Toxicity Of PM Research Articles

Chemical Speciation of Fe and Ni in Residual Oil Fly Ash Fine Particulate Matter Using X-ray Absorption Spectroscopy

Epidemiological studies have linked residual oil fly ash fine particulate matter with aerodynamic diameter <2.5 μm (ROFA PM(2.5)) to morbidity and mortality from cardiovascular and respiratory illnesses. Bioavailable transition metals within PM have been cited as one of the components that induce such illnesses. By combining synchrotron-based X-ray absorption spectroscopy with leaching experiment, we studied the effect of residual oil compositions and combustion conditions on the speciation of Fe and Ni in ROFA PM(2.5) and the implication of these species for human health and environment. PM(2.5) samples were obtained from two types of combustors, a fire tube boiler (FTB) and a refractory line combustor (RLC). The study reveals that only Fe(2)(SO(4))(3)·nH(2)O is present in RLC PM(2.5) while Fe(2)(SO(4))(3)·nH(2)O predominates in FTB PM(2.5) with inclusion of varying amounts of nickel ferrite. The finding that RLC PM(2.5) is more bioavailable and hence more toxic than FTB PM(2.5) is significant. The reduction of toxicity of FTB PM(2.5) is due to the immobilization of a portion of Fe and Ni in the formation of an insoluble NiFe(2)O(4). This may explain the variation of toxicity from exposure to different ROFA PM(2.5). Additionally, the speciation data are sought for developing emission inventories for source apportionment study and understanding the mechanism of PM formation.

Toxicological properties of emission particles from heavy duty engines powered by conventional and bio-based diesel fuels and compressed natural gas

BackgroundOne of the major areas for increasing the use of renewable energy is in traffic fuels e.g. bio-based fuels in diesel engines especially in commuter traffic. Exhaust emissions from fossil diesel fuelled engines are known to cause adverse effects on human health, but there is very limited information available on how the new renewable fuels may change the harmfulness of the emissions, especially particles (PM). We evaluated the PM emissions from a heavy-duty EURO IV diesel engine powered by three different fuels; the toxicological properties of the emitted PM were investigated. Conventional diesel fuel (EN590) and two biodiesels were used − rapeseed methyl ester (RME, EN14214) and hydrotreated vegetable oil (HVO) either as such or as 30% blends with EN590. EN590 and 100% HVO were also operated with or without an oxidative catalyst (DOC + POC). A bus powered by compressed natural gas (CNG) was included for comparison with the liquid fuels. However, the results from CNG powered bus cannot be directly compared to the other situations in this study.ResultsHigh volume PM samples were collected on PTFE filters from a constant volume dilution tunnel. The PM mass emission with HVO was smaller and with RME larger than that with EN590, but both biofuels produced lower PAH contents in emission PM. The DOC + POC catalyst greatly reduced the PM emission and PAH content in PM with both HVO and EN590. Dose-dependent TNFα and MIP-2 responses to all PM samples were mostly at the low or moderate level after 24-hour exposure in a mouse macrophage cell line RAW 264.7. Emission PM from situations with the smallest mass emissions (HVO + cat and CNG) displayed the strongest potency in MIP-2 production. The catalyst slightly decreased the PM-induced TNFα responses and somewhat increased the MIP-2 responses with HVO fuel. Emission PM with EN590 and with 30% HVO blended in EN590 induced the strongest genotoxic responses, which were significantly greater than those with EN590 + cat or 100% HVO. The emission PM sample from the CNG bus possessed the weakest genotoxic potency but had the strongest oxidative potency of all the fuel and catalyst combinations. The use of 100% HVO fuel had slightly weaker and 100% RME somewhat stronger emission PM induced ROS production, when compared to EN590.ConclusionsThe harmfulness of the exhaust emissions from vehicle engines cannot be determined merely on basis of the emitted PM mass. The study conditions and the engine type significantly affect the toxicity of the emitted particles. The selected fuels and DOC + POC catalyst affected the PM emission from the heavy EURO IV engine both qualitative and quantitative ways, which influenced their toxicological characteristics. The plain HVO fuel performed very well in emission reduction and in lowering the overall toxicity of emitted PM, but the 30% blend of HVO in EN590 was no better in this respect than the plain EN590. The HVO with a DOC + POC catalyst in the EURO IV engine, performed best with regard to changes in exhaust emissions. However some of the toxicological parameters were significantly increased even with these low emissions.

Influence of soil ageing on bioavailability and ecotoxicity of lead carried by process waste metallic ultrafine particles

Ultrafine particulate matters enriched with metals are emitted into the atmosphere by industrial activities and can impact terrestrial and aquatic ecosystems. Thus, this study investigated the environmental effects of process particles from a lead-recycling facility after atmospheric deposition on soils and potential run-off to surface waters. The toxicity of lead-enriched PM for ecosystems was investigated on lettuce and bacteria by (i) germination tests, growth assays, lead transfer to plant tissues determination and (ii) Microtox analysis. The influence of ageing and soil properties on metal transfer and ecotoxicity was studied using three different soils and comparing various aged, spiked or historically long-term polluted soils. Finally, lead availability was assessed by 0.01 M CaCl 2 soil extraction. The results showed that process PM have a toxic effect on lettuce seedling growth and on Vibrio fischeri metabolism. Soil–PM interactions significantly influence PM ecotoxicity and bioavailability; the effect is complex and depends on the duration of ageing. Solubilisation or stabilisation processes with metal speciation changes could be involved. Finally, Microtox and phytotoxicity tests are sensitive and complementary tools for studying process PM ecotoxicity.

Concentration and Photochemistry of PAHs, NPAHs, and OPAHs and Toxicity of PM2.5 during the Beijing Olympic Games

Atmospheric particulate matter with diameter <2.5 um (PM(2.5)) was collected at Peking University (PKU) in Beijing, China before, during, and after the 2008 Olympics and analyzed for black carbon (BC), organic carbon (OC), lower molecular weight (MW < 300) and MW302 Polycyclic Aromatic Hydrocarbons (PAHs), nitrated PAHs (NPAHs) and oxygenated PAHs (OPAHs). In addition, the direct and indirect acting mutagenicity of the PM(2.5) and the potential for DNA damage to human lung cells were also measured. Significant reductions in BC (45%), OC (31%), MW< 300 PAH (26-73%), MW 302 PAH (22-77%), NPAH (15-68%), and OPAH (25-53%) concentrations were measured during the source control and Olympic periods. However, the mutagenicity of the PM(2.5) was significantly reduced only during the Olympic period. The PAH, NPAH, and OPAH composition of the PM(2.5) was similar throughout the study, suggesting similar sources during the different periods. During the source control period, the parent PAH concentrations were correlated with NO, CO, and SO(2) concentrations, indicating that these PAHs were associated with both local and regional emissions. However, the NPAH and OPAH concentrations were only correlated with the NO concentrations, indicating that the NPAH and OPAH were primarily associated with local emissions. The relatively high 2-nitrofluoranthene/1-nitropyrene ratio (25-46) and 2-nitrofluoranthene/2-nitropyrene ratio (3.4-4.8), suggested a predominance of photochemical formation of NPAHs through OH-radical-initiated reactions in the atmosphere. On average, the ∑NPAH and ∑OPAH concentrations were 8% of the parent PAH concentrations, while the direct-acting mutagenicity (due to the NPAH and OPAH) was 200% higher than the indirect-acting mutagenicity (due to the PAH). This suggests that NPAH and OPAH make up a significant portion of the overall mutagenicity of PM(2.5) in Beijing.

Effect of Advanced Aftertreatment for PM and NOx Reduction on Heavy-Duty Diesel Engine Ultrafine Particle Emissions

Four heavy-duty and medium-duty diesel vehicles were tested in six different aftertreament configurations using a chassis dynamometer to characterize the occurrence of nucleation (the conversion of exhaust gases to particles upon dilution). The aftertreatment included four different diesel particulate filters and two selective catalytic reduction (SCR) devices. All DPFs reduced the emissions of solid particles by several orders of magnitude, but in certain cases the occurrence of a volatile nucleation mode could increase total particle number emissions. The occurrence of a nucleation mode could be predicted based on the level of catalyst in the aftertreatment, the prevailing temperature in the aftertreatment, and the age of the aftertreatment. The particles measured during nucleation had a high fraction of sulfate, up to 62% of reconstructed mass. Additionally the catalyst reduced the toxicity measured in chemical and cellular assays suggesting a pathway for an inverse correlation between particle number and toxicity. The results have implications for exposure to and toxicity of diesel PM.

Spatial and Temporal Variability of Coarse (PM10−2.5) Particulate Matter Concentrations in the Los Angeles Area

Recent epidemiological and toxicological studies suggest that coarse particulate matter (CPM, particles smaller than 10 and larger than 2.5 μm in diameter, PM 10−2.5 ) concentrations may be associated with adverse health outcomes at levels similar to or larger than those associated with PM 2.5 concentrations. CPM may consist of several, mechanically generated, potentially toxic components, including re-suspended road dust, industrial materials, trace metals, and bio-aerosols. In an effort to better understand and quantify the linkage between sources, composition and the toxicity of coarse PM, 10 sampling sites were set-up in the Los Angeles area. Sites within this diverse monitoring network were selected to encompass urban, rural, coastal, inland, near-freeway, community-based, upwind pollutant “source” and downwind pollutant “receptor” sites to fully characterize the range of likely conditions. At each location, a 24 h time-integrated coarse PM sample was collected once per week for one year in order to ...

Mouse lung inflammation after instillation of particulate matter collected from a working dairy barn

Coarse and fine particulate matter (PM 2.5–10 and PM 2.5, respectively) are regulated ambient air pollutants thought to have major adverse health effects in exposed humans. The role of endotoxin and other bioaerosol components in the toxicity of PM from ambient air is controversial. This study evaluated the inflammatory lung response in mice instilled intratracheally with PM 2.5–10 and PM 2.5 emitted from a working dairy barn, a source presumed to have elevated concentrations of endotoxin. PM 2.5–10 was more pro-inflammatory on an equal weight basis than was PM 2.5; both fractions elicited a predominantly neutrophilic response. The inflammatory response was reversible, with a peak response to PM 2.5–10 observed at 24 h after instillation, and a return to control values by 72 h after instillation. The major active pro-inflammatory component in whole PM 2.5–10, but not in whole PM 2.5, is heat-labile, consistent with it being endotoxin. A heat treatment protocol for the gradual inactivation of biological materials in the PM fractions over a measurable time course was developed and optimized in this study using pure lipopolysaccharide (LPS) as a model system. The time course of heat inactivation of pure LPS and of endotoxin activity in PM 2.5–10 as measured by Limulus bioassay is identical. The active material in both PM 2.5–10 and PM 2.5 remained in the insoluble fraction when the whole PM samples were extracted with physiological saline solution. Histological analysis of lung sections from mice instilled with PM 2.5–10 or PM 2.5 showed evidence of inflammation consistent with the cellular responses observed in lung lavage fluid. The major pro-inflammatory components present in endotoxin-rich PM were found in the insoluble fraction of PM 2.5–10; however, in contrast with PM 2.5–10 isolated from ambient air in the Central Valley of California, the active components in the insoluble fraction were heat-labile.

The relationship between physicochemical characterization and the potential toxicity of fine particulates (PM 2.5) in Shanghai atmosphere

Fine particulate matter with aerodynamic diameter less than 2.5 μm (PM 2.5) was collected at urban and suburban sites in Shanghai from April 2005 to March 2006. Average mass concentrations of PM 2.5 ranged from 43.5 to 149 μg m −3 in the urban area and 21.7 to 159 μg m −3 in suburban area. The mass levels of PM 2.5 sampled at urban and suburban sites showed seasonal variation with much higher values in winter and spring, lower values in summer, and the lowest in autumn. The results of environmental scanning electron microscopy (ESEM) showed that Shanghai PM 2.5 was consisted of soot aggregates, coal fly ashes, minerals, bio-particles and unidentified particles. Inductively coupled plasma atomic mission spectrum (ICP-AES) results showed total elements in Shanghai PM 2.5 increased gradually from summer to winter and remained at a relatively high level in spring. There was a significant difference in the mass of elements in PM 2.5 collected in urban and in suburban atmosphere. Enrichment factor (EF) analysis results demonstrated that K, Na, Ca, Mg, Al, Fe, Ba and Sr originated from natural sources, while As, Cu, Zn, Pb, Cd, Mn, Ni and Se were emitted from anthropogenic sources. The plasmid DNA assay showed that potential toxicity of Shanghai PM 2.5 collected at urban and suburban sampling sites, and in different seasons, varied greatly. Toxicity of the Shanghai urban winter PM 2.5 sample was much stronger compared to any of the other samples. Heavy metals in Shanghai PM 2.5, including Cu, Zn, Pb, Cd, Cr, Mn, and Ni, might have synergic-effects on plasmid DNA damage.

Cellular evaluation of the toxicity of combustion derived particulate matter: influence of particle grinding and washing on cellular response

There is increasing interest in continual monitoring of air for the presence of inhalation health hazards, such as particulate matter, produced through combustion of fossil fuels. Currently there are no means to rapidly evaluate the relative toxicity of materials or to reliably predict potential health impact due to the complexity of the composition, size, and physical properties of particulate matter. This research evaluates the feasibility of utilizing cell cultures as the biological recognition element of an inhalation health monitoring system. The response of rat lung type II epithelial (RLE-6TN) cells to a variety of combustion derived particulates and their components has been evaluated. The focus of the current work is an evaluation of how particles are delivered to a cellular sensing array and to what degree does washing or grinding of the particles impacts the cellular response. There were significant differences in the response of these lung cells to PM’s of varying sources. Mechanical grinding or washing was found to alter the toxicity of some of these particulates; however these effects were strongly dependent on the fuel source. Washing reduced toxicity of oil PM’s, but had little effect on those from diesel or coal. Mechanical grinding could significantly increase the toxicity of coal PM’s, but not for oil or diesel.

Evaluation of micronucleus induction of sand dust storm fine particles (PM 2.5) in human blood lymphocytes

Sand dust storms are common phenomena in the arid and semi-arid regions. Previous studies have demonstrated that the airborne air fine particulate matter (PM 2.5, particulates with an aerodynamic diameter ≤2.5 μm) and its extracts can induce human genetic damage of lymphocytes such as micronucleus formation, chromosomal aberration and so on. However, little is known about the health risks associated with sand dust storm PM 2.5 and its extracts. The aim of the present study is to investigate the micronucleus induction of sand dust storm PM 2.5 (include its organic and inorganic extract) from two different towns on human lymphocytes. The samples of normal PM 2.5 and sand dust storm PM 2.5 were collected in Wuwei (Gansu Province) and Baotou (Inner Mongolia), China. The cytochalasin-B cytokinesis-block test was employed and the cells were treated with 0, 33, 100, 300 μg ml −1 sand dust storm PM 2.5 or normal ambient air PM 2.5 suspension (physiological saline as solvent control), or inorganic extract (0, 75, 150, 300 μg ml −1, physiological saline as solvent control) or organic extract (0, 20, 40, 80 μg ml −1, DMSO as solvent control) at the beginning of the cell culture. Both sand dust storm and normal PM 2.5 and their extract treatment cultures revealed an increase in the frequency of micronucleus. With the increase of treatment concentrations the frequency of micronucleus increased and the nuclear division index (NDI) values declined in a dose–response manner ( P < 0.01). In the same concentrates, the frequency of micronucleus of normal ambient air PM 2.5 and its extract were significant higher than those of sand dust storm PM 2.5 ( P < 0.01) except the treatment of Wuwei sample at higher doses, the treatment of inorganic extract of PM 2.5 at the highest dose (300 μg ml −1) and the treatment of organic extract of PM 2.5 at the higher dose (40 and 80 μg ml −1) either in Baotou or in Wuwei ( P > 0.05). The toxicity of sand dust storm PM 2.5 and its extract at high dose is very potent. The frequency of micronucleus of normal PM 2.5 (include its organic extract) from Baotou were higher than those of Wuwei especially in low and middle dose ( P < 0.05), but the treatment results of sand dust storm PM 2.5 (include its all extract) was not significantly different between the towns ( P > 0.05).

Effects of Concentrated Ambient Particles on Heart Rate Variability in Spontaneously Hypertensive Rats

In the present study, the cardiovascular toxicity of PM(2.5) was determined in spontaneously hypertensive (SH) rats using the standard deviation of normal-to-normal intervals (SDNN) and root mean square of successive differences of adjacent normal-to-normal intervals (RMSSD) as outcome measurements. Four SH rats implanted with radiotelemetry transmitters were repeatedly exposed to concentrated PM(2.5) in nose-only exposure chambers. Gravimetric analysis revealed the mean post-concentrating mass concentration of particles during the 5 h of exposure was 202 mug/m(3). Using each animal as its own control and linear mixed-effects model, to adjust for circadian nature and individual differences, we found that SDNN decreased by 15% initially then gradually decreased to 60% of the initial value at the end of exposure. Our results indicate that concentrated PM(2.5) may decrease SDNN on SH rats during PM exposure. The study also showed that SDNN is more sensitive to PM induced effects than RMSSD.

Toxicity of tire debris extracts on human lung cell line A549

TD, produced by tire wear, is a significant constituent of PM 10 in urban areas where traffic related emissions are predominant. TD contains a lot of chemicals which can affect human respiratory system and it has received little attention until now, even the toxicity of PM has been extensively documented. A549 cells, a human alveolar lung cells, were exposed for 24, 48, 72 h to 10, 50, 60, 75 μg/ml of TD organic extract. MTT and Trypan Blue assays were used to evaluate cytotoxicity and Comet Assay to evidence DNA damage. TD extracts induced a dose-dependent increase in cell mortality and DNA damage. A significant toxicity was observed when cells were exposed to 60 μg/ml for 72 h. Moreover cell morphology observed at ultra structural level, was severely affected at the highest dose.

Oil fly ash-induced elevation of plasma fibrinogen levels in rats.

Particulate matter air pollution (PM) has been associated with morbidity and mortality from ischemic heart disease and stroke in humans. It has been hypothesized that alveolar inflammation, resulting from exposure to PM, may induce a state of blood hypercoagulability, triggering cardiovascular events in susceptible individuals. Previous studies in our laboratory have demonstrated acute lung injury with alveolar inflammation in rats following exposure to residual oil fly ash (ROFA), an emission source particulate. In addition, increased mortality has been documented following exposure to ROFA in rats with preexistent cardiopulmonary disease. ROFA's toxicity derives from its soluble metal content, which appears also to drive the toxicity of ambient PM. The present study was conducted to test the hypothesis that exposure of rats to a toxic PM, like ROFA, would adversely alter hemostatic parameters and cardiovascular risk factors thought to be involved in human epidemiologic findings. Sixty-day-old male Sprague-Dawley rats were exposed by intratracheal instillation (IT) to varying doses (0.3, 1. 7, or 8.3 mg/kg) of ROFA, 8.3 mg/kg Mt. Saint Helen's volcanic ash (MSH, control particle), or 0.3 ml saline (SAL, control). At 24 h post-IT, activated partial thromboplastin time (APTT), prothrombin time (PT), plasma fibrinogen (PF), plasma viscosity (PV), and complete blood count (CBC) were performed on venous blood samples. No differences from control were detected in APTT and PT in ROFA-exposed rats; however, ROFA exposure did result in elevated PF, at 8.3 mg/kg only. In addition, PV values were elevated in both ROFA and MSH-exposed rats relative to SAL-control rats, but not significantly. Although no changes were detected in APTT and PT, alteration of important hematologic parameters (notably fibrinogen) through PM induction of an inflammatory response may serve as biomarkers of cardiovascular risk in susceptible individuals.

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.

Partial nodular transformation of the liver with patent ductus venosus: J.S. Lentz, I.R. Wanless, E.A. Roberts, Dept. of Pathology, Toronto Western Hospital, and Division of Gastroenterology, Hospital for Sick Children, University of Toronto, Toronto, M5T 2S8

Polygonum multiflorum Thunb.(PM), (known as Heshouwu (何首乌) in China) is one of the most important and well mentioned Chinese medicinal herbs in the literature for its use in blackening hair, nourishing liver and kidney, anti-aging, anti-hyperlipidemia, antioxidant, anti-inflammatory, anticancer, hepatoprotection, cardio-protection and improving age-related cognitive dysfunction. The purpose of this review is to give a comprehensive and recent update on PM: new compounds or isolated for the first time, potential hepatotoxic compounds and their mechanisms. Moreover, future perspectives and challenges in the future study of this plant are conversed which will make a new base for further study on PM.A comprehensive review of relevant published literature on PM using the scientific databases SCOPUS, PubMed, and Science Direct was done.PM is broadly produced in many provinces of China and well known in other Eastern Asian Countries for its ethno-medical uses. Previous phytochemical investigation of PM had led to the isolation of more than 175 compounds including recently isolated 70 new compounds. Most of the new compounds isolated after 2015 are majorly dianthrone glycosides and stilbene glycosides. Processing has also a significant effect on chemical composition, pharmacological activities, and toxicity of PM. PM-induced liver injury is increasing after the first report in Hong Kong in 1996. Hepatotoxicity of PM was constantly reported in Japan, Korea, China, Australia, Britain, Italy, and other countries although its toxicity is related to idiosyncratic hepatotoxicity. More interestingly, although there is indispensable interest to predict idiosyncratic hepatotoxicity of PM and understand its mechanisms, the responsible hepatotoxic compounds and mechanisms of liver damage induced by PM are still not clear. There is a big controversy on the identification of the most responsible constituent. Anthraquinone and stilbene compounds in PM, mainly emodine and TSG are mentioned in the literature to be the main responsible hepatotoxic compounds. However, comparing the two compounds, which one is the more critical toxic agent for PM-induced hepatotoxicity is not well answered. Affecting different physiological and metabolic pathways such as oxidative phosphorylation and TCA cycle pathway, metabolic pathways, bile acid excretion pathway and genetic polymorphisms are among the mechanisms of hepatotoxicity of PM.Deeper and effective high throughput experimental studies are still research hotspots to know the most responsible constituent and the mechanism of PM-induced hepatotoxicity.