Combustion-generated Particulate Matter Research Articles

Investigating the oxidative reactivity and nanostructural characteristics of diffusion flame generated soot using methyl crotonate and methyl butyrate blended diesel fuels

Combustion-generated particulate matter has a consequential fallout on climate, environment, and human health. Thus, comprehension of soot formation and mitigation processes using biodiesel additives is a focal point of modern combustion research. This study presents an intricate investigation of enhanced oxidative reactivity and its dependence on the soot nanostructural properties induced by distinctive blending of a saturated and an unsaturated biodiesel surrogates namely, methyl butyrate (MB) and methyl crotonate (MC) respectively with pure diesel. 25% MB-75% diesel fuel resulted in the lowest sooting propensity and lowest activation energy (155.4 ± 2 kJ/mol) for soot oxidation in comparison to pure diesel fuel and diesel soot (175.1 ± 2 kJ/mol). The soot was collected using a smoke point apparatus involving a wick-fed laminar diffusion flame at atmospheric pressure after meticulous observation of the smoke points. The detailed nanostructural characterization of the flame generated soots were performed using high-resolution transmission electron microscopy, X-ray diffraction, elemental analysis and Raman spectroscopy. BET surface area analysis, and thermogravimetric analysis were carried out for surface area distinction and activation energy calculations respectively. It revealed that, addition of MB to diesel resulted in improved fuel combustion with reduction in primary soot particle diameter, greater inter-planar separation, increased fringe tortuosity and greater crystal structure disorder resulting in its enhanced reactivity with O2. The 25% MC-75% diesel blend resulted in relatively greater sooting propensity while its soot exhibited lower crystal structure disorder and greater activation energy (165.0 ± 2 kJ/mol) for O2 induced oxidation compared to 25% MB-75% diesel, possibly due to the resonance stabilized radical (RSRs) formation that altered the fuel combustion chemistry. Therefore, this study successfully depicts that the structural differences in the surrogate fuels do influence the soot formation and oxidation kinetics. These structural effects therefore need to be considered when formulating the global multiphase kinetic models for biodiesel-diesel fuel combustion.11Dedicated to Prof. Purnakala Samant on the occasion of her 50th birthday celebration.

Excitation–Emission Matrix Spectroscopy for Analysis of Chemical Composition of Combustion Generated Particulate Matter

Analysis of particulate matter (PM) is important for the assessment of human exposures to potentially harmful agents, notably combustion-generated PM. Specifically, polycyclic aromatic hydrocarbons (PAHs) found in ultrafine PM have been linked to cardiovascular diseases and carcinogenic and mutagenic effects. In this study, we quantify the presence and concentrations of PAHs with lower molecular weight (LMW, 126 < MW < 202) and higher molecular weight (HMW, 226 < MW < 302), i.e., smaller and larger than Pyrene, in combustion-generated PM using excitation-emission matrix (EEM) fluorescence spectroscopy. Laboratory combustion PM samples were generated in a laminar diffusion inverted gravity flame reactor (IGFR) operated on ethylene and ethane. Fuel dilution by Ar in 0% to 90% range controlled the flame temperature. The colder flames result in lower PM yields however, the PM PAH content increases significantly. Temperature thresholds for PM transition from low to high organic carbon content were characterized based on the maximum flame temperature (Tmax,c ∼ 1791 to 1857 K) and the highest soot luminosity region temperature (T*c ∼ 1600 to 1650K). Principal component regression (PCR) analysis of the EEM spectra of IGFR samples correlates to GCMS data with R2 = 0.988 for LMW and 0.998 for HMW PAHs. PCR-EEM analysis trained on the IGFR samples was applied to PM samples from woodsmoke and diesel exhaust, the model accurately predicts HMW PAH concentrations with R2 = 0.976 and overestimates LMW PAHs.

"Are we forgetting the smallest, sub 10 nm combustion generated particles?".

Although mass emissions of combustion-generated particulate matter have been substantially reduced by new combustion technology, there is still a great concern about the emissions of huge numbers of sub-10 nm particles with insignificant mass. These particles have up to orders of magnitude higher surface area to mass ratios compared to larger particles, have surfaces covered with adsorbed volatile and semi-volatile organic species or even are constituted by such species. Currently there is only very little information available on exposure and related health effects specific for smaller particles and first evidences for long-term health effects has only been recently published. However, the fact that these nanoparticles are not easily measured at the exhausts and in the atmosphere and that their biological activity is obscure does not mean that we can overlook them. There is an urgent need to develop i) reliable methods to measure sub-10 nm particles at the exhaust and in the atmosphere and ii) a robust correlation between the chemical structure of the molecules making up combustion-generated nanoparticles and health burden of new combustion technologies. Our attention has to turn to this new class of combustion-generated nanoparticles, which might be the future major constituents of air pollution.

Exposure to Deepwater Horizon Crude Oil Burnoff Particulate Matter Induces Pulmonary Inflammation and Alters Adaptive Immune Response.

The ″in situ burning" of trapped crude oil on the surface of Gulf waters during the 2010 Deepwater Horizon (DWH) oil spill released numerous pollutants, including combustion-generated particulate matter (PM). Limited information is available on the respiratory impact of inhaled in situ burned oil sail particulate matter (OSPM). Here we utilized PM collected from in situ burn plumes of the DWH oil spill to study the acute effects of exposure to OSPM on pulmonary health. OSPM caused dose-and time-dependent cytotoxicity and generated reactive oxygen species and superoxide radicals in vitro. Additionally, mice exposed to OSPM exhibited significant decreases in body weight gain, systemic oxidative stress in the form of increased serum 8-isoprostane (8-IP) levels, and airway inflammation in the form of increased macrophages and eosinophils in bronchoalveolar lavage fluid. Further, in a mouse model of allergic asthma, OSPM caused increased T helper 2 cells (Th2), peribronchiolar inflammation, and increased airway mucus production. These findings demonstrate that acute exposure to OSPM results in pulmonary inflammation and alteration of innate/adaptive immune responses in mice and highlight potential respiratory effects associated with cleaning up an oil spill.

Mitochondrial-Mediated Apoptosis Pathway in Alveolar Epithelial Cells Exposed to the Metals in Combustion-Generated Particulate Matter

Previously a significant mitochondrial impairment was identified in alveolar epithelial cells exposed to metals adsorbed to combustion-generated particulate matter (PM). Due to the critical role of mitochondria in apoptosis, the aim of this study was to investigate the pro-apoptotic potential of metals present in oil fly ash (OFA). A549 cells were exposed to water-soluble components of an OFA sample, containing vanadium [V(IV)], iron [Fe(III)], and nickel [Ni(II)] (68.8, 110.4, and 18 μM, respectively). Experiments were also performed using individual metal solutions. Apoptosis was detected and the mitochondrial role was assessed by a caspase-9 inhibitor (Z-LEHD-FMK). To determine whether the presence of impaired mitochondria in unexposed daughter cells increased apoptosis, an in vitro model was developed that allowed determination of effects until the third cell generation. To specifically examine the toxicity of vanadium (V), that characterize the airborne pollutant examined in this study, p53involvement and metabolic impairment through changes in HIF-1α and Glut-1 expression were determined. OFA and individual metal solutions produced significant apoptosis in the progeny of exposed cells, triggering the intrinsic apoptosis pathway. In apoptosis induced by poorly genotoxic metal V, p53 did not play a significant role. However, V exposure increased nuclear translocation of HIF-1α and expression of the Glut-1 receptor, indicating metabolic impairment due to metal-induced mitochondrial dysfunction. Overall, these results improve our knowledge of the pathogenic role that airborne metals and in particular V exerted in respiratory epithelium.

Model Combustion-Generated Particulate Matter Containing Persistent Free Radicals Redox Cycle to Produce Reactive Oxygen Species

Particulate matter (PM) is emitted during thermal decomposition of waste. During this process, aromatic compounds chemisorb to the surface of metal-oxide-containing PM, forming a surface-stabilized environmentally persistent free radical (EPFR). We hypothesized that EPFR-containing PM redox cycle to produce ROS and that this redox cycle is maintained in biological environments. To test our hypothesis, we incubated model EPFRs with the fluorescent probe dihydrorhodamine (DHR). Marked increases in DHR fluorescence were observed. Using a more specific assay, hydroxyl radicals ((•)OH) were also detected, and their level was further increased by cotreatment with thiols or ascorbic acid (AA), known components of epithelial lining fluid. Next, we incubated our model EPFR in bronchoalveolar lavage fluid (BALF) or serum. Detection of EPFRs and (•)OH verified that PM generate ROS in biological fluids. Moreover, incubation of pulmonary epithelial cells with EPFR-containing PM increased (•)OH levels compared to those in PM lacking EPFRs. Finally, measurements of oxidant injury in neonatal rats exposed to EPFRs by inhalation suggested that EPFRs induce an oxidant injury within the lung lining fluid and that the lung responds by increasing antioxidant levels. In summary, our EPFR-containing PM redox cycle to produce ROS, and these ROS are maintained in biological fluids and environments. Moreover, these ROS may modulate toxic responses of PM in biological tissues such as the lung.

Impacts of Traffic-Related and Woodsmoke Air Pollution on Endothelial Function and Systemic Inflammation

Background: Evidence links combustion-generated particulate matter (PM) with cardiovascular morbidity. Both traffic-related air pollution (TRAP) and residential wood combustion (RWC) may be important, but few studies have compared their impacts. Aims: We evaluated the effects of HEPA filtration and indoor PM2.5 on reactive hyperemia index (RHI) and inflammation (C-reactive protein [CRP] and IL-6) among individuals residing in Vancouver areas impacted by either TRAP or RWC. We aimed to test HEPA efficacy and to introduce similar PM2.5 exposure contrasts in all homes. Methods: In this randomized, single-blind crossover study we enrolled 83 healthy adults (44 homes), from the general population. Each home was monitored over two consecutive weeks (one with HEPA and one with “placebo” filtration). RHI was measured after each week and blood samples were collected at baseline and after each week. Effects were estimated from mixed models with PM2.5 effects reported per median within-home contrast (2.4 µg/m3). Results: This analysis included 51 participants with complete PM2.5, RHI, and blood measurements. Participants in TRAP- (N=34) and RWC-impacted areas (N=17) had similar BMI, baseline CRP, time spent at home, and PM2.5 levels, but TRAP-exposed participants were younger. HEPA filters reduced average indoor PM2.5 levels by 39%, and 92% of homes had reductions, but in intent to treat analysis filtration was not associated with changes in cardiovascular outcomes. PM2.5 was not associated with CRP in the full population; however, PM2.5 reductions were associated with lower CRP among TRAP-impacted (19.2% decrease, 95% CI: 3.2%–37.4%) but not RWC-impacted (11.6% increase, -37.3%–23.5%) participants. There were no associations with RHI or IL-6. Conclusions: Indoor PM2.5 reductions were associated with decreases in CRP, a marker of systemic inflammation, only among those in areas impacted by TRAP. This supports the hypothesis that traffic-related PM2.5 has greater inflammatory effects than other combustion PM.

Emerging mechanistic targets in lung injury induced by combustion-generated particles.

The mechanism for biological effect following exposure to combustion-generated particles is incompletely defined. The identification of pathways regulating the acute toxicological effects of these particles provides specific targets for therapeutic manipulation in an attempt to impact disease following exposures. Transient receptor potential (TRP) cation channels were identified as "particle sensors" in that their activation was coupled with the initiation of protective responses limiting airway deposition and inflammatory responses, which promote degradation and clearance of the particles. TRPA1, V1, V4, and M8 have a capacity to mediate adverse effects after exposure to combustion-generated particulate matter (PM); relative contributions of each depend upon particle composition, dose, and deposition. Exposure of human bronchial epithelial cells to an organic extract of diesel exhaust particle was followed by TRPV4 mediating Ca(++) influx, increased RAS expression, mitogen-activated protein kinase signaling, and matrix metalloproteinase-1 activation. These novel pathways of biological effect can be targeted by compounds that specifically inhibit critical signaling reactions. In addition to TRPs and calcium biochemistry, humic-like substances (HLS) and cell/tissue iron equilibrium were identified as potential mechanistic targets in lung injury after particle exposure. In respiratory epithelial cells, iron sequestration by HLS in wood smoke particle (WSP) was associated with oxidant generation, cell signaling, transcription factor activation, and release of inflammatory mediators. Similar to WSP, cytotoxic insoluble nanosized spherical particles composed of HLS were isolated from cigarette smoke condensate. Therapies that promote bioelimination of HLS and prevent the disruption of iron homeostasis could function to reduce the harmful effects of combustion-generated PM exposure.

Radical-Containing Ultrafine Particulate Matter Initiates Epithelial-to-Mesenchymal Transitions in Airway Epithelial Cells

Environmentally persistent free radicals (EPFRs) in combustion-generated particulate matter (PM) are capable of inducing pulmonary pathologies and contributing to the development of environmental asthma. In vivo exposure of infant rats to EPFRs demonstrates their ability to induce airway hyperresponsiveness to methacholine, a hallmark of asthma. However, the mechanisms by which combustion-derived EPFRs elicit in vivo responses remain elusive. In this study, we used a chemically defined EPFR consisting of approximately 0.2 μm amorphrous silica containing 3% cupric oxide with the organic pollutant 1,2-dichlorobenzene (DCB-230). DCB-230 possesses similar radical content to urban-collected EPFRs but offers several advantages, including lack of contaminants and chemical uniformity. DCB-230 was readily taken up by BEAS-2B and at high doses (200 μg/cm(2)) caused substantial necrosis. At low doses (20 μg/cm(2)), DCB-230 particles caused lysosomal membrane permeabilization, oxidative stress, and lipid peroxidation within 24 hours of exposure. During this period, BEAS-2B underwent epithelial-to-mesenchymal transition (EMT), including loss of epithelial cell morphology, decreased E-cadherin expression, and increased α-smooth muscle actin (α-SMA) and collagen I production. Similar results were observed in neonatal air-liquid interface culture (i.e., disruption of epithelial integrity and EMT). Acute exposure of infant mice to DCB-230 resulted in EMT, as confirmed by lineage tracing studies and evidenced by coexpression of epithelial E-cadherin and mesenchymal α-SMA proteins in airway cells and increased SNAI1 expression in the lungs. EMT in neonatal mouse lungs after EPFR exposure may provide an explanation for epidemiological evidence supporting PM exposure and increased risk of asthma.

Airway remodeling in chronic alcohol C57BL/6 mice with inhalation co-exposure to combustion-generated particulate matter

Airway remodeling in chronic alcohol C57BL/6 mice with inhalation co-exposure to combustion-generated particulate matter

On the characterization of nanoparticles emitted from combustion sources related to understanding their effects on health and climate

This work describes the use of well-controlled laboratory flames to produce aerosols of organic carbon (OC) as model particles representative of the OC fraction of combustion-generated particulate matter emissions in fresh exhausts. Water–particle interactions are explored in two specific cases. In the first case, particles are exposed to saturated environments and come into direct contact with liquid water by bubbling flame samples through a column of water. This case is representative of particle–liquid interactions relevant to wet removal routes by particle interception by rain or fog droplets or in biological systems covered with biological fluids composed mostly of water. In the second case, the particles are exposed to sub-saturated vapors with H2O concentrations representative of cloud-forming atmospheres. The particles’ capacity to serve as atmospheric cloud condensation nuclei (CCN) by rapid growth to droplets was measured and compared to NaCl particles, which are highly soluble particles with well known activation diameters. The results show measureable interactions with water in highly saturated conditions. However, in sub-saturated environments, no growth by water condensation was observed, and fresh emissions of OC nanoparticles are not likely to act as CCN in atmospherically relevant humidity.

CARDIOVASCULAR MORTALITY AND OCCUPATIONAL EXPOSURE IN AN ALUMINUM COHORT

Background and aims: Increased risk of cardiovascular mortality related to combustion-generated particulate matter (PM) in air pollution has become a major public health concern. Although occupational exposures to PM can be orders of magnitude higher than ambient levels, evidence regarding cardiovascular disease risk associated with workplace exposure to PM is scant. Methods: We examined cardiovascular mortality from 1996 to 2008 in a cohort of over 11,700 aluminum workers which has been under observation for over a decade. Individual level exposure metrics for total PM and PM2.5 are being developed for the cohort based on job histories and personal sampling results in smelters, refining and fabrication facilities. Results: Initial analyses using broad classifications of plant type (smelter vs other) show no increased risk of all-cause mortality among those who worked in a smelter. Thirty percent of the deaths were due to cardiovascular disease (CVD). Stratifying by active versus inactive person-time, we found a 14% increased risk for death from CVD (N = 78) and a 28% increased risk for death from ischemic heart disease (N = 55) for active workers who worked at smelters, although all confidence intervals include the null. Conclusions: Higher peak and mean PM exposures occurred at smelting facilities compared to refining and fabrication facilities, lending support to the hypothesis that there is an exposure-response association between quantitative exposures to PM and CVD mortality.

The application of profluorescent nitroxides to detect reactive oxygen species derived from combustion-generated particulate matter: Cigarette smoke – A case study

Reactive oxygen species (ROS) and related free radicals are considered to be key factors underpinning the various adverse health effects associated with exposure to ambient particulate matter. Therefore, measurement of ROS is a crucial factor for assessing the potential toxicity of particles. In this work, a novel profluorescent nitroxide, BPEAnit, was investigated as a probe for detecting particle-derived ROS. BPEAnit has a very low fluorescence emission due to inherent quenching by the nitroxide group, but upon radical trapping or redox activity, a strong fluorescence is observed. BPEAnit was tested for detection of ROS present in mainstream and sidestream cigarette smoke. In the case of mainstream cigarette smoke, there was a linear increase in fluorescence intensity with an increasing number of cigarette puffs, equivalent to an average of 101 nmol ROS per cigarette based on the number of moles of the probe reacted. Sidestream cigarette smoke sampled from an environmental chamber exposed BPEAnit to much lower concentrations of particles, but still resulted in a clearly detectible increase in fluorescence intensity with sampling time. It was calculated that the amount of ROS was equivalent to 50 ± 2 nmol per mg of particulate matter; however, this value decreased with ageing of the particles in the chamber. Overall, BPEAnit was shown to provide a sensitive response related to the oxidative capacity of the particulate matter. These findings present a good basis for employing the new BPEAnit probe for the investigation of particle-related ROS generated from cigarette smoke as well as from other combustion sources.

Copper Oxide-Based Model of Persistent Free Radical Formation on Combustion-Derived Particulate Matter

We have found that environmentally persistent free radicals (PFRs) are formed by adsorption of substituted aromatic molecular precursors on the surface of cupric oxide-containing particles at temperatures between 100 and 400 degrees C. This temperature range corresponds to the conditions in the postflame, cool zone of combustion, and thermal processes. Depending upon the nature of the precursor and the adsorption temperature, both substituted phenoxyl and semiquinone radicals are formed. The PFRs are formed through a mechanism of initial physisorption, followed by chemisorption via elimination of water or hydrogen chloride, and electron transfer resulting in the simultaneous reduction of Cu(II) to Cu(I) and formation of the PFR. The PFRs are still observable by electron paramagnetic resonance (EPR) after exposure to air for more than a day. Their lifetimes under vacuum appear to be infinite. Other redox-active transition metals such as iron are expected to also mediate or catalyze the formation of PFRs. The properties of the observed radicals are consistent with radicals previously observed on airborne and combustion-generated particulate matter. We propose a catalytic biochemical cycle for both the particle-associated semiquinone and phenoxyl PFRs that result in the formation of hydroxyl radical and other reactive oxygen species (ROS). This suggests that combustion-generated, particle-associated PFRs may be responsible for the oxidative stress resulting in cardiopulmonary disease and probably cancer that has been attributed to exposure to airborne fine particles.

Origin and Health Impacts of Emissions of Toxic By-Products and Fine Particles from Combustion and Thermal Treatment of Hazardous Wastes and Materials

High-temperature, controlled incineration and thermal treatment of contaminated soils, sediments, and wastes at Superfund sites are often preferred methods of remediation of contaminated sites under the Comprehensive Environmental Response, Compensation, and Liability Act of 1980 and related legislation. Although these methods may be executed safely, formation of toxic combustion or reaction by-products is still a cause of concern. Emissions of polycyclic aromatic hydrocarbons (PAHs); chlorinated hydrocarbons (CHCs), including polychlorinated dibenzo-p-dioxins and dibenzofurans; and toxic metals (e.g., chromium VI) have historically been the focus of combustion and health effects research. However, fine particulate matter (PM) and ultrafine PM, which have been documented to be related to cardiovascular disease, pulmonary disease, and cancer, have more recently become the focus of research. Fine PM and ultrafine PM are effective delivery agents for PAHs, CHCs, and toxic metals. In addition, it has recently been realized that brominated hydrocarbons (including brominated/chlorinated dioxins), redox-active metals, and redox-active persistent free radicals are also associated with PM emissions from combustion and thermal processes. In this article, we discuss the origin of each of these classes of pollutants, the nature of their association with combustion-generated PM, and the mechanisms of their known and potential health impacts.

The role of combustion-generated radicals in the toxicity of PM 2.5

Electron paramagnetic resonance analyses of samples of ambient, fine particulate matter (PM2.5), as well as fly-ashes and soots from a wood-burning fireplace, a boiler cofired with chlorinated organics, a pilot-scale hazardous waste incinerator, and laboratory combustion of various halocarbons reveal that they contain stable free radicals. All of the radical systems were indefinitely stable in air. Extracts of PM2.5 and the incinerator ash caused damage to DNA, both in vitro and in cell systems. Cellular damage to DNA was prevented by addition of the enzymes superoxide dismutase and/or catalase that destroy the superoxide radical and hydrogen peroxide, respectively. This type of DNA damage and protection is observed for the semiquinone radicals in cigarette tar. Therefore, we have tentatively assigned the structure of the observed radicals as semiquinones. In solution, semiquinone radicals undergo redox cycling, reducing oxygen and forming superoxide radical and hydrogen peroxide, and ultimately the hydroxyl radical that can initiate DNA damage. Since ambient PM2.5 is primarily composed of combustion-generated particulate matter, our results imply that combustion sources produce semiquinone-type radicals that persist on fine particles in the atmosphere. The fine particles provide a carrier for deposit of the radicals deep in the human respiratory tract. These radicals then initiate immune system responses that can trigger the production of further radicals as well as other species that can damage DNA or induce damage to the respiratory tract.