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Thermal treatment of perfluoroalkyl and polyfluoroalkyl substances (PFASs) presents a promising opportunity to halt the PFAS cycle. However, how co-occurring materials such as granular activated carbon (GAC) influence thermal decomposition products of PFASs, and underlying mechanisms remain unclear. We studied the pyrolysis of two potassium salts of perfluoroalkanesulfonates (PFSAs, CnF2n+1SO3K), perfluorobutanesulfonate (PFBS-K), and perfluorooctanesulfonate (PFOS-K), with or without GAC. PFBS-K is more stable than PFOS-K for pure standards, but when it is adsorbed onto GAC, its thermal stabilities and decomposition behaviors are similar. Temperatures and heating rates can significantly influence the decomposition mechanisms and products for pure standards, while these effects are less pronounced when PFSAs are adsorbed onto GAC. We further studied the underlying decomposition mechanisms. Pure standards of CnF2n+1SO3K can decompose directly in their condense phase by reactions: F(CF2)nSO3K → F(CF2)n-2CF═CF2 + KFSO3 or F(CF2)nSO3K → F(CF2)n- + K+ + SO3. GAC appears to facilitate breakage of the C-S bond to release SO2 at temperatures as low as 280 °C. GAC promotes fluorine mineralization through functional reactive sites. SiO2 is particularly important for the surface-mediated mineralization of PFASs into SiF4. These findings offer valuable insights into optimizing thermal treatment strategies for PFAS-contaminated waste.

Sulfur-containing volatile organic compounds emitted during wildfire events, such as dimethyl sulfide, are known to form secondary aerosols containing inorganic sulfate (SO4 2-) and surfactant-like organic compounds; however, little is known about the fate of sulfur in other emitted reduced organosulfur species. This study aimed to determine the sulfurous product distribution resulting from the nighttime oxidation of thiophene as a model system. Ion chromatography (IC) and aerosol mass spectrometry (a mini aerosol mass spectrometer, mAMS) were used to constrain the proportions of sulfurous compounds produced under wildfire-relevant conditions ([NO2]/[O3] = 0.1). With constraints from IC, results indicated that the sulfurous particle mass consisted of 30.3 ± 6.6% SO4 2-, while mAMS fractionation attributed 24.5 ± 1.6% of total sulfate signal to SO4 2-, 15.4 ± 1.9% to organosulfates, and 60.1 ± 0.9% to sulfonates. Empirical formulas of organosulfur products were identified as C1-C8 organosulfates and sulfonates using complementary mass spectrometry techniques. This study highlights the nighttime oxidation of thiophene and its derivatives as a source of SO4 2- and particulate organosulfur compounds, which have important implications for the atmospheric sulfur budget and aerosol/droplet physical and chemical properties.

The molybdenum- and tungsten-containing formate dehydrogenases from a variety of microorganisms catalyze the reversible interconversion of formate and CO2; several, in fact, function as CO2 reductases in the reverse direction under physiological conditions. CO2 reduction catalyzed by these enzymes occurs under mild temperature and pressure rather than the elevated conditions required for current industrial processes. Given the contemporary importance of remediation of atmospheric CO2 to address global warming, there has been considerable interest in the application of these enzymes in bioreactors. Equally important, understanding the detailed means by which these biological catalysts convert CO2 to formate, a useful and easily transported feedstock chemical, might also inspire the development of a new generation of highly efficient, biomimetic synthetic catalysts. Here we have examined the ability of the FdsDABG formate dehydrogenase from Cupriavidus necator to catalyze the exchange of solvent oxygen into product CO2 during the course of formate oxidation under single-turnover conditions. Negligible incorporation of 18O is observed when the experiment is performed in H218O, indicating that bicarbonate cannot be the immediate product of the enzyme-catalyzed reaction, as previously concluded. These results, in conjunction with the observation that the reductive half-reaction exhibits mildly acid-catalyzed rather than base-catalyzed chemistry, are consistent with a reaction mechanism involving direct hydride transfer from formate to the enzymes molybdenum center, directly yielding CO2. Our results are inconsistent with any mechanism in which the initial product formed on oxidation of formate is bicarbonate.

The production of e-cigarette aerosols through vaping processes is known to cause the formation of various free radicals and reactive oxygen species (ROS). Despite the well-known oxidative potential and cytotoxicity of fresh vaping emissions, the effects of chemical aging on exhaled vaping aerosols by indoor atmospheric oxidants are yet to be elucidated. Terpenes are commonly found in e-liquids as flavor additives. In the presence of indoor ozone (O3), e-cigarette aerosols that contain terpene flavorings can undergo chemical transformations, further producing ROS and reactive carbonyl species. Here, we simulated the aging process of the e-cigarette emissions in a 2 m3 FEP film chamber with 100 ppbv of O3 exposure for an hour. The aged vaping aerosols, along with fresh aerosols, were collected to detect the presence of ROS. The aged particles exhibited 2- to 11-fold greater oxidative potential, and further analysis showed that these particles formed a greater number of radicals in aqueous conditions. The aging process induced the formation of various alkyl hydroperoxides (ROOH), and through iodometric quantification, we saw that our aged vaping particles contained significantly greater amounts of these hydroperoxides than their fresh counterparts. Bronchial epithelial cells exposed to aged vaping aerosols exhibited an upregulation of the oxidative stress genes, HMOX-1 and GSTP1, indicating the potential for inhalation toxicity. This work highlights the indirect danger of vaping in environments with high ground-level O3, which can chemically transform e-cigarette aerosols into new particles that can induce greater oxidative damage than fresh e-cigarette aerosols. Given that the toxicological characteristics of e-cigarettes are mainly associated with the inhalation of fresh aerosols in current studies, our work may provide a perspective that characterizes vaping exposure under secondhand or thirdhand conditions as a significant health risk.

Light-absorbing secondary organic aerosols (SOAs), also known as secondary brown carbon (BrC), are major components of wildfire smoke that can have a significant impact on the climate system; however, how environmental factors such as relative humidity (RH) influence their formation is not fully understood, especially for heterocyclic precursors. We conducted chamber experiments to investigate secondary BrC formation from the nighttime oxidation of furan and pyrrole, two primary heterocyclic precursors in wildfires, in the presence of pre-existing particles at RH < 20% and ∼ 50%. Our findings revealed that increasing RH significantly affected the size distribution dynamics of both SOAs, with pyrrole SOA showing a stronger potential to generate ultrafine particles via intensive nucleation processes. Higher RH led to increased mass fractions of oxygenated compounds in both SOAs, suggesting enhanced gas-phase and/or multiphase oxidation under humid conditions. Moreover, higher RH reduced the mass absorption coefficients of both BrC, contrasting with those from homocyclic precursors, due to the formation of non-absorbing high-molecular-weight oxygenated compounds and the decreasing mass fractions of molecular chromophores. Overall, our findings demonstrate the unique RH dependence of secondary BrC formation from heterocyclic precursors, which may critically modulate the radiative effects of wildfire smoke on climate change.

The chemical and optical properties of secondary organic aerosols (SOA) have been widely studied through environmental chamber experiments, and some of the results have been parametrized in atmospheric models to help understand their radiative effects and climate influence. While most chamber studies investigate the aerosol formed from a single volatile organic compound (VOC), the potential interactions between reactive intermediates derived from VOC mixtures are not well understood. In this study, we investigated the SOA formed from pure and mixtures of anthropogenic (phenol and 1-methylnaphthalene) and/or biogenic (longifolene) VOCs using continuous-flow, high-NOx photooxidation chamber experiments to better mimic ambient conditions. SOA optical properties, including single scattering albedo (SSA), mass absorption coefficient (MAC), and refractive index (RI) at 375 nm, and chemical composition, including the formation of oxygenated organic compounds, organic-nitrogen compounds (including organonitrates and nitro-organics), and the molecular structure of the major chromophores, were explored. Additionally, the imaginary refractive index values of SOA in the multi-VOC system were predicted using a linear-combination assumption and compared with the measured values. When two VOCs were oxidized simultaneously, we found evidence for changes in SOA chemical composition compared to SOA formed from single-VOC systems, and this change led to nonlinear effects on SOA optical properties. The nonlinear effects were found to vary between different systems.

The light absorption properties of brown carbon (BrC), which are linked to molecular chromophores, may play a significant role in the Earths energy budget. While nitroaromatic compounds have been identified as strong chromophores in wildfire-driven BrC, other types of chromophores remain to be investigated. Given the electron-withdrawing nature of carbonyls ubiquitous in the atmosphere, we characterized carbonyl chromophores in BrC samples from the nighttime oxidation of furan and pyrrole derivatives, which are important but understudied precursors of secondary organic aerosols primarily found in wildfire emissions. Various carbonyl chromophores were characterized and quantified in BrC samples, and their ultraviolet-visible spectra were simulated by using time-dependent density functional theory. Our findings suggest that chromophores with carbonyls bonded to nitrogen (i.e., imides and amides) derived from N-containing heterocyclic precursors substantially contribute to BrC light absorption. The quantified N-containing carbonyl chromophores contributed to over 40% of the total light absorption at wavelengths below 350 nm and above 430 nm in pyrrole BrC. The contributions of chromophores to total light absorption differed significantly by wavelength, highlighting their divergent importance in different wavelength ranges. Overall, our findings highlight the significance of carbonyl chromophores in secondary BrC and underscore the need for further investigation.

Fluoroalkylether substances (ether PFAS) constitute a large group of emerging PFAS with uncertain environmental fate. Among them, GenX is the well-known alternative to perfluorooctanoic acid and one of the six proposed PFAS to be regulated by the U.S. Environmental Protection Agency. This study investigated the structure-biodegradability relationship for 12 different ether PFAS with a carboxylic acid headgroup in activated sludge communities. Only polyfluorinated ethers with at least one -CH2- moiety adjacent to or a C=C bond in the proximity of the ether bond underwent active biotransformation via oxidative and hydrolytic O-dealkylation. The bioreactions at ether bonds led to the formation of unstable fluoroalcohol intermediates subject to spontaneous defluorination. We further demonstrated that this aerobic biotransformation/defluorination could complement the advanced reduction process in a treatment train system to achieve more cost-effective treatment for GenX and other recalcitrant perfluorinated ether PFAS. These findings provide essential insights into the environmental fate of ether PFAS, the design of biodegradable alternative PFAS, and the development of cost-effective ether PFAS treatment strategies.

Despite previous studies indicating the thermal stability of vitamin E acetate (VEA) at low temperatures, VEA has been shown to readily decompose into various degradation products such as alkenes, long-chain alcohols, and carbonyls such as duroquinone (DQ) at vaping temperatures of

BACKGROUND: Exposure to diesel exhaust particles (DEP) has been linked to a variety of adverse health effects, including increased morbidity and mortality from cardiovascular diseases, chronic obstructive pulmonary disease (COPD), metabolic syndrome, and lung cancer. The epigenetic changes caused by air pollution have been associated with increased health risks. However, the exact molecular mechanisms underlying the lncRNA-mediated pathogenesis induced by DEP exposure have not been revealed. METHODS: Through RNA-sequencing and integrative analysis of both mRNA and lncRNA profiles, this study investigated the role of lncRNAs in altered gene expression in healthy and diseased human primary epithelial cells (NHBE and DHBE-COPD) exposed to DEP at a dose of 30 μg/cm2. RESULTS: We identified 503 and 563 differentially expressed (DE) mRNAs and a total of 10 and 14 DE lncRNAs in NHBE and DHBE-COPD cells exposed to DEP, respectively. In both NHBE and DHBE-COPD cells, enriched cancer-related pathways were identified at mRNA level, and 3 common lncRNAs OLMALINC, AC069234.2, and LINC00665 were found to be associated with cancer initiation and progression. In addition, we identified two cis-acting (TMEM51-AS1 and TTN-AS1) and several trans-acting lncRNAs (e.g. LINC01278, SNHG29, AC006064.4, TMEM51-AS1) only differentially expressed in COPD cells, which could potentially play a role in carcinogenesis and determine their susceptibility to DEP exposure. CONCLUSIONS: Overall, our work highlights the potential importance of lncRNAs in regulating DEP-induced gene expression changes associated with carcinogenesis, and individuals suffering from COPD are likely to be more vulnerable to these environmental triggers.

In this study, the regulated emissions, gaseous toxics, and the physical, chemical, and toxicological properties of particulate matter (PM) emissions from a legacy off-road diesel engine operated on hydrogenated vegetable oil (HVO) and HVO blends with biodiesel were investigated. This is one of the very few studies currently available examining the emissions and potential health effects of HVO and its blends with biodiesel from diesel engines. Extended testing was conducted over the nonroad transient cycle (NRTC) and the 5-mode D2 ISO 8718 cycle. Nitrogen oxide (NOx) emissions showed statistically significant reductions for HVO compared to diesel, whereas the biodiesel blends statistically significant increases in NOx emissions. PM and solid particle number reductions with pure HVO and the biodiesel blends were also observed. Low-molecular weight polycyclic aromatic hydrocarbons (PAHs) were the dominant species in the exhaust for all fuels, with pure HVO and the biodiesel blends showing lower concentrations of these pollutants compared to diesel fuel. Our results showed that the oxidative stress and cytotoxicity in PM emissions decreased with the use of biofuels. Notable correlations were observed between PM emissions and oxidative stress and cytotoxicity, especially elemental carbon and particle-phase PAH emissions.

In late 2019, the outbreak of e-cigarette or vaping-associated lung injuries (EVALIs) in the United States demonstrated to the public the potential health risks of vaping. While studies since the outbreak have identified vitamin E acetate (VEA), a diluent of tetrahydrocannabinol (THC) in vape cartridges, as a potential contributor to lung injuries, the molecular mechanisms through which VEA may cause damage are still unclear. Recent studies have found that the thermal degradation of e-liquids during vaping can result in the formation of products that are more toxic than the parent compounds. In this study, we assessed the role of duroquinone (DQ) in VEA vaping emissions that may act as a mechanism through which VEA vaping causes lung damage. VEA vaping emissions were collected and analyzed for their potential to generate reactive oxygen species (ROS) and induce oxidative stress-associated gene expression in human bronchial epithelial cells (BEAS-2B). Significant ROS generation by VEA vaping emissions was observed in both acellular and cellular systems. Furthermore, exposure to vaping emissions resulted in significant upregulation of NQO1 and HMOX-1 genes in BEAS-2B cells, indicating a strong potential for vaped VEA to cause oxidative damage and acute lung injury; the effects are more profound than exposure to equivalent concentrations of DQ alone. Our findings suggest that there may be synergistic interactions between thermal decomposition products of VEA, highlighting the multifaceted nature of vaping toxicity.

Nearly two years after vitamin E acetate (VEA) was identified as the potential cause of the 2019-2020 outbreak of e-cigarette, or vaping product-associated lung injuries (EVALI), the toxicity mechanisms of VEA vaping are still yet to be fully understood. Studies since the outbreak have found that e-liquids such as VEA undergo thermal degradation during the vaping process to produce various degradation products, which may pose a greater risk of toxicity than exposure to unvaped VEA. Additionally, a wide range of customizable parameters-including the model of e-cigarette used, puffing topography, or the applied power/temperature used to generate aerosols-have been found to influence the physical properties and chemical compositions of vaping emissions. However, the impact of heating coil temperature on the chemical composition of VEA vaping emissions has not been fully assessed. In this study, we investigated the emission product distribution of VEA vaping emissions produced at temperatures ranging from 176 to 356°C, corresponding to a variable voltage vape pen set at 3.3 to 4.8V. VEA degradation was found to be greatly enhanced with increasing temperature, resulting in a shift towards the production of lower molecular weight compounds, such as the redox active duroquinone (DQ) and short-chain alkenes. Low temperature vaping of VEA resulted in the production of long-chain molecules, such as phytol, exposure to which has been suggested to induce lung damage in previous studies. Furthermore, differential product distribution was observed in VEA degradation products generated from vaping and from pyrolysis using a tube furnace in the absence of the heating coil at equivalent temperatures, suggesting the presence of external factors such as metals or oxidation that may enhance VEA degradation during vaping. Overall, our findings indicate that vaping behavior may significantly impact the risk of exposure to toxic vaping products and potential for vaping-related health concerns.

BackgroundExisting studies on the health effects of e-cigarettes focused on e-cigarette users themselves. To study the corresponding effects on passive vapers, it is crucial to quantify e-cigarette chemicals deposited in their airways.ObjectiveThis study proposed an innovative approach to estimate the deposited dose of e-cigarette chemicals in the passive vapers' airways. The effect of the distance between active and passive vapers on the deposited dose was also examined.MethodsThe chemical constituent analysis was conducted to detect Nicotine and flavoring agents in e-cigarette aerosol. The Mobile Aerosol Lung Deposition Apparatus (MALDA) was employed to conduct aerosol respiratory deposition experiments in real-life settings to generate real-time data.ResultsFor e-cigarette aerosol in the ultrafine particle regime, the deposited doses in the alveolar region were on average 3.2 times higher than those in the head-to-TB airways, and the deposited dose in the passive vaper's airways increased when being closer to the active vaper.SignificanceWith prolonged exposure and close proximity to active vapers, passive vapers may be at risk for potential health effects of harmful e-cigarette chemicals. The methodology developed in this study has laid the groundwork for future research on exposure assessment and health risk analysis for passive vaping.

It has been demonstrated that propylene glycol (PG), vegetable glycerin (VG), and flavoring chemicals can thermally degrade to form carbonyls during vaping, but less is known about carbonyl emissions produced by transformation of flavoring chemicals and the interactive effects among e-liquid constituents. This study characterized carbonyl composition and levels in vaping emissions of PG-VG (e-liquid base solvents) and four e-liquid formulations flavored with trans-2-hexenol, benzyl alcohol, l-(-)-menthol, or linalool. Utilizing gas chromatography (GC)- and liquid chromatography (LC)-mass spectrometry (MS) methods, 14 carbonyls were identified and quantified. PG-VG emitted highest levels of formaldehyde, acetaldehyde, and acrolein. However, flavored e-liquids contributed to the production of a wider variety of carbonyls, with some carbonyls directly corresponding to the oxidation of alcohol moieties in flavoring compounds (e.g., trans-2-hexenol and benzyl alcohol transformed into trans-2-hexenal and benzaldehyde, respectively). Detections of formaldehyde-GSH and trans-2-hexenal-GSH adducts signify interactions of carbonyls with biological nucleophiles. The global reactivity descriptors (I, A, μ, η, and ω) and condensed Fukui parameters (fk0, fk-, fk+, and dual-descriptor) were computed to elucidate site reactivities of selected simple and α,β-unsaturated carbonyls found in vaping emissions. Overall, this study highlights carbonyl emissions and reactivities and their potential health risk effects associated with vaping.

The C-F bond is one of the strongest single bonds in nature. Although microbial reductive dehalogenation is well known for the other organohalides, no microbial reductive defluorination has been documented for perfluorinated compounds except for a single, nonreproducible study on trifluoroacetate. Here, we report on C-F bond cleavage in two C6 per- and polyfluorinated compounds via reductive defluorination by an organohalide-respiring microbial community. The reductive defluorination was demonstrated by the release of F- and the formation of the corresponding product when lactate was the electron donor, and the fluorinated compound was the sole electron acceptor. The major dechlorinating species in the seed culture, Dehalococcoides, were not responsible for the defluorination as no growth of Dehalococcoides or active expression of Dehalococcoides-reductive dehalogenases was observed. It suggests that minor phylogenetic groups in the community might be responsible for the reductive defluorination. These findings expand our fundamental knowledge of microbial reductive dehalogenation and warrant further studies on the enrichment, identification, and isolation of responsible microorganisms and enzymes. Given the wide use and emerging concerns of fluorinated organics (e.g., per- and polyfluoroalkyl substances), particularly the perfluorinated ones, the discovery of microbial defluorination under common anaerobic conditions may provide valuable insights into the environmental fate and potential bioremediation strategies of these notorious contaminants.

Exposure to fine particulate matter (PM2.5), of which secondary organic aerosol (SOA) is a major constituent, is linked to adverse health outcomes, including cardiovascular disease, lung cancer, and preterm birth. Atmospheric oxidation of isoprene, the most abundant nonmethane hydrocarbon emitted into Earth's atmosphere primarily from vegetation, contributes to SOA formation. Isoprene-derived SOA has previously been found to alter inflammatory/oxidative stress genes. MicroRNAs (miRNAs) are epigenetic regulators that serve as post-transcriptional modifiers and key mediators of gene expression. To assess whether isoprene-derived SOA alters miRNA expression, BEAS-2B lung cells were exposed to laboratory-generated isoprene-derived SOA constituents derived from the acid-driven multiphase chemistry of authentic methacrylic acid epoxide (MAE) or isomeric isoprene epoxydiols (IEPOX) with acidic sulfate aerosol particles. These IEPOX- and MAE-derived SOA constituents have been shown to be measured in large quantities within PM2.5 collected from isoprene-rich areas affected by acidic sulfate aerosol particles derived from human activities. A total of 29 miRNAs were identified as differentially expressed when exposed to IEPOX-derived SOA and 2 when exposed to MAE-derived SOA, a number of which are inflammatory/oxidative stress associated. These results suggest that miRNAs may modulate the inflammatory/oxidative stress response to SOA exposure, thereby advancing the understanding of airway cell epigenetic response to SOA.

Dimethyl selenide (DMSe) is one of the major volatile organoselenium compounds released from aquatic and terrestrial environments through microbial transformation and plant metabolism. The detailed processes of DMSe leading to secondary organic aerosol (SOA) formation and the pulmonary health effects induced by inhalation of DMSe-derived SOA remain largely unknown. In this study, we characterized the chemical composition and formation yields of SOA produced from the oxidation of DMSe with OH radicals and O3 in controlled chamber experiments. Further, we profiled the transcriptome-wide gene expression changes in human airway epithelial cells (BEAS-2B) after exposure to DMSe-derived SOA. Our analyses indicated a significantly higher SOA yield resulting from the OH-initiated oxidation of DMSe. The oxidative potential of DMSe-derived SOA, as measured by the dithiothreitol (DTT) assay, suggested the presence of oxidizing moieties in DMSe-derived SOA at levels higher than typical ambient aerosols. Utilizing RNA sequencing (RNA-Seq) techniques, gene expression profiling followed by pathway enrichment analysis revealed several major biological pathways perturbed by DMSe-derived SOA, including elevated genotoxicity, DNA damage, and p53-mediated stress responses, as well as downregulated cholesterol biosynthesis, glycolysis, and interleukin IL-4/IL-13 signaling. This study highlights the significance of DMSe-derived SOA as a stressor in human airway epithelial cells.

Twelve undescribed sesquiterpenoids, fomitopins A-L (1-12), were isolated via bioassay-guided purification from the bracket fungus Fomitopsis pinicola (Sw.) P. Karst, and this fungus have been reported to exhibit anti-microbial and anti-inflammatory activities. The structures of 1-12 were elucidated by spectroscopic and spectrometric analyses and their absolute configurations were further confirmed by ECD simulations. Ten isolated compounds were evaluated for their anti-inflammatory potential and compound 11 exhibited the most significant inhibition of superoxide anion generation and elastase release with IC50 values of 0.81 ± 0.15 and 0.74 ± 0.12 μM. These newly purified sesquiterpenoids could be potential candidates for further anti-inflammatory studies.

Traffic-related particulate matter (PM) is a major source of outdoor air pollution worldwide. It has been recently hypothesized to cause cardiometabolic syndrome, including cardiovascular dysfunction, obesity, and diabetes. The environmental and toxicological factors involved in the processes, and the detailed mechanisms remain to be explored. The objective of this study is to assess the current scientific evidence of traffic-related PM-induced cardiometabolic syndrome. We conducted a literature review by searching the keywords of "traffic related air pollution", "particulate matter", "human health", and "metabolic syndrome" from 1980 to 2018. This resulted in 25 independent research studies for the final review. Both epidemiological and toxicological findings reveal consistent correlations between traffic-related PM exposure and the measured cardiometabolic health endpoints. Smaller sizes of PM, particularly ultrafine particles, are shown to be more harmful due to their greater concentrations, reactive compositions, longer lung retention, and bioavailability. The active components in traffic-related PM could be attributed to metals, black carbon, elemental carbon, polyaromatic hydrocarbons, and diesel exhaust particles. Existing evidence points out that the development of cardiometabolic symptoms can occur through chronic systemic inflammation and increased oxidative stress. The elderly (especially for women), children, genetically susceptible individuals, and people with pre-existing conditions are identified as vulnerable groups. To advance the characterization of the potential health risks of traffic-related PM, additional research is needed to investigate the detailed chemical compositions of PM constituents, atmospheric transformations, and the mode of action to induce adverse health effects. Furthermore, we recommend that future studies could explore the roles of genetic and epigenetic factors in influencing cardiometabolic health outcomes by integrating multi-omics approaches (e.g., genomics, epigenomics, and transcriptomics) to provide a comprehensive assessment of biological perturbations caused by traffic-related PM.

Secondary organic aerosol (SOA) derived from the photochemical oxidation of isoprene contributes a substantial mass fraction to atmospheric fine particulate matter (PM2.5). The formation of isoprene SOA is influenced largely by anthropogenic emissions through multiphase chemistry of its multigenerational oxidation products. Considering the abundance of isoprene SOA in the troposphere, understanding mechanisms of adverse health effects through inhalation exposure is critical to mitigating its potential impact on public health. In this study, we assessed the effects of isoprene SOA on gene expression in human airway epithelial cells (BEAS-2B) through an air-liquid interface exposure. Gene expression profiling of 84 oxidative stress and 249 inflammation-associated human genes was performed. Our results show that the expression levels of 29 genes were significantly altered upon isoprene SOA exposure under noncytotoxic conditions (p < 0.05), with the majority (22/29) of genes passing a false discovery rate threshold of 0.3. The most significantly affected genes belong to the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) transcription factor network. The Nrf2 function is confirmed through a reporter cell line. Together with detailed characterization of SOA constituents, this study reveals the impact of isoprene SOA exposure on lung responses and highlights the importance of further understanding its potential health outcomes.

In the southeastern US, substantial emissions of isoprene from deciduous trees undergo atmospheric oxidation to form secondary organic aerosol (SOA) that contributes to fine particulate matter (PM2.5). Laboratory studies have revealed that anthropogenic pollutants, such as sulfur dioxide (SO2), oxides of nitrogen (NO x ), and aerosol acidity, can enhance SOA formation from the hydroxyl radical (OH)-initiated oxidation of isoprene; however, the mechanisms by which specific pollutants enhance isoprene SOA in ambient PM2.5 remain unclear. As one aspect of an investigation to examine how anthropogenic pollutants influence isoprene-derived SOA formation, high-volume PM2.5 filter samples were collected at the Birmingham, Alabama (BHM), ground site during the 2013 Southern Oxidant and Aerosol Study (SOAS). Sample extracts were analyzed by gas chromatography-electron ionization-mass spectrometry (GC/EI-MS) with prior trimethylsilylation and ultra performance liquid chromatography coupled to electrospray ionization high-resolution quadrupole time-of-flight mass spectrometry (UPLC/ESI-HR-QTOFMS) to identify known isoprene SOA tracers. Tracers quantified using both surrogate and authentic standards were compared with collocated gas- and particle-phase data as well as meteorological data provided by the Southeastern Aerosol Research and Characterization (SEARCH) network to assess the impact of anthropogenic pollution on isoprene-derived SOA formation. Results of this study reveal that isoprene-derived SOA tracers contribute a substantial mass fraction of organic matter (OM) (~ 7 to ~ 20 %). Isoprene-derived SOA tracers correlated with sulfate ( SO42- ) (r2 = 0.34, n = 117) but not with NO x . Moderate correlations between methacrylic acid epoxide and hydroxymethyl-methyl-α-lactone (together abbreviated MAE/HMML)-derived SOA tracers with nitrate radical production (P[NO3]) (r2 = 0.57, n = 40) were observed during nighttime, suggesting a potential role of the NO3 radical in forming this SOA type. However, the nighttime correlation of these tracers with nitrogen dioxide (NO2) (r2 = 0.26, n = 40) was weaker. Ozone (O3) correlated strongly with MAE/HMML-derived tracers (r2 = 0.72, n = 30) and moderately with 2-methyltetrols (r2 = 0.34, n = 15) during daytime only, suggesting that a fraction of SOA formation could occur from isoprene ozonolysis in urban areas. No correlation was observed between aerosol pH and isoprene-derived SOA. Lack of correlation between aerosol acidity and isoprene-derived SOA is consistent with the observation that acidity is not a limiting factor for isoprene SOA formation at the BHM site as aerosols were acidic enough to promote multiphase chemistry of isoprene-derived epoxides throughout the duration of the study. All in all, these results confirm previous studies suggesting that anthropogenic pollutants enhance isoprene-derived SOA formation.

Aromatic organosulfates are identified and quantified in fine particulate matter (PM2.5) from Lahore, Pakistan, Godavari, Nepal, and Pasadena, California. To support detection and quantification, authentic standards of phenyl sulfate, benzyl sulfate, 3-and 4-methylphenyl sulfate and 2-, 3-, and 4-methylbenzyl sulfate were synthesized. Authentic standards and aerosol samples were analyzed by ultra-performance liquid chromatography (UPLC) coupled to negative electrospray ionization (ESI) quadrupole time-of-flight (ToF) mass spectrometry. Benzyl sulfate was present in all three locations at concentrations ranging from 4 - 90 pg m-3. Phenyl sulfate, methylphenyl sulfates and methylbenzyl sulfates were observed intermittently with abundances of 4 pg m-3, 2-31 pg m-3, 109 pg m-3, respectively. Characteristic fragment ions of aromatic organosulfates include the sulfite radical (•SO3-, m/z 80) and the sulfate radical (•SO4-,m/z 96). Instrumental response factors of phenyl and benzyl sulfates varied by a factor of 4.3, indicating that structurally-similar organosulfates may have significantly different instrumental responses and highlighting the need to develop authentic standards for absolute quantitation organosulfates. In an effort to better understand the sources of aromatic organosulfates to the atmosphere, chamber experiments with the precursor toluene were conducted under conditions that form biogenic organosulfates. Aromatic organosulfates were not detected in the chamber samples, suggesting that they form through different pathways, have different precursors (e.g. naphthalene or methylnaphthalene), or are emitted from primary sources.

Secondary organic aerosol (SOA) formation from 2-methyl-3-buten-2-ol (MBO) photooxidation has recently been observed in both field and laboratory studies. Similar to the level of isoprene, the level of MBO-derived SOA increases with elevated aerosol acidity in the absence of nitric oxide; therefore, an epoxide intermediate, (3,3-dimethyloxiran-2-yl)methanol (MBO epoxide), was synthesized and tentatively proposed to explain this enhancement. In this study, the potential of the synthetic MBO epoxide to form SOA via reactive uptake was systematically examined. SOA was observed only in the presence of acidic aerosol. Major SOA constituents, 2,3-dihydroxyisopentanol and MBO-derived organosulfate isomers, were chemically characterized in both laboratory-generated SOA and in ambient fine aerosol collected from the BEACHON-RoMBAS field campaign during the summer of 2011, where MBO emissions are substantial. Our results support the idea that epoxides are potential products of MBO photooxidation leading to the formation of atmospheric SOA and suggest that reactive uptake of epoxides may explain acid enhancement of SOA observed from other biogenic hydrocarbons.