Urban Air Particulate Matter Research Articles

An investigation into the relationship between the major chemical components of particulate matter in urban air

Particulate matter (PM) generally comprises such chemical components as inorganic ions, organic carbon (OC), elemental carbon (EC), and metals. In terms of environmental studies, these major chemical components of particulate matter (MCP) are important in understanding PM distribution, behaviors and source apportionment. In this study, the MCP fractions of total suspended particles (TSP) were measured at an urban residential area in Seoul, Korea from February to December in 2009. The behavior of each individual MCP was studied in order to explain their relationship to environmental conditions and sources. The MCP measured during this study period was able to account between 54% (spring) to 67% (fall) of total TSP composition. During the study period, it was found that the TSP sampled comprised mostly: anions, OC, cations, EC, and metals in decreasing order of abundance. Although such relative ordering seems to remain fairly constant over time, the relative balance of this relationship may be altered by variations in environmental conditions.

Ecotoxicological characterisation of exhaust particulates from diesel-powered light-duty vehicles

Abstract Diesel exhaust is one of the major sources of fine and ultrafine particulate matter in urban air. Toxicity of diesel-powered engine emissions has been quite widely assessed, however, much less information is available on their ecotoxicity. In our study the kinetic version of the Vibrio fischeri bioluminescence inhibition bioassay, based on the ISO 21338:2010 standard, was used to characterise the ecotoxicity of diesel-powered cars. The method is sensitive enough to test the ecotoxic effect of the emission of individual vehicles. In general, significant positive correlation was found between ecotoxicity (expressed as Toxic Unit /TU/values) and total carbon (TC) as well as between TU and polycyclic aromatic hydrocarbon (PAH) concentrations.

Background concentrations of xerophilic fungi and particulate matter in urban air

Aim: In the present study the background spore concentrations of airborne culturable xerophilic fungi and particulate matter of 0.3-10.0 µm were evaluated in the urban air. Also, the concentrations...

Ecotoxicity and genotoxicity assessment of exhaust particulates from diesel-powered buses

Diesel exhaust is one of the major sources of fine and ultra-fine particulate matter in urban air. Toxicity of diesel-powered engine emissions has been quite widely assessed; however, much less information is available on their ecotoxicity. In our study, the kinetic version of the Vibrio fischeri bioluminescence inhibition bioassay based on the ISO 21338:2010 standard was used to characterise the ecotoxicity of diesel-powered buses. It is a direct contact test in which solid samples are tested in suspension and test organisms are in direct contact with toxic particles. The age of the selected buses fell into a wide range; the oldest one was produced in 1987. Diesel engines of different emission standards (Euro0-Euro4) were included. Measured EC50 values of Euro0-Euro1 engine emissions fell into the same range, 1.24-0.96μgml(-1), respectively. On the contrary, emission of Euro4 vehicle proved to be non-toxic. Genotoxic potential of the samples was also estimated, using the colorimetric SOS-chromotest™. Genotoxicity was detected also for Euro0 and Euro1 buses, showing correlation with the ecotoxic potential. The fact that the particulates from Euro4 vehicles did not show ecotoxic/genotoxic effect implies that replacing old Euro1 and Euro2 buses can be a highly effective solution for reducing environmental hazard of automotive emissions. The whole-aerosol testing method is a cheap alternative that can be used in engine developments and emission control.

Persistent activation of DNA damage signaling in response to complex mixtures of PAHs in air particulate matter

Complex mixtures of polycyclic aromatic hydrocarbons (PAHs) are present in air particulate matter (PM) and have been associated with many adverse human health effects including cancer and respiratory disease. However, due to their complexity, the risk of exposure to mixtures is difficult to estimate. In the present study the effects of binary mixtures of benzo[a]pyrene (BP) and dibenzo[a,l]pyrene (DBP) and complex mixtures of PAHs in urban air PM extracts on DNA damage signaling was investigated. Applying a statistical model to the data we observed a more than additive response for binary mixtures of BP and DBP on activation of DNA damage signaling. Persistent activation of checkpoint kinase 1 (Chk1) was observed at significantly lower BP equivalent concentrations in air PM extracts than BP alone. Activation of DNA damage signaling was also more persistent in air PM fractions containing PAHs with more than four aromatic rings suggesting larger PAHs contribute a greater risk to human health. Altogether our data suggests that human health risk assessment based on additivity such as toxicity equivalency factor scales may significantly underestimate the risk of exposure to complex mixtures of PAHs. The data confirms our previous findings with PAH-contaminated soil (Niziolek-Kierecka et al., 2012) and suggests a possible role for Chk1 Ser317 phosphorylation as a biological marker for future analyses of complex mixtures of PAHs.

Acute systemic and lung inflammation in C57Bl/6J mice after intratracheal aspiration of particulate matter from small-scale biomass combustion appliances based on old and modern technologies

Inflammation is regarded as an important mechanism behind mortality and morbidity experienced by cardiorespiratory patients exposed to urban air particulate matter (PM). Small-scale biomass combustion is an important source of particulate air pollution. In this study, we investigated association between inflammatory responses and chemical composition of PM1 emissions from seven different small-scale wood combustion appliances representing old and modern technologies. Healthy C57Bl/6J mice were exposed by intratracheal aspiration to single dose (10 mg/kg) of particulate samples. At 4 and 18 h after the exposure, bronchoalveolar lavage fluid (BALF) as well as serum was collected for subsequent analyses of inflammatory indicators (interleukin (IL)-6, IL-1β, IL-12, and IL-10; tumor necrosis factor-α (TNF-α); keratinocyte-derived chemoattractant (KC), and interferon-γ (IFN-γ)) in multiplexing assay. When the responses to the PM1 samples were compared on an equal mass basis, the PM from modern technology appliances increased IL-6, KC, and IL-1β levels significantly in BALF at 4 and 18 h after the exposure. In contrast, these responses were seen only at 4 h time point in serum. Increased cytokine concentrations correlated with metal-rich ash related compounds which were more predominant in the modern technology furnaces emissions. These particles induced both local and systemic inflammation. Instead, polycyclic hydrocarbon (PAH) rich PM1 samples from old technology (OT) evoked only minor inflammatory responses. In conclusion, the combustion technology largely affects the toxicological and chemical characteristics of the emissions. The large mass emissions of old combustion technology should be considered, when evaluating the overall harmfulness between the appliances. However, even the small emissions from modern technologies may pose significant toxic risks.

The concentrations of culturable microorganisms in relation to particulate matter in urban air

The ambient air consists not only of gases but also of bioaerosols and particulate matter. The concentrations of particulate matter in relation to the culturable microorganisms in the urban ambient air and their dependence on air temperature and relative humidity were investigated. The seasonal distribution of particles sizes, the concentrations of aerobic mesophilic bacteria and xerophilic fungi in the air were evaluated. Moreover, the identification of the fungal genera Cladosporium, Aspergillus and Penicillium were conducted.Within one year at 177 days particle and microorganism concentrations in the ambient air were recorded in the city centre of Graz/Austria.The results show that the concentrations of fine particles and coarse particles were the highest in winter and decreased continuously to a minimum in the summer months depending on temperature and air humidity. The concentrations of xerophilic fungi showed no correlation to the different particle concentrations. The spore concentrations of Cladosporium spp. showed the same results of xerophilic fungi whereas the genera Penicillium and Aspergillus increased with the increase of fine particles. The concentrations of mesophilic bacteria were positively correlated with all particle counts. The maximum mesophilic bacteria concentrations were found in the winter months.Further studies are required to evaluate the concentrations of specific microorganisms in the natural environment in relation to the particulate matter.

Environmental impacts of rapid urbanization in China: a showcase of recent research developments

Urbanization is taking an unprecedented rate in China, and it is projected that some 350 million people will be added to the country’s urban population by 2025, and 1 billion people will live in Chinese cities by 2030 (Zhu et al. 2011). For the first time in history, China will have over 50 % of its 1.3 billion population living in cities this year. This is remarkable for China, an ancient and more agriculturebased civilization. In many ways, urbanization will improve the quality of sanitary conditions, better health care systems, the efficiency of public transport, and will provide the population with more access to modern civilization. However, it is also clear that urbanization will, in the same time, bring many negative impacts on the environment and human health, as recently highlighted by Zhu et al. (2011). To overcome the negative environmental impacts of rapid urbanization in China is becoming one of the major themes of environmental studies in China. Urban ecosystem is human-dominated, and the changes in environmental quality and the health of urban ecosystems are largely driven and determined by concentrated human consumption of energy and natural resources. In this special issue, we publish 11 papers to illustrate some of the recent endeavors in investigating the status of urban environmental quality and the impacts of urbanization on environmental changes, as well as technologies to mitigate the negative impacts of urbanization. Two review papers are included in this issue, one by Guo-Ping Sheng provides an overview on wastewater discharge and urbanization in China, and the other one by Chen et al. provides Chinese perspectives of sewage sludge utilization. Four papers examined the current status of environmental quality, such as the occurrence of micropollutants (perfluoroalkyl and estrogenic compounds), sediment quality in urban river systems, particulate matter in urban air, etc. The paper by Jun Yang addresses the issue of aquatic ecosystem health by looking at algal community and trophic state. One paper (by Xinhu Li) looks at the spatial features of the relationship between human health and urbanization. There are also two papers which report some new technological developments that help lessen these environmental problems. In recent years, publications related to “urbanization and China” have increased dramatically, from 21 in 2000 to 337 in 2010 (Web of Science, accessed on 11 March 2012). Therefore, by no means will this special issue provide a full picture of urban environmental studies in China; rather, it serves as a window to showcase the recent developments in urban environmental studies.

Seasonal variability of bacteria in fine and coarse urban air particulate matter

The current knowledge about the microbial communities associated with airborne particulate matter, particularly in urban areas, is limited. This study aims to fill this gap by describing the microbial community associated with coarse (PM10) and fine (PM2.5) particulate matter using pyrosequencing. Particulate matter was sampled on Teflon filters over 3 months in summer and 3 months in winter in Milan (Italy), and the hypervariable V3 region of the gene 16S rRNA amplified from the DNA extracted from the filters. The results showed large seasonal variations in the microbial communities, with plant-associated bacteria dominating in summer and spore-forming bacteria in winter. Bacterial communities from PM10 and PM2.5 were also found to differ from each other by season. In all samples, a high species richness, comparable with that of soils, but a low evenness was found. The results suggest that not only can the sources of the particulate influence the presence of specific bacterial groups but also that environmental factors and stresses can shape the bacterial community.

Airborne Particles in Swansea, UK: Their Collection and Characterization

Urban air particulate matter (PM) has previously been associated with a variety of adverse health effects. It is now believed that the smallest particles, ultrafine or nanoparticles, are linked to the greatest health effects. The physicochemistry of these particles is likely to provide information regarding their toxicity. Therefore, the aim of this study was to further the understanding of the heterogeneous and changing particle concentrations in urban air, in conjunction with gaining an understanding of the physicochemistry of the particles. A Dekati electrical low-pressure impactor was used to collect the particles and real-time data in a busy traffic corridor in Swansea, Wales, over a period of 10 nonconsecutive weeks. Particle concentrations in the street canyon were analyzed and particle physicochemistries investigated using a variety of techniques. Particle number concentrations were found to vary both diurnally and from day to day in the traffic corridor. Of all particles, the nano to fine size fraction was consistently identified in the highest concentrations (maximum: 140,000 particles cm−3). Particle physicochemistry was found to vary as a function of size, with larger particles exhibiting a greater variety of morphologies (and consequently particle types) and associated metals.

Oxidative damage induced by carcinogenic polycyclic aromatic hydrocarbons and organic extracts from urban air particulate matter

We investigated the role of oxidative damage in the mechanism of action of selected individual carcinogenic PAHs (c-PAHs: benzo[ a]pyrene, B[ a]P; dibenzo[ a, l]pyrene, DB[ a, l]P), an artificial mixture of c-PAHs (c-PAHs mix) and extractable organic matter (EOM) from urban air particulate matter (PM). Two cell lines (human hepatoma cells, HepG2; human diploid lung fibroblasts, HEL) were treated for 24 and 48 h with various concentrations of compounds and mixtures. A panel of oxidative stress markers included 8-oxodeoxyguanosine (8-oxodG), 15-F 2t-isoprostane (15-F 2t-IsoP) and protein carbonyl groups. The response of the cell lines to the test compounds was substantially different. In HepG2 cells, oxidative damage to DNA was generally not induced by individual c-PAHs and the c-PAHs mix, but EOM increased 8-oxodG levels in these cells. In HEL cells, none of the compounds induced oxidative DNA damage. Lipid peroxidation, measured as the level of 15-F 2t-IsoP, was induced by c-PAHs in HepG2 cells only after 48 h of incubation, while the effect of EOM was detected already after 24 h. In HEL cells, individual c-PAHs and the c-PAH mix generally decreased 15-F 2t-IsoP levels. This effect was even stronger for EOM treatment. Protein oxidation, assessed as carbonyl levels in cell lysates, was not induced after 24 h of treatment with any compound in either cell line. Individual c-PAHs and the c-PAH mix generally induced protein oxidation in both cell lines after 48 h treatment, with the exception of DB[ a, l]P in HepG2 cells. Oxidative damage to proteins caused by EOM was generally increased in HepG2 cells after 48 h of incubation, while in HEL cells the effect was observed for only one dose of EOM. In summary, our results demonstrate the ability of EOM to induce oxidative damage to DNA and lipids after 24 h of treatment, and to proteins after 48 h, in HepG2 cells, while the effect of c-PAHs was substantially less. The induction of oxidative stress by c-PAHs and EOM in HEL cells was weak.

Modest vasomotor dysfunction induced by low doses of C60 fullerenes in apolipoprotein E knockout mice with different degree of atherosclerosis

BackgroundExposure to small size particulate matter in urban air is regarded as a risk factor for cardiovascular effects, whereas there is little information about the impact on the cardiovascular system by exposure to pure carbonaceous materials in the nano-size range. C60 fullerenes are nano-sized particles that are expected to have a widespread use, including cosmetics and medicines.MethodsWe investigated the association between intraperitoneal injection of pristine C60 fullerenes and vasomotor dysfunction in the aorta of 11–13 and 40–42 weeks old apolipoprotein E knockout mice (apoE-/-) with different degree of atherosclerosis.ResultsThe aged apoE-/-mice had lower endothelium-dependent vasorelaxation elicited by acetylcholine in aorta segments mounted in myographs and the phenylephrine-dependent vasoconstriction response was increased. One hour after an intraperitoneal injection of 0.05 or 0.5 mg/kg of C60 fullerenes, the young apoE-/- mice had slightly reduced maximal endothelium-dependent vasorelaxation. A similar tendency was observed in the old apoE-/- mice. Hampered endothelium-independent vasorelaxation was also observed as slightly increased EC50 of sodium nitroprusside-induced vasorelaxation response in young apoE-/- mice.ConclusionTreatment with C60 fullerenes affected mainly the response to vasorelaxation in young apoE-/- mice, whereas the vasomotor dysfunction in old apoE-/- mice with more advanced atherosclerosis was less affected by acute C60 fullerene treatment. These findings represent an important step in the hazard characterization of C60 fullerenes by showing that intraperitoneal administration is associated with a moderate decrease in the vascular function of mice with atherosclerosis.

Inflammation and short-term cardiopulmonary effects of particulate matter

Correlations between short-term exposures to urban air particulate matter (PM) and increased morbidity and mortality for various cardiopulmonary diseases have been explained by the pro-inflammatory and pro-thrombotic effects of PM. This review updates a recent one by Scapellato and Lotti () and discusses the correlations between PM exposures, inflammatory endpoints and functional changes. Panel studies and controlled exposures to PM of various sizes in either healthy individuals, asthmatics and patients with coronary heart diseases, do not provide strong evidence of an inflammatory pathophysiology of PM toxicities. Contradictory results among reviewed studies could be explained by difficulties in dissecting inflammation brought about by PM from that of the ongoing diseases. However, other mechanisms, such as neurological ones, might be more relevant and co-exist with inflammation.

Reactive matrix clean-up of naturally occurring perylene in young lignite

Young lignite from two locations in Sendai City, Japan, were analyzed for polynuclear aromatic compounds (PACs). Lignite samples were extracted with toluene and PACs were isolated by a compound-class-selective, reactive matrix clean-up. This clean-up separates all compounds of polynuclear aromatic structure, for example hydrocarbons and ketones and their primary metabolites, from interfering organic compounds. The result of this isolation procedure is, therefore, a group of a large number of polycyclic compounds with different functional groups. Further analysis is done by glass capillary gas chromatography. Perylene was identified as the only compound obtained by the reactive matrix clean-up of lignite samples from both locations. Concentrations were in the range of 1-10 mg kg(-1). Conversely, PACs resulting from particulate emissions from fossil fuel combustion always contain isomeric PAHs (polynuclear aromatic hydrocarbons) with some polycyclic aromatic ketones and thousands of primary and secondary metabolites at very low concentrations. This was demonstrated for a sample of urban air particulate matter, which is the source of PAC contamination of surface soil. The absence of accompanying PAHs and polynuclear aromatic ketones in the lignite samples confirms that perylene did not originate from a combustion process. It is assumed that the high concentrations of perylene are the result of a reduction of perylene quinone. Thus, the high perylene content of the lignite samples investigated is of biogenic origin.

Chemical Compositions Responsible for Inflammation and Tissue Damage in the Mouse Lung by Coarse and Fine Particulate Samples from Contrasting Air Pollution in Europe

Inflammation is regarded as an important mechanism in mortality and morbidity associated with exposures of cardiorespiratory patients to urban air particulate matter. We investigated the association of the chemical composition and sources of urban air fine (PM2.5−0.2) and coarse (PM10−2.5) particulate samples with the inflammatory activity in the mouse lung. The particulate samples were collected during selected seasons in six European cities using a high-volume cascade impactor. Healthy C57BL/6J mice were intratracheally instilled with a single dose (10 mg/kg) of the particulate samples. At 4, 12, and 24 h after the exposure, the lungs were lavaged and the bronchoalveolar lavage fluid (BALF) was assayed for indicators of inflammation and tissue damage: cell number, total protein, and cytokines (tumor necrosis factor [TNF]-α, interleukin [IL]-6, and KC). Dicarboxylic acids and transition metals, especially Ni and V, in PM2.5−0.2 correlated positively and some secondary inorganic ions (NO3-, NH4+) negatively with the inflammatory activity. Total organic matter and SO42- had no consistent correlations. In addition, the soil-derived constituents (Ca2+, Al, Fe, Si) showed positive correlations with the PM2.5−0.2-induced inflammatory activity, but their role in PM10−2.5 remained obscure, possibly due to largely undefined biogenic material. Markers of poor biomass and coal combustion, i.e., monosaccharide anhydrides and As, were associated with elevated PAH contents in PM2.5−0.2 and a consistent immunosuppressive effect. Overall, our results support epidemiological findings that the local sources of incomplete combustion and resuspended road dust are important in urban air particulate pollution-related health effects.

Toward Distinguishing Woodsmoke and Diesel Exhaust in Ambient Particulate Matter

Particulate matter (PM) from biomass burning and diesel exhaust has distinct X-ray spectroscopic, carbon specific signatures, which can be employed for source apportionment. Characterization of the functional groups of a wide selection of PM samples (woodsmoke, diesel soot, urban air PM) was carried out using the soft X-ray spectroscopy capabilities at the synchrotron radiation sources in Berkeley (ALS) and Brookhaven (NSLS). The spectra reveal that diesel exhaust particulate (DEP) matter is made up from a semigraphitic solid core and soluble organic matter, predominantly with carboxylic functional groups. Woodsmoke PM has no or a less prevalent, graphitic signature, instead it contains carbon-hydroxyl groups. Using these features to apportion the carbonaceous PM in ambient samples we estimate that the relative contribution of DEP to ambient PM in an urban area such as Lexington, KY and St. Louis, MO is 7% and 13.5%, respectively. These values are comparable to dispersion modeling data from nonurban and urban areas in California, and with elemental carbon measurements in urban locations such as Boston, MA, Rochester, NY, and Washington, DC.

Temporal variation in the genotoxic potential of urban air particulate matter

The main aim of this study was to compare the genotoxic potential of organic extracts from urban air particles collected in three different sampling periods in the center of Prague (Czech Republic). For this purpose, we analyzed the DNA adduct forming activity of extractable organic matter (EOM) from urban air particles <10 μm (PM10) in the human hepatoma cell line HepG2. DNA adducts were analyzed by 32P-postlabelling with nuclease P1 enrichment. PM10 concentrations were 36.9 μg/m 3, 62.6 μg/m 3 and 39.0 μg/m 3, in summer 2000, winter 2001 and winter 2005, respectively. The corresponding EOM contents were 5.0 μg/m 3 (13.9% of PM10), 14.9 μg/m 3 (23.8%) and 6.7 μg/m 3 (17.2%). The total DNA adduct levels induced by 10 μg EOM/ml were 4.7, 19.5 and 37.2 adducts/10 8 nucleotides in summer 2000, winter 2001 and winter 2005, respectively. However, when the EOM quantities per cubic meter of air were taken into consideration, the summer sample exhibited a 10-fold lower genotoxicity than did those of winter, while the difference between the winter samples was not significant: 23.4 in summer 2000, 291 in winter 2001 and 249 in winter 2005 (in relative units). Although the PM10 concentration in air and the EOM content in particles in winter 2005 were significantly lower than in winter 2001, the genotoxic potential of the ambient air in these samples was almost equal. There were significant positive correlations between the B[ a]P and c-PAH content in EOM from various sampling periods and the total DNA adduct levels detected in the EOM-treated samples. These findings support the hypothesis that the B[ a]P and c-PAH content in EOM is the most important factor that determines its genotoxic potential. Thus, estimating the genotoxic potential of the ambient air and predicting health risk should be based mainly on the c-PAH concentration and the biological activity of the extracts, while the mass of particles and the EOM content do not seem to be crucial determinants of ambient air genotoxicity.

Myocardial infarction in Swedish subway drivers

Particulate matter in urban air is associated with the risk of myocardial infarction in the general population. Very high levels of airborne particles have been detected in the subway system of Stockholm, as well as in several other large cities. This situation has caused concern for negative health effects among subway staff. The aim of this study was to investigate whether there is an increased incidence of myocardial infarction among subway drivers. Data from a population-based case-control study of men aged 40-69 in Stockholm County in 1976-1996 were used. The study included all first events of myocardial infarction in registers of hospital discharges and deaths. The controls were selected randomly from the general population. National censuses were used for information on occupation. Altogether, 22 311 cases and 131 496 controls were included. Among these, 54 cases and 250 controls had worked as subway drivers. The relative risk of myocardial infarction among subway drivers was not increased. It was 0.92 [95% confidence interval (95% CI) 0.68-1.25] when the subway drivers were compared with other manual workers and 1.06 (95% CI 0.78-1.43) when the subway drivers were compared with all other gainfully employed men. Subgroup analyses indicated no influence on the risk of myocardial infarction from the duration of employment, latency time, or time since employment stopped. Subway drivers in Stockholm do not have a higher incidence of myocardial infarction than other employed persons.

Dose and Time Dependency of Inflammatory Responses in the Mouse Lung to Urban Air Coarse, Fine, and Ultrafine Particles From Six European Cities

We investigated the dose and time dependency of inflammatory and cytotoxic responses to size-segregated urban air particulate samples in the mouse lung. Coarse (PM10−2.5), fine (PM2.5−0.2), and ultrafine (PM0.2) particles were collected in six European cities (Duisburg, Prague, Amsterdam, Helsinki, Barcelona, Athens) in selected seasons using a modified Harvard high-volume cascade impactor. Healthy C57Bl/6J mice were intratracheally exposed to the particulate samples in a 24-h dose-response study (1, 3, and 10 mg/kg) and in 4-, 12-, and 24-h time course studies (10 mg/kg). After the exposures, the lungs were lavaged and the bronchoalveolar lavage fluid (BALF) was assayed for indicators of inflammation and tissue damage: total cell number, cell differential, total protein, and lactate dehydrogenase (LDH) and cytokine (tumor necrosis alpha [TNF-α], interleukin-6 [IL-6], and keratinocyte-derived chemokine [KC]) concentrations. In general, PM10−2.5 samples had higher inflammatory activity than PM2.5−0.2 samples. PM0.2 samples showed negligible inflammatory activity. PM10−2.5 and PM2.5−0.2 samples caused large increases in BALF cytokine concentrations at 4 h, but not at 12 or 24 h, after exposure. The BALF total cell number and total protein concentrations increased significantly at 12 h for both the PM10−2.5 and PM2.5−0.2 samples, but only PM10−2.5 samples produced consistent, significant increases at 24 h after exposure. There was more heterogeneity in BALF cytokine and neutrophil cell number responses to PM2.5−0.2 samples than to PM10−2.5 samples between the sampling campaigns. Thus, particle size, sources, and atmospheric transformation processes affect the inflammatory activity and response duration of urban air particulate matter in the mouse lung.

Heterogeneities in Inflammatory and Cytotoxic Responses of RAW 264.7 Macrophage Cell Line to Urban Air Coarse, Fine, and Ultrafine Particles From Six European Sampling Campaigns

We investigated the cytotoxic and inflammatory activities of size-segregated particulate samples (particulate matter, PM) from contrasting air pollution situations in Europe. Coarse (PM10−2.5), fine (PM2.5−0.2), and ultrafine (PM0.2) particulate samples were collected with a modified Harvard high-volume cascade impactor (HVCI). Mouse RAW 264.7 macrophages were exposed to the samples for 24 h. Selected inflammatory mediators, nitric oxide (NO) and cytokines (tumor necrosis factor alpha [TNFα], interleukin 6 [IL-6], macrophage inflammatory protein-2 [MIP-2]), were measured together with cytotoxicity (MTT test), and analysis of apoptosis and cell cycle (propidium iodide staining). The PM10−2.5 samples had a much higher inflammatory activity than the PM2.5−0.2 and PM0.2 samples, but the PM2.5−0.2 samples showed the largest differences in inflammatory activity, and the PM0.2 samples in cytotoxicity, between the sampling campaigns. The PM2.5−0.2 samples from traffic environments in springtime Barcelona and summertime Athens had the highest inflammatory activities, which may be related to the high photochemical activity in the atmosphere during the sampling campaigns. The PM0.2 sample from wintertime Prague with proven impacts from local coal and biomass combustion had very high cytotoxic and apoptotic activities and caused a distinct cell cycle arrest. Thus, particulate size, sources, and atmospheric transformation processes affect the toxicity profile of urban air particulate matter. These factors may explain some of the heterogeneity observed in particulate exposure-response relationships of human health effects in epidemiological studies.