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The overlap between the geographic distribution of COVID-19 outbreaks and pollution levels confirmed a correlation between exposure to atmospheric particulate matter (PM) and the SARS-CoV-2 pandemic. The RAS system is essential in the pathogenesis of inflammatory diseases caused by pollution: the ACE/AngII/AT1 axis activates a pro-inflammatory pathway, which is counteracted by the ACE2/Ang(1-7)/MAS axis, which activates an anti-inflammatory and protective pathway. However, ACE2 is also known to act as a receptor through which SARS-CoV-2 enters host cells to replicate. Furthermore, in vivo systems have demonstrated that exposure to PM increases ACE2 expression. In this study, the effects of acute and sub-acute exposure to ultrafine particles (UFP), originating from different anthropogenic sources (DEP and BB), on the levels of ACE2, ACE, COX-2, HO-1, and iNOS in the lungs and other organs implicated in the pathogenesis of COVID-19 were analyzed in the in vivo BALB/c male mice model. Exposure to UFP alters the levels of ACE2 and/or ACE in all examined organs, and exposure to sub-acute DEP also results in the release of s-ACE2. Furthermore, as evidenced in this and our previous works, COX-2, HO-1, and iNOS levels also demonstrated organ-specific alterations. These proteins play a pivotal role in the UFP-induced inflammatory and oxidative stress responses, and their dysregulation is linked to the development of severe symptoms in individuals infected with SARS-CoV-2, suggesting a heightened vulnerability or a more severe clinical course of the disease. UFP and SARS-CoV-2 share common pathways; therefore, in a "risk stratification" concept, daily exposure to air pollution may significantly increase the likelihood of developing a severe form of COVID-19, explaining, at least in part, the greater lethality of the virus observed in highly polluted areas. [ABSTRACT FROM AUTHOR]

Constituents of air pollution, the ultrafine particles (UFP) with a diameter of ≤0.1 μm, are considerably related to traffic emissions. Several studies link air pollution to Alzheimer's disease (AD), yet the exact relationship between the two remains poorly understood. Mitochondria are known targets of environmental toxicants, and their dysfunction is associated with neurodegenerative diseases. The olfactory mucosa (OM), located at the rooftop of the nasal cavity, is directly exposed to the environment and in contact with the brain. Mounting evidence suggests that the UFPs can impact the brain directly through the olfactory tract. By using primary human OM cultures established from nasal biopsies of cognitively healthy controls and individuals diagnosed with AD, we aimed to decipher the effects of traffic-related UFPs on mitochondria. The UFP samples were collected from the exhausts of a modern heavy-duty diesel engine (HDE) without aftertreatment systems, run with renewable diesel (A0) and petroleum diesel (A20), and from an engine of a 2019 model diesel passenger car (DI-E6d) equipped with state-of-the-art aftertreatment devices and run with renewable diesel (Euro6). OM cells were exposed to three different UFPs for 24-h and 72-h, after which cellular processes were assessed on the functional and transcriptomic levels. Our results show that UFPs impair mitochondrial functions in primary human OM cells by hampering oxidative phosphorylation (OXPHOS) and redox balance, and the responses of AD cells differ from cognitively healthy controls. RNA-Seq and IPA® revealed inhibition of OXPHOS and mitochondrial dysfunction in response to UFPs A0 and A20. Functional validation confirmed that A0 and A20 impair cellular respiration, decrease ATP levels, and disturb redox balance by altering NAD and glutathione metabolism, leading to increased ROS and oxidative stress. RNA-Seq and functional assessment revealed the presence of AD-related alterations in human OM cells and that different fuels and engine technologies elicit differential effects.

The overlap between the geographic distribution of COVID-19 outbreaks and pollution levels confirmed a correlation between exposure to atmospheric particulate matter (PM) and the SARS-CoV-2 pandemic. The RAS system is essential in the pathogenesis of inflammatory diseases caused by pollution: the ACE/AngII/AT1 axis activates a pro-inflammatory pathway, which is counteracted by the ACE2/Ang(1-7)/MAS axis, which activates an anti-inflammatory and protective pathway. However, ACE2 is also known to act as a receptor through which SARS-CoV-2 enters host cells to replicate. Furthermore, in vivo systems have demonstrated that exposure to PM increases ACE2 expression. In this study, the effects of acute and sub-acute exposure to ultrafine particles (UFP), originating from different anthropogenic sources (DEP and BB), on the levels of ACE2, ACE, COX-2, HO-1, and iNOS in the lungs and other organs implicated in the pathogenesis of COVID-19 were analyzed in the in vivo BALB/c male mice model. Exposure to UFP alters the levels of ACE2 and/or ACE in all examined organs, and exposure to sub-acute DEP also results in the release of s-ACE2. Furthermore, as evidenced in this and our previous works, COX-2, HO-1, and iNOS levels also demonstrated organ-specific alterations. These proteins play a pivotal role in the UFP-induced inflammatory and oxidative stress responses, and their dysregulation is linked to the development of severe symptoms in individuals infected with SARS-CoV-2, suggesting a heightened vulnerability or a more severe clinical course of the disease. UFP and SARS-CoV-2 share common pathways; therefore, in a “risk stratification” concept, daily exposure to air pollution may significantly increase the likelihood of developing a severe form of COVID-19, explaining, at least in part, the greater lethality of the virus observed in highly polluted areas.

Background: While epidemiologic evidence links higher levels of exposure to fine particulate matter (PM2.5) to decreased cognitive function, fewer studies have investigated links with traffic-related air pollution (TRAP), and none have examined ultrafine particles (UFP, ≤100 nm) and late-life dementia incidence. Objective: To evaluate associations between TRAP exposures (UFP, black carbon [BC], and nitrogen dioxide [NO2]) and late-life dementia incidence. Methods: We ascertained dementia incidence in the Seattle-based Adult Changes in Thought (ACT) prospective cohort study (beginning in 1994) and assessed ten-year average TRAP exposures for each participant based on prediction models derived from an extensive mobile monitoring campaign. We applied Cox proportional hazards models to investigate TRAP exposure and dementia incidence using age as the time axis and further adjusting for sex, self-reported race, calendar year, education, socioeconomic status, PM2.5, and APOE genotype. We ran sensitivity analyses where we did not adjust for PM2.5 and other sensitivity and secondary analyses where we adjusted for multiple pollutants, applied alternative exposure models (including total and size-specific UFP), modified the adjustment covariates, used calendar year as the time axis, assessed different exposure periods, dementia subtypes, and others. Results: We identified 1,041 incident all-cause dementia cases in 4,283 participants over 37,102 person-years of follow-up. We did not find evidence of a greater hazard of late-life dementia incidence with elevated levels of long-term TRAP exposures. The estimated hazard ratio of all-cause dementia was 0.98 (95 % CI: 0.92–1.05) for every 2000 pt/cm3 increment in UFP, 0.95 (0.89–1.01) for every 100 ng/m3 increment in BC, and 0.96 (0.91–1.02) for every 2 ppb increment in NO2. These findings were consistent across sensitivity and secondary analyses. Discussion: We did not find evidence of a greater hazard of late-life dementia risk with elevated long-term TRAP exposures in this population-based prospective cohort study.

Objective: To assess the spatiotemporal heterogeneity of lung-deposited particle surface area concentration (LDSA), while testing the long-term performance of a prototype of low-cost-low-maintenance LDSA sensors. One factor hampering epidemiological studies on fine to ultrafine particles (F-to-UFP) exposure is exposure error due to their high spatiotemporal heterogeneity, not reflected in particle mass. Though LDSA shows consistent associations between F-to-UFP exposure and health effects, LDSA data are limited.Methods: We measured LDSA in a network of ten sensors, including urban, suburban, and rural environments in Zurich, Switzerland. With traffic counts, traffic co-pollutant concentrations, and meteorological parameters, we assessed the drivers of the LDSA observations.Results: LDSA reflected the high spatiotemporal heterogeneity of F-to-UFP. With micrometeorological influences, local sources like road traffic, restaurants, air traffic, and residential combustion drove LDSA. The temporal pattern of LDSA reflected that of the local sources.Conclusion: LDSA may be a viable metric for inexpensively characterizing F-to-UFP exposure. The tested devices generated sound data and may significantly contribute to filling the LDSA exposure data gap, providing grounds for more statistically significant epidemiological studies and regulation of F-to-UFP.

Constituents of air pollution, the ultrafine particles (UFP) with a diameter of ≤0.1 μm, are considerably related to traffic emissions. Several studies link air pollution to Alzheimer's disease (AD), yet the exact relationship between the two remains poorly understood. Mitochondria are known targets of environmental toxicants, and their dysfunction is associated with neurodegenerative diseases. The olfactory mucosa (OM), located at the rooftop of the nasal cavity, is directly exposed to the environment and in contact with the brain. Mounting evidence suggests that the UFPs can impact the brain directly through the olfactory tract. By using primary human OM cultures established from nasal biopsies of cognitively healthy controls and individuals diagnosed with AD, we aimed to decipher the effects of traffic-related UFPs on mitochondria. The UFP samples were collected from the exhausts of a modern heavy-duty diesel engine (HDE) without aftertreatment systems, run with renewable diesel (A0) and petroleum diesel (A20), and from an engine of a 2019 model diesel passenger car (DI-E6d) equipped with state-of-the-art aftertreatment devices and run with renewable diesel (Euro6). OM cells were exposed to three different UFPs for 24-h and 72-h, after which cellular processes were assessed on the functional and transcriptomic levels. Our results show that UFPs impair mitochondrial functions in primary human OM cells by hampering oxidative phosphorylation (OXPHOS) and redox balance, and the responses of AD cells differ from cognitively healthy controls. RNA-Seq and IPA® revealed inhibition of OXPHOS and mitochondrial dysfunction in response to UFPs A0 and A20. Functional validation confirmed that A0 and A20 impair cellular respiration, decrease ATP levels, and disturb redox balance by altering NAD and glutathione metabolism, leading to increased ROS and oxidative stress. RNA-Seq and functional assessment revealed the presence of AD-related alterations in human OM cells and that different fuels and engine technologies elicit differential effects., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Sectional physics-based aerosol models imply a computational effort that hinders their use in building digital twins, real-time predictive control, and computer-based iterative optimization versus black-box approaches. The innovation of this paper lies in the proposal of a novel systematic methodology to optimize the number of size bins in sectional reduced-order models for particle concentration simulations. This allows its application in indoor air quality management and overcomes generalizability and data-dependency issues of black-box models. This method, based on k-means clustering, aims to ensure precision when tackling relatively fast fine and ultrafine particle simulations targeting the reduction of time and resource consumption from experimentally-determined aerosol size distribution time series. Consequently, three tests were carried out using combustion aerosols inside a custom-designed emission chamber to simulate emission hotspots in non-commercial and occupational settings. 2-, 3-, 4-, and 5-cluster classifications were evaluated for data coming from 13 particle size bins through silhouette analysis and the study of their temporal profiles. Results show that the 4-cluster classification summarizes the behavior of data in the 10–420 nm range, ensuing up to a 77 % improvement in the model's computational demand. Moreover, this method allows an accurate definition of the necessary size ranges to calculate nanoparticle concentrations inside the chamber and facilitates the interpretation of aerosol behavior and processes through the resulting clusters' temporal profiles. • K-means clustering method applied to indoor fine and ultrafine particle size range. • Providing a method for optimized sectional modeling for indoor environment management. • K-means simplifies aerosol bins and enhances data interpretation. • Method tested in a confined emission chamber with combustion aerosols. • Results show a reduction from 13 to 4 size bins in the 10–420 nm range. This article addresses the gap between the precision required in physics-based indoor air quality models and the need for low-computation models for digital twins, predictive control, and computer-based iterative optimization to deploy occupational health assessment tools effectively. [ABSTRACT FROM AUTHOR]

Abstract Background The aim of this study is to make a comparison of a new small sized nanoparticle monitoring instrument, Nanoscan SMPS, with more traditional large size instruments, known to be precise and accurate [Scanning Mobility Particle Sampler (SMPS) and Fast Mobility Particle Sizer (FMPS)], and with an older small size instrument with bulk measurements of 10–1000 nm particles (CPC3007). The comparisons are made during simulated exposure scenarios relevant to occupational hygiene studies. Methods Four scenarios were investigated: metal inert gas (MIG) welding, polyvinyl chloride (PVC) welding, cooking, and candle-burning. Ratios between results are compaed and Pearsson correlations analysis was performed. Results The highest correlation between the results is found between Nanoscan and SMPS, with Pearsson correlation coefficients above 0.9 for all scenarios. However, Nanoscan tended to overestimate the results from the SMPS; the ratio between the UFP concentrations vary between 1.44 and 2.01, and ratios of total concentrations between 1.18 and 2.33. CPC 3007 did not show comparable results with the remaining instruments. Conclusion Based on the results of this study, the choice of measurement equipment may be crucial when evaluating measurement results against a reference value or a limit value for nanoparticle exposure. This stresses the need for method development, standardisation, and harmonisation of particle sampling protocols before reference values are introduced. Until this is established, the SMPS instruments are the most reliable for quantification of the concentrations of UFP, but in a more practical occupational hygiene context, the Nanoscan SMPS should be further tested.

Ultrafine particles (UFP; diameter less than 100 nm) are ubiquitous in urban air, and an acknowledged risk to human health. At the same time, little is known about the immission situation at typical urban sites such as high-traffic roads, residential areas with a high amount of solid fuels for home heating or commercial and industrial areas due to missing legal requirements for measurements of UFP. Therefore, UFP were measured and evaluated in the (sub-)urban background as well as on spots influenced by these various anthropogenic local sources in the city of Augsburg, Germany, for the year 2017. In particular, the spatial and temporal correlations of the UFP concentrations between the seven measurement sites, the quantification and valuation of the contribution of local emitters with regard to their diurnal, weekly and seasonal variations and the influence of meteorological conditions on the formation and dispersion of UFP were investigated. Our analysis results demonstrate that urban UFP concentrations show a pronounced temporal and spatial variability. The mean concentration level of UFP varies between below 8,000 ultrafine particles/cm3 at the suburban background site and above 16,700 ultrafine particles/cm3 at the measurement station located next to a busy street canyon. At this particularly traffic-exposed measurement station, maximum concentrations of over 50,000 ultrafine particles/cm3 were measured. The additional UFP load caused by intensive traffic volume during evening rush hour in connection with the unfavourable exchange processes in the street canyon can be quantified to concentrations of 14,000 ultrafine particles/cm3 on average (compared to the immission situation of the urban background). An aggravating effect is brought about by inversion weather conditions in connection with air-polluted easterly winds, low wind speeds, lack of precipitation and very low mixing layer heights, such as over Augsburg at the end of January 2017, and cause peak concentrations of UFP.

• Focus: Dementia incidence and exposure to traffic-related air pollution (TRAP). • Study design: Community-based prospective cohort study in Seattle, WA, age 65+. • Exposure: predicted UFP, BC, and NO 2 from an extensive monitoring campaign. • Result: No evidence of a greater hazard of dementia incidence with TRAP exposures. • Conclude: Sensitivity and secondary analyses were in agreement; replication needed. While epidemiologic evidence links higher levels of exposure to fine particulate matter (PM 2.5) to decreased cognitive function, fewer studies have investigated links with traffic-related air pollution (TRAP), and none have examined ultrafine particles (UFP, ≤100 nm) and late-life dementia incidence. To evaluate associations between TRAP exposures (UFP, black carbon [BC], and nitrogen dioxide [NO 2 ]) and late-life dementia incidence. We ascertained dementia incidence in the Seattle-based Adult Changes in Thought (ACT) prospective cohort study (beginning in 1994) and assessed ten-year average TRAP exposures for each participant based on prediction models derived from an extensive mobile monitoring campaign. We applied Cox proportional hazards models to investigate TRAP exposure and dementia incidence using age as the time axis and further adjusting for sex, self-reported race, calendar year, education, socioeconomic status, PM 2.5 , and APOE genotype. We ran sensitivity analyses where we did not adjust for PM 2.5 and other sensitivity and secondary analyses where we adjusted for multiple pollutants, applied alternative exposure models (including total and size-specific UFP), modified the adjustment covariates, used calendar year as the time axis, assessed different exposure periods, dementia subtypes, and others. We identified 1,041 incident all-cause dementia cases in 4,283 participants over 37,102 person-years of follow-up. We did not find evidence of a greater hazard of late-life dementia incidence with elevated levels of long-term TRAP exposures. The estimated hazard ratio of all-cause dementia was 0.98 (95 % CI: 0.92–1.05) for every 2000 pt/cm3 increment in UFP, 0.95 (0.89–1.01) for every 100 ng/m3 increment in BC, and 0.96 (0.91–1.02) for every 2 ppb increment in NO 2. These findings were consistent across sensitivity and secondary analyses. We did not find evidence of a greater hazard of late-life dementia risk with elevated long-term TRAP exposures in this population-based prospective cohort study. [ABSTRACT FROM AUTHOR]

Although regular exercise improves overall well-being, increased physical activity results in enhanced breathing which consequently leads to elevated exposure to a variety of air pollutants producing adverse effects. It is well-known that one of these ambient air contaminants is ultrafine particles (UFP). Thus, this study aimed to (1) examine exposure to particle number concentrations (PNC) in size ranging from N20–1000 nm in different sport environments and (2) estimate the respective inhalation doses across varying activity scenarios based upon the World Health Organization recommendations for physical activity. PNC were continuously monitored (TSI P-Trak™ condensation particle counter) outdoors (Out1–Out2) and indoors (Ind1–Ind2; fitness clubs) over 4 weeks. Outdoor PNC (total median 12 563 # cm–3; means of 20 367 # cm–3 at Out1 and 7 122 # cm–3 at Out2) were approximately 1.6-fold higher than indoors (total median 7 653 # cm–3; means of 11 861 # cm–3 at Ind1 and 14 200 # cm–3 at Ind2). The lowest doses were inhaled during holistic group classes (7.91 × 107–1.87 × 108 # per kg body weight) whereas exercising with mixed cardio and strength training led to approximately 1.8-fold higher levels. In order to optimize the health benefit of exercises, environmental characteristics of the locations at which physical activities are conducted need to be considered. [ABSTRACT FROM AUTHOR]

Abstract Due to the negative health impacts, significant efforts have been directed towards investigating ultrafine particle (UFP) exposure in various indoor environments. As children spend approximately one third of their time in schools, educatory environments deserve particular attention; however, majority of past research has focused on UFP assessment in classrooms. Thus, this work aims to expand the characterization of UFP in primary schools by considering different indoor and outdoor school microenvironments and estimating inhalation doses for the respective students (6–11yrs old). Real-time UFP measurements were daily conducted (9:00–17:30) in 20 primary schools in Oporto (January–April 2014; October–February 2015) in classrooms, canteens, gyms, libraries, and concurrently outdoors. Overall, UFP concentrations showed large temporal and spatial variations. For classrooms (n = 73), median UFP (1.56 × 103–16.8 × 103 # cm−3) were lower than the corresponding levels in ambient air of schools (1.79 × 103–24.1 × 103 # cm−3). Outdoor emissions contributed to indoor UFP (indoor-to-outdoor ratios I/O of 0.0.30–0.85), but ventilation, room characteristics and its occupancy were identified as important parameters contributing to overall indoor UFP levels. Considering specific indoor school microenvironments, canteens were the microenvironment with the highest UFP levels (5.47 × 103–36.4 × 103 # cm−3), cooking conducted directly on school grounds resulted in significantly elevated UFP in the respective classrooms (p < 0.05); the lowest UFP were found in libraries (4.45 × 103–8.50 × 103 # cm−3) mostly due to the limited occupancies. Although students spend majority of their school time in classrooms (66–71%), classroom exposure was not consistently the predominant contributor to school total UFP inhalation dose (29–75%). Outdoor exposure contributed 23–70% of school dose (depending on UFP levels in ambient levels and/or conducted activities) whereas short periods of lunch break accounted for 8–40%. Therefore, when evaluating UFP exposure in educatory settings other microenvironments beyond classrooms should be an integral part of the study. Graphical abstract Image 1 Highlights • Ultrafine particles (UFP) assessed in various primary school microenvironments. • Overall UFP in classrooms (n = 73) were lower than the corresponding outdoor levels. • Ventilation, room characteristics and occupancy influenced indoor UFP levels. • Canteens exhibited the highest UFP levels, especially when meals cooked in schools. • Outdoor exposure contributed large part (∼up to 70%) of total school UFP dose. This work fills a gap providing information on levels of ultrafine particles in different indoor and outdoor microenvironments of primary schools. [ABSTRACT FROM AUTHOR]

This study evaluated how exposure to the ubiquitous air pollution component, ultrafine particles (UFPs), alters the olfactory bulb (OB) transcriptome. The study utilised a whole-body inhalation chamber to simulate real-life conditions and focused on UFPs due to their high translocation and deposition ability in OBs as well as their prevalence in ambient air. Female C57BL/6J mice were exposed to clean air or to freshly generated combustion derived UFPs for two weeks, after which OBs were dissected and mRNA transcripts were investigated using RNA sequencing analysis. For the first time, transcriptomics was applied to determine changes in mRNA expression levels occurring after subacute exposure to UFPs in the OBs. We found forty-five newly described mRNAs to be involved in air pollution-induced responses, including genes involved in odorant binding, synaptic regulation, and myelination signalling pathway, providing new gene candidates for future research. This study provides new insights for the environmental science and neuroscience fields and nominates future research directions. • UFP exposure alters gene expression in the olfactory bulb of mice. • Elevated expression of odorant binding proteins is observed in UFP-exposed olfactory bulb. • Immune defence protein, Bpifa1, shows increased expression after UFP exposure. • UFP exposure may disrupt neural functioning via the myelination pathway. • Study paves the way for new air pollution exposure biomarker identification. [ABSTRACT FROM AUTHOR]

Cooking is one of the main sources of indoor air pollutants, and may even exceed the contribution from outdoor sources. This pilot study examines the use of different flow-rate fans during cooking and tests whether continuing to run the fan after cooking significantly improves pollutant removal rates and integrated exposures. Tests were carried out in the Canadian Centre for Housing Technology's twin research houses, in Ottawa, Ontario. We completed the same cooking protocol 60 times on a gas stove, testing 6 different flow rates on three different over-the-range exhaust fans, while continuously measuring UFP, PM 2.5 , NO 2 , and NO. The fan was operated during cooking for all tests and then either turned off or left on after cooking for the duration of the three hour test. We estimated decay rates, source emission rates, and integrated exposures to measured pollutants following the cooking test. The results showed that while leaving the fan on after cooking generally increased decay rates, it had a relatively small effect on integrated exposures compared to the effects of fan flow rate and the specific fan used during cooking. For PM 2.5 , the effect of running an exhaust fan for 15 min after cooking was similar in magnitude to the impact of a 100 cfm increase in the flow rate used while cooking: both were associated with a decrease in 15-min integrated exposure of roughly 3  μg m −3 . This suggests that one can partially compensate for a low flow rate exhaust fan by continuing to run the fan after cooking. [ABSTRACT FROM AUTHOR]

Objective: To assess the spatiotemporal heterogeneity of lung-deposited particle surface area concentration (LDSA), while testing the long-term performance of a prototype of low-cost-low-maintenance LDSA sensors. One factor hampering epidemiological studies on fine to ultrafine particles (F-to-UFP) exposure is exposure error due to their high spatiotemporal heterogeneity, not reflected in particle mass. Though LDSA shows consistent associations between F-to-UFP exposure and health effects, LDSA data are limited. Methods: We measured LDSA in a network of ten sensors, including urban, suburban, and rural environments in Zurich, Switzerland. With traffic counts, traffic co-pollutant concentrations, and meteorological parameters, we assessed the drivers of the LDSA observations. Results: LDSA reflected the high spatiotemporal heterogeneity of F-to-UFP. With micrometeorological influences, local sources like road traffic, restaurants, air traffic, and residential combustion drove LDSA. The temporal pattern of LDSA reflected that of the local sources. Conclusion: LDSA may be a viable metric for inexpensively characterizing F-to-UFP exposure. The tested devices generated sound data and may significantly contribute to filling the LDSA exposure data gap, providing grounds for more statistically significant epidemiological studies and regulation of F-to-UFP., Competing Interests: Author MF was employed by the company Naneos Particle Solution GmbH. The remaining authors declare that they do not have any conflicts of interest., (Copyright © 2023 Edebeli, Spirig, Fluck, Fierz and Anet.)

A mobile laboratory unit (MOBILAB) with on-board instrumentation (Scanning Mobility Particle Sizer, SMPS; Ambient NOx analyzer) was used to measure size-resolved particle number concentrations (PNCs) of quasi-ultrafine particles (UFPs, 9–372 nm), along with NOx, in road microenvironments. On-road measurements were carried out in and around a large Greek urban agglomeration, the Thessaloniki Metropolitan Area (TMA). Two 2-week measurement campaigns were conducted during the warm period of 2011 and the cold period of 2012. During each sampling campaign, MOBILAB was driven through a 5-day inner-city route and a second 5-day external route covering in total a wide range of districts (urban, urban background, industrial and residential), and road types (major and minor urban roads, freeways, arterial and interurban roads). All routes were conducted during working days, in morning and in afternoon hours under real-world traffic conditions. Spatial classification of MOBILAB measurements involved the assignment of measurement points to location bins defined by the aspect ratio of adjacent urban street canyons (USCs). Source apportionment was further carried out, by applying Positive Matrix Factorization (PMF) to particle size distribution data. Apportioned PMF factors were interpreted, by employing a two-step methodology, which involved (a) statistical association of PMF factor contributions with 12 h air-mass back-trajectories ending at the TMA during MOBILAB measurements, and (b) Multiple Linear Regression (MLR) using PMF factor contributions as the dependent variables, while relative humidity, solar radiation flux, and vehicle speed were used as the independent variables. The applied data analysis showed that low-speed cruise and high-load engine operation modes are the two dominant sources of UFPs in most of the road microenvironments in the TMA, with significant contributions from background photochemical processes during the warm period, explaining the reversed seasonal variation of UFP concentrations, compared to those observed in cities across Northern Europe. It was also demonstrated that town planning exerts a profound effect on the mitigation of traffic emissions. [ABSTRACT FROM AUTHOR]

Background: Air pollution is a major global environmental risk factor. Since people spend most of their time indoors, the sole measure of outdoor concentrations is not sufficient to assess total exposure to air pollution. Therefore, the arising interest by the international community to indoor-outdoor relationships has led to the development of various techniques for the study of emission and exchange parameters among ambient and non-ambient pollutants. However, a standardised method is still lacking due to the complex release and dispersion of pollutants and the site conditions among studies. Methods: This review attempts to fill this gap to some extent by focusing on the analysis of the variety of site-specific approaches for the assessment of particulate matter in work and life environments. Results: First, the main analogies and differences between indoor and outdoor particles emerging from several studies are briefly described. Commonly-used indicators, sampling methods, and other approaches are compared. Second, recommendations for further studies based on recent results in order to improve the assessment and management of those issues are provided. Conclusions: This review is a step towards a comprehensive understanding of indoor and outdoor exposures which may stimulate the development of innovative tools for further epidemiological and multidisciplinary research.

Membrane transporters are important for maintaining brain homeostasis by regulating the passage of solutes into, out of, and within the brain. Growing evidence suggests neurotoxic effects of air pollution exposure and its contribution to neurodegenerative disorders, including Alzheimer's disease (AD), yet limited knowledge is available on the exact cellular impacts of exposure. This study investigates how exposure to ubiquitous solid components of air pollution, ultrafine particles (UFPs), influence brain homeostasis by affecting protein levels of membrane transporters. Membrane transporters were quantified and compared in brain cortical samples of wild-type and the 5xFAD mouse model of AD in response to subacute exposure to inhaled UFPs. The cortical ASCT1 and ABCB1 transporter levels were elevated in wild-type and 5xFAD mice subjected to a 2-week UFP exposure paradigm, suggesting impairment of brain homeostatic mechanisms. This study provides new insight on the molecular mechanisms underlying adverse effects of air pollution on the brain. • Ultrafine particulate matter induces changes in brain transporter protein levels. • Subacute exposure to air pollution increases ABCB1 and ASCT1 transporter levels. • The changes were found in both wildtype mice and 5xFAD model of Alzheimer's disease. [ABSTRACT FROM AUTHOR]

Urban canyons increase overall air pollution concentrations at the street level. Yet, due to the difficulty in characterizing such geometric features over a regional area, they are rarely included in the evaluation of population exposures. This study combines measurements of ultrafine particles (UFP) with land-use regression techniques in order to capture the determinants of near-road concentrations of UFP while specifically accounting for urban canyon effects. Using the mean UFP concentration measured within a set of urban canyons (over 1000 road segments) as the dependent variable, we investigated the effects of a number of urban canyon descriptors (width, height, contiguity, vegetation, and road class) through a multivariate linear regression. Our models are adjusted for the effects of meteorology. The signs and values of the regression coefficients are qualitatively consistent with what is already known about urban canyons: increased building height (b height = 0.004; 95% CI: 0.001, 0.007) along with decreased canyon width (b width = −0.007; 95% CI: −0.012, −0.002) serve to worsen the air quality therein, while increased tree cover (b trees = −1.762; 95% CI: −2.236, −1.289) improves air quality. We also observed that the difference in UFP levels on both sides of the canyon increased with increasing street width (b width = 0.113; 95% CI: 0.061, 0.165), and with wind direction more perpendicular to the street. We conclude that it is possible to include urban canyon effects in the development of air pollution exposure surfaces thus refining the assessment of population exposure to air pollution in urban microenvironments. [ABSTRACT FROM AUTHOR]

Exposure to the ambient particulate matters (PM) has been associated with the morbidity and mortality of cardiopulmonary diseases. Compared with coarse particles, ultrafine particles (UFP) absorb or condense higher concentration of toxic air pollutants and are easily inhaled into the lung. However, the combined effects of UFP and air pollutants on human health are still poorly understood. In this study, a co-exposure in vitro model of amorphous silica nanoparticles (nano-SiO2) and methyl mercury (MeHg) was established to investigate their combined effects and the potential joint action type. Lung adenocarcinoma cells (A549) were exposed to either nano-SiO2 or MeHg alone, or a combination of both. Factorial design was applied to analyze their potential joint action type. Higher interfacial energy was observed in the mixed solution of nano-SiO2 and MeHg. The intracellular content of both silicon and mercury in combination group were much higher than those in single exposure groups. In addition, the co-exposure of nano-SiO2 and MeHg enhanced the reactive oxygen species (ROS) generation, lipid peroxidation and reduced the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-px). The excessive oxidative stress led to oxidative DNA damage as well as cellular apoptosis. Factorial design analysis demonstrated that additive and synergistic interactions were responsible for the combined toxicity of nano-SiO2 and MeHg. [ABSTRACT FROM AUTHOR]

Exposure to particulate matter (PM), a component of urban air pollution, may cause adverse effects in the brain. Although the exact mechanisms involved are unknown, both oxidative and inflammatory responses have been reported. Since the main route of exposure to particulate matter is through inhalation, there is a potential for compounds to directly enter the brain and alter normal cellular function. Enhancement in both oxidative stress and neuroinflammatory markers has been observed in neurodegenerative disorders and PM-induced potentiation of these events may accelerate the disease process. The objective of this pilot study was to use normal human brain cells, a model system which has not been previously used, to assess cell-type-specific responses after exposure to ultrafine particles (UFP). Human microglia, neurons, and astrocytes were grown separately or as co-cultures and then exposed to aqueous UFP suspensions. Reactive Oxygen Species (ROS) formation and the proinflammatory cytokine tumor necrosis factor alpha (TNF-α) were measured as markers of oxidative stress or inflammation respectively. Our results revealed that after exposure to 2µg/ml of particles, normal human neurons exhibit a decrease in ROS formation and an increase in TNF-α. The observed decrease in ROS formation persisted in the presence of glial cells, which contrasts previous studies done in rodent cells reporting that PM-induced microglial activation modulates neuronal responses. Our study indicates that human CNS cells may respond differently compared to rodent cells and that their use may be more predictive in risk assessment. [ABSTRACT FROM AUTHOR]

Abstract: Proximity to road traffic involves higher health risks because of atmospheric pollutants. In addition to outdoor air, indoor air quality contributes to overall exposure. In the framework of the BREATHE study, indoor and outdoor air pollution was assessed in 39 schools in Barcelona. The study quantifies indoor and outdoor air quality during school hours of the BREATHE schools. High levels of fine particles (PM2.5), nitrogen dioxide (NO2), equivalent black carbon (EBC), ultrafine particle (UFP) number concentration and road traffic related trace metals were detected in school playgrounds and indoor environments. PM2.5 almost doubled (factor of 1.7) the usual urban background (UB) levels reported for Barcelona owing to high school-sourced PM2.5 contributions: [1] an indoor-generated source characterised mainly by organic carbon (OC) from organic textile fibres, cooking and other organic emissions, and by calcium and strontium (chalk dust) and; [2] mineral elements from sand-filled playgrounds, detected both indoors and outdoors. The levels of mineral elements are unusually high in PM2.5 because of the breakdown of mineral particles during playground activities. Moreover, anthropogenic PM components (such as OC and arsenic) are dry/wet deposited in this mineral matter. Therefore, PM2.5 cannot be considered a good tracer of traffic emissions in schools despite being influenced by them. On the other hand, outdoor NO2, EBC, UFP, and antimony appear to be good indicators of traffic emissions. The concentrations of NO2 are 1.2 times higher at schools than UB, suggesting the proximity of some schools to road traffic. Indoor levels of these traffic-sourced pollutants are very similar to those detected outdoors, indicating easy penetration of atmospheric pollutants. Spatial variation shows higher levels of EBC, NO2, UFP and, partially, PM2.5 in schools in the centre than in the outskirts of Barcelona, highlighting the influence of traffic emissions. Mean child exposure to pollutants in schools in Barcelona attains intermediate levels between UB and traffic stations. [Copyright &y& Elsevier]

Abstract: Background: Increasing evidence suggests that ultrafine particles (UFPs) may contribute to cardiorespiratory morbidity. We examined the relationship between near road UFPs and several traffic and built environment factors to identify predictors that may be used to estimate exposures in population-based studies. Black carbon (BC) was also examined. Methods: Data were collected on up to 6 occasions at 73 sites in Montreal, Canada over 6-week period during summer, 2012. After excluding highly correlated variables, road width, truck ratio (trucks/total traffic), building height, land zoning parameters, and meteorological factors were evaluated. Random-effect models were used to estimate percent changes in UFP and BC concentrations with interquartile changes in each candidate predictor adjusted for meteorological factors. Results: Mean pollutant concentrations varied substantially across sites (UFP range: 1977–94, 798particles/cm3; BC range: 29–9460ng/m3). After adjusting for meteorology, interquartile increases in road width (14%, 95% CI: 0, 30), building height (13%, 95% CI: 5, 22), and truck ratio (13%, 95% CI: 3, 23) were the most important predictors of mean UFP concentrations. Road width (28%, 95% CI: 9, 51) and industrial zoning (18%, 95% CI: 2, 37) were the strongest predictors of maximum UFP concentrations. Industrial zoning (35%, 95% CI: 9, 67) was the strongest predictor of BC. Conclusions: A number of traffic and built environmental factors were identified as important predictors of near road UFP and BC concentrations. Exposure models incorporating these factors may be useful in evaluating the health effects of traffic related air pollution. [Copyright &y& Elsevier]

Abstract: Ultrafine particles (UFP) have complex spatial and temporal patterns that can be difficult to characterize, especially in areas with multiple source types. In this study, we utilized mobile monitoring and statistical modeling techniques to determine the contributions of both roadways and aircraft to spatial and temporal patterns of UFP in the communities surrounding an airport. A mobile monitoring campaign was conducted in five residential areas surrounding T.F. Green International Airport (Warwick, RI, USA) for one week in both spring and summer of 2008. Monitoring equipment and geographical positioning system (GPS) instruments were carried following scripted walking routes created to provide broad spatial coverage while recognizing the complexities of simultaneous spatial and temporal heterogeneity. Autoregressive integrated moving average models (ARIMA) were used to predict UFP concentrations as a function of distance from roadway, landing and take-off (LTO) activity, and meteorology. We found that distance to the nearest Class 2 roadway (highways and connector roads) was inversely associated with UFP concentrations in all neighborhoods. Departures and arrivals on a major runway had a significant influence on UFP concentrations in a neighborhood proximate to the end of the runway, with a limited influence elsewhere. Spatial patterns of regression model residuals indicate that spatial heterogeneity was partially explained by traffic and LTO terms, but with evidence that other factors may be contributing to elevated UFP close to the airport grounds. Regression model estimates indicate that mean traffic contributions exceed mean LTO contributions, but LTO activity can dominate the contribution during some minutes. Our combination of monitoring and statistical modeling techniques demonstrated contributions from major surrounding runways and LTO activity to UFP concentrations near a mid-sized airport, providing a methodology for source attribution within a community with multiple distinct sources. [Copyright &y& Elsevier]

Abstract: Background: Iron and steel industry is an important source of air pollution emissions. Few studies have investigated cardiovascular effects of air pollutants emitted from steel plants. Objective: We examined the influence of outdoor air pollution in the vicinity of a steel plant on cardiovascular physiology in Sault Ste. Marie, Canada. Methods: Sixty-one healthy, non-smoking subjects (females/males=33/28, median age 22 years) spent 5 consecutive 8-hour days outdoors in a residential area neighbouring a steel plant, or on a college campus approximately 5 kilometres away from the plant, and then crossed over to the other site with a 9-day washout. Mid day, subjects underwent daily 30-minute moderate intensity exercise. Blood pressure (BP) and pulse rate were determined daily and post exercise at both sites. Flow-mediated vasodilation (FMD) was determined at the site near the plant. Air pollution was monitored at both sites. Mixed-effects regressions were run for statistical associations, adjusting for weather variables. Results: Concentrations of ultrafine particles, sulphur dioxide (SO2), nitrogen dioxide (NO2) and carbon monoxide (CO) were 50–100% higher at the site near the plant than at the college site, with minor differences in temperature, humidity, and concentrations of particulate matter ≤2.5μm in size (PM2.5) and ozone (O3). Resting pulse rate [mean (95% confidence interval)] was moderately higher near the steel plant [+1.53bpm (0.31, 2.78)] than at the college site, male subjects having the highest pulse rate elevation [+2.77bpm (0.78, 4.76)]. Resting systolic and diastolic BP and pulse pressure, and post-exercise BP and pulse rate were not significantly different between two sites. Interquartile range concentrations of SO2 (2.9ppb), NO2 (5.0ppb) and CO (0.2ppm) were associated with increased pulse rate [0.19bpm (−0.00, 0.38), 0.86bpm (0.03, 1.68), and 0.11bpm (0.00, 0.22), respectively], ultrafine particles (10,256count/cm3) associated with increased pulse pressure [0.85mmHg (0.23, 1.48)], and NO2 and CO inversely associated with FMD [−0.14% (−0.31, 0.02), −0.02% (−0.03, −0.00), respectively]. SO2 during exercise was associated with increased pulse rate [0.26bpm (0.01, 0.51)]. Conclusion: Air quality in residential areas near steel plants may influence cardiovascular physiology. [Copyright &y& Elsevier]

Growing evidence links traffic-related air pollution (TRAP) to adverse health effects. We designed an innovative and extensive mobile monitoring campaign to characterize TRAP exposure levels for the Adult Changes in Thought (ACT) study, a Seattle-based cohort. The campaign measured particle number concentration (PNC) to capture ultrafine particles (UFP), black carbon (BC), nitrogen dioxide (NO 2 ), fine particulate matter (PM 2.5 ), and carbon dioxide (CO 2 ) at 309 roadside sites within a large, 1200 land km 2 (463 mi 2 ) area representative of the cohort. We collected about 29 two-minute measurements at each site during all seasons, days of the week, and most times of the day over a 1-year period. Validation showed good agreement between our BC, NO 2 , and PM 2.5 measurements and monitoring agency sites ( R 2 = 0.68-0.73). Universal kriging-partial least squares models of annual average pollutant concentrations had cross-validated mean square error-based R 2 (and root mean square error) values of 0.77 (1177 pt/cm 3 ) for PNC, 0.60 (102 ng/m 3 ) for BC, 0.77 (1.3 ppb) for NO 2 , 0.70 (0.3 μg/m 3 ) for PM 2.5 , and 0.51 (4.2 ppm) for CO 2 . Overall, we found that the design of this extensive campaign captured the spatial pollutant variations well and these were explained by sensible land use features, including those related to traffic.

In epidemiological studies, ultrafine particle (UFP) data from a single monitoring site are generally used as a measure of population exposure potentially resulting in exposure misclassification. From August 2009 to October 2010, 1-week campaigns were conducted during each season. The temporal and spatial variations of UFP number size distributions were investigated at 12 monitoring sites distributed across a 9 × 9 km urban area in Rochester, New York using a Fast Mobility Particle Sizer spectrometer. The overall average number concentrations of 5.6- to 560-nm particles in summer, winter, spring, and fall were 9,025, 10,939, 4,955, and 14,485 cm, respectively. Coefficients of divergence and correlation coefficients were calculated between site pairs to assess the spatial heterogeneity in the particle number size distributions. Moderate spatial divergence and uniform temporal variation were found for the chosen sites. Elevated UFP number concentrations were observed near highways, off-road diesel engines, and residential wood combustion sources, indicating significant contributions to the UFP exposure of people living adjacent to these sources. Our results suggest that one stationary monitoring site may not represent the actual human UFP exposure over a whole urban area. [ABSTRACT FROM AUTHOR]

Abstract: A new parameterization for size resolved ultrafine particles (UFP) traffic emissions is proposed based on the results of PARTICULATES project (). It includes the emission factors from the (total number of particles, #/km/veh), the shape of the corresponding particle size distribution given in PARTICULATES and data for the traffic activity. The output of the model UFPEM (UltraFine Particle Emission Model) is a sum of continuous distributions of ultrafine particles emissions per vehicle type (passenger cars and heavy duty vehicles), fuel (petrol and diesel) and average speed representative for urban, rural and highway driving. The results from the parameterization are compared with measured total number of ultrafine particles and size distributions in a tunnel in Antwerp (Belgium). The measured UFP concentration over the entire campaign shows a close relation to the traffic activity. The modelled concentration is found to be lower than the measured in the campaign. The average emission factor from the measurement is 4.29E+14 #/km/veh whereas the calculated is around 30% lower. A comparison of emission factors with literature is done as well and in overall a good agreement is found. For the size distributions it is found that the measured distributions consist of three modes — Nucleation, Aitken and accumulation and most of the ultrafine particles belong to the Nucleation and the Aitken modes. The modelled Aitken mode (peak around 0.04–0.05μm) is found in a good agreement both as amplitude of the peak and the number of particles whereas the modelled Nucleation mode is shifted to smaller diameters and the peak is much lower that the observed. Time scale analysis shows that at 300m in the tunnel coagulation and deposition are slow and therefore neglected. The UFPEM emission model can be used as a source term in dispersion models. [Copyright &y& Elsevier]

Epidemiological studies reveal that air pollution exposure may exacerbate neurodegeneration. Ultrafine particles (UFPs) are pollutants that remain unregulated in ambient air by environmental agencies. Due to their small size (<100 nm), UFPs have the most potential to cross the bodily barriers and thus impact the brain. However, little information exists about how UFPs affect brain function. Alzheimer's disease (AD) is the most common form of dementia, which has been linked to air pollutant exposure, yet limited information is available on the mechanistic connection between them. This study aims to decipher the effects of UFPs in the brain and periphery using the 5xFAD mouse model of AD. In our study design, AD mice and their wildtype littermates were subjected to 2-weeks inhalation exposure of UFPs in a whole-body chamber. That subacute exposure did not affect the amyloid-beta accumulation. However, when multiple cytokines were analyzed, we found increased levels of proinflammatory cytokines in the brain and periphery, with a predominant alteration of interferon-gamma in response to UFP exposure in both genotypes. Following exposure, mitochondrial superoxide dismutase was significantly upregulated only in the 5xFAD hippocampi, depicting oxidative stress induction in the exposed AD mouse group. These data demonstrate that short-term exposure to inhaled UFPs induces inflammation without affecting amyloid-beta load. This study provides a better understanding of adverse effects caused by short-term UFP exposure in the brain and periphery, also in the context of AD., (Copyright © 2022 University of Eastern Finland. Published by Elsevier B.V. All rights reserved.)

Significant efforts have been directed towards addressing the adverse health effects of atmospheric particles, emphasizing the relevance of indoor exposure. Homes represent an indoor environment where human spend the majority of their time. Thus, the objective of this work was to concurrently assess different matrix of indoor particles considering both mass (PM 10 , PM 2.5) and number (N 20-1000) concentrations in indoor and outdoor air of homes (n = 65). Real-time measurements (PM 10 , PM 2.5 , UFP) were conducted simultaneously during 48 h in dwellings situated in Oporto, Portugal. In 75% of homes, indoor PM 2.5 (mean = 53 μg m−3) exceeded limit of 25 μg m−3, for PM 10 (mean = 57 μg m−3) 41% of homes demonstrated average levels higher than 50 μg m−3, thus indicating potential risks. Indoor PM 10 was mostly (82–99%) composed of PM 2.5 , both PM were highly correlated (|rs|>0.9655), thus suggesting the similar origin. Indoor PM originated from infiltrations of outdoor emissions; ∼70% of homes exhibited indoor to outdoor (I/O) ratio < 1. On the contrary, UFP indoors (mean = 13.3 × 103 # cm−3) were higher than outdoors (mean = 10.0 × 103 # cm−3). Indoor UFP spatially varied as follows: kitchens > living rooms > bedrooms. UFP indoors were poorly correlated (|rs| = 0.456) with outdoor concentrations, I/O ratios showed that indoor UFP predominantly originated from indoor emission sources (combustions). Therefore, in order to reduce exposure to UFP and protect public health, the primary concerns should be focused on controlling emissions from indoor sources. Image 1 • Indoor UFP were poorly correlated with PM (|r s |<0.552–0.594). • Indoor UFP were approximately 30% higher indoors that outdoors (|r s | = 0.456). • Indoor UFP mainly originated from indoor sources (mean I/O = 1.59, range 0.27–6.67). • Indoor PM 2.5 mostly resulted from outdoor emissions infiltrations (mean I/O = 0.88). • PM 2.5 and PM 10 exceeded WHO daily limits in 75% and 41% of homes, respectively. This work fills a gap providing concurrent information on different PM mass/number size fractions (PM 10 , PM 2.5 and UFP) in indoor and outdoor air of home environments. [ABSTRACT FROM AUTHOR]

Accurate assessment of particulate matter (PM) dose and respiratory deposition is essential to better understand the risks of exposure to PM and, consequently, to develop the respective risk-control strategies. In homes, this is especially relevant in regards to ultrafine particles (UFP; <0.1 μm) which origin in these environments is mostly due to indoor sources. Thus, this study aimed to estimate inhalation doses for different PM mass/number size fractions (i.e., PM 10 , PM 2.5 and UFP) in indoor air of residential homes and to quantify the deposition (total, regional and lobar) in human respiratory tract for both newborn children and mothers. Indoor real-time measurements of PM 10 , PM 2.5 and UFP were conducted in 65 residential homes situated in Oporto metropolitan area (Portugal). Inhalation doses were estimated based on the physical characteristics of individual subjects and their activity patterns. The multi-path particle dosimetry model was used to quantify age-specific depositions in human respiratory tract. The results showed that 3-month old infants exhibited 4-fold higher inhalation doses than their mothers. PM 10 were primarily deposited in the head region (87%), while PM 2.5 and UFP depositions mainly occurred in the pulmonary area (39% and 43%, respectively). Subject age affected the pulmonary region and the total lung deposition; higher deposition being observed among the newborns. Similarly, lower lobes (left lobe: 37% and right lobe: 30%) received higher PM deposition than upper and middle lobes; right lobes lung are prone to be more susceptible to respiratory problems, since asymmetric deposition was observed. Considering that PM-related diseases occur at specific sites of respiratory system, quantification of site-specific particle deposition should be predicted in order to better evidence the respective health outcomes resulting from inhaled PM. Unlabelled Image • Inhalation dose and deposition of PM 10 , PM 2.5 , and UFP estimated in child and adults. • Newborns (3 months) exhibited 4-fold higher inhalation doses than their mothers. • PM 10 deposited in head region, PM 2.5 and UFP depositions occurred in pulmonary area. • Lower lobes received higher PM deposition than upper and middle lobes. • Right lobes lung are prone to be more susceptible to respiratory problems. [ABSTRACT FROM AUTHOR]

Conducting aerobic activity on regular basis is recognised as one of the steps to maintain healthier lifestyle. The positive outcomes though can be outweighed if conducted in polluted atmosphere. Furthermore, the specific inhalation during exercising, which results in bypass of nasal filtration systems and deeper penetration into the respiratory system, might result in higher risks especially to pollutants such as ultrafine particles (UFP), which aerodynamic particle diameter are <100 nm. Thus, this work aims to evaluate UFP levels at sites used for conducting physical sport activities outdoors and to estimate the respective inhalation doses considering various scenarios and different physical activities. Monitoring of UFP was conducted during three weeks (May–June 2015) at four different sites (S1–S4) regularly used to conduct physical exercising. The results showed that UFP highly varied (medians 5.1–20.0 × 103 # cm−3) across the four sites, with the highest UFP obtained when exercising next to trafficked streets whereas S3 and S4 (a garden and city park) exhibited 2–4 times lower UFP. In view of the obtained UFP concentrations, the estimated inhalation doses ranged 1.73 × 108–3.81 × 108 # kg−1 when conducting moderately intense sport activities and 1.93 × 108–5.95 × 108 # kg−1 for highly intense ones. Highly intense activities (i.e. running) led to twice higher UFP exposure; children and youths (5–17 yrs old) experienced 203–267% higher doses. Considering the age– and gender– differences, estimated UFP doses of males were 1.1–2.8 times higher than of females. Finally, UFP inhalation doses estimated for walking (commuting to work and/or schools) were 1.6–7.5 times lower than when conducting sport activities. Thus to protect public health and to promote healthy and physically active lifestyle, strategies to minimize the negative impacts of air pollution should be developed and implemented. Image 1 • Ultrafine particles levels (UFP) while exercising outdoors were monitored. • The obtained UFP ranged between 5.1 and 20.0 × 103 # cm−3 across four sites. • At trafficked streets UFP levels were 2–4 times higher than at a park and a garden. • UFP levels were associated with meteorological parameters (T, RH, wind speed). • Estimated inhalation doses were ∼ twice higher for highly intense sport activities. This work fills a gap providing information on levels of ultrafine particles during conducting different outdoor physical activities. [ABSTRACT FROM AUTHOR]

Significant efforts have been directed towards addressing the adverse health effects of atmospheric particles, emphasizing the relevance of indoor exposure. Homes represent an indoor environment where human spend the majority of their time. Thus, the objective of this work was to concurrently assess different matrix of indoor particles considering both mass (PM 10 , PM 2.5 ) and number (N 20-1000 ) concentrations in indoor and outdoor air of homes (n = 65). Real-time measurements (PM 10 , PM 2.5 , UFP) were conducted simultaneously during 48 h in dwellings situated in Oporto, Portugal. In 75% of homes, indoor PM 2.5 (mean = 53 μg m -3 ) exceeded limit of 25 μg m -3 , for PM 10 (mean = 57 μg m -3 ) 41% of homes demonstrated average levels higher than 50 μg m -3 , thus indicating potential risks. Indoor PM 10 was mostly (82-99%) composed of PM 2.5 , both PM were highly correlated (|rs|>0.9655), thus suggesting the similar origin. Indoor PM originated from infiltrations of outdoor emissions; ∼70% of homes exhibited indoor to outdoor (I/O) ratio < 1. On the contrary, UFP indoors (mean = 13.3 × 10 3 # cm -3 ) were higher than outdoors (mean = 10.0 × 10 3 # cm -3 ). Indoor UFP spatially varied as follows: kitchens > living rooms > bedrooms. UFP indoors were poorly correlated (|rs| = 0.456) with outdoor concentrations, I/O ratios showed that indoor UFP predominantly originated from indoor emission sources (combustions). Therefore, in order to reduce exposure to UFP and protect public health, the primary concerns should be focused on controlling emissions from indoor sources., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Exposure to ambient particulate matter (PM) has been linked to adverse pulmonary and cardiovascular health effects. Activation of both inflammatory and oxidative stress pathways has been observed and may be a probable cause of these outcomes. We tested the hypothesis that in human monocytes, PM-induced oxidative and inflammatory responses are interrelated. A human monocytic cell line (THP-1) was used to determine if dose and differentiation state plays a role in the cellular response after a 24hr exposure to particles. Primary human monocytes derived from eight female, non-smoker donors (aged: 21, 24, 27, 28, 48, 49, 54 & 60yo) were used to determine if the age of donors modulates the response. Cells were treated with aqueous suspensions of ambient ultrafine particles (UFP, defined as smaller than 0.2µm in size) or a media control for 24hr. After exposure, reactive oxygen species (ROS) formation was increased irrespective of dose or differentiation state of THP-1 cells. In the primary human monocytes, ROS formation was not significantly changed. The release of the proinflammatory cytokine, tumor necrosis factor alpha (TNF-α), was dose-dependent and greatest in differentiated compared to undifferentiated THP-1 cells exposed to UFP. In the Primary human monocytes, TNF-α secretion was increased irrespective of the age of the donor. Our results suggest that after a 24hr exposure to particles, general reactive oxygen species formation was nonspecific and uncorrelated to cytokine secretion which was consistently enhanced. Cytokines play an important role in orchestrating many immune responses and thus the ability of ambient particles to enhance robust secretion of a proinflammatory cytokine from primary human monocytes, and how this may influence the response to pathogens and alter disease states, needs to be further evaluated., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Background: Ultrafine particles (UFP) of biogenic and anthropogenic origin occur in high numbers in the ambient atmosphere. In addition, aerosols containing ultrafine powders are used for the inhalation therapy of various diseases. All these facts make it necessary to obtain comprehensive knowledge regarding the exact behavior of UFP in the respiratory tract., Methods: Theoretical simulations of local UFP deposition are based on previously conducted inhalation experiments, where particles with various sizes (0.04, 0.06, 0.08, and 0.10 µm) were administered to the respiratory tract by application of the aerosol bolus technique. By the sequential change of the lung penetration depth of the inspired bolus, different volumetric lung regions could be generated and particle deposition in these regions could be evaluated. The model presented in this contribution adopted all parameters used in the experiments. Besides the obligatory comparison between practical and theoretical data, also advanced modeling predictions including the effect of varying functional residual capacity (FRC) and respiratory flow rate were conducted., Results: Validation of the UFP deposition model shows that highest deposition fractions occur in those volumetric lung regions corresponding to the small and partly alveolated airways of the tracheobronchial tree. Particle deposition proximal to the trachea is increased in female probands with respect to male subjects. Decrease of both the FRC and the respiratory flow rate results in an enhancement of UFP deposition., Conclusions: The study comes to the conclusion that deposition of UFP taken up via bolus inhalation is influenced by a multitude of factors, among which lung morphometry and breathing conditions play a superior role., Competing Interests: The author has no conflicts of interest to declare.

Background: Inhaled ultrafine particles (UFP) may induce greater adverse respiratory effects than larger particles occurring in the ambient atmosphere. Due to this potential of UFP to act as triggers for diverse lung injuries medical as well as physical research has been increasingly focused on the exact deposition behavior of the particles in lungs of various probands. Main purpose of the present study was the presentation of experimental and theoretical data of total, regional, and local UFP deposition in the lungs of men and women., Methods: Both experiments and theoretical simulations were carried out by using particle sizes of 0.04, 0.06, 0.08, and 0.10 µm [number median diameters (NMD)]. Inhalation of UFP took place by application of predefined tidal volumes (500, 750, and 1,000 mL) and respiratory flow rates (150, 250, 375, and 500 mL·s(-1)). For male subjects a functional residual capacity (FRC) of 3,911±892 mL was measured, whereas female probands had a FRC of 3,314±547 mL. Theoretical predictions were based on (I) a stochastic model of the tracheobronchial tree; (II) particle transport computations according to a random walk algorithm; and (III) empirical formulae for the description of UFP deposition., Results: Total deposition fractions (TDF) are marked by a continuous diminution with increasing particle size. Whilst particles measuring 0.04 µm in size deposit in the respiratory tract by 40-70%, particles with a size of 0.10 µm exhibit deposition values ranging from 20% to 45%. Except for the largest particles studied here TDF of female probands are higher than those obtained for male probands. Differences between experimental and theoretical results are most significant for 0.10 µm particles, but never exceed 20%. Predictions of regional (extrathoracic, tracheobronchial, alveolar) UFP deposition show clearly that females tend to develop higher tracheobronchial and alveolar deposition fractions than males. This discrepancy is also confirmed by airway generation-specific deposition, which is permanently higher in women than in men., Conclusions: From the experimental data and modeling predictions it can be concluded that females bear a slightly higher potential to develop lung insufficiencies after exposure to UFP than males. Besides higher deposition fractions occurring in female subjects, also total lung deposition dose is noticeably enhanced.