solvent extracted PM did not. Platelet responses to the physiological agonist thrombin were approximately twice as potent in the spin-down preparation as in the multi-solvent extract. We conclude (1) the method of filter extraction can influence the degree of biological response, (2) for SacPM the minimal effective dose is 27.5–50 µg based on neutrophil recruitment, and (3) P450s are upregulated differently in airways and lung parenchyma in response to PAH-containing PM.

Atmospheric particles are frequently collected onto filter and impactor substrates for studies related to the composition, health effects and climate impact of ambient particulate matter (PM). Many of these studies require extraction of that PM from the substrates but available methods have low extraction efficiencies that may lead to compositional and thus toxicity bias. Here, novel PM extraction methods are presented that (a) maximize extraction efficiency, (b) minimize compositional biases in extracted PM, relative to sampled PM and (c) minimize extraction artifacts. Method development was based upon strengths and weaknesses of existing SOPs and current requirements in the field of aerosol health effects research. Extraction objectives were accomplished using a combination of sonication in solvents of varying polarity, selective filtration, liquid-liquid extraction of water-based extracts, solvent removal and final reconstitution of the total extracted PM. Relying largely on intensive gravimetric analyses and comparison to existing SOPs, the new technique has been fully validated on nearly 40 different size-segregated, source-oriented samples collected during two separate seasons in Fresno, CA. Compared to existing methods, and depending on the source, compositionally-specific increases in extraction efficiencies of 10-40% and 20-50% were obtained for the ultrafine and submicron fine PM fractions, respectively, indicating significant increases in total extraction efficiency and significant decreases in compositional bias. © 2014 Elsevier Ltd.

Analysis of chemical constituents from mass spectrometry of aerosols involves non-negative matrix factorization, an approximation of high-dimensional data in lower-dimensional space. The associated optimization problem is non-convex, resulting in crude approximation errors that are not accessible to scientists. To address this shortcoming, we introduce a new methodology for user-guided error-aware data factorization that entails an assessment of the amount of information contributed by each dimension of the approximation, an effective combination of visualization techniques to highlight, filter, and analyze error features, as well as a novel means to interactively refine factorizations. A case study and the domain-expert feedback provided by the collaborating atmospheric scientists illustrate that our method effectively communicates errors of such numerical optimization results and facilitates the computation of high-quality data factorizations in a simple and intuitive manner.

Vehicle exhaust is rich in polycyclic aromatic hydrocarbons (PAH) and can be a dominant contributor to ultrafine urban particulate matter (PM). Exposure to ultrafine PM is correlated with respiratory infections and asthmatic symptoms in young children. The lung undergoes substantial growth, alveolarization, and cellular maturation within the first years of life, which may be impacted by environmental pollutants such as PM. PAHs in PM can serve as ligands for the aryl hydrocarbon receptor (AhR) that induces expression of certain isozymes in the cytochrome P-450 superfamily, such as CYP1A1 and CYP1B1, localized in specific lung cell types. Although AhR activation and induction has been widely studied, its context within PM exposure and impact on the developing lung is poorly understood. In response, we have developed a replicable ultrafine premixed flame particle (PFP) generating system and used in vitro and in vivo models to define PM effects on AhR activation in the developing lung. We exposed 7-day neonatal and adult rats to a single 6-h PFP exposure and determined that PFPs cause significant parenchymal toxicity in neonates. PFPs contain weak AhR agonists that upregulate AhR-xenobiotic response element activity and expression and are capable inducers of CYP1A1 and CYP1B1 expression in both ages with different spatial and temporal patterns. Neonatal CYP1A1 expression was muted and delayed compared with adults, possibly because of differences in the enzyme maturation. We conclude that the inability of neonates to sufficiently adapt in response to PFP exposure may, in part, explain their susceptibility to PFP and urban ultrafine PM.

The study of aerosol composition for air quality research involves the analysis of high-dimensional single particle mass spectrometry data. We describe, apply, and evaluate a novel interactive visual framework for dimensionality reduction of such data. Our framework is based on non-negative matrix factorization with specifically defined regularization terms that aid in resolving mass spectrum ambiguity. Thereby, visualization assumes a key role in providing insight into and allowing to actively control a heretofore elusive data processing step, and thus enabling rapid analysis meaningful to domain scientists. In extending existing black box schemes, we explore design choices for visualizing, interacting with, and steering the factorization process to produce physically meaningful results. A domain-expert evaluation of our system performed by the air quality research experts involved in this effort has shown that our method and prototype admits the finding of unambiguous and physically correct lower-dimensional basis transformations of mass spectrometry data at significantly increased speed and a higher degree of ease.

Current particulate matter regulations control the mass concentration of particles in the atmosphere regardless of composition, but some primary and/or secondary particulate matter components are no doubt more or less toxic than others. Testing direct emissions of pollutants from different sources neglects atmospheric transformations that may increase or decrease their toxicity. This work describes a system that conditionally samples particles from the atmosphere depending on the sources or source combinations that predominate at the sampling site at a given time. A single particle mass spectrometer (RSMS-II), operating in the 70-150 nm particle diameter range, continuously provides the chemical composition of individual particles. The mass spectra indicate which sources are currently affecting the site. Ten ChemVol samplers are each assigned one source or source combination, and the RSMS-II controls which one operates depending on the sources or source combinations observed. By running this system for weeks at a time, sufficient sample is collected by the ChemVols for comparative toxicological studies. This paper describes the instrument and algorithmic design, implementation, and first results from operating this system in Fresno, CA, during summer 2008 and winter 2009.

Single-particle mass spectrometry data collected during the Pittsburgh Supersite experiment was used to isolate an episode on 27 October 2001 when the measurement site was primarily influenced by emissions from coal combustion sources. Results showed that (a) 60–80% of the particles detected during this event belonged to the Na/Si/K/Ca/Fe/Ga/Pb particle class associated with coal combustion emissions, (b) observation of this class was an isolated event occurring only during the hours of 06:00–14:00 EST, and (c) the detection of these particles was highly correlated with shifts in wind direction. Coincident SMPS, TEOM PM2.5, SO2, NOx, and O3 measurements were in excellent agreement with the single-particle results in terms of both identifying and characterizing this event. The three most likely point sources of these particles were isolated and Gaussian plume dispersion models were used in reverse to predict their particle number, particle mass, and gas phase emissions. Calculated mass emission rates were in general agreement with the US EPA National Emissions Inventory (NEI) database emissions estimates and the Title V PM10 limit. The largest of the three sources emits about 2.4×1017 fine and ultrafine particles per second.

The EPA regulates ambient particulate matter (PM) because substantial associations have been established between PM and health impacts. Presently, regulatory compliance involves broad control of PM emission sources based on mass concentration rather than chemical composition, although PM toxicity is likely to vary depending upon PM physicochemical properties. The overall objective of this study was to help inform source-specific PM emission control regulations. For the first time, source-oriented PM was collected from the atmosphere in Fresno, CA, onto 38 source/size substrates. Mice were exposed via oropharyngeal aspiration to equivalent mass doses [50 μg] of two size fractions: ultrafine (Dp < 0.17μm) and submicron fine (0.17 < Dp < 1 μm) during summer and winter seasons. At 24 hours post-exposure, cellular and biochemical indicators of pulmonary inflammation were evaluated in the bronchoalveolar lavage fluid. Significant inflammatory responses were elicited by vehicle, regional background, and cooking PM sources that were dependent on season and particle size. This is the first study of source-oriented toxicity of atmospheric PM and supports source-specific emissions control strategies.

© 2015 Elsevier Ltd. Collection and subsequent extraction of particulate matter (PM) from filter substrates is a common requirement for invivo and invitro toxicological studies, as well as chemical analyses such as ion chromatography and inductively coupled plasma mass spectrometry. Several filter extraction protocols exist and different laboratories employ different methods, potentially biasing inter-study comparisons. Previous studies have shown significant differences in extraction efficiency between techniques and identified the relevant extraction artifacts. However, a comprehensive inter-comparison of different methods based on the chemical composition of the extracted PM has never been conducted. In the current study, an exhaustive suite of chemical analyses is performed on PM extracted from glass micro-fiber filters using techniques commonly employed in different laboratories: Multi-solvent extraction (MSE) and spin-down extraction (SDE). PM samples were collected simultaneously during field studies conducted in an urban and rural setting using a high-volume PM2.5 sampler. Results show remarkable compositional variance between the PM extracts for all chemical components analyzed, including metals, water soluble ions, polycyclic aromatic hydrocarbons, non-aromatic organics, elemental carbon and organic carbon. Mass closure was greater than 90% for MSE but deviated substantially for SDE. Detailed retrospective gravimetric analysis of archived SDE samples revealed that a process-based loss of PM mass is the root cause of the differences. These losses are shown to be compositionally biased, both externally between different PM mixtures and internally within a given PM mixture. In combination, the results of this study are the first to demonstrate (i) an exhaustive chemical characterization of a single PM extract, (ii) the significance of directly characterizing the extracted PM used in toxicological studies, (iii) the existence of substantial compositional biases between different filter extraction techniques and (iv) the importance of standardizing filter extraction objectives and procedures to avoid introducing study bias into toxicological studies.

A single particle mass spectrometer, RSMS-3, and a MOUDI were deployed during the Pittsburgh Air Quality Study (PAQS), July 2001–September 2002, to obtain size resolved measurements of elemental composition for particulate matter (PM) within the Pittsburgh area. Elemental mass distributions from analysis of the MOUDI stages were directly compared to those constructed using the single particle data, in conjunction with coincident SMPS measurements, for specific days within the PAQS. Results from one episode on 27 October 2001 showed that approximately 80% of the metal containing particles detected on this day belonged to the Na/Si/K/Ca/Fe/Ga/Pb particle class. The density and shape factor of these particles were estimated to be 3.9±0.8 g/cc and 1.5±0.2, respectively, and the relative sensitivity factors for individual metals showed little variation with respect to particle diameter over the size range of 70–800 nm. Compared to the 27 October 2001 episode, there was a larger degree of variability in the metal containing particles detected during another episode on 14 March 2002. The Ca and Pb mass distributions from this day represent an ensemble of externally mixed particles. Estimates of particle density were provided for the dominant particle types, including EC/OC/Ca, Al/Si/Ca/Fe, EC/OC/Pb and Na/K/Zn/Pb, and estimates of particle shape factor were provided for the EC/OC/Ca and Na/K/Zn/Pb classes. Comparison with the 27 October 2001 Ca and Pb mass distributions revealed that the RSMS data reconstructed the MOUDI mass much better from the Ca/Pb containing particles detected on 14 March 2002 than those observed on 27 October 2001, suggesting that the single particle instrument sensitivity to both Ca and Pb depends on the particle matrix.

During the Pittsburgh Air Quality Study (PAQS), July 2001–September 2002, three co-located instruments analyzed the composition of ambient particulate matter (PM): (1) A single particle mass spectrometer, RSMS-3, was deployed to obtain high-temporal-resolution measurements of single particle size (>1.1 μm) and composition which were correlated with meteorological data to identify sources; (2) PM2.5 and PM10 were collected on cellulose filters using high-volume (hi-vol) samplers, followed by microwave-assisted digestion and analysis by inductively coupled plasma–mass spectrometry (ICP–MS). Positive matrix factorization (PMF) was used to identify possible source categories; and (3) a micro-orifice uniform-deposit impactor (MOUDI) obtained size-distributed samples of PM. Several days of MOUDI filters were selected for microwave-assisted digestion and analysis by ICP–MS. In this paper, sources identified using the single particle data were compared to the PMF results for the hi-vol/ICP–MS data. The strengths of each method were combined to hypothesize the most likely sources of various elements in ambient PM in Pittsburgh. In the final results, Mo and Cr are attributed to local specialty steel facilities; Fe, Mn, Zn, and K are attributed to a steel mill SE of the monitoring station; internally mixed Pb-containing particles are attributed to a major source to the NW; and Ga is attributed to coal combustion sources to the NW. There is a notable lack of oil combustion sources. The MOUDI data were used to resolve discrepancies between the single particle and hi-vol/ICP–MS data concerning the detection of Ti and Se. The hi-vol data showed appreciable Ti and Se masses, but RSMS-3 was unable to detect significant numbers of Ti-containing particles because of their large size, while we hypothesize that the volatility of Se caused it to be distributed more evenly over all emitted particles such that the amount of Se in any individual particle is below the limit of detection.

© 2014 Taylor & Francis Group, LLC. Ambient particulate matter (PM) originates from a range of sources and differs in composition with respect to season, time of day, and particle size. In this study, ambient PM samples in the ultrafine and submicrometer fine range were tested for the potential to exacerbate a murine model of allergic airway inflammation when exposure occurs solely during allergic sensitization, but not during subsequent allergen challenge. Temporally resolved and size-segregated PM samples were used to understand how summer or winter, day or night, and ambient ultrafine and submicrometer fine particle size influence PMs ability to exacerbate allergic inflammation. PM was collected in urban Fresno, CA. BALB/c mice were exposed to PM and house dust mite allergen (HDM) via intranasal aspiration on d 1, 3, and 5. HDM challenge occurred on d 12-14, with inflammation assessed 24 h following final challenge. While season or particle size did not predict allergic inflammation, daytime ultrafine and submicrometer fine particles significantly increased total cellular inflammation, specifically lymphocyte and eosinophil infiltration, compared to allergic controls. Further studies examined PM-mediated changes within the lung during the period where allergen sensitization occurred by measuring direct effects of PM on pulmonary oxidative stress and inflammation. Pulmonary levels of heme oxygenase-1 (HO-1), a biomarker of oxidative stress, but not cellular inflammation, demonstrated a remarkable correlation with the degree of allergic inflammation in animals sensitized to allergen and PM concomitantly, suggesting acute PM-mediated HO-1 levels may serve as a predictive indicator of a particles ability to exacerbate allergic airway inflammation.

Recent epidemiological evidence supports the hypothesis that health effects from inhalation of ambient particulate matter (PM) are governed by more than just the mass of PM inhaled. Both specific chemical components and sources have been identified as important contributors to mortality and hospital admissions, even when these endpoints are unrelated to PM mass. Sources may cause adverse health effects via their ability to produce reactive oxygen species, possibly due to the transition metal content of the PM. Our goal is to quantify the oxidative potential of ambient particle sources collected during two seasons in Fresno, CA using the dithiothreitol (DTT) assay. We collected PM from different sources or source combinations into different ChemVol (CV) samplers in real time using a novel source-oriented sampling technique based on single particle mass spectrometry. We segregated the particles from each source-oriented mixture into two size fractions – ultrafine (Dp ≤ 0.17 μm) and submicron fine (0.17 μm ≤ Dp ≤ 1.0 μm) – and measured metals and the rate of DTT loss in each PM extract. We find that the mass-normalized oxidative potential of different sources varies by up to a actor of 8 and that submicron fine PM typically has a larger mass-normalized oxidative potential than ultrafine PM from the same source. Vehicular Emissions, Regional Source Mix, Commute Hours, Daytime Mixed Layer and Nighttime Inversion sources exhibit the highest mass-normalized oxidative potential. When we apportion the volume-normalized oxidative potential, which also accounts for the source's prevalence, cooking sources account for 18–29% of the total DTT loss while mobile (traffic) sources account for 16–28%. When we apportion DTT activity for total PM sampled to specific chemical compounds, soluble copper accounts for roughly 50% of total air-volume-normalized oxidative potential, soluble manganese accounts for 20%, and other unknown species, likely including quinones and other organics, account for 30%. During nighttime, soluble copper and manganese largely explain the oxidative potential of PM, while daytime has a larger contribution from unknown (likely organic) species.

[1] A synthesis of data and analyses identified eight separate wildfire events (five in boreal Canada and three in the western United States) that impacted the Pittsburgh Supersite, as well as Toronto, during June and July 2002. These data also revealed a larger structure in the nature of pollution episodes in Pittsburgh characterized by alternating periods of stagnation and cleansing. Stagnation resulted in significant and sustained increases in pollutant concentrations that were eventually flushed by clean air transported from Canada. Stagnation events were further characterized by decreases in wind speed, increases in ambient temperature, and enhanced atmospheric processing. Reverse trends were observed during the “clean” periods. Wildfire emissions consistently arrived immediately prior to the stagnation events and tended to be trapped and recirculated by the associated surface high pressure system, prolonging their impact. These receptor site dynamics were correlated to the structure and propagation of transient extratropical synoptic-scale waves, which were characterized by eastward propagating transcontinental trough-ridge-trough configurations. Temporal patterns observed in the Pittsburgh data (a repeating sequence of long-range transport followed by stagnation and then flushing) were in phase with alternating synoptic structures of the propagating waves. Northwesterly subsiding flow between the ridge and trough transported wildfire emissions from the injection height above the fires down into the Pittsburgh and Toronto air sheds. As the wave propagated, the surface high associated with the upper-level ridge passed Pittsburgh, initiating a stagnation event. The cold front associated with the approaching trough flushed the stagnant air but reset the sequence of events as emissions from new wildfires were again transported behind the front. The sequence consistently repeated throughout the study period with a frequency directly correlated to the frequency of extratropical wave formation. Stagnation severity was related to the speed and maturity of the synoptic disturbances while wildfire impact severity corresponded to fire size.

[1] A suite of particulate, gaseous and meteorological measurements during the Pittsburgh Supersite experiment were used to characterize the impact of the 2002 Quebec wildfires on pollutant concentrations and physical and chemical processes dominant in the region. Temporal trends in the number distribution of wildfire particles (isolated using Rapid Single-ultrafine-particle Mass Spectrometry data) combined with CO, NOx and O3 mixing ratios identified two separate periods (Periods I and II) when the measurement site was directly impacted by plumes of relatively unprocessed wildfire emissions; i.e., increases in primary ultrafine wildfire particles, CO and NOx concomitant with a decrease in O3 from intraplume NOx titration. Carbonaceous particle number distributions predominantly associated with vehicular emissions, PM2.5 sulfate mass concentration and SO2 mixing ratio resolved individual components of local and regional sources. Single particle signatures indicated a period of intense atmospheric processing following Period II that caused rapid growth of the ultrafine mode due to simultaneous sulfate and secondary organic mass accumulation, resulting in significant changes to particle physical and chemical properties. Particle growth was concurrent with large increases in O3 and maxima in incoming solar radiation and ambient temperature and is posited to have occurred in situ as the air mass, containing a mixture of urban and wildfire emissions, was advected past the site. In total, the current work demonstrates significant added severity for pollution episodes in an area already burdened by large anthropogenic emission rates due to the impact of the 2002 Quebec wildfires. High levels of atmospheric processing increased sulfate accumulation and SOA formation and brought PM2.5 mass concentrations close to, and O3 mixing ratios in excess of, the National Ambient Air Quality Standards. Projections of increasing wildfire activity under a warming climate may increase the frequency and severity of such events.

[1] Approximately 236,000 single particle mass spectra were collected throughout the duration of the Pittsburgh Supersite experiment using the third-generation rapid single particle mass spectrometer (RSMS-3). The instrument was operated semicontinuously for 306 days, sampling particles with aerodynamic diameters in the range of 30–1100 nm and collecting both positive and negative ion spectra, particle size, and time of detection for each particle measured. The entire data set has been fully processed and analyzed. Spectra have been clustered into 20 distinct particle classes on the basis of the distribution of their positive ion mass peaks. Negative ion spectra were classified independently within each positive ion class. Frequency of occurrence versus particle size, month of the year, and wind direction has also been calculated for the full data set, as well as within each class. Results indicate a rich array of multicomponent ultrafine particles composed primarily of carbon and ammonium nitrate. Approximately 54% of all the particles measured fell into the carbonaceous ammonium nitrate (CAN) class. These particles were observed in all size bins and from most wind directions for the entirety of this study. Ubiquitous sources throughout the area, including vehicular emissions and secondary organic aerosol formation, are considered to be responsible for a larger fraction of these particles. In terms of particle number, metal containing aerosol dominated the remainder of the particle classes identified. These particles were rich in K+, Na+, Fe+, and Pb+ and to a lesser extent, Ga+ and Zn+. They tended to be smaller in size and were highly correlated with specific wind directions, facilitating the isolation of specific sources.

A field evaluation of versatile aerosol concentration enrichment system (VACES) coupled to a rapid single- particle mass spectrometer (RSMS-3) was conducted as part of the U. S. Environmental Protection Agency Supersite program in Pittsburgh during March 2002. RSMS- 3 hit rate increases were measured, and possible particle composition changes introduced by the VACES were examined in the single- particle mass spectra. The hit rates increased by 5 - 20 times at particle sizes ranging from 40 to 640 nm. VACES only enhances the hit rate by about a factor of 2 for large particle sizes because the RSMS-3 flow rates for these particles did not match the optimum operating condition of VACES. During the 3 days of measurements most of the particles were a mixture of carbonaceous material and ammonium nitrate with a variation across the spectrum from particles that were mostly carbonaceous to particles that were mostly ammonium nitrate. Both ambient and concentrated carbonaceous and ammonium nitrate composition distributions were indistinguishable with RSMS-3, suggesting that VACES introduces an insignificant artifact for those particles.