Urban Air Particles Research Articles

Investigation of sources of atmospheric dust in Guiyang City, southwest China using rare earth element patterns

Rare earth elements (REE) of atmospheric dust were used in many investigations to trace the potential sources of environmental materials. In this study, we collected atmospheric dry deposition samples monthly from May of 2009 to January of 2011 over one and half year in a typical karst urban area of Guiyang city, southwest China, and measured the contents of REE to trace the sources. The total REE contents (∑REE) of the dusts ranged from 9.48 to 181 mg kg−1, with an average of 93.9 mg kg−1. The ∑REE content of atmospheric dusts is similar to the contents of local soils. All the dust samples showed slighter Ce and Eu anomalies, and the dusts deposited in dry season showed slightly positive Ce anomaly. PAAS (post-Archean Australian shale) normalized REE patterns showed that there was significant difference between the dusts of dry seasons and wet seasons. The values of PAAS-normalized LaN/YbN, LaN/SmN and GdN/YbN of atmospheric dusts were closer to those of local soils collected in dry seasons, whereas the REE characteristics and patterns of dusts were similar to anthropogenic urban air particulates in wet seasons, demonstrating that dusts were mainly originated from anthropogenic inputs.

Structural Features and Pro-Inflammatory Effects of Water-Soluble Organic Matter in Inhalable Fine Urban Air Particles.

The impact of inhalable fine particulate matter (PM2.5, aerodynamic diameter <2.5 μm) on public health is of great concern worldwide. Knowledge on their harmful effects are mainly due to studies carried out with whole air particles, with the contribution of their different fractions remaining largely unknown. Herein, a set of urban PM2.5 samples were collected during daytime and nighttime periods in autumn and spring, aiming to address the seasonal and day-night variability of water-soluble organic matter (WSOM) composition. In vitro analysis of the oxidative and pro-inflammatory potential of WSOM samples was carried out in both acute (24 h) and chronic (3 weeks) exposure setups using Raw264.7 macrophages as cell model. Findings revealed that the structural composition of WSOM samples differs between seasons and in a day-night cycle. Cell exposure resulted in an increase in the transcription of the cytoprotective Hmox1 and pro-inflammatory genes Il1b and Nos2, leading to a moderate pro-inflammatory status. These macrophages showed an impaired capacity to subsequently respond to a strong pro-inflammatory stimulus such as bacterial lipopolysaccharide, which may implicate a compromised capacity to manage harmful pathogens. Further investigation on aerosol WSOM could help to constrain the mechanisms of WSOM-induced respiratory diseases and contribute to PM2.5 regulations.

The effect of talc particles on phagocytes in co-culture with ovarian cancer cells

Talc and titanium dioxide are naturally occurring water-insoluble mined products usually available in the form of particulate matter. This study was prompted by epidemiological observations suggesting that perineal use of talc powder is associated with increased risk of ovarian cancer, particularly in a milieu with higher estrogen. We aimed to test the effects of talc vs. control particles on the ability of prototypical macrophage cell lines to curb the growth of ovarian cancer cells in culture in the presence of estrogen.We found that murine ovarian surface epithelial cells (MOSEC), a prototype of certain forms of ovarian cancer, were present in larger numbers after co-culture with macrophages treated to a combination of talc and estradiol than to either agent alone or vehicle. Control particles (titanium dioxide, concentrated urban air particulates or diesel exhaust particles) did not have this effect. Co-exposure of macrophages to talc and estradiol has led to increased production of reactive oxygen species and changes in expression of macrophage genes pertinent in cancer development and immunosurveillance. These findings suggest that in vitro exposure to talc, particularly in a high-estrogen environment, may compromise immunosurveillance functions of macrophages and prompt further studies to elucidate this mechanism.

Chronic exposure to urban air pollution from Buenos Aires: the ocular mucosa as an early biomarker.

Air pollution represents a major health problem in megacities, bringing about 8 million deaths every year. The aim of the study was to evaluate in vivo the ocular and respiratory mucosa biological response after chronic exposure to urban air particles from Buenos Aires (UAP-BA). BALB/c mice were exposed to UAP-BA or filtered air for 1, 6, 9, and 12months. After exposure, histology, histomorphometry, and IL-6 proinflammatory cytokine level were evaluated in the respiratory and ocular mucosa. Total cell number and differential cell count were determined in the brochoalveolar lavage fluid. In the lung, chronic exposure to UAP-BA induced reduction of the alveolar space, polymorhonuclear cell recruitment, and goblet cell hyperplasia. In the ocular surface, UAP-BA induced an initial mucin positive cells rise followed by a decline through time, while IL-6 level increased at the latest point-time assayed. Our results showed that the respiratory and the ocular mucosas respond differently to UAP-BA. Being that lung and ocular mucosa diseases may be triggered and/or exacerbated by chronic exposure to urban air PM, the inhabitants of Buenos Aires whom are chronically exposed to environmental urban air pollution may be considered a subpopulation at risk. Based on our results, we propose the ocular mucosa as a reliable and more accessible surrogate for pulmonary mucosa environmental toxicity that might also serve as an earlier biomarker for air pollution adverse impact on health.

Exposure to Particles and Nitrogen Dioxide Among Workers in the Stockholm Underground Train System

ObjectivesExposure to fine particles in urban air has been associated with a number of negative health effects. High levels of fine particles have been detected at underground stations in big cities. We investigated the exposure conditions in four occupational groups in the Stockholm underground train system to identify high-exposed groups and study variations in exposure.MethodsPM1 and PM2.5 were measured during three full work shifts on 44 underground workers. Fluctuations in exposure were monitored by a real-time particle monitoring instrument, pDR, DataRAM. Qualitative analysis of particle content was performed using inductively coupled plasma mass spectrometry. Nitrogen dioxide was measured using passive monitors.ResultsFor all underground workers, the geometric mean (GM) of PM1 was 18 μg/m3 and of PM2.5 was 37 μg/m3. The particle exposure was highest for cleaners/platform workers, and the GM of PM1 was 31.6 μg/m3 [geometric standard deviation (GSD), 1.6] and of PM2.5 was 76.5 μg/m3 (GSD, 1.3); the particle exposure was lowest for ticket sellers, and the GM of PM1 was 4.9 μg/m3 (GSD, 2.1) and of PM2.5 was 9.3 μg/m3 (GSD, 1.5). The PM1 and PM2.5 levels were five times higher in the underground system than at the street level, and the particles in the underground had high iron content. The train driver's nitrogen dioxide exposure level was 64.1 μg/m3 (GSD, 1.5).ConclusionsCleaners and other platform workers were statistically significantly more exposed to particles than train drivers or ticket sellers. Particle concentrations (PM2.5) in the Stockholm underground system were within the same range as in the New York underground system but were much lower than in several older underground systems around the world.

Direct and Indirect Effect of Air Particles Exposure Induce Nrf2-Dependent Cardiomyocyte Cellular Response In Vitro.

Air particulate matter has been associated with adverse effects in the cardiorespiratory system leading to cytotoxic and pro-inflammatory effects. Particulate matter-associated cardiac effects may be direct or indirect. While direct interactions may occur when inhaled ultrafine particles and/or particle components cross the air-blood barrier reaching the cardiac tissue, indirect interactions may occur as the result of pulmonary inflammation and consequently the release of inflammatory and oxidative mediators into the blood circulation. The aim of the study is to investigate the direct or indirectly the effect of Urban Air particles from downtown Buenos Aires (UAP-BA) and residual oil fly ash (ROFA), a surrogate of ambient air pollution, on cardiomyocytes (HL-1 cells). HL-1 cultured cells were directly exposed to particulate matter [UAP-BA (10-200µg/ml), ROFA (1-100µg/ml)] or indirectly exposed to conditioned media (CM) from particle-exposed alveolar macrophages (AM). Metabolic activity, reactive oxygen species (ROS), and Nrf2 expression were assessed by MTT, DHR 123, and immunocytochemistry techniques, respectively. We found that direct exposure of cardiomyocytes to UAP-BA or ROFA increased ROS generation but the oxidative damage did not alter metabolic activity likely by a concomitant increase in the cytoplasmic and nuclear Nrf2 expression. However, indirect exposure through CM caused a marked reduction on cardiac metabolic activity probably due to the rise in ROS generation without Nrf2 translocation into the cell nuclei. In this in vitro model, our results indicate both direct and indirect PM effects on cardiomyocytes cells in culture. Our findings employing lung and cardiomyocytes cells provide support to the hypothesis that particle-induced cardiac alteration may possibly involve lung-derived mediators.

Combustion Particle-Induced Changes in Calcium Homeostasis: A Contributing Factor to Vascular Disease?

Air pollution is the leading environmental risk factor for disease and premature death in the world. This is mainly due to exposure to urban air particle matter (PM), in particular, fine and ultrafine combustion-derived particles (CDP) from traffic-related air pollution. PM and CDP, including particles from diesel exhaust (DEP), and cigarette smoke have been linked to various cardiovascular diseases (CVDs) including atherosclerosis, but the underlying cellular mechanisms remain unclear. Moreover, CDP typically consist of carbon cores with a complex mixture of organic chemicals such as polycyclic aromatic hydrocarbons (PAHs) adhered. The relative contribution of the carbon core and adhered soluble components to cardiovascular effects of CDP is still a matter of discussion. In the present review, we summarize evidence showing that CDP affects intracellular calcium regulation, and argue that CDP-induced impairment of normal calcium control may be a critical cellular event through which CDP exposure contributes to development or exacerbation of cardiovascular disease. Furthermore, we highlight in vitro research suggesting that adhered organic chemicals such as PAHs may be key drivers of these responses. CDP, extractable organic material from CDP (CDP-EOM), and PAHs may increase intracellular calcium levels by interacting with calcium channels like transient receptor potential (TRP) channels, and receptors such as G protein-coupled receptors (GPCR; e.g., beta-adrenergic receptors [βAR] and protease-activated receptor 2 [PAR-2]) and the aryl hydrocarbon receptor (AhR). Clarifying a possible role of calcium signaling and mechanisms involved may increase our understanding of how air pollution contributes to CVD.

Petroleum coke exposure leads to altered secretome profiles in human lung models.

Petroleum coke (PC) is a coal-like product that is produced during the refinement of crude oil and bituminous sand. Fugitive dust from open storage of PC in urban areas is a potential human health concern. Animal inhalation studies suggest that PC leads to an adverse pulmonary histopathology, including areas of fibrosis and chronic inflammation; however, little is known about its impact on human health. In order to identify biomarkers and cellular pathways that are associated with exposure, we performed two-dimensional liquid chromatography-mass spectrometric analyses on secreted proteins from two human lung culture models. A total of 2795 proteins were identified and relatively quantified from an immortalized cell line and 2406 proteins from primary cultures that were either mock treated or exposed to particulate matter with a diameter of 2.5-10 μm PC or filtered urban air particulates for 16 h. Pathway analysis on secretomes from primary lung cultures indicated that PC exposure suppressed the secretion of proteins involved in the organization of the extracellular matrix and epithelial differentiation. Because these cellular processes could facilitate fibrosis, we performed chronic 12-day exposure studies on three-dimensional human lung cultures consisting of epithelia and stromal fibroblasts. Relative to mock-treated cells, matrix metallopeptidase 9 levels in the conditioned media were lower by 4 days postexposure and remained suppressed for the duration of the experiment. Immunocytochemical staining of collagen III, a marker associated with fibrosis, showed increased accumulation in the epithelial layer and at the air-liquid interface.

Short-term effects of ultrafine particles on daily mortality by primary vehicle exhaust versus secondary origin in three Spanish cities

BackgroundEvidence on the short-term effects of ultrafine particles (with diameter<100nm, UFP) on health is still inconsistent. New particles in ambient urban air are the result of direct emissions and also the formation of secondary UFP from gaseous precursors. We segregated UFP into these two components and investigated their impact on daily mortality in three Spanish cities affected by different sources of air pollution. MethodsWe separated the UFP using a method based on the high correlation between black carbon (BC) and particle number concentration (N). The first component accounts for aerosol constituents emitted by vehicle exhaust (N1) and the second for the photochemical new particle formation enhancements (N2). We applied city-specific Poisson regression models, adjusting for long-term trends, temperature and population dynamics. ResultsMean BC levels were higher in Barcelona and Tenerife (1.8 and 1.2μg·m−3, respectively) than in Huelva (0.8μg·m−3). While mean UFP concentrations were similar in the three cities, from which N1 was 40% in Barcelona, 46% in Santa Cruz de Tenerife, and 27% in Huelva. We observed an association with N1 and daily mortality in Barcelona, by increasing approximately 1.5% between lags 0 and 2, per an interquartile increase (IQR) of 3277cm−3, but not with N2. A similar pattern was found in Santa Cruz de Tenerife, although none of the associations were significant. Conversely, in the industrial city of Huelva mortality was associated with N2 at lag 0, by increasing 3.9% per an IQR of 12,032·cm−3. ConclusionThe pattern and origin of UFP determines their short-term effect on human health. BC is possibly the better parameter to evaluate the health effects of particulate vehicle exhaust emissions, although in areas influenced by domestic solid fuel combustion this should also be taken into account.

In vitro toxicoproteomic analysis of A549 human lung epithelial cells exposed to urban air particulate matter and its water-soluble and insoluble fractions

BackgroundToxicity of airborne particulate matter (PM) is difficult to assess because PM composition is complex and variable due to source contribution and atmospheric transformation. In this study, we used an in vitro toxicoproteomic approach to identify the toxicity mechanisms associated with different subfractions of Ottawa urban dust (EHC-93).MethodsA549 human lung epithelial cells were exposed to 0, 60, 140 and 200 μg/cm2 doses of EHC-93 (total), its insoluble and soluble fractions for 24 h. Multiple cytotoxicity assays and proteomic analyses were used to assess particle toxicity in the exposed cells.ResultsThe cytotoxicity data based on cellular ATP, BrdU incorporation and LDH leakage indicated that the insoluble, but not the soluble, fraction is responsible for the toxicity of EHC-93 in A549 cells. Two-dimensional gel electrophoresis results revealed that the expressions of 206 protein spots were significantly altered after particle exposures, where 154 were identified by MALDI-TOF-TOF-MS/MS. The results from cytotoxicity assays and proteomic analyses converged to a similar finding that the effects of the total and insoluble fraction may be alike, but their effects were distinguishable, and their effects were significantly different from the soluble fraction. Furthermore, the toxic potency of EHC-93 total is not equal to the sum of its insoluble and soluble fractions, implying inter-component interactions between insoluble and soluble materials resulting in synergistic or antagonistic cytotoxic effects. Pathway analysis based on the low toxicity dose (60 μg/cm2) indicated that the two subfractions can alter the expression of those proteins involved in pathways including cell death, cell proliferation and inflammatory response in a distinguishable manner. For example, the insoluble and soluble fractions differentially affected the secretion of pro-inflammatory cytokines such as MCP-1 and IL-8 and distinctly altered the expression of those proteins (e.g., TREM1, PDIA3 and ENO1) involved in an inflammatory response pathway in A549 cells.ConclusionsThis study demonstrated the impact of different fractions of urban air particles constituted of various chemical species on different mechanistic pathways and thus on cytotoxicity effects. In vitro toxicoproteomics can be a valuable tool in mapping these differences in air pollutant exposure-related toxicity mechanisms.

Transgenerational transmission of asthma risk after exposure to environmental particles during pregnancy.

Exposure to environmental particles during pregnancy increases asthma susceptibility of the offspring. We tested the hypothesis that this transmission continues to F2 and F3 generations and occurs via epigenetic mechanisms. We compared allergic susceptibility of three generations of BALB/c offspring after a single maternal exposure during pregnancy to diesel exhaust particles or concentrated urban air particles. After pregnant dams received intranasal instillations of particle suspensions or control, their F1, F2, and F3 offspring were tested in a low-dose ovalbumin protocol for sensitivity to allergic asthma. We found that the elevated susceptibility after maternal exposure to particles during pregnancy persists into F2 and, with lesser magnitude, into F3 generations. This was evident from elevated eosinophil counts in bronchoalveolar lavage (BAL) fluid, histopathological changes of allergic airway disease, and increased BAL levels of IL-5 and IL-13. We have previously shown that dendritic cells (DCs) can mediate transmission of risk upon adoptive transfer. Therefore, we used an enhanced reduced representation bisulfite sequencing protocol to quantify DNA methylation in DCs from each generation. Distinct methylation changes were identified in F1, F2, and F3 DCs. The subset of altered loci shared across the three generations were not linked to known allergy genes or pathways but included a number of genes linked to chromatin modification, suggesting potential interaction with other epigenetic mechanisms (e.g., histone modifications). The data indicate that pregnancy airway exposure to diesel exhaust particles (DEP) triggers a transgenerationally transmitted asthma susceptibility and suggests a mechanistic role for epigenetic alterations in DCs in this process.

Target and suspect screening of OH-PAHs in air particulates using liquid chromatography-orbitrap high resolution mass spectrometry

Up until now, the methods used for determination of hydroxylated polycyclic aromatic hydrocarbons in air particulate samples have been target methods, only determining compounds with available reference standards. In this present study, a combined target and suspect screening strategy for the analysis of hydroxylated polycyclic aromatic hydrocarbons was developed, utilizing liquid chromatography coupled to orbitrap high resolution mass spectrometry. The target screening included simultaneous determination of nine hydroxylated polycyclic aromatic hydrocarbons, while additional eight hydroxylated polycyclic aromatic hydrocarbon masses were screened for using the suspect screening. The target screening was validated with respect to linearity, limits of detection and quantification and matrix effects. The calibration curves ranged from 0.01 to 10ng/mL, the method limits of detection and quantification were in the rage of 0.001– 0.018pg/m3 and 0.006 – 0.061pg/m3, respectively, while matrix effects ranged from 83% to 104%. For the suspect screening, a list with expected precursor ions created from suspect monoisotopic masses was used. The suspects were then identified by the accurate exact mass, with a mass accuracy threshold <5ppm, molecular formula, isotopic pattern, and mass spectra (fragments) and also semi-quantified in order to obtain information on their relative levels in different matrixes. The developed strategy was applied on five air particulate samples collected from an urban background and five samples from a car tunnel in Stockholm (Sweden). In total 20 hydroxylated polycyclic aromatic hydrocarbons were detected, of which nine compounds were determined using the target screening and 11 were tentatively identified and semi-quantified using the suspect screening strategy. The concentrations of the target compounds ranged from 20.7 to 96.9pg/m3, for most of the analytes the concentrations in particles from car tunnel were slightly higher than in urban air particles. The levels of most of the tentatively identified compounds were also slightly higher in particles from the car tunnel.

Atmospheric Polycyclic and Nitropolycyclic Aromatic Hydrocarbons in an Iron-manufacturing City

Total suspended particulates (TSP) in the atmosphere were collected for 2 weeks during winter in Muroran, Hokkaido, Japan, a typical iron-manufacturing city. The concentrations of polycyclic aromatic hydrocarbons (PAHs) and nitropolycyclic aromatic hydrocarbons (NPAHs) in TSP were determined by high-performance liquid chromatography (HPLC) using fluorescence and chemiluminescence detectors, respectively. No relationship was observed between the atmospheric PAH and NPAH concentration, or the atmospheric PAH and TSP concentration. However, there was a tendency that the atmospheric PAH concentration was higher when the wind blew from the coke-oven plant. Furthermore, the concentration ratios of 1-nitropyrene to pyrene, which is a suitable indicator of the contribution made by automobiles and coal combustion systems to urban air particulates, were smaller in Muroran and the values were close to those observed in particulates from coal combustion systems. Therefore, these results show that the PAH and NPAH compositions for Muroran are characteristic of an iron-manufacturing city.

Acute exposure to Buenos Aires air particles (UAP-BA) induces local and systemic inflammatory response in middle-aged mice: A time course study

Exposure to air particulate matter (PM) is associated with increased cardiovascular morbimortality. However, PM doesn't affect equally to all people, being the old cohort the most susceptible and studied. We hypothesized that another specific life phase, the middle-aged subpopulation, may be negatively affected. Therefore, the aim of this study was to analyze in vivo the acute biological impact of two environmental particles, Urban Air Particles from Buenos Aires and Residual Oil Fly Ash, on the cardiorespiratory system of middle-aged mice, evaluating oxidative metabolism and inflammation. Both PM provoked a local and systemic inflammatory response, leading to a reduced alveolar area in the lung, an epicard inflammation in the heart, an increment of IL-6, and a reduction on PON 1 activity in serum of middle-aged animals. The positive correlation of local parameters with systemic markers of oxidative stress and inflammation could be responsible for associations of cardiovascular morbimortality in this subpopulation.

Investigating the water-soluble organic functionality of urban aerosols using two-dimensional correlation of solid-state 13C NMR and FTIR spectral data

Two-dimensional (2D) correlation spectroscopy, applied to one-dimensional solid-state cross polarization magic angle spinning (CP-MAS) 13C nuclear magnetic resonance (NMR), Fourier transform infrared coupled to attenuated total reflectance (FTIR-ATR), and the combination of CP-MAS 13C NMR and FTIR-ATR data, has been used to glean new structural information on the most hydrophobic water-soluble organic matter (WSOM) from fine urban air particles collected during different seasons. CP-MAS 13C NMR analysis confirmed that unsubstituted saturated aliphatics, aromatics, oxygenated aliphatics, and carboxylic acids accounted for most (84–92%) of the characterized carbon functional groups. Applying 2D correlation spectroscopy to CP-MAS 13C NMR and FTIR-ATR spectra indicates an increase in the contribution of hydroxyl and carboxylic groups to the aliphatic component with increasing air temperature, suggesting the photo-chemical origin of these WSOM structures. Urban samples from colder periods are clearly impacted by biomass combustion sources, although the presence of aged and processed organic aerosols cannot be ruled out. Using 2D FTIR-13C NMR hetero-spectral correlation spectroscopy, it has been demonstrated that the studied WSOM samples consists of at least two different classes of compounds: (i) an aliphatic component rich in both carboxylic and hydroxyl functional groups, and (ii) lignin-derived structures.

Emissions of fluorides from welding processes

The levels of fluoride airborne particulates emitted from welding processes were investigated. They were sampled with the patented IOM Sampler, developed by J. H. Vincent and D. Mark at the Institute of Occupational Medicine (IOM), personal inhalable sampler for simultaneous collection of the inhalable and respirable size fractions. Ion chromatography with conductometric detection was used for quantitative analysis. The efficiency of fluoride extraction from the cellulose filter of the IOM sampler was examined using the standard sample of urban air particle matter SRM-1648a. The best results for extraction were obtained when water and the anionic surfactant N-Cetyl-N-N-N-trimethylammonium bromide (CTAB) were used in an ultrasonic bath. The limits of detection and quantification for the whole procedure were 8μg/L and 24μg/L, respectively. The linear range of calibration was 0.01–10mg/L, which corresponds to 0.0001–0.1mg of fluorides per m3 in collection of a 20L air sample. The concentration of fluorides in the respirable fraction of collected air samples was in the range of 0.20–1.82mg/m3, while the inhalable fraction contained 0.23–1.96mg/m3 of fluorides during an eight-hour working day in the welding room.

Monitoring urban air quality with a diffusion charger based electrical particle sensor

Urban air contains considerable amounts of harmful gaseous substances and aerosol particles. In this study, a recently introduced diffusion charger based PPS-M particle sensor (Pegasor Oy, Tampere, Finland) was evaluated for outdoor air quality measurements in urban environment. The PPS-M particle sensor was used in two stationary air quality measurement stations, one located in the roadside environment and the other in residential area, and in a mobile laboratory. The sampling of urban aerosol to the PPS-M sensor was performed without any pre-conditioning of aerosol. The sensor response to PM2.5 varied between the measurements, being between 7 and 30fA/(μg/m3) depending on the aerosol source. The highest PM2.5 response was observed in the roadside study for exhaust particles while the lowest PM2.5 response was observed for large long range transported aerosol particles having relatively large mean particle size. The sensor signal was found to produce very linear response, with only minimal deviation, to the lung deposited particle surface area concentration (from 4.5 to 6fA/(μm2/cm3)) and to the condensation sink of urban air particles (from 1.0×104 to 1.2×104fAcm3). The sensor response to particle number concentration was defined to be 0.0044fA/(1/cm3) in roadside environment. In this environment, the signal was found to correlate also with NO and NO2 concentrations of roadside air due to the same origin of particulate and gaseous pollutants. Similar correlation between NOx and the PPS-M signal was not observed in residential area.

Tire tread wear particles in ambient air—a previously unknown source of human exposure to the biocide 2-mercaptobenzothiazole

Urban particulate matter (PM), asphalt, and tire samples were investigated for their content of benzothiazole and benzothiazole derivates. The purpose of this study was to examine whether wear particles, i.e., tire tread wear or road surface wear, could contribute to atmospheric concentrations of benzothiazole derivatives. Airborne particulate matter (PM10) sampled at a busy street in Stockholm, Sweden, contained on average 17 pg/m(3) benzothiazole and 64 pg/m(3) 2-mercaptobenzothiazole, and the total suspended particulate-associated benzothiazole and 2-mercaptobenzothiazole concentrations were 199 and 591 pg/m(3), respectively. This indicates that tire tread wear may be a major source of these benzothiazoles to urban air PM in Stockholm. Furthermore, 2-mercaptobenzothiazole was determined in urban air particulates for the first time in this study, and its presence in inhalable PM10 implies that the human exposure to this biocide is underestimated. This calls for a revision of the risk assessments of 2-mercaptobenzothiazole exposure to humans which currently is limited to occupational exposure.

Range-finding risk assessment of inhalation exposure to nanodiamonds in a laboratory environment.

This study considers fundamental methods in occupational risk assessment of exposure to airborne engineered nanomaterials. We discuss characterization of particle emissions, exposure assessment, hazard assessment with in vitro studies, and risk range characterization using calculated inhaled doses and dose-response translated to humans from in vitro studies. Here, the methods were utilized to assess workers’ risk range of inhalation exposure to nanodiamonds (NDs) during handling and sieving of ND powder. NDs were agglomerated to over 500 nm particles, and mean exposure levels of different work tasks varied from 0.24 to 4.96 µg·m−3 (0.08 to 0.74 cm−3). In vitro-experiments suggested that ND exposure may cause a risk for activation of inflammatory cascade. However, risk range characterization based on in vitro dose-response was not performed because accurate assessment of delivered (settled) dose on the cells was not possible. Comparison of ND exposure with common pollutants revealed that ND exposure was below 5 μg·m−3, which is one of the proposed exposure limits for diesel particulate matter, and the workers’ calculated dose of NDs during the measurement day was 74 ng which corresponded to 0.02% of the modeled daily (24 h) dose of submicrometer urban air particles.

Direct and indirect air particle cytotoxicity in human alveolar epithelial cells

Air particulate matter has been associated with adverse impact on the respiratory system leading to cytotoxic and proinflammatory effects. The biological mechanisms behind these associations may be initiated by inhaled small size particles, particle components (soluble fraction) and/or mediators released by particle-exposed cells (conditioned media).The effect of Urban Air Particles from Buenos Aires (UAP-BA) and Residual Oil Fly Ash (ROFA) a surrogate of ambient air pollution, their Soluble Fractions (SF) and Conditioned Media (CM) on A549 lung epithelial cells was examined. After 24h exposure to TP (10 and 100μg/ml), SF or CM, several biological parameters were assayed on cultured A549 cells. We tested cell viability by MTT, superoxide anion (O2-) generation by NBT and proinflammatory cytokine (TNFα, IL-6 and IL-8) production by ELISA.UAP-BA particles or its SF (direct effect) did not modify cell viability and generation of O2- for any of the doses tested. On the contrary, UAP-BA CM (indirect effect) reduced cell viability and increased both generation of O2- and IL-8 production. Exposure to ROFA particles, SF or ROFA CM reduced proliferation and O2- but, stimulated IL-8. It is worth to note that UAP-BA and ROFA depicted distinct effects on particle-exposed A549 cells implicating morphochemical dependence. These in vitro findings support the hypothesis that particle-induced lung inflammation and disease may involve lung-derived mediators.