Ultrafine Carbon Particles Research Articles

CARCINOGENIC EFFECT OF VARIOUS TYPES OF SMOKE

All types of smoke are carcinogenic. Increasing air smoke is a serious global problem. Knowledge on carcinogenic effects of various types of smoke is necessary to work out effective preventive measures.
 The purpose of the review is to characterize the general characteristics and peculiarities of the carcinogenic effects of various types of smoke. The most significant carcinogens of all types of smoke are polycyclic aromatic hydrocarbons, heavy metals and carbon microparticles. Any smoke is an etiological factor for respiratory tract cancer, and systemic neoplasms (tumors of hematopoietic and lymphoid tissues, central and peripheral nervous systems, soft tissues and skeleton). Tobacco smoke may be involved in the pathogenesis of cervical cancer due to the induction of local immunosuppression and specific tropic nitrosamines. Exhaust fumes due to high benzene content may cause hematological malignancies, especially leukemia in children. Wildfire smoke, due to significant amounts of ultra-fine carbon particles PM0.1, contributes to the development of central nervous system tumors. Severe contamination with natural and artificial radionuclides makes wildfire smoke a factor of high carcinogenic danger for the human population globally. Prevention of malignant neoplasms caused by smoke requires government measures to promote smoking cessation, hybrid and electric engines in automobiles, as well as wildfire prevention, early detection and extinction. Effective respirators and indoor air filters should be used for personal protection. To relieve environmentally caused oxidative stress, herbal medicines and food products that stimulate autophagy, as well as transfer factors for immunodeficiency correction, are recommended.

Black Carbon along a Highway and in a Residential Neighborhood during Rush-Hour Traffic in a Cold Climate

Short-term exposure to ultra-fine Black Carbon (BC) particles produced during incomplete fuel combustion of wood and fossil fuel has been linked to respiratory and cardiovascular diseases, hospitalizations and premature deaths. The goal of this research was to assess traffic-related BC in a cold climate along an urban highway and 300 m into an adjacent residential neighborhood. BC was measured with an aethalometer (MA350, Aethlabs) along the main traffic artery in geothermally heated Reykjavík, the capital of Iceland (64.135° N–21.895° W, 230,000 inhabitants). Stationary monitoring confirmed that traffic was the dominant source of roadside BC in winter, averaging 1.0 ± 1.1 µg/m3 (0.6 and 1.1 µg/m3 median and interquartile range; 28,000 vehicles/day). Inter-day variations in BC were primarily correlated to the atmospheric lapse rate and wind speed, both during stationary and mobile campaigns. During winter stills, BC levels surpassed 10 µg/m3 at intersections and built up to 5 µg/m3 during the afternoon in the residential neighborhood (adjacent to the highway with 43,000 vehicles/day). The BC penetrated deeply into the neighborhood, where the lowest concentration was 1.8 µg/m3 within 300 m. BC concentration was highly correlated to nitrogen dioxide (r > 0.8) monitored at the local Urban Traffic Monitoring site.

Intensification of flotation separation process of residual carbon from coal gasification fine slag using ultrafine carbon particles conditioning

ABSTRACT Coal gasification fine slag (CGFS) is a high-ash product with high content of residual carbon. Flotation is a common method to separate residual carbon from CGFS. However, conventional flotation is difficult to effectively remove residual carbon due to the intimate interlock between carbon and ash components in CGFS and the developed pore structure of residual carbon. In this work, a separation method was proposed using ultrafine carbon particles during conditioning to achieve the intensification of ash-carbon flotation separation from CGFS. The flotation results showed that employing ultrafine carbon particles conditioning pulp effectively increase the removal rate of unburned carbon by nearly 20%. To investigate the mechanism of the effect of variable contents of ultrafine carbon particles on the decarburization performance of CGFS, the mercury intrusion porosimeter and a self-made laboratory attachment process observation system were used, indicating that the proposed method reduced the cumulative pore volume of CGFS from 1.27 to 1.09, a 15% decrease. During the conditioning process, the ultrafine carbon particles could follow the fluid flow into the residual carbon pores, which prevented the flotation reagent entering the pores. Thus, this avoids waste of flotation reagents and improves flotation performance.

Pulmonary translocation of ultrafine carbon particles in COPD and IPF patients

Objective Epidemiological studies indicate association between elevated air pollution and adverse health effects. Several mechanisms have been suggested, including translocation of inhaled ultrafine carbon (UFC) particles into the bloodstream. Previous studies in healthy subjects have shown no significant pulmonary translocation of UFC-particles. This study aimed to assess if UFC-particles translocate from damaged alveolar compartment in subjects suffering from chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). Methods Eleven COPD and nine IPF subjects were exposed to a 100 nm UFC-particle-aerosol labeled with Indium-111. Activity in the body was followed up for 10 days using gamma camera planar-imaging as well as in blood and urine samples. Results The pulmonary central to periphery activity ratio was significantly higher for COPD as compared to IPF subjects at exposure, 1.8 and 1.4, respectively and remained constant throughout the test period. Ten days after exposure, the estimated median pulmonary translocation of UFC particles was 22.8 and 25.8% for COPD and IPF, respectively. Bound activity was present in blood throughout the test period, peaking at 24-h postinhalation with a median concentration of 5.6 and 8.9 Bq/ml for the COPD and IPF, respectively. Median bound activity excreted in urine (% of inhaled) after 10 days was 1.4% in COPD and 0.7% in IPF. Activity accumulation in liver and spleen could not be demonstrated. Conclusions Our results suggest that UFC particles leak through the damaged alveolar barrier to the bloodstream in COPD and IPF patients probably distributing in a wide spectrum of whole-body tissues.

Lung deposited surface area of atmospheric aerosol particles at three observatories in Japan

The lung deposited surface area (LDSA) measured by diffusion charging (DC) method has been recently receiving increased attention as it is believed to accurately represent the surface reactivity of the particles, including ultrafine particles. To characterize regional and seasonal behaviors of the LDSA in the atmosphere and the factors controlling them, we measured the LDSA concentrations, using the DC method, and other physicochemical properties at three sites in Japan, including urban and rural areas. Comparisons among the three sites in the same season showed the highest LDSA concentration at the urban site Fukuoka, due to high concentrations and low particle sizes. In addition, this urban site frequently recorded high LDSA concentrations with high specific LDSAs, which represents the high contribution of ultrafine particles to the LDSA concentration. This is because the site was dominated by ultrafine black carbon particles emitted from surrounding cities, along with low contribution of long-range transported particles from the continent. In contrast, the dominance of these transported particles, which is typically observed at the three sites during this season, caused the specific LDSA to fall within a low and narrow range. However, even at rural areas, the active formation of organic particles in the summer caused high specific LDSAs, although their concentrations were low. Thus, the particles in urban areas, where ultrafine particles are probably emitted with high concentration from surrounding cities, have the potential to cause a greater adverse effect on human health even for the identical LDSA concentration. In addition, our observations showed that the LDSA of atmospheric aerosol particles measured by the DC method can be roughly represented by the theoretical LDSA of particles assuming spherical shape. Our characterizations using the specific LDSAs provide useful information for applying the LDSAs as the toxicity indicator of atmospheric aerosol particles, including ultrafine particles.

Capturing of gaseous and particulate pollutants into liquid phase by a water/oil column using microbubbles

A new method was developed to remove gaseous and particulate pollutants by capturing them in water using microbubbles. The capture efficiency of gaseous toluene and ultrafine carbon particles, which are hydrophobic substances, was remarkably improved compared to water-only conditions by adding a small amount of oily substances (4% volume fraction of water) to the water surface. The physicochemical properties of four types of oily substances were investigated. Rapeseed and mineral oil exhibited good capture efficiency during a capture experiment of high-concentration gaseous toluene for 96 h. Additionally, a long-term continuous capture experiment for 24 days revealed that the capture mechanisms of rapeseed and mineral oil were different. The toluene concentration in rapeseed oil reached saturation in the middle of the experiment while the capture efficiency of mineral oil remained constant. It was also shown that the emulsion formation greatly affected the capture of rapeseed oil. Thus, it is expected that a new gaseous pollutant treatment technology that can capture and remove gaseous/particulate pollutants regardless of their hydrophilic/hydrophobic properties could be developed in the future.

A human embryonic stem cell-based in vitro model revealed that ultrafine carbon particles may cause skin inflammation and psoriasis

Air pollution has been linked to many health issues, including skin conditions, especially in children. Among all the atmospheric pollutants, ultrafine particles have been deemed very dangerous since they can readily penetrate the lungs and skin, and be absorbed into the bloodstream. Here, we employed a human embryonic stem cell (hESC)-based differentiation system towards keratinocytes, to test the effects of ultrafine carbon particles, which mimic ambient ultrafine particles, at environment related concentrations. We found that 10 ng/mL to 10 μg/mL ultrafine carbon particles down-regulated the expression of the pluripotency marker SOX2 in hESCs. Moreover, 1 μg/mL to 10 μg/mL carbon particle treatments disrupted the keratinocyte differentiation, and up-regulated inflammation- and psoriasis-related genes, such as IL-1β, IL-6, CXCL1, CXCL2, CXCL3, CCL20, CXCL8, and S100A7 and S100A9, respectively. Overall, our results provide a new insight into the potential developmental toxicity of atmospheric ultrafine particles.

Environmental Radio‐Toxins as Possible Radio‐biomarkers for Diseases of the CNS

A hypothesis is presented identifying environmental radon (EnRn) progeny as a radio‐biomarker of use in studies of the brain and central nervous system (CNS) diseases such as Alzheimer's (AD) and Parkinson's (PD). The long‐lived environmental radon progeny, Pb‐210/Po‐210, in air and soil is a common radio‐biomarker in plants and animals. Hydrocarbon combustion in power plants and internal combustion engines produce copious quantities of ultrafine carbon particles that entrain heavy metals such as Pb‐210 found in air of the combustion process. The UFP's laden with Pb‐210 are readily taken up in the lungs and transported by the blood throughout the body including the brain and CNS. The more numerous small UFP's (<10nm) can be transferred across the blood‐brain and cellular barriers into cells where Pb‐210 is permanently deposited. The Pb+2 ions can mimic Ca+2 in brain and CNS cellular action potential systems providing a pathway into the cells and producing deleterious biochemical effects, additionally with radioactive Pb‐210 there are cellular radiation effects. Within the context of the proposed hypothesis data of diseased brain tissues containing Pb‐210/Po‐210 showed selective deposition in the brain proteins in AD and brain lipids in PD, with increased Po‐210 in MS colon tissueSupport or Funding InformationThis abstract is an end result of over 40 years of collaborative studies of environment radon progeny in humans. Collaboration among scientists from academia, government and private industry is noted.The support programs are too numerous to mention, but have been recognized in peer‐reviewed publications associated with the work.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Ultrafine particles and ozone perturb norepinephrine clearance rather than centrally generated sympathetic activity in humans

Cardiovascular risk rapidly increased following exposure to air pollution. Changes in human autonomic regulation have been implicated based on epidemiological associations between exposure estimates and indirect autonomic nervous system measurements. We conducted a mechanistic study to test the hypothesis that, in healthy older individuals, well-defined experimental exposure to ultrafine carbon particles (UFP) increases sympathetic nervous system activity and more so with added ozone (O3). Eighteen participants (age >50 years, 6 women) were exposed to filtered air (Air), UFP, and UFP + O3 combination for 3 hours during intermittent bicycle ergometer training in a randomized, crossover, double-blind fashion. Two hours following exposure, respiration, electrocardiogram, blood pressure, and muscle sympathetic nerve activity (MSNA) were recorded at supine rest, during deep breathing, and during a Valsalva manoeuvre. Catechols and inflammatory marker levels were measured in venous blood samples. Induced sputum was obtained 3.5 h after exposure. Combined exposure to UFP + O3 but not UFP alone, caused a significant increase in sputum neutrophils and circulating leucocytes. Norepinephrine was modestly increased while the ratio between plasma dihydroxyphenylglycol (DHPG) and norepinephrine levels, a marker for norepinephrine clearance, was reduced with UFP + O3. Resting MSNA was not different (47 ± 12 with Air, 47 ± 14 with UFP, and 45 ± 14 bursts/min with UFP + O3). Indices of parasympathetic heart rate control were unaffected by experimental air pollution. Our study suggests that combined exposure to modest UFP and O3 levels increases peripheral norepinephrine availability through decreased clearance rather than changes in central autonomic activity. Pulmonary inflammatory response may have perturbed pulmonary endothelial norepinephrine clearance.

Effects of neonatal inhalation exposure to ultrafine carbon particles on pathology and behavioral outcomes in C57BL/6J mice

BackgroundRecent epidemiological studies indicate early-life exposure to air pollution is associated with adverse neurodevelopmental outcomes. Previous studies investigating neonatal exposure to ambient fine and ultrafine particles have shown sex specific inflammation-linked pathological changes and protracted learning deficits. A potential contributor to the adverse phenotypes from developmental exposure to particulate matter observed in previous studies may be elemental carbon, a well-known contributor to pollution particulate. The present study is an evaluation of pathological and protracted behavioral alterations in adulthood following subacute neonatal exposure to ultrafine elemental carbon. C57BL/6J mice were exposed to ultrafine elemental carbon at 50 μg/m3 from postnatal days 4–7 and 10–13 for 4 h/day. Behavioral outcomes measured were locomotor activity, novel object recognition (short-term memory), elevated plus maze (anxiety-like behavior), fixed interval (FI) schedule of food reward (learning, timing) and differential reinforcement of low rate (DRL) schedule of food reward (impulsivity, inability to inhibit responding). Neuropathology was assessed by measures of inflammation (glial fibrillary-acidic protein), myelin basic protein expression in the corpus callosum, and lateral ventricle area.ResultsTwenty-four hours following the final exposure day, no significant differences in anogenital distance, body weight or central nervous system pathological markers were observed in offspring of either sex. Nor were significant changes observed in novel object recognition, elevated plus maze performance, FI, or DRL schedule-controlled behavior in either females or males.ConclusionThe limited effect of neonatal exposure to ultrafine elemental carbon suggests this component of air pollution is not a substantial contributor to the behavioral alterations and neuropathology previously observed in response to ambient pollution particulate exposures. Rather, other more reactive constituent species, organic and/or inorganic, gas-phase components, or combinations of constituents may be involved. Defining these neurotoxic components is critical to the formulation of better animal models, more focused mechanistic assessments, and potential regulatory policies for air pollution.

Pure ultra-fine carbon particles do not exert pro-coagulation and inflammatory effects on microvascular endothelial cells.

Pro-thrombotic and inflammatory changes play an important role in cardiovascular morbidity and mortality, resulting from short-term exposure to fine particulate air-pollution. Part of those effects has been attributed to the ultra-fine particles (UFPs) that pass through the lung and directly contact blood-exposed and circulating cells. Despite UFP-induced platelet activation, it is unclear whether the penetrated particles exert any direct effect on endothelial cells. While exposure levels are boosting as a result of world-wide increases in economic development and desertification, which create more air-polluted regions, as well as increase in demands for synthetic UFPs in medicine and various industries, further studies on the health effects of these particles are required. In this study, human pulmonary and cardiac microvascular endothelial cells (MECs) have been exposed to 0.1, 1, 10, and 100μg/ml suspensions of either a natural (carbon black) or a synthetic (multi-walled carbon nano-tubes) type of UFPs, in vitro. As a result, no changes in the levels of coagulation factor VIII, Von Willebrand factor, Interleukin 8, and P-selectin measured in the cells' supernatant were observed prior to and 6, 12, and 24h after exposure. In parallel, the spatio-temporal effect of UFPs on cardiac MECs was evaluated by Transmission Electron Microscopy. Despite phagocytic uptake of pure UFPs observed on cellular sections of the treated cells, Weibel-Palade bodies remained intact in shape and similar in number when compared with the untreated cells. Our work shows that carbon itself is a non-toxic carrier for endothelial cells.

Variations in Condensation Properties of Mixed Smoke from Biomass Burning at Different Smoke Evolution Stages

The variations in the optical-microphysical properties of the mixed wood smoke are studied in the Large Aerosol Chamber, Institute of Atmospheric Optics, Siberian Branch, Russian Academy of Sciences (volume of 1800 m3) during long-term (6-day) smoke aging under the conditions of periodic impacts of relative air humidity varying in the range 45–95%. Spectral nephelometric measurements of angular scattering and solution of the inverse problem were used to analyze the dynamics of the size distributions and complex refractive indices for ultrafine, medium-sized, and coarse fractions of particles, as well as effective particle radius, lidar scattering parameter, and single scattering albedo in the visible spectral range. It is found that both quantitative and qualitative features of the variations in the aerosol optical-microphysical parameters substantially change at different smoke aging stages as functions of air humidity. It is shown that, during aging of the mixed smoke, the key factors of the variations in smoke properties are the physical-chemical heterogeneity of three fractions of smoke particles, as well as the physical processes of coagulation migration of ultrafine black carbon particles (<100 nm in size) across the size spectrum and the condensational wetting of smoke particles. The interrelated effect (“interference”) of these processes on the particle structure determines the main features of the dynamics of the disperse composition and absorption properties of smoke particles.

Ignitability of Diesel Fuel with an Inclusion of Ultrafine Carbon Particles

Nanosize carbon fuel additions were synthesized by the action of an electric discharge on a diesel fuel. Depending on the discharge regime, variously shaped carbon particles, including planar graphitized ones, were formed in the fuel. Ignitability of the produced samples was assessed by the method of initiation of a foamed fuel sample by a lowcurrent electric arc. The modified fuel showed the improvement of the ignition characteristics in the presence of a nanodispersed solid phase.

Aerosol particle mixing state, refractory particle number size distributions and emission factors in a polluted urban environment: Case study of Metro Manila, Philippines

Ultrafine soot particles (black carbon, BC) in urban environments are related to adverse respiratory and cardiovascular effects, increased cases of asthma and premature deaths. These problems are especially pronounced in developing megacities in South-East Asia, Latin America, and Africa, where unsustainable urbanization ant outdated environmental protection legislation resulted in severe degradation of urban air quality in terms of black carbon emission. Since ultrafine soot particles do often not lead to enhanced PM10 and PM2.5 mass concentration, the risks related to ultrafine particle pollution may therefore be significantly underestimated compared to the contribution of secondary aerosol constituents. To increase the awareness of the potential toxicological relevant problems of ultrafine black carbon particles, we conducted a case study in Metro Manila, the capital of the Philippines.Here, we present a part of the results from a detailed field campaign, called Manila Aerosol Characterization Experiment (MACE, 2015). Measurements took place from May to June 2015 with the focus on the state of mixing of aerosol particles. The results were alarming, showing the abundance of externally mixed refractory particles (soot proxy) at street site with a maximum daily number concentration of approximately 15000 #/cm3. That is up to 10 times higher than in cities of Western countries. We also found that the soot particle mass contributed from 55 to 75% of total street site PM2.5. The retrieved refractory particle number size distribution appeared to be a superposition of 2 ultrafine modes at 20 and 80 nm with a corresponding contribution to the total refractory particle number of 45 and 55%, respectively. The particles in the 20 nm mode were most likely ash from metallic additives in lubricating oil, tiny carbonaceous particles and/or nucleated and oxidized organic polymers, while bigger ones (80 nm) were soot agglomerates. To the best of the authors' knowledge, no other studies reported such high number concentration of ultrafine refractory particles under ambient conditions. Inverse modeling of emission factors of refractory particle number size distributions revealed that diesel-fed public utility Jeepneys, commonly used for public transportation, are responsible for 94% of total roadside emitted refractory particle mass.The observed results showed that the majority of urban pollution in Metro Manila is dominated by carbonaceous aerosol. This suggests that PM10 or PM2.5 metrics do not fully describe possible health related effects in this kind of urban environments. Extremely high concentrations of ultrafine particles have been and will continue to induce adverse health related effects, because of their potential toxicity. We imply that in megacities, where the major fraction of particulates originates from the transport sector, PM10 or PM2.5 mass concentration should be complemented by legislative measurements of equivalent black carbon mass concentration.

Ultrafine, fine, and black carbon particle concentrations in California child-care facilities.

Although many U.S. children spend time in child care, little information exists on exposures to airborne particulate matter (PM) in this environment, even though PM may be associated with asthma and other respiratory illness, which is a key concern for young children. To address this data gap, we measured ultrafine particles (UFP), PM2.5 , PM10 , and black carbon in 40 California child-care facilities and examined associations with potential determinants. We also tested a low-cost optical particle measuring device (Dylos monitor). Median (interquartile range) concentrations for indoor UFP, gravimetric PM2.5 , real-time PM2.5 , gravimetric PM10 , and black carbon over the course of a child-care day were 14000 (11000-29000) particles/cm3 , 15 (9.6-21) μg/m3 , 15 (11-23) μg/m3 , 48 (33-73) μg/m3 , and 0.43 (0.25-0.65) ng/m3 , respectively. Indoor black carbon concentrations were inversely associated with air exchange rate (Spearman's rho=-.36) and positively associated with the sum of all Gaussian-adjusted traffic volume within a one-kilometer radius (Spearman's rho=.45) (P-values <.05). Finally, the Dylos may be a valid low-cost alternative to monitor PM levels indoors in future studies. Overall, results indicate the need for additional studies examining particle levels, potential health risks, and mitigation strategies in child-care facilities.

Ultrafine carbon particles promote rotenone-induced dopamine neuronal loss through activating microglial NADPH oxidase

BackgroundAtmospheric ultrafine particles (UFPs) and pesticide rotenone were considered as potential environmental risk factors for Parkinson's disease (PD). However, whether and how UFPs alone and in combination with rotenone affect the pathogenesis of PD remains largely unknown. MethodsUltrafine carbon black (ufCB, a surrogate of UFPs) and rotenone were used individually or in combination to determine their roles in chronic dopaminergic (DA) loss in neuron-glia, and neuron-enriched, mix-glia cultures. Immunochemistry using antibody against tyrosine hydroxylase was performed to detect DA neuronal loss. Measurement of extracellular superoxide and intracellular reactive oxygen species (ROS) were performed to examine activation of NADPH oxidase. Genetic deletion and pharmacological inhibition of NADPH oxidase and MAC-1 receptor in microglia were employed to examine their role in DA neuronal loss triggered by ufCB and rotenone. ResultsIn rodent midbrain neuron-glia cultures, ufCB and rotenone alone caused neuronal death in a dose-dependent manner. In particularly, ufCB at doses of 50 and 100μg/cm2 induced significant loss of DA neurons. More importantly, nontoxic doses of ufCB (10μg/cm2) and rotenone (2nM) induced synergistic toxicity to DA neurons. Microglial activation was essential in this process. Furthermore, superoxide production from microglial NADPH oxidase was critical in ufCB/rotenone-induced neurotoxicity. Studies in mix-glia cultures showed that ufCB treatment activated microglial NADPH oxidase to induce superoxide production. Firstly, ufCB enhanced the expression of NADPH oxidase subunits (gp91phox, p47phox and p40phox); secondly, ufCB was recognized by microglial surface MAC-1 receptor and consequently promoted rotenone-induced p47phox and p67phox translocation assembling active NADPH oxidase. ConclusionufCB and rotenone worked in synergy to activate NADPH oxidase in microglia, leading to oxidative damage to DA neurons. Our findings delineated the potential role of ultrafine particles alone and in combination with pesticide rotenone in the pathogenesis of PD.

Surface microstructure and properties of Cu-C powder metallurgical alloy induced by high-current pulsed electron beam

This paper investigates the microstructure and properties of Cu-6C powder metallurgy (PM) alloys irradiated by high-current pulse electron beam (HCPEB). After 20-pulsed HCPEB irradiation, the surface was melted completely and the remelted layer was formed in 2–3 μm thickness, which consisting of ultrafine Cu grains. Within the near irradiated surface, high-density dislocations and vacancy clusters were observed which provide a large amount of paths for carbon atoms to diffuse into Cu matrix, and it leads to the formation of the supersaturated solid solution, causing Cu lattice parameter expansion. In addition, the extreme rapid cycle generated the ultrafine carbon particles at the surface of Cu-6C metallic matrix. The results of microhardness measurements and sliding wear resistance testing indicated that the irradiated sample exhibited better properties than the initial one. The ultrafine carbon particles played an important role in the antifriction properties, which was attributed to the formation of carbonic tribolayer on the hard surface.

Structure and phase composition of deposited tantalum–carbon films

Ion plasma sputtering and the subsequent codeposition of ultrafine tantalum and carbon particles were used to prepare coatings with 4.6–71.5 at % C. Structural studies of the coatings showed the existence of carbon solid solutions in β Ta at carbon contents to 4.6 at %, carbon solid solutions in α Ta at carbon contents of 4.6–10.3 at %, and direct synthesis of TaC at carbon contents of 44.7–71.5 at %. During heat treatments to 700°C, the substantial concentration widening of regions of the existence of Ta2C and TaC was found. The lattice parameters of hexagonal Ta2C and fcc TaC carbides were determined for composition ranges of the existence of phases during heating to 700°C. Upon heating above 600°C, the progressive transition of quasiamorphous Ta2C carbide into the crystalline Ta2C carbide was found to take place. The possibility of applying the direct synthesis of TaC carbide in engineering was noted.

Aerosol–computational fluid dynamics modeling of ultrafine and black carbon particle emission, dilution, and growth near roadways

Abstract. Many studies have shown that on-road vehicle emissions are the dominant source of ultrafine particles (UFPs; diameter &lt; 100 nm) in urban areas and near-roadway environments. In order to advance our knowledge on the complex interactions and competition among atmospheric dilution, dispersion, and dynamics of UFPs, an aerosol dynamics–computational fluid dynamics (CFD) coupled model is developed and validated against field measurements. A unique approach of applying periodic boundary conditions is proposed to model pollutant dispersion and dynamics in one unified domain from the tailpipe level to the ambient near-road environment. This approach significantly reduces the size of the computational domain, and therefore allows fast simulation of multiple scenarios. The model is validated against measured turbulent kinetic energy (TKE) and horizontal gradient of pollution concentrations perpendicular to a major highway. Through a model sensitivity analysis, the relative importance of individual aerosol dynamical processes on the total particle number concentration (N) and particle number–size distribution (PSD) near a highway is investigated. The results demonstrate that (1) coagulation has a negligible effect on N and particle growth, (2) binary homogeneous nucleation (BHN) of H2SO4–H2O is likely responsible for elevated N closest to the road, and (3) N and particle growth are very sensitive to the condensation of semi-volatile organics (SVOCs), particle dry deposition, and the interaction between these processes. The results also indicate that, without the proper treatment of the atmospheric boundary layer (i.e., its wind profile and turbulence quantities), the nucleation rate would be underestimated by a factor of 5 in the vehicle wake region due to overestimated dilution. Therefore, introducing atmospheric boundary layer (ABL) conditions to activity-based emission models may potentially improve their performance in estimating UFP traffic emissions.

Ultrafine carbon particle mediated cardiovascular impairment of aged spontaneously hypertensive rats.

BackgroundStudies provide compelling evidences for particulate matter (PM) associated cardiovascular health effects. Elderly individuals, particularly those with preexisting conditions like hypertension are regarded to be vulnerable. Experimental data are warranted to reveal the molecular pathomechanism of PM related cardiovascular impairments among aged/predisposed individuals. Thus we investigated the cardiovascular effects of ultrafine carbon particles (UfCP) on aged (12–13 months) spontaneously hypertensive rats (SHRs) and compared the findings with our pervious study on adult SHRs (6–7 months) to identify age related predisposition events in cardiovascular compromised elderly individuals.MethodsAged SHRs were inhalation exposed to UfCP for 24 h (~180 μg/m3) followed by radio-telemetric assessment for blood pressure (BP) and heart rate (HR). Bronchoalveolar lavage (BAL) fluid cell differentials, interleukin 6 (IL-6) and other proinflammatory cytokines; serum C-reactive protein (CRP) and haptoglobin (HPT); and plasma fibrinogen were measured. Transcript levels of hemeoxygenase 1 (HO-1), endothelin 1 (ET1), endothelin receptors A, B (ETA, ETB), tissue factor (TF), and plasminogen activator inhibitor-1 (PAI-1) were measured in the lung and heart to assess oxidative stress, endothelial dysfunction and coagulation cascade.ResultUfCP exposed aged SHRs exhibited increased BP (4.4%) and HR (6.3%) on 1st recovery day paralleled by a 58% increase of neutrophils and 25% increase of IL-6 in the BAL fluid. Simultaneously higher CRP, HPT and fibrinogen levels in exposed SHRs indicate systemic inflammation. HO-1, ET1, ET-A, ET-B, TF and PAI-1 were induced by 1.5-2.0 folds in lungs of aged SHRs on 1st recovery day. However, in UfCP exposed adult SHRs these markers were up-regulated (2.5-6 fold) on 3rd recovery day in lung without detectable pulmonary/systemic inflammation.ConclusionsThe UfCP induced pulmonary and systemic inflammation in aged SHRs is associated with oxidative stress, endothelial dysfunction and disturbed coagulatory hemostasis. UfCP exposure increased BP and HR in aged SHRs rats which was associated with lung inflammation, and increased expression of inflammatory, vasoconstriction and coagulation markers as well as systemic changes in biomarkers of thrombosis in aged SHRs. Our study provides further evidence for potential molecular mechanisms explaining the increased risk of particle mediated cardiac health effects in cardiovascular compromised elderly individuals.