Ambient ultrafine particles exacerbate oxygen desaturation during sleep in patients with chronic obstructive pulmonary disease: New insights into the effect spectrum of ultrafine particles on susceptible populations.

The health effects of ultrafine particles (UFPs) are of growing global concern, but the epidemiological evidence remains limited. Sleep-disordered breathing (SDB) characterized by hypoxemia is a prevalent condition linked to many debilitating chronic diseases. However, the role of UFPs in the development of SDB is lacking. Therefore, this prospective panel study was performed to specifically investigate the association of short-term exposure to UFPs with SDB parameters in patients with chronic obstructive pulmonary disease (COPD). Ninety-one COPD patients completed 226 clinical visits in Beijing, China. Personal exposure to ambient UFPs of 0-7 days was estimated based on infiltration factor and time-activity pattern. Real-time monitoring of sleep oxygen saturation, spirometry, respiratory questionnaires and airway inflammation detection were performed at each clinical visit. Generalized estimating equation was used to estimate the effects of UFPs. Exposure to UFPs was significantly associated with increased oxygen desaturation index (ODI) and percent of the time with oxygen saturation below 90 % (T90), with estimates of 21.50 % (95%CI: 6.38 %, 38.76 %) and 18.75 % (95%CI: 2.83 %, 37.14 %), respectively, per 3442 particles/cm3 increment of UFPs at lag 0-3 h. Particularly, UFPs' exposure within 0-7 days was positively associated with the concentration of alveolar nitric oxide (CaNO), and alveolar eosinophilic inflammation measured by CaNO exceeding 5 ppb was associated with 29.63 % and 33.48 % increases in ODI and T90, respectively. In addition, amplified effects on oxygen desaturation were observed in current smokers. Notably, individuals with better lung function and activity tolerance were more affected by ambient UFPs due to longer time spent outdoors. To our knowledge, this is the first study to link UFPs to hypoxemia during sleep and uncover the key role of alveolar eosinophilic inflammation. Our findings provide new insights into the effect spectrum of UFPs and potential environmental and behavioral intervention strategies to protect susceptible populations.

Male-Biased Vulnerability of Mouse Brain Tryptophan/Kynurenine and Glutamate Systems to Adolescent Exposures to Concentrated Ambient Ultrafine Particle Air Pollution.

Air pollution (AP) exposures have been associated with numerous neurodevelopmental and psychiatric disorders, including autism spectrum disorder, attention deficit hyperactivity disorder and schizophrenia, all male-biased disorders with onsets from early life to late adolescence/early adulthood. While prior experimental studies have focused on effects of AP exposures during early brain development, brain development actually extends well into early adulthood. The current study in mice sought to extend the understanding of developmental brain vulnerability during adolescence, a later but significant period of brain development and maturation to the ultrafine particulate (UFPs) component of AP, considered its most reactive component. Additionally, it examined adolescent response to UFPs when preceded by earlier developmental exposures, to ascertain the trajectory of effects and potential enhancement or mitigation of adverse consequences. Outcomes focused on shared features associated with multiple neurodevelopmental disorders. For this purpose, C57Bl/6J mice of both sexes were exposed to ambient concentrated UFPs or filtered air from PND (postnatal day) 4-7 and PND10-13, and again at PND39-42 and 45-49, resulting in 3 exposure postnatal/adolescent treatment groups per sex: Air/Air, Air/UFP, and UFP/UFP. Features common to neurodevelopmental disorders were examined at PND50. Mass exposure concentration from postnatal exposure averaged 44.34 µg/m3 and the adolescent exposure averaged 49.18 µg/m3. Male brain showed particular vulnerability to UFP exposures in adolescence, with alterations in frontal cortical and striatal glutamatergic and tryptophan/serotonergic neurotransmitters and concurrent reductions in levels of astrocytes in corpus callosum and in serum cytokine levels, with combined exposures resulting in significant reductions in corpus callosum myelination and serum corticosterone. Reductions in serum corticosterone in males correlated with reductions in neurotransmitter levels, and reductions in striatal glutamatergic function specifically correlated with reductions in corpus callosum astrocytes. UFP-induced changes in neurotransmitter levels in males were mitigated by prior postnatal exposure, suggesting potential adaptation, whereas reductions in corticosterone and in corpus callosum neuropathological effects were further strengthened by combined postnatal and adolescent exposures. UFP-induced changes in females occurred primarily in striatal dopamine systems and as reductions in serum cytokines only in response to combined postnatal and adolescent exposures. Findings in males underscore the importance of more integrated physiological assessments of mechanisms of neurotoxicity. Further, these findings provide biological plausibility for an accumulating epidemiologic literature linking air pollution to neurodevelopmental and psychiatric disorders. As such, they support a need for consideration of the regulation of the UFP component of air pollution.

Physicochemical Characterization of the Particulate Matter in New Jersey/New York City Area, Resulting from the Canadian Quebec Wildfires in June 2023.

The global increase in wildfires, primarily driven by climate change, significantly affects air quality and health. Wildfire-emitted particulate matter (WFPM) is linked to adverse health effects, yet the toxicological mechanisms are not fully understood given its physicochemical complexity and the lack of spatiotemporal exposure data. This study focuses on the physicochemical characterization of WFPM from a Canadian wildfire in June 2023, which affected over 100 million people in the US Northeast, particularly around New Jersey/New York. Aerosol systems were deployed to characterize WFPM during the 3 day event, revealing unprecedented mass concentrations mainly in the WFPM0.1 and WFPM0.1-2.5 size fractions. Peak WFPM2.5 concentrations reached 317 µg/m3, nearly 10 times the National Ambient Air Quality Standard (NAAQS) 24 h average limit. Chemical analysis showed a high organic-to-total carbon ratio (96%), consistent with brown carbon wildfires nanoparticles. Large concentrations of high-molecular-weight PAHs were found predominantly bound to WFPM0.1, with retene, a molecular marker of biomass burning and a known teratogen, being the most abundant (>70%). Computational modeling estimated a total lung deposition of 9.15 mg over 72 h, highlighting the health risks of WFPM, particularly due to its long-distance travel capability and impact on densely populated areas.

Associations between fine particulate matter, gene expression, and promoter methylation in human bronchial epithelial cells exposed within a classroom under air-liquid interface.

Associations between indoor air pollution from fine particulate matter (PM with aerodynamic diameter dp < 2.5 µm) and human health are poorly understood. Here, we analyse the concentration-response curves for fine and ultrafine PM, the gene expression, and the methylation patterns in human bronchial epithelial cells (BEAS-2B) exposed at the air-liquid interface (ALI) within a classroom in downtown Rome. Our results document the upregulation of aryl hydrocarbon receptor (AhR) and genes associated with xenobiotic metabolism (CYP1A1 and CYP1B1) in response to single exposure of cells to fresh urban aerosols at low fine PM mass concentrations within the classroom. This is evidenced by concentrations of ultrafine particles (UFPs, dp < 0.1 µm), polycyclic aromatic hydrocarbons (PAH), and ratios of black carbon (BC) to organic aerosol (OA). Additionally, an interleukin 18 (IL-18) down-regulation was found during periods of high human occupancy. Despite the observed gene expression dysregulation, no changes were detected in the methylation levels of the promoter regions of these genes, indicating that the altered gene expression is not linked to changes in DNA methylation and suggesting the involvement of another epigenetic mechanism in the gene regulation. Gene expression changes at low exposure doses have been previously reported. Here, we add the possibility that lung epithelial cells, when singly exposed to real environmental concentrations of fine PM that translate into ultra-low doses of treatment, may undergo epigenetic alteration in the expression of genes related to xenobiotic metabolism. Our findings provide a perspective for future indoor air quality regulations. We underscore the potential role of indoor UFPs as carriers of toxic molecules with low-pressure weather conditions, when rainfall and strong winds may favour low levels of fine PM.

A review on vulnerable atmospheric aerosol nanoparticles: Sources, impact on the health, ecosystem and management strategies.

The Earth's atmosphere contains ultrafine particles known as aerosols, which can be either liquid or solid particles suspended in gas. These aerosols originate from both natural sources and human activities, termed primary and secondary sources respectively. They have significant impacts on the environment, particularly when they transform into ultrafine particles or aerosol nanoparticles, due to their extremely fine atomic structure. With this context in mind, this review aims to elucidate the fundamentals of atmospheric-derived aerosol nanoparticles, covering their various sources, impacts, and methods for control and management. Natural sources such as marine, volcanic, dust, and bioaerosols are discussed, along with anthropogenic sources like the combustion of fossil fuels, biomass, and industrial waste. Aerosol nanoparticles can have several detrimental effects on ecosystems, prompting the exploration and analysis of eco-friendly, sustainable technologies for their removal or mitigation.Despite the adverse effects highlighted in the review, attention is also given to the generation of aerosol-derived atmospheric nanoparticles from biomass sources. This finding provides valuable scientific evidence and background for researchers in fields such as epidemiology, aerobiology, and toxicology, particularly concerning atmospheric nanoparticles.

Neurotoxicity of fine and ultrafine particulate matter: A comprehensive review using a toxicity pathway-oriented adverse outcome pathway framework.

Fine particulate matter (PM2.5) can cause brain damage and diseases. Of note, ultrafine particles (UFPs) with an aerodynamic diameter less than or equal to 100 nm are a growing concern. Evidence has suggested toxic effects of PM2.5 and UFPs on the brain and links to neurological diseases. However, the underlying mechanism has not yet been fully illustrated due to the variety of the study models, different endpoints, etc. The adverse outcome pathway (AOP) framework is a pathway-based approach that could systematize mechanistic knowledge to assist health risk assessment of pollutants. Here, we constructed AOPs by collecting molecular mechanisms in PM-induced neurotoxicity assessments. We chose particulate matter (PM) as a stressor in the Comparative Toxicogenomics Database (CTD) and identified the critical toxicity pathways based on Ingenuity Pathway Analysis (IPA). We found 65 studies investigating the potential mechanisms linking PM2.5 and UFPs to neurotoxicity, which contained 2, 675 genes in all. IPA analysis showed that neuroinflammation signaling and glucocorticoid receptor signaling were the common toxicity pathways. The upstream regulator analysis (URA) of PM2.5 and UFPs demonstrated that the neuroinflammation signaling was the most initially triggered upstream event. Therefore, neuroinflammation was recognized as the MIE. Strikingly, there is a clear sequence of activation of downstream signaling pathways with UFPs, but not with PM2.5. Moreover, we found that inflammation response and homeostasis imbalance were key cellular events in PM2.5 and emphasized lipid metabolism and mitochondrial dysfunction, and blood-brain barrier (BBB) impairment in UFPs. Previous AOPs, which only focused on phenotypic changes in neurotoxicity upon PM exposure, we for the first time propose AOP framework in which PM2.5 and UFPs may activate pathway cascade reactions, resulting in adverse outcomes associated with neurotoxicity. Our toxicity pathway-based approach not only advances risk assessment for PM-induced neurotoxicity but shines a spotlight on constructing AOP frameworks for new chemicals.

Ambient Particulate Matter Induces In Vitro Toxicity to Intestinal Epithelial Cells without Exacerbating Acute Colitis Induced by Dextran Sodium Sulfate or 2,4,6-Trinitrobenzenesulfonic Acid.

Inflammatory bowel disease (IBD) is an immunologically complex disorder involving genetic, microbial, and environmental risk factors. Its global burden has continued to rise since industrialization, with epidemiological studies suggesting that ambient particulate matter (PM) in air pollution could be a contributing factor. Prior animal studies have shown that oral PM10 exposure promotes intestinal inflammation in a genetic IBD model and that PM2.5 inhalation exposure can increase intestinal levels of pro-inflammatory cytokines. PM10 and PM2.5 include ultrafine particles (UFP), which have an aerodynamic diameter of <0.10 µm and biophysical and biochemical properties that promote toxicity. UFP inhalation, however, has not been previously studied in the context of murine models of IBD. Here, we demonstrated that ambient PM is toxic to cultured Caco-2 intestinal epithelial cells and examined whether UFP inhalation affected acute colitis induced by dextran sodium sulfate and 2,4,6-trinitrobenzenesulfonic acid. C57BL/6J mice were exposed to filtered air (FA) or various types of ambient PM reaerosolized in the ultrafine size range at ~300 µg/m3, 6 h/day, 3-5 days/week, starting 7-10 days before disease induction. No differences in weight change, clinical disease activity, or histology were observed between the PM and FA-exposed groups. In conclusion, UFP inhalation exposure did not exacerbate intestinal inflammation in acute, chemically-induced colitis models.

Variability in personal exposure to ultrafine and fine particles by microenvironment among adolescents in Cincinnati.

Personal exposure to air pollution is influenced by an individual's time-activity patterns, but data regarding personal exposure to air pollution among children populations is lacking. The objective of this study was to characterize personal exposure to both PM2.5 and ultrafine particles (UFPs) using two portable real-time monitors, combined with GPS logging, and describe the relationship between these exposures across time and microenvironments among adolescents with asthma. Participants completed personal exposure monitoring for seven consecutive days and PM2.5 and UFP concentrations experienced in five microenvironments were determined using GPS location and mobility data. Average UFP and PM2.5 exposure varied across microenvironments with the highest average UFP exposure concentrations observed in transit (10,910 ± 27,297 p/cc), though correlations between UFP and PM2.5 concentrations in transit were low (0.24) and did not reach statistical significance (p > 0.05). We calculated exposure time ratios for each participant. Across participants, UFP exposures within the transit environment demonstrated the highest ratio (average exposure-time ratio = 1.91) though only 3 % of overall sampling time among all participants was monitored in transit (74/2840 h). We did not observe similar trends among PM2.5 exposures. The correlations between UFP and PM2.5 exposures varied throughout the day, with an overall correlation ranging from moderate to high among participants. Identifying microenvironments and activities where high exposure to PM occurs may offer potential targets for interventions to reduce overall exposures among sensitive groups.

Airborne Nanoparticle Concentrations Are Associated with Increased Mortality Risk in Canada's Two Largest Cities.

RATIONALE: Outdoor fine particulate air pollution (PM2.5) contributes to millions of deaths around the world each year, but much less is known about the long-term health impacts of other particulate air pollutants including ultrafine particles (a.k.a. nanoparticles) which are in the nanometer size range (<100 nm), widespread in urban environments, and not currently regulated. OBJECTIVES: Estimate the associations between long-term exposure to outdoor ultrafine particles and mortality. METHODS: Outdoor air pollution levels were linked to the residential addresses of a large, population-based cohort from 2001 - 2016. Associations between long-term exposure to outdoor ultrafine particles and nonaccidental and cause-specific mortality were estimated using Cox proportional hazards models. MEASUREMENTS: An increase in long-term exposure to outdoor ultrafine particles was associated with an increased risk of nonaccidental mortality (Hazard Ratio = 1. 073, 95% Confidence Interval = 1. 061, 1. 085) and cause-specific mortality, the strongest of which was respiratory mortality (Hazard Ratio = 1.174, 95% Confidence Interval = 1.130, 1.220). MAIN RESULTS: Long-term exposure to outdoor ultrafine particles was associated with increased risk of mortality. We estimated the mortality burden for outdoor ultrafine particles in Montreal and Toronto, Canada to be approximately 1100 additional nonaccidental deaths every year. Furthermore, we observed possible confounding by particle size which suggests that previous studies may have underestimated or missed important health risks associated with ultrafine particles. CONCLUSIONS: As outdoor ultrafine particles are not currently regulated, there is great potential for future regulatory interventions to improve population health by targeting these common outdoor air pollutants.

Indoor and outdoor air quality in street corner kiosks in a large metropolitan area.

Poor air quality in workplaces constitutes a great concern on human health as a good fraction of our time is spent at work. In Greece, very unique workplaces are the street corner kiosks, which are freestanding boxes placed on sidewalks next to city streets and vehicular traffic, where one can find many consumer goods. As such, its employees are exposed to both outdoor and indoor air pollutants. Very few studies have examined the occupational exposure of kiosk workers to air pollutants, and thus the magnitude of this unique indoor and outdoor exposure remains unknown. The objective of this study is to investigate and compare the levels of indoor and outdoor particulate matter (PM10 and PM2.5), ultrafine particles (UFPs) and black carbon (BC) in different kiosks located in Athens, Greece, in urban-traffic and urban-background environments. Continuous measurements of the above-mentioned pollutants were carried out on a 24-h basis over 7 consecutive days at three kiosks from September to October 2019. Indoor PM10 concentrations in the urban kiosk ranged from 19.0 to 44.0 µg/m3, PM2.5 values ranged from 14.0 to 33.0 µg/m3, whereas BC concentrations ranged from 1.2 to 7.0 µg/m3 and UFPs from almost 9.5 to 47.0 × 103 pt/cm3. Outdoor PM10 and PM2.5 measurements ranged from 29.0 to 59.0 µg/m3 and from 22.0 to 39.0 µg/m3, respectively. BC outdoor concentrations ranged from 1.1 to 2.2 µg/m3. The mean hazard quotient (HQ) for PM10 (4.9) and PM2.5 (4.7) among all participants was >1. The health risk of exposure to PM10 and PM2.5 was found to be at moderate hazard levels, although in some cases we observed HQ values higher than 10 due to high PM10 and PM2.5 concentrations in the kiosks. Overall our study indicates that people working at kiosks can be exposed to very high concentrations on particulate pollution depending on a number of factors including the traffic that strongly depends on location and the time of the day.

The role of nanoparticles in bleed air in the etiology of Aerotoxic Syndrome: A review of cabin air-quality studies of 2003-2023.

Aerotoxic Syndrome may develop as a result of chronic, low-level exposure to organophosphates (OPs) and volatile organic compounds in the airplane cabin air, caused by engine oil leaking past wet seals. Additionally, acute high-level exposures, so-called "fume events," may occur. However, air quality monitoring studies concluded that levels of inhaled chemicals might be too low to cause adverse effects. The presence of aerosols of nanoparticles (NPs) in bleed air has often been described. The specific hypothesis is a relation between NPs acting as a vector for toxic compounds in the etiology of the Aerotoxic Syndrome. These NPs function as carriers for toxic engine oil compounds leaking into the cabin air. Inhaled by aircrew NPs carrying soluble and insoluble components deposit in the alveolar region, where they are absorbed into the bloodstream. Subsequently, they may cross the blood-brain barrier and release their toxic compounds in the central nervous system. Olfactory absorption is another route for NPs with access to the brain. To study the hypothesis, all published in-flight measurement studies (2003-2023) of airborne volatile (and low-volatile) organic pollutants in cabin air were reviewed, including NPs (10-100 nm). Twelve studies providing data for a total of 387 flights in 16 different large-passenger jet aircraft types were selected. Maximum particle number concentrations (PNC) varied from 104 to 2.8 × 106 #/cm3 and maximum mass concentrations from 9 to 29 µg/m3. NP-peaks occurred after full-power take-off, in tailwind condition, after auxiliary power unit (APU) bleed air introduction, and after air conditioning pack failure. Chemical characterization of the NPs showed aliphatic hydrocarbons, black carbon, and metallic core particles. An aerosol mass-spectrometry pattern was consistent with aircraft engine oil. It is concluded that chronic exposure of aircrew to NP-aerosols, carrying oil derivatives, maybe a significant feature in the etiology of Aerotoxic Syndrome. Mobile NP measuring equipment should be made available in the cockpit for long-term monitoring of bleed air. Consequently, risk assessment of bleed air should include monitoring and analysis of NPs, studied in a prospective cohort design.

Antisolvent precipitation for the synergistic preparation of ultrafine particles of nobiletin under ultrasonication-homogenization and evaluation of the inhibitory effects of α-glucosidase and porcine pancreatic lipase in vitro.

To further enhance the application of nobiletin (an important active ingredient in Citrus fruits), we used ultrasonic homogenization-assisted antisolvent precipitation to create ultrafine particles of nobiletin (UPN). DMSO was used as the solvent, and deionized water was used as the antisolvent. When ultrasonication (670 W) and homogenization (16000 r/min) were synergistic, the solution concentration was 57 mg/mL, and the minimum particle size of UPN was 521.02 nm. The UPN samples outperformed the RN samples in terms of the inhibition of porcine pancreatic lipase, which was inhibited (by 500 mg/mL) by 68.41 % in the raw sample, 90.34 % in the ultrafine sample, and 83.59 % in the positive control, according to the data. Fourier transform infrared spectroscopy analysis revealed no chemical changes in the samples before or after preparation. However, the crystallinity of the processed ultrafine nobiletin particles decreased. Thus, this work offers significant relevance for applications in the realm of food chemistry and indirectly illustrates the expanded application potential of nobiletin.

Indoor Emissions Contributed the Majority of Ultrafine Particles in Chinese Urban Residences.

Ultrafine particle (UFP) pollution should be controlled to reduce its effects on health. The design of control measures is limited owing to the uncertainty of source contributions in Chinese residences, where indoor UFP pollution is more severe than in Western residences. Herein, a source-specific, time-dependent UFP concentration model was developed by applying an infiltration factor model incorporating coagulation effects. A Monte Carlo framework with the UFP concentration model was employed to estimate the probabilistic distribution of source contributions in Chinese residences. The input parameter distributions were determined based on our survey and previous studies. The annually averaged indoor UFP concentration was estimated at (2.75 ± 1.71) × 104 #/cm3, ranging from 2.35 × 103 to 1.27 × 105 #/cm3 outside the kitchen, and at (5.48 ± 3.08) × 104 #/cm3, ranging from 2.90 × 103 to 1.94 × 105 #/cm3 in the kitchen. Indoor sources contributed more to indoor UFPs, accounting for 61% in the nonkitchen and 80% in the kitchen, surpassing their contribution to indoor PM2.5 in Chinese residences. Meanwhile, the indoor UFP emission contributions were higher than those in the United States, Canada, and Germany, owing to higher emissions from cooking and cigarette smoking. These results will aid in elucidating human exposure to UFPs and in designing more targeted control measures.

A traffic-induced shift of ultrafine particle sources under COVID-19 soft lockdown in a subtropical urban area.

During the unprecedented COVID-19 city lockdown, a unique opportunity arose to dissect the intricate dynamics of urban air quality, focusing on ultrafine particles (UFPs) and volatile organic compounds (VOCs). This study delves into the nuanced interplay between traffic patterns and UFP emissions in a subtropical urban setting during the spring-summer transition of 2021. Leveraging meticulous roadside measurements near a traffic nexus, our investigation unravels the intricate relationship between particle number size distribution (PNSD), VOCs mixing ratios, and detailed vehicle activity metrics. The soft lockdown era, marked by a 20-27% dip in overall traffic yet a surprising surge in early morning motorcycle activity, presented a natural experiment. We observed a consequential shift in the urban aerosol regime: the decrease in primary emissions from traffic substantially amplified the role of aged particles and secondary aerosols. This shift was particularly pronounced under stagnant atmospheric conditions, where reduced dilution exacerbated the influence of alternative emission sources, notably solvent evaporation, and was further accentuated with the resumption of normal traffic flows. A distinct seasonal trend emerged as warmer months approached, with aromatic VOCs such as toluene, ethylbenzene, and xylene not only increasing but also significantly contributing to more frequent particle growth events. These findings spotlight the criticality of targeted strategies at traffic hotspots, especially during periods susceptible to weak atmospheric dilution, to curb UFP and precursor emissions effectively. As we stand at the cusp of widespread vehicle electrification, this study underscores the imperative of a holistic approach to urban air quality management, embracing the complexities of primary emission reductions and the resultant shifts in atmospheric chemistry.

Particle number size distributions and concentrations in transportation environments: a review.

Ambient air ultrafine particles (UFP, particles with a diameter <100 nm) have gained significant attention in World Health Organization (WHO) air quality guidelines and European legislation. This review explores UFP concentrations and particle number size distributions (PNC-PNSD) in various transportation hotspots, including road traffic, airports, harbors, trains, and urban commuting modes (walking, cycling, bus, tram, and subway). The results highlight the lack of information on personal exposure at harbors and railway stations, inside airplanes and trains, and during various other commuting modes. The different lower particle size limits of the reviewed measurements complicate direct comparisons between them. Emphasizing the use of instruments with detection limits ≤10 nm, this review underscores the necessity of following standardized UFP measurement protocols. Road traffic sites are shown to exhibit the highest PNC within cities, with PNC and PNSD in commuting modes driven by the proximity to road traffic and weather conditions. In closed environments, such as cars, buses, and trams, increased external air infiltration for ventilation correlates with elevated PNC and a shift in PNSD toward smaller diameters. Airports exhibit particularly elevated PNCs near runways, raising potential concerns about occupational exposure. Recommendations from this study include maintaining a substantial distance between road traffic and other commuting modes, integrating air filtration into ventilation systems, implementing low-emission zones, and advocating for a general reduction in road traffic to minimize daily UFP exposure. Our findings provide important insights for policy assessments and underscore the need for additional research to address current knowledge gaps.

Hidden danger: The long-term effect of ultrafine particles on mortality and its sociodemographic disparities in New York State.

Although previous studies have shown increased health risks of particulate matters, few have evaluated the long-term health impacts of ultrafine particles (UFPs or PM0.1, ≤ 0.1 µm in diameter). This study assessed the association between long-term exposure to UFPs and mortality in New York State (NYS), including total non-accidental and cause-specific mortalities, sociodemographic disparities and seasonal trends. Collecting data from a comprehensive chemical transport model and NYS Vital Records, we used the interquartile range (IQR) and high-level UFPs (≥75 % percentile) as indicators to link with mortalities. Our modified difference-in-difference model controlled for other pollutants, meteorological factors, spatial and temporal confounders. The findings indicate that long-term UFPs exposure significantly increases the risk of non-accidental mortality (RR=1.10, 95 % CI: 1.05, 1.17), cardiovascular mortality (RR=1.11, 95 % CI: 1.05, 1.18) particularly for cerebrovascular (RR=1.21, 95 % CI: 1.10, 1.35) and pulmonary heart diseases (RR=1.33, 95 % CI: 1.13, 1.57), and respiratory mortality (borderline significance, RR=1.09, 95 % CI: 1.00, 1.18). Hispanics (RR=1.13, 95 % CI: 1.00, 1.29) and non-Hispanic Blacks (RR=1.40, 95 % CI: 1.16, 1.68) experienced significantly higher mortality risk after exposure to UFPs, compared to non-Hispanic Whites. Children under five, older adults, non-NYC residents, and winter seasons are more susceptible to UFPs' effects.

Harnessing AI to unmask Copenhagen's invisible air pollutants: A study on three ultrafine particle metrics.

Ultrafine particles (UFPs) are airborne particles with a diameter of less than 100 nm. They are emitted from various sources, such as traffic, combustion, and industrial processes, and can have adverse effects on human health. Long-term mean ambient average particle size (APS) in the UFP range varies over space within cities, with locations near UFP sources having typically smaller APS. Spatial models for lung deposited surface area (LDSA) within urban areas are limited and currently there is no model for APS in any European city. We collected particle number concentration (PNC), LDSA, and APS data over one-year monitoring campaign from May 2021 to May 2022 across 27 locations and estimated annual mean in Copenhagen, Denmark, and obtained additionally annual mean PNC data from 6 state-owned continuous monitors. We developed 94 predictor variables, and machine learning models (random forest and bagged tree) were developed for PNC, LDSA, and APS. The annual mean PNC, LDSA, and APS were, respectively, 5523 pt/cm3, 12.0 µm2/cm3, and 46.1 nm. The final R2 values by random forest (RF) model were 0.93 for PNC, 0.88 for LDSA, and 0.85 for APS. The 10-fold, repeated 10-times cross-validation R2 values were 0.65, 0.67, and 0.60 for PNC, LDSA, and APS, respectively. The root mean square error for final RF models were 296 pt/cm3, 0.48 µm2/cm3, and 1.60 nm for PNC, LDSA, and APS, respectively. Traffic-related variables, such as length of major roads within buffers 100-150 m and distance to streets with various speed limits were amongst the highly-ranked predictors for our models. Overall, our ML models achieved high R2 values and low errors, providing insights into UFP exposure in a European city where average PNC is quite low. These hyperlocal predictions can be used to study health effects of UFPs in the Danish Capital.

Long-term trends of black carbon and particle number concentrations and their vehicle emission factors in Stockholm.

Black carbon (BC) and particle number (PN) concentrations are usually high in cities due to traffic emissions. European mitigation policies, including Euro emission standards, have been implemented to curb these emissions. We analyzed BC and PN (particle diameter Dp > 4 nm) concentrations in Stockholm spanning the years 2013-2019 (BC) and 2009-2019 (PN) measured at street canyon and rooftop sites to assess the effectiveness of the implemented policies. Combining these data with inverse dispersion modeling, we estimated BC and PN emission factors (EFBC and EFPN) for the mixed fleet, reflecting real-world driving conditions. The pollutants showed decreasing trends at both sites, but PN concentrations remained high at the canyon site considering the World Health Organization (WHO) recommendations. BC concentrations declined more rapidly than PN concentrations, showing a -9.4% and -4.9% annual decrease at the canyon and -7.2% and -0.5% at the rooftop site in the years 2013-2019. The EFBC and EFPN trends showed that the mitigation strategies for reducing particulate emissions for on-road vehicles were successful over the study period. However, the introduction of biofuels in the vehicle fleet -ethanol and later rapeseed methyl ester (RME)- increased the concentrations of particles with Dp < 10 nm before the adoption of particulate filters in the exhausts. Stricter Euro emission regulations, especially with diesel particulate filters (DPF) in Euro 5, 6, and VI vehicles, led to 66% decrease in EFBC and 55% in EFPN. Real-world EFBC surpassed HBEFA (Handbook Emission Factors for Road Transport) database values by 2.4-4.8 times; however, direct comparisons between real-world and HBEFA EFPN are difficult due to differences in lower cut-off sizes and measurement techniques. Our results underscore the necessity for revising the HBEFA database, updating laboratory testing methods and portable emission measuring systems (PEMS) measurements to account for liquid condensate contributions to PN measurements.

Personal exposure to ultrafine particles in multiple microenvironments among adolescents.

BACKGROUND: Experimental studies suggest ultrafine particles (UFPs), the smallest size fraction of particulate matter, may be more toxic than larger particles, however personal sampling studies in children are lacking. OBJECTIVE: The objective of this analysis was to examine individual, housing, and neighborhood characteristics associated with personal UFP concentrations as well as the differences in exposures that occur within varying microenvironments. METHODS: We measured weekly personal UFP concentrations and GPS coordinates in 117 adolescents ages 13-17 to describe exposures across multiple microenvironments. Individual, home, and neighborhood characteristics were collected by caregiver completed questionnaires. RESULTS: Participants regularly exposed to secondhand tobacco smoke had significantly higher indoor concentrations of UFPs compared to participants who were not. We observed that the 'home' microenvironment dominated the relative contribution of overall UFP concentrations and sampling time, however, relative proportion of integrated UFP exposure were higher in 'other' environments. IMPACT STATEMENT: In this study, we employed a novel panel study design, involving real-time measurement of UFP exposure within the multiple microenvironments of adolescents. We found a combination of personal sampling and detailed activity patterns should be used in future studies to accurately describe exposure-behavior relationships.

The combined effect of ultrafine particles of cobalt and manganese oxides and Origanum vulgare herb extract on ruminal digestion in vitro.

Background and Aim: At present, detailed studies are being conducted to confirm the safety of the use of metal-containing ultrafine particles (UFP) in animal feeding, preventing the possibility of negative effects on productive qualities and physiological state, as well as on the environment and final consumer, that is, humans. Thus, the purpose of this research was to study the safety of cobalt- and manganese-containing UFP (UFP Co3O4, Mn2O3 UFP) together with Origanum vulgare (PB) herb extract in a bioluminescence inhibition test, as well as the effect of this composition on ruminal digestion in vitro. Materials and Methods: The safety of the studied samples was determined using a multifunctional microplate analyzer TECAN Infinite F200 (Tecan Austria GmbH, Austria), recording the luminescence value of the bacterial strain Escherichia coli K12 TG11 (Ecolum, JSC NVO Immunotech, Russia). Dry matter (DM) digestibility studies were performed using the in vitro method on an "artificial rumen" model using an ANKOM Daisy II incubator unit (AD II; USA). The number of protozoa in ruminal fluid was counted in a Goryaev chamber. The bacterial mass was assessed by differential centrifugation followed by drying. This method is based on differences in the sedimentation rate of particles that differ in size and density. Results: UFP Co3O4 and Mn2O3 at concentrations above 1.5 × 10-5 and 1.9 × 10-3 mol/L, respectively, have a pronounced bactericidal effect, suppressing more than 50% of the luminescence of E. coli K12 TG1. The combined use of UFP metals and plant extract increases the luminescence of the test object, indicating its safety. The combined use of UFP and PB increases the digestibility of feed DM in vitro and the number of protozoa in 1 mL of ruminal fluid; however, the combination of UFP Mn2O3 + PB (13.8%) yielded the best result, which is recommended for further in vivo research. Conclusion: Origanum vulgare extract reduces the toxicity of UFP Co3O4 and Mn2O3 in vitro, indicating that their combined use is safer.