Search

Nanoparticle emissions from transport are of considerable importance because of their dominance in terms of particle number concentration in most urban atmospheres. Nanoparticles may carry toxic substances, posing a serious threat to pedestrians, passengers and residents. The road sector has been studied intensively in both academia and industry and considerable knowledge has already been gathered. Shipping is also a significant source of nanoparticles both at the global and the European level and may be responsible for cardiopulmonary diseases and lung cancer at the global level, while ship emissions are known as one of the least regulated sources of pollutants. Aviation nanoparticle emissions have also received increasing attention in recent years because of the rapid growth of air transport volumes and the expected expansion to meet capacity needs for future years. Exhaust nanoparticle emissions from diesel rail transport are not very well known and only a few sources addressing actual emission rates are available. All modes of transport are sources of non-exhaust nanoparticle number emission associated with the tire, brake, and road/rail surface wear and tear. This paper provides a literature review to identify the different aerosol modes (i.e., primary, delayed primary, and secondary) from each transport source (road, shipping, aviation, rail), in both laboratory and field tests and to explore their toxicity relevance. The review focuses on nanoparticles (, This work was funded by European Union’s Horizon 2020 Research and Innovation programme, under grant agreement № 954377.

Relevant in vitro assays that can simulate exposure to nanoparticles (NPs) via inhalation are urgently needed. Presently, the most common method employed is to expose lung cells under submerged conditions, but the cellular responses to NPs under such conditions might differ from those observed at the more physiological air-liquid interface (ALI). The aim of this study was to investigate the cytotoxic and inflammatory potential of CeO2 NPs (NM-212) in a co-culture of A549 lung epithelial cells and differentiated THP-1 cells in both ALI and submerged conditions. Cellular dose was examined quantitatively using inductively coupled plasma mass spectrometry (ICP-MS). The role of serum and LPS-priming for IL-1β release was further tested in THP-1 cells in submerged exposure. An aerosol of CeO2 NPs was generated by using the PreciseInhale® system, and NPs were deposited on the co-culture using XposeALI®. No or minor cytotoxicity and no increased release of inflammatory cytokines (IL-1β, IL-6, TNFα, MCP-1) were observed after exposure of the co-culture in ALI (max 5 µg/cm2) or submerged (max 22 µg/cm2) conditions. In contrast, CeO2 NPs cause clear IL-1β release in monocultures of macrophage-like THP-1, independent of the presence of serum and LPS-priming. This study demonstrates a useful approach for comparing effects at various in-vitro conditions.

Personal monitors based on unipolar diffusion charging (miniDiSC/DiSCmini, NanoTracer, Partector) can be used to assess the individual exposure to nanoparticles in different environments. The charge acquired by the aerosol particles is nearly proportional to the particle diameter and, by coincidence, also nearly proportional to the alveolar lung-deposited surface area (LDSA), the metric reported by all three instruments. In addition, the miniDiSC/DiSCmini and the NanoTracer report particle number concentration and mean particle size. In view of their use for personal exposure studies, the comparability of these personal monitors was assessed in two measurement campaigns. Altogether 29 different polydisperse test aerosols were generated during the two campaigns, covering a large range of particle sizes, morphologies and concentrations. The data provided by the personal monitors were compared with those obtained from reference instruments: a scanning mobility particle sizer (SMPS) for LDSA and mean particle size and a ultrafine particle counter (UCPC) for number concentration. The results indicated that the LDSA concentrations and the mean particle sizes provided by all investigated instruments in this study were in the order of ± 30% of the reference value obtained from the SMPS when the particle sizes of the test aerosols generated were within 20–400 nm and the instruments were properly calibrated. Particle size, morphology and concentration did not have a major effect within the aforementioned limits. The comparability of the number concentrations was found to be slightly worse and in the range of ± 50% of the reference value obtained from the UCPC. In addition, a minor effect of the particle morphology on the number concentration measurements was observed. The presence of particles > 400 nm can drastically bias the measurement results of all instruments and all metrics determined. © 2016 Elsevier B.V.

To study the relationship between exposure to airborne particles in a pulp and paper mill and markers of inflammation and coagulation in blood. Personal sampling of inhalable dust was performed for 72 subjects working in a Swedish pulp and paper mill. Stationary measurements were used to study concentrations of total dust, respirable dust, PM10 and PM2.5, the particle surface area and the particle number concentrations. Markers of inflammation, interleukins (IL-1b, IL-6, IL-8, and IL-10), C-reactive protein (CRP), serum amyloid A (SAA), and fibrinogen and markers of coagulation factor VIII, von Willebrand, plasminogen activator inhibitor, and D-dimer were measured in plasma or serum. Sampling was performed on the last day of the work free period of 5 days, before and after the shift the first day of work and after the shifts the second and third day. In a mixed model analysis, the relationship between particulate exposures and inflammatory markers was determined. Sex, age, smoking, and BMI were included as covariates. The average 8-h time-weighted average (TWA) air concentration levels of inhalable dust were 0.30 mg/m(3), range 0.005-3.3 mg/m(3). The proxies for average 8-h TWAs of respirable dust were 0.045 mg/m(3). Significant and consistent positive relations were found between several exposure metrics (PM 10, total and inhalable dust) and CRP, SAA and fibrinogen taken post-shift, suggesting a dose-effect relationship. This study supports a relationship between occupational particle exposure and established inflammatory markers, which may indicate an increased risk of cardiovascular disease. Funding Agencies|Swedish Research Council for Health, Working Life and Welfare [2006-0152]

Relevant in vitro assays that can simulate exposure to nanoparticles (NPs) via inhalation are urgently needed. Presently, the most common method employed is to expose lung cells under submerged conditions, but the cellular responses to NPs under such conditions might differ from those observed at the more physiological air-liquid interface (ALI). The aim of this study was to investigate the cytotoxic and inflammatory potential of CeO2 NPs (NM-212) in a co-culture of A549 lung epithelial cells and differentiated THP-1 cells in both ALI and submerged conditions. Cellular dose was examined quantitatively using inductively coupled plasma mass spectrometry (ICP-MS). The role of serum and LPS-priming for IL-1&beta, release was further tested in THP-1 cells in submerged exposure. An aerosol of CeO2 NPs was generated by using the PreciseInhale&reg, system, and NPs were deposited on the co-culture using XposeALI&reg, No or minor cytotoxicity and no increased release of inflammatory cytokines (IL-1&beta, IL-6, TNF&alpha, MCP-1) were observed after exposure of the co-culture in ALI (max 5 &micro, g/cm2) or submerged (max 22 &micro, g/cm2) conditions. In contrast, CeO2 NPs cause clear IL-1&beta, release in monocultures of macrophage-like THP-1, independent of the presence of serum and LPS-priming. This study demonstrates a useful approach for comparing effects at various in-vitro conditions.

Studies using advanced toxicological methods enabling in vitro conditions that are more realistic are currently needed for understanding the risks of pulmonary exposure to airborne nanoparticles. Owing to the carcinogenicity of certain nickel compounds, the increased production of nickel nanoparticles (Ni‐NPs) raises occupational safety concerns. The aim of this study was to investigate the genotoxicity of airborne Ni‐NPs using a recently developed air–liquid interface exposure system. The wild‐type Chinese hamster lung fibroblast cell line (V79) was used and cytotoxicity, DNA damage and mutagenicity were studied by testing colony forming efficiency, alkaline DNA unwinding and HPRT mutation assays, respectively. Additionally, co‐exposure to a PARP‐1 inhibitor was performed to test possible involvement of base excision repair (BER) in repair of Ni‐induced DNA damage. The results showed that cell viability was reduced significantly (to 45% and 46%) after 48 hours Ni‐NP exposure at concentrations of 0.15 and 0.32 μg cm−2. DNA damage was significantly increased after Ni‐NP exposure in the presence of the BER inhibitor indicating that Ni‐NP‐induced DNA damages are subsequently repaired by BER. Furthermore, there was no increased HPRT mutation frequency following Ni‐NP exposure. In conclusion, this study shows that Ni‐NP treatment of lung fibroblasts in an air–liquid interface system that mimics real‐life exposure, results in increased DNA strand breaks and reduced cellular viability. These DNA lesions were repaired with BER in an error‐free manner without resulting in mutations. This study also underlines the importance of appropriate quantification of the actual exposure concentrations during air–liquid interface exposure studies., The aim of this study was to investigate the genotoxicity of airborne Ni nanoparticles using a recently developed air‐liquid interface exposure system that mimics real‐life exposure. Cytotoxicity, DNA damage and mutagenicity were in the V79 cell line. Ni nanoparticle exposure of the cells in the air‐liquid interface resulted in increased DNA strand breaks and reduced cellular viability at concentrations of 0.15 and 0.32 μg cm −2. These DNA lesions were repaired with BER in an error‐free manner without resulting in mutations

There is currently a need to develop and test in vitro systems for predicting the toxicity of nanoparticles. One challenge is to determine the actual cellular dose of nanoparticles after exposure.In this study, human epithelial lung cells (A549) were exposed to airborne Cu particles at the air-liquid interface (ALI). The cellular dose was determined for two different particle sizes at different deposition conditions, including constant and pulsed Cu aerosol flow.Airborne polydisperse particles with a geometric mean diameter (GMD) of 180 nm [geometric standard deviation (GSD) 1.5, concentration 10(5) particles/mL] deposited at the ALI yielded a cellular dose of 0.4-2.6 μg/cm(2) at pulsed flow and 1.6-7.6 μg/cm(2) at constant flow. Smaller polydisperse particles in the nanoregime (GMD 80 nm, GSD 1.5, concentration 10(7) particles/mL) resulted in a lower cellular dose of 0.01-0.05 μg/cm(2) at pulsed flow, whereas no deposition was observed at constant flow. Exposure experiments with and without cells showed that the Cu particles were partly dissolved upon deposition on cells and in contact with medium.Different cellular doses were obtained for the different Cu particle sizes (generated with different methods). Furthermore, the cellular doses were affected by the flow conditions in the cell exposure system and the solubility of Cu. The cellular doses of Cu presented here are the amount of Cu that remained on the cells after completion of an experiment. As Cu particles were partly dissolved, Cu (a nonnegligible contribution) was, in addition, present and analyzed in the nourishing medium present beneath the cells. This study presents cellular doses induced by Cu particles and demonstrates difficulties with deposition of nanoparticles at the ALI and of partially soluble particles.

Occupational exposure to airborne nickel is associated with an elevated risk for respiratory tract diseases including lung cancer. Therefore, the increased production of Ni-containing nanoparticles necessitates a thorough assessment of their physical, chemical, as well as toxicological properties. The aim of this study was to investigate and compare the characteristics of nickel metal (Ni) and nickel oxide (NiO) particles with a focus on Ni release, reactive oxygen species (ROS) generation, cellular uptake, cytotoxicity and genotoxicity. Four Ni-containing particles of both nano-size (Ni-n and NiO-n) and micron-size (Ni-m1 and Ni-m2) were tested. The released amount of Ni in solution was notably higher in artificial lysosomal fluid (e.g. 80-100 wt% for metallic Ni) than in cell medium after 24h (ca. 1-3 wt% for all particles). Each of the particles was taken up by the cells within 4 h and they remained in the cells to a high extent after 24 h post-incubation. Thus, the high dissolution in ALF appeared not to reflect the particle dissolution in the cells. Ni-m1 showed the most pronounced effect on cell viability after 48 h (alamar blue assay) whereas all particles showed increased cytotoxicity in the highest doses (20-40 μg cm2) when assessed by colony forming efficiency (CFE). Interestingly an increased CFE, suggesting higher proliferation, was observed for all particles in low doses (0.1 or 1 μg cm-2). Ni-m1 and NiO-n were the most potent in causing acellular ROS and DNA damage. However, no intracellular ROS was detected for any of the particles. Taken together, micron-sized Ni (Ni-m1) was more reactive and toxic compared to the nano-sized Ni. Furthermore, this study underlines that the low dose effect in terms of increased proliferation observed for all particles should be further investigated in future studies.

Continuous daily measurements of airborne particles were conducted during specific periods at an underground platform within the subway system of the city center of Stockholm, Sweden. Main emphasis was placed on number concentration, particle size distribution, soot content (analyzed as elemental and black carbon) and surface area concentration. Conventional measurements of mass concentrations were conducted in parallel as well as analysis of particle morphology, bulk- and surface composition. In addition, the presence of volatile and semi volatile organic compounds within freshly collected particle fractions of PM 10 and PM 2.5 were investigated and grouped according to functional groups. Similar periodic measurements were conducted at street level for comparison. The investigation clearly demonstrates a large dominance in number concentration of airborne nano-sized particles compared to coarse particles in the subway. Out of a mean particle number concentration of 12 000 particles/cm 3 (7500 to 20 000 particles/cm 3 ), only 190 particles/cm 3 were larger than 250 nm. Soot particles from diesel exhaust, and metal-containing particles, primarily iron, were observed in the subway aerosol. Unique measurements on freshly collected subway particle size fractions of PM 10 and PM 2.5 identified several volatile and semi-volatile organic compounds, the presence of carcinogenic aromatic compounds and traces of flame retardants. This interdisciplinary and multi-analytical investigation aims to provide an improved understanding of reported adverse health effects induced by subway aerosols.

The number and mass distribution of airborne particles were recorded in several industrial plants. From the data obtained, particle deposition was estimated in three regions of the respiratory trac ...

Different methodological settings can influence particle characteristics and toxicity in nanotoxicology. The aim of this study was to investigate how serum proteins and sonication of Cu nanoparticle suspensions influence the properties of the nanoparticles and toxicological responses on human lung epithelial cells. This was investigated by using methods for particle characterization (photon correlation spectroscopy and TEM) and Cu release (atomic absorption spectroscopy) in combination with assays for analyzing cell toxicity (MTT-, trypan blue- and Comet assay). The results showed that sonication of Cu nanoparticles caused decreased cell viability and increased Cu release compared to non-sonicated particles. Furthermore, serum in the cell medium resulted in less particle agglomeration and increased Cu release compared with medium without serum, but no clear difference in toxicity was detected. Few cells showed intracellular Cu nanoparticles due to fast release/dissolution processes of Cu. In conclusion; sonication can affect the toxicity of nanoparticles. This work was partly supported by the Swedish Research Council for Environment, Agricultural Sciences, and Spatial Planning (FORMAS), AForsk (Angpanneföreningen’s Foundation for Research and Development), and Environmental Cancer Risk, Nutrition, and Individual Susceptibility (ECNIS), a Network of Excellence operating within the European Union 6th Framework Program, Priority 5: “Food, Quality and Safety” (Contract No. 513943).

An interdisciplinary and multianalytical research effort is undertaken to assess the toxic aspects of thoroughly characterized nano- and micrometer-sized particles of oxidized metallic copper and copper(II) oxide in contact with cultivated lung cells, as well as copper release in relevant media. All particles, except micrometer-sized Cu, release more copper in serum-containing cell medium (supplemented Dulbecco's minimal essential medium) compared to identical exposures in phosphate-buffered saline. Sonication of particles for dispersion prior to exposure has a large effect on the initial copper release from Cu nanoparticles. A clear size-dependent effect is observed from both a copper release and a toxicity perspective. In agreement with greater released amounts of copper per quantity of particles from the nanometer-sized particles compared to the micrometer-sized particles, the nanometer particles cause a higher degree of DNA damage (single-strand breaks) and cause a significantly higher percentage of cell death compared to cytotoxicity induced by micrometer-sized particles. Cytotoxic effects related to the released copper fraction are found to be significantly lower than the effects related to particles. No DNA damage is induced by the released copper fraction.

The use of refined toxicological methods is currently needed for characterizing the risks of airborne nanoparticles (NPs) to human health. To mimic pulmonary exposure, we have developed an air–liquid interface (ALI) exposure system for direct deposition of airborne NPs on to lung cell cultures. Compared to traditional submerged systems, this allows more realistic exposure conditions for characterizing toxicological effects induced by airborne NPs. The purpose of this study was to investigate how the deposition of silver NPs (AgNPs) is affected by different conditions of the ALI system. Additionally, the viability and metabolic activity of A549 cells was studied following AgNP exposure. Particle deposition increased markedly with increasing aerosol flow rate and electrostatic field strength. The highest amount of deposited particles (2.2 μg cm–2) at cell‐free conditions following 2 h exposure was observed for the highest flow rate (390 ml min–1) and the strongest electrostatic field (±2 kV). This was estimated corresponding to deposition efficiency of 94%. Cell viability was not affected after 2 h exposure to clean air in the ALI system. Cells exposed to AgNPs (0.45 and 0.74 μg cm–2) showed significantly (P < 0.05) reduced metabolic activities (64 and 46%, respectively). Our study shows that the ALI exposure system can be used for generating conditions that were more realistic for in vitro exposures, which enables improved mechanistic and toxicological studies of NPs in contact with human lung cells.Copyright © 2016 The Authors Journal of Applied Toxicology Published by John Wiley & Sons Ltd., An electrostatic airliquid interface exposure system was developed to assess the effects of pulmonary exposure to airborne nanoparticles. An applied electrostatic field strength and aerosol flow rate can be adjusted for achieving different particle doses. The highest amount of deposited particles was 2.2 μg cm2. Silver nanoparticles were found to cause cytotoxicity after 2 h exposure to 0.45 and 0.74 μg(Ag+)/cm2.

An increased understanding of nanoparticle toxicity and its impact on human health is essential to enable a safe use of nanoparticles in our society. The aim of this study is to investigate the role of a Trojan horse type mechanism for the toxicity of Ag-nano and CuO-nano particles and their corresponding metal ionic species (using CuCl2 and AgNO3), i.e., the importance of the solid particle to mediate cellular uptake and subsequent release of toxic species inside the cell. The human lung cell lines A549 and BEAS-2B are used and cell death/membrane integrity and DNA damage are investigated by means of trypan blue staining and the comet assay, respectively. Chemical analysis of the cellular dose of copper and silver is performed using atomic absorption spectroscopy. Furthermore, transmission electron microscopy, laser scanning confocal microscopy, and confocal Raman microscopy are employed to study cellular uptake and particle-cell interactions. The results confirm a high uptake of CuO-nano and Ag-nano compared to no, or low, uptake of the soluble salts. CuO-nano induces both cell death and DNA damage whereas CuCl2 induces no toxicity. The opposite is observed for silver, where Ag-nano does not cause any toxicity, whereas AgNO3 induces a high level of cell death. In conclusion: CuO-nano toxicity is predominantly mediated by intracellular uptake and subsequent release of copper ions, whereas no toxicity is observed for Ag-nano due to low release of silver ions within short time periods.

To study the possible relationship between inhalation of airborne particles in the work environment and inflammatory markers in blood.Total dust was sampled in the breathing zone of 73 subjects working with welding, cutting, grinding and in foundries such as iron, aluminium, and concrete. Stationary measurements were used to study different size fractions of particles including respirable dust, particulate matter (PM)(10) and PM(2.5), the particle number concentration, the number of particles deposited in the alveoli, and total particle surface area concentration. Inflammatory markers such as interleukin-6 (IL-6), C-reactive protein (CRP), fibrinogen, d-dimer, and urate were measured in plasma or serum before the first shift after the summer vacation and after the first, second, and fourth shift.The mean level of total dust in the breathing zone was 0.93 mg/m(3). The proxies for mean respirable dust fraction was 0.27 mg/m(3), PM(10) 0.60 mg/m(3), and PM(2.5) was 0.31 mg/m(3). The IL-6 values increased by 50% after the first day, but decreased after shift on the second and fourth day. CRP did not increase after the first shift but increased by 17% after the second shift. Other biomarkers were unaffected. A multiple linear regression analysis of a subgroup of 47 subjects showed a statistically significant positive relationship between particle exposure and post-shift IL-6.This study supports previous investigations observing increases of IL-6 at air concentrations of PM(10) or PM(2.5) between 0.13 and 0.3 mg/m(3) among healthy subjects. This increase of IL-6 may indicate an increased risk of coronary heart disease.

Ultrafine particles are considered as a possible cause of some of the adverse health effects caused by airborne particles. In this study, the particle characteristics were measured in seven Swedish industrial plants, with a special focus on the ultrafine particle fraction. Number concentration, size distribution, surface area concentration, and mass concentration were measured at 10 different job activities, including fettling, laser cutting, welding, smelting, core making, moulding, concreting, grinding, sieving powders, and washing machine goods. A thorough particle characterization is necessary in workplaces since it is not clear yet which choice of ultrafine particle metric is the best to measure in relation to health effects. Job activities were given a different order of rank depending on what particle metric was measured. An especially high number concentration (130 x 10(3) cm(-3)) and percentage of ultrafine particles (96%) were found at fettling of aluminium, whereas the highest surface area concentration (up to 3800 mum(2) cm(-3)) as well as high PM10 (up to 1 mg m(-3)) and PM1 (up to 0.8 mg m(-3)) were found at welding and laser cutting of steel. The smallest geometric mean diameter (22 nm) was found at core making (geometric standard deviation: 1.9).

An epidemiologic study has demonstrated that asphalt workers show increased loss of lung function and an increase of biomarkers of inflammation over the asphalt paving season. The aim of this study was to investigate which possible agent(s) causes the inflammatory reaction, with emphasis on ultrafine particles. The workers' exposure to total dust, polycyclic aromatic hydrocarbons, and NO(2) was determined by personal sampling. Exposure to ultrafine particles was measured by means of particle counters and scanning mobility particle sizer mounted on a van following the paving machine. The fractions of organic and elemental carbon were determined. Asphalt paving workers were exposed to ultrafine particles with medium concentration of about 3.4 x 10(4)/cm(3). Ultrafine particles at the paving site originated mainly from asphalt paving activities and traffic exhaust; most seemed to originate from asphalt fumes. Oil mist exceeded occupational limits on some occasions. Diesel particulate matter was measured as elemental carbon, which was low, around 3 microg/m(3). NO(2) and total dust did not exceed limits. Asphalt pavers were exposed to relatively high concentrations of ultrafine particles throughout their working day, with possible adverse health effects.

Objectives Study the relationship between inhalation of airborne particles in a pulp and paper mill and markers of inflammation and coagulation in blood. Method Personal sampling of inhalable dust was performed for 72 subjects working in a Swedish pulp and paper mill. Stationary measurements were used to study different particle size fractions including respirable dust, PM10 , PM2.5, the particle surface area and particle number concentrations of ultrafine particles. Markers of inflammation such as interleukins (IL-1b, IL-6, IL-8, and IL-10), C-reactive protein (CRP), serum amyloid A (SAA), and fibrinogen and markers of coagulation such as factor VIII, von Willebrand factor vWF), plasminogen activator inhibitor (PAI-1), and D-dimer were determined before the first shift after a work free period of normally five days and after the first, second and third shift Results The average 8hr-TWA level of inhalable dust in was 0.30 mg/m3, range 0.005–3.3 mg/m3.The proxies for 8hr-TWAs of respirable dust was 0.045 mg/m3, PM10 0.17 mg/m3 and PM2.5 0.08 mg/m3. No significant increase of markers of inflammation or coagulation in blood during the working week was noted after a non-exposure period of five days. In a multiple regression analysis adjustments were made for sex, age, smoking, BMI, and blood group. Significant positive correlations were found between several particle exposure metrics and CRP, SAA and fibrinogen taken pre- and post-shift day 1, suggesting a dose-effect relationship. Conclusions These relations between particle exposure and inflammatory markers may indicate an increased risk of cardiovascular disease.