Investigation of the Mechanism of Oxidative Potential Increase in Atmospheric Particulate Matter during Photoaging: Important Role of Aromatic Nitrogenous Compounds.

Particulate matter (PM) undergoing various aging processes in the atmosphere changes its toxicity. However, the mechanism of toxicity evolution is not fully clarified currently. This study demonstrates that photoaging promotes an increase in the oxidative potential (OP) of atmospheric PM by about 30%, and the increased OP is mainly attributed to the production of secondary organic compounds, while water-soluble metal ions contribute only 11%. The OP of nonextractable matters (NEMs) of atmospheric PM was mostly increased after photoaging, followed by water-soluble matters (WSMs). NEM can produce quinone-like functional groups and secondary persistent free radicals during photoaging, which are most likely to produce reactive oxygen species (ROS). For WSM, the conversion of low-oxidation humic-like substances (HULIS) to high-oxidation HULIS is the main reason for the increase in OP. Quinones, nitrophenols, and N-containing heterocycles are the OP contributors produced during the conversion process. Among them, quinones are the main secondary oxidizing active compounds, while nitro-phenolic compounds and N-containing heterocyclic compounds may play a catalyst-like role, facilitating the production of oxidizing active compounds and ROS in the newly converted high-oxidation HULIS. This study clarifies the secondary OP generation mechanism and provides new insights into the uncertainty of PM toxicity during atmospheric aging.

Analysis of PM2.5 inorganic and organic constituents to resolve contributing sources in Seoul, South Korea and Beijing, China and their possible associations with cytokine IL-8.

China and South Korea are the most polluted countries in East Asia due to significant urbanization and extensive industrial activities. As neighboring countries, collaborative management plans to maximize public health in both countries can be helpful in reducing transboundary air pollution. To support such planning, PM2.5 inorganic and organic species were determined in simultaneously collected PM2.5 integrated filters. The resulting data were used as inputs to positive matrix factorization, which identified nine sources at the ambient air monitoring sites in both sites. Secondary nitrate, secondary sulfate/oil combustion, soil, mobile, incinerator, biomass burning, and secondary organic carbon (SOC) were found to be sources at both sampling sites. Industry I and II were only identified in Seoul, whereas combustion and road dust sources were only identified in Beijing. A subset of samples was selected for exposure assessment. The expression levels of IL-8 were significantly higher in Beijing (167.7 pg/mL) than in Seoul (72.7 pg/mL). The associations between the PM2.5 chemical constituents and its contributing sources with PM2.5-induced inflammatory cytokine (interleukin-8, IL-8) levels in human bronchial epithelial cells were investigated. For Seoul, the soil followed by the secondary nitrate and the biomass burning showed increase with IL-8 production. However, for the Beijing, the secondary nitrate exhibited the highest association with IL-8 production and SOC and biomass burning showed modest increase with IL-8. As one of the highest contributing sources in both cities, secondary nitrate showed an association with IL-8 production. The soil source having the strongest association with IL-8 production was found only for Seoul, whereas SOC showed a modest association only for Beijing. This study can provide the scientific basis for identifying the sources to be prioritized for control to provide effective mitigation of particulate air pollution in each city and thereby improve public health.

Association of fine particulate matter and residential green space with rheumatoid arthritis.

BACKGROUND: Fine particulate matter (PM2.5) is a recognized risk factor for respiratory and cardiovascular diseases, but the association between PM2.5 and rheumatoid arthritis (RA) is still controversial. Additionally, evidence on the relationship of green space with RA is scarce. This study aimed to investigate the separate and combined associations of PM2.5 and green space with risk of RA. METHODS: Our study involved 30,684 participants from the Yinzhou cohort in Ningbo, China. PM2.5 concentrations were determined using a land-use regression model. Residential green space was assessed using the Normalized Difference Vegetation Index (NDVI) and Enhanced Vegetation Index (EVI) from satellite images. We employed the Cox proportional hazard model to evaluate the relationships of PM2.5 and green space with RA. RESULTS: During the 176,894 person-years of follow-up period, 354 cases of RA were identified. Hazard ratio (HR) and the corresponding 95% confidence interval (95% CI) for every interquartile range (IQR) increase in PM2.5 were 1.23 (95% CI: 1.02, 1.49). Compared with lower exposure to residential green space, individuals living in areas with more green space had a decreased risk of RA (HR was 0.80 (95% CI: 0.70, 0.92), 0.80 (95% CI: 0.70, 0.92), and 0.79 (95% CI: 0.70, 0.89) for 250m, 500m, and 1000m NDVI buffers, respectively). Similar results were observed for the association between EVI and RA. Furthermore, a significant multiplicative interaction was observed between PM2.5 and green space (NDVI 250m and EVI 250m). No mediating effect of PM2.5 on the relationship between green space and RA was observed. CONCLUSION: Our findings indicated that living in areas with higher green space was linked to a reduced risk of RA, whereas living in areas with higher PM2.5 was associated with an increased risk of RA. The beneficial effect of high green space may be offset by exposure to PM2.5.

Long-term exposure to ambient fine particulate matter constituents and mortality from total and site-specific gastrointestinal cancer.

BACKGROUND: Ambient fine particulate matter (PM2.5) exposure has been associated with an increased risk of gastrointestinal cancer mortality, but the attributable constituents remain unclear. OBJECTIVES: To investigate the association of long-term exposure to PM2.5 constituents with total and site-specific gastrointestinal cancer mortality using a difference-in-differences approach in Jiangsu province, China during 2015-2020. METHODS: We split Jiangsu into 53 spatial units and computed their yearly death number of total gastrointestinal, esophagus, stomach, colorectum, liver, and pancreas cancer. Utilizing a high-quality grid dataset on PM2.5 constituents, we estimated 10-year population-weighted exposure to black carbon (BC), organic carbon (OC), sulfate, nitrate, ammonium, and chloride in each spatial unit. The effect of constituents on gastrointestinal cancer mortality was assessed by controlling time trends, spatial differences, gross domestic product (GDP), and seasonal temperatures. RESULTS: Overall, 524,019 gastrointestinal cancer deaths were ascertained in 84.77 million population. Each interquartile range increment of BC (0.46 µg/m3), OC (4.56 µg/m3), and nitrate (1.41 µg/m3) was significantly associated with a 27%, 26%, and 34% increased risk of total gastrointestinal cancer mortality, respectively, and these associations remained significant in PM2.5-adjusted models and constituent-residual models. We also identified robust associations of BC, OC, and nitrate exposures with site-specific gastrointestinal cancer mortality. The mortality risk generally displayed increased trends across the total exposure range and rose steeper at higher levels. We did not identify robust associations for sulfate, ammonium, or chlorine exposure. Higher mortality risk ascribed to constituent exposures was identified in total gastrointestinal and liver cancer among women, stomach cancer among men, and total gastrointestinal and stomach cancer among low-GDP regions. CONCLUSIONS: This study offers consistent evidence that long-term exposure to PM2.5-bound BC, OC, and nitrate is associated with total and site-specific gastrointestinal cancer mortality, indicating that these constituents need to be controlled to mitigate the adverse effect of PM2.5 on gastrointestinal cancer mortality.

An investigation of inequalities in exposure to PM2.5 air pollution across small areas in Ireland.

The link between exposure to air pollution and adverse effects on human health is well documented. Yet, in a European context, research on the spatial distribution of air pollution and the characteristics of areas is relatively scarce, and there is a need for research using different spatial scales, a wider variety of socioeconomic indicators (such as ethnicity) and new methodologies to assess these relationships. This study uses comprehensive data on a wide range of demographic and socioeconomic indicators, matched to data on PM2.5 concentrations for small areas in Ireland, to assess the relationship between social vulnerability and PM2.5 air pollution. Examining a wide range of socioeconomic indicators revealed some differentials in PM2.5 concentration levels by measure and by rural and urban classification. However, statistical modelling using concentration curves and concentration indices did not present substantial evidence of inequalities in PM2.5 concentrations across small areas. In common with other western European countries, an overall decline in the levels of PM2.5 between 2011 and 2016 was observed in Ireland, though the data indicates that almost all small areas in Ireland were found to have exceeded the World Health Organization (WHO)'s PM2.5 annual guideline (of 5 µg/m3), calling for greater policy efforts to reduce air pollution in Ireland. The recent Clean Air Strategy contains a commitment to achieve the WHO guideline limits for PM2.5 by 2040, with interim targets at various points over the next two decades. Achieving these targets will require policy measures to decarbonise home heating, promote active travel and the transition to electric vehicles, and further regulations on burning fossil fuels and enforcing environmental regulations more tightly. From a research and information-gathering perspective, installing more monitoring stations at key points could improve the quality and spatial dimension of the data collected and facilitate the assessment of the implementation of the measures in the Clean Air Strategy.

Interleukin-37 relieves PM2.5-triggered lung injury by inhibiting autophagy through the AKT/mTOR signaling pathway in vivo and in vitro.

Autophagy mediates PM2.5-related lung injury (LI) and is tightly linked to inflammation and apoptosis processes. IL-37 has been demonstrated to regulate autophagy. This research aimed to examine the involvement of IL-37 in the progression of PM2.5-related LI and assess whether autophagy serves as a mediator for its effects.To create a model of PM2.5-related LI, this research employed a nose-only PM2.5 exposure system and utilized both human IL-37 transgenic mice and wild-type mice. The hIL-37tg mice demonstrated remarkable reductions in pulmonary inflammation and pathological LI compared to the WT mice. Additionally, they exhibited activation of the AKT/mTOR signaling pathway, which served to regulate the levels of autophagy and apoptosis.Furthermore, in vitro experiments revealed a dose-dependent upregulation of autophagy and apoptotic proteins following exposure to PM2.5 DMSO extraction. Simultaneously, p-AKT and p-mTOR expression was found to decrease. However, pretreatment with IL-37 demonstrated a remarkable reduction in the levels of autophagy and apoptotic proteins, along with an elevation of p-AKT and p-mTOR. Interestingly, pretreatment with rapamycin, an autophagy inducer, weakened the therapeutic impact of IL-37. Conversely, the therapeutic impact of IL-37 was enhanced when treated with 3-MA, a potent autophagy inhibitor. Moreover, the inhibitory effect of IL-37 on autophagy was successfully reversed by administering AKT inhibitor MK2206. The findings suggest that IL-37 can inhibit both the inflammatory response and autophagy, leading to the alleviation of PM2.5-related LI. At the molecular level, IL-37 may exert its anti autophagy and anti apoptosis effects by activating the AKT/mTOR signaling pathway.

Hidden health effects and economic burden of stroke and coronary heart disease attributed to ambient air pollution (PM2.5) in Tehran, Iran: Evidence from an assessment and forecast up to 2030.

Air pollution is one of the main causes of global disease burden, especially in low-income and middle-income countries. Estimation of the current situation and prediction of the future health effects of death and incidence of stroke and coronary heart disease (CHD) attributed to PM2.5 were done using BenMAP-CE software. Estimating and forecasting the economic burden of these diseases were done in 4 scenarios: Stability of the current PM2.5 concentration, annual 10 % reduction of PM2.5 concentration, reduction to 5 µg/m3, and reduction to 12 µg/m3, with three approaches for calculating the economic burden in mortality costs, including the human capital(HC), years of life lost(YLL) and value of statistical life(VSL) was performed. With the stability of the PM2.5 concentration, the economic burden of stroke attributed to PM2.5 with the approach of calculating the cost of death with the HC, the YLL, and VSL will reach from 64, 82 and 172 million USD in 2020-849, 1120 and 2703 million USD in 2030 and these costs for CHD in the mentioned approaches of calculating the cost of death will reach respectively from 499, 568 and 898 million USD in 2020-7096, 8088, and 13,621 million USD in 2030. We find that the morbidity economic burden (including direct, indirect, and intangible costs) of stroke compared to the cost of death with the HC, and YLL approaches are 67.58 times, 3.15 times respectively, and in the VSL approach is 47.32 % of stroke death cost. Also, the costs of CHD morbidity economic burden compared to the cost of death in the method of calculating the cost of death with the HC, YLL, and VSL approaches are 42.09, 7.25, and 1.16 times, respectively. This study provides comprehensive baseline information for health policymakers to understand the benefits of air pollution control policies globally, especially in LMICs.

A longitudinal study on the effect of PM2.5 components on blood pressure in the hypertensive patients from 2011 to 2019.

Extensive research has established the link between PM2.5 exposure and blood pressure (BP) levels among normal individuals. However, the association between PM2.5 components and BP levels in hypertensive patients has not been fully explored. In this study, 12 971 hypertensive cases from Jinchang cohort (in Jinchang City, China) with nearly 9 years of follow-up were enrolled. Based on the linear mixed-effect model, the effects of fine particulate matter (PM2.5) and five major components [sulfate (SO42-), nitrate (NO3-), ammonium (NH4+), black carbon (BC) and organic matter (OM)]on BP [systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and pulse pressure (PP)]were evaluated by single-component model, component-joint model and component-residual model, respectively. A positive correlation was found between PM2.5 as well as its components (SO42-, NO3-, NH4+, BC and OM) exposure and BP levels. The effects of SO42-, BC and OM on BP were observed to be the most robust among the three models. Based on the results of interaction effects and stratified analysis, the effect of BC exposure on SBP, and the effect of PM2.5 and its five components on PP were greater in female than in males. Compared with elderly hypertensive patients, OM had more significant effects on SBP, DBP and MAP in young and (or) middle-aged hypertensive patients. During the heating season, the effect of PM2.5 and its components on BP was grater compared to the non-heating season. Meanwhile, PM2.5 and its components have a greater influence on BP in patients with hypertension combined with diabetes. Therefore, the findings suggested that both PM2.5 exposure and its components had a significant effect on BP in patients with hypertension. Women and young and middle-aged hypertensive patient were the sensitive population. The implementation of source control and reduction of PM2.5 emission (mainly for SO42-, BC and OM) may be of great significance to control BP level and could reduce the risk of cardiovascular disease in patients with hypertension.

Wearable Sensor Node for Safety Improvement in Workplaces: Technology Assessment in a Simulated Environment.

Personal protective equipment (PPE) has been universally recognized for its role in protecting workers from injuries and illnesses. Smart PPE integrates Internet of Things (IoT) technologies to enable continuous monitoring of workers and their surrounding environment, preventing undesirable events, facilitating rapid emergency response, and informing rescuers of potential hazards. This work presents a smart PPE system with a sensor node architecture designed to monitor workers and their surroundings. The sensor node is equipped with various sensors and communication capabilities, enabling the monitoring of specific gases (VOC, CO2, CO, O2), particulate matter (PM), temperature, humidity, positional information, audio signals, and body gestures. The system utilizes artificial intelligence algorithms to recognize patterns in worker activity that could lead to risky situations. Gas tests were conducted in a special chamber, positioning capabilities were tested indoors and outdoors, and the remaining sensors were tested in a simulated laboratory environment. This paper presents the sensor node architecture and the results of tests on target risky scenarios. The sensor node performed well in all situations, correctly signaling all cases that could lead to risky situations.

Particulate Matter-Induced Neurotoxicity: Unveiling the Role of NOX4-Mediated ROS Production and Mitochondrial Dysfunction in Neuronal Apoptosis.

Urban air pollution, a significant environmental hazard, is linked to adverse health outcomes and increased mortality across various diseases. This study investigates the neurotoxic effects of particulate matter (PM), specifically PM2.5 and PM10, by examining their role in inducing oxidative stress and subsequent neuronal cell death. We highlight the novel finding that PM increases mitochondrial ROS production via stimulating NOX4 activity, not through its expression level in Neuro-2A cells. Additionally, PMs provoke ROS production via increasing the expression and activity of NOX2 in SH-SY5Y human neuroblastoma cells, implying differential regulation of NOX proteins. This increase in mitochondrial ROS triggers the opening of the mitochondrial permeability transition pore (mPTP), leading to apoptosis through key mediators, including caspase3, BAX, and Bcl2. Notably, the voltage-dependent anion-selective channel 1 (VDAC1) increases at 1 µg/mL of PM2.5, while PM10 triggers an increase from 10 µg/mL. At the same concentration (100 µg/mL), PM2.5 causes 1.4 times higher ROS production and 2.4 times higher NOX4 activity than PM10. The cytotoxic effects induced by PMs were alleviated by NOX inhibitors GKT137831 and Apocynin. In SH-SY5Y cells, both PM types increase ROS and NOX2 levels, leading to cell death, which Apocynin rescues. Variability in NADPH oxidase sources underscores the complexity of PM-induced neurotoxicity. Our findings highlight NOX4-driven ROS and mitochondrial dysfunction, suggesting a potential therapeutic approach for mitigating PM-induced neurotoxicity.

PM2.5 associates with blood pressure: a Mendelian randomization analysis.

The relationship between fine particulate matter (PM2.5) and blood pressure (BP) is a controversial issue. We conducted a two-sample Mendelian randomization (MR) analysis and identified 58 genome-wide significant single-nucleotide polymorphisms associated with PM2.5 as instrument variables. Inverse-variance weighted (IVW) was used as the primary analysis approach. MR-Egger, weighted median, simple model, and weighted model methods were selected for quality control. We found a significant negative causal association of higher genetically predicted PM2.5 levels with lower systolic BP (SBP), while no causal relationship was identified between PM2.5 and diastolic BP (DBP). For each 1 standard deviation increase in genetically predicted PM2.5 levels, the beta value (95% CI) of SBP was -0.14 (-0.25, -0.03) for IVW (p=0.02), and -0.13 (-0.22, -0.04) for weighted median (p=0.005). Increased PM2.5 concentrations can lead to decreased SBP levels. Our findings provided novel insights into the controversial topic on the causal relationship between PM2.5 and BP.

Spatial-temporal distribution and source analysis of atmospheric particulate-bound cadmium from 1998 to 2021 in China.

Cadmium (Cd) is one of the most serious atmospheric heavy metal pollutants in China. PM2.5, PM10, and total suspended particle (TSP) are all important media for population Cd exposure. However, no studies so far have systematically explored the spatial and temporal distribution of atmospheric Cd bound to all these media in China, and the specific industrial sectors that contribute to the airborne Cd level are still unclear at present. In this study, we constructed the spatial and temporal distribution of PM (PM2.5, PM10, and TSP) binding Cd concentrations in China. Quantitative source apportionment of atmospheric Cd was carried out by analyzing the association of 23 industrial or energy-consuming sectors with Cd concentrations. Our results showed PM2.5, PM10, and TSP binding Cd concentrations decreased by 5.8%, 5.9%, and 6.1% per year at the national level, respectively. High PM-Cd concentrations were concentrated and distributed mainly in central and northwestern China. In addition, the medians of atmospheric PM2.5, PM10, and TSP binding Cd concentrations at the national level were 0.0026 µg/m3, 0.0036 µg/m3, and 0.0042 µg/m3, respectively. The main sources of PM-Cd include nonferrous metal smelting (Zn, Pb, Al) (47%), glass production (13%), pesticide production (12%), cement production (10%), and coal consumption (9%). This study analyzes comprehensively the atmospheric PM-bound Cd pollution, identifies the major industrial sectors that affect atmospheric Cd concentrations at the macroscale for the first time, and provides a basis for further reduction in the atmospheric Cd pollution.

Seasonal anomaly of particulate matter concentration in an equatorial climate: Evaluating the transboundary impact from neighboring provinces on Padang City, Indonesia.

This study investigated the anomalous seasonal variations in particulate matter (PM) concentrations-specifically PM2.5 and PM10-in Padang City, Indonesia, situated within the Equatorial climate zone. A one-year dataset of half-hourly PM measurements from January to December 2023, collected by the Air Quality Monitoring System (AQMS) managed by the Environmental Agency of West Sumatra (DLH), was utilized. Maps of hotspots and air mass backward trajectories were used to identify possible transboundary emissions affecting Padang City. Despite the region experiencing nearly continuous rainfall, significant elevations in PM levels were observed during the typically drier months of August to October. Specifically, PM2.5 levels peaked at 36.57 µg/m3 and PM10 at 39.58 µg/m3 in October, significantly higher than in other months and indicating a substantial deviation from the typical expectations for equatorial climates. These results suggest that the high PM concentrations are not solely due to local urban emissions or normal seasonal variations but are also significantly influenced by transboundary smoke from peatland fires and agricultural burning in neighboring provinces such as Bengkulu, Riau, Jambi, and South Sumatra. Backward trajectory analysis further confirmed the substantial impact of regional activities on degradation of air quality in Padang City. The study underscores the need for integrated air quality management that includes both local and transboundary pollution sources. Enhanced monitoring, public engagement, and inter-regional collaboration are emphasized as crucial strategies for mitigating the adverse effects of PM pollution in equatorial regions like Padang City.

Satellite or ground-based measurements for air pollutants (PM2.5, PM10, SO2, NO2, O3) data and their health hazards: which is most accurate and why?

Air pollution is growing at alarming rates on regional and global levels, with significant consequences for human health, ecosystems, and change in climatic conditions. The present 12 weeks (4 October 2021, to 26 December 2021) study revealed the different ambient air quality parameters, i.e., PM2.5, PM10, SO2, NO2, and O3 over four different sampling stations of Delhi-NCR region (Dwarka, Knowledge park III, Sector 125, and Vivek Vihar), India, by using satellite remote sensing data (MERRA-2, OMI, and Aura Satellite) and different ground-based instruments. The ground-based observation revealed the mean concentration of PM2.5 in Dwarka, Knowledge park III, Sector 125, and Vivek Vihar as 279 µg m-3, 274 µg m-3, 294 µg m-3, and 365 µg m-3, respectively. The ground-based instrumental concentration of PM2.5 was greater than that of satellite observations, while as for SO2 and NO2, the mean concentration of satellite-based monitoring was higher as compared to other contaminants. Negative and positive correlations were observed among particulate matter, trace gases, and various meteorological parameters. The wind direction proved to be one of the prominent parameter to alter the variation of these pollutants. The current study provides a perception into an observable behavior of particulate matter, trace gases, their variation with meteorological parameters, their health hazards, and the gap between the measurements of satellite remote sensing and ground-based measurements.

Exposure to ambient fine particulate matter components during pregnancy and early childhood and its association with asthma, allergies, and sensitization in school-age children.

BACKGROUND: Exposure to fine particulate matter (PM2.5) has been associated with allergic diseases, including asthma. However, information about the effects of specific PM2.5 components is limited. This study aimed to investigate the relationship of exposure to chemical components of PM2.5 during pregnancy and early childhood with the development of asthma, allergies, and sensitization in school-age children. METHODS: This study included 2,408 children in the second grade of elementary school. Questionnaire surveys of respiratory/allergic symptoms and measurements of serum total IgE and specific IgE levels to house dust mite (HDM) and animal proteins were conducted. Exposures to ambient PM2.5 mass, sulfate (SO42-), nitrate (NO3-), ammonium (NH4+), elemental carbon (EC), and organic carbon (OC) of PM2.5 in participants' residences from conception to age six were estimated using predictive models. Multiple logistic regression analysis was used to analyze the association of respiratory/allergic symptoms and allergen sensitization with estimated exposure concentrations, after adjustment for survey year, sex, season of birth, feeding method during infancy, presence of siblings, history of lower respiratory tract infection, use of childcare facilities, passive smoking, presence of pets, mother's age, history of allergic diseases, smoking during pregnancy, and annual household income. RESULTS: No significant association was found between PM2.5 and its component concentrations and asthma. However, wheezing significantly increased with mean NO3- concentrations during pregnancy (odds ratio of 1.64 [95% confidence interval: 1.10, 2.47] for an interquartile range increase). Significant associations were also found between EC in the second trimester of pregnancy and PM2.5, NO3-, EC, and OC concentrations in early childhood. Higher PM2.5, SO4-, and NH4+ concentrations during the second trimester increased the risk of rhinitis. Sensitizations to HDM and animal proteins were significantly associated with exposure to components such as SO42- and NH4+ during pregnancy but not with postnatal exposure. CONCLUSIONS: Exposures to NO3-, EC, and OC during pregnancy and early childhood were associated with wheezing. SO42- and NH4+ exposures during pregnancy were associated with sensitization to HDM and animal proteins. Asthma was not associated with exposure to PM2.5 and its main components at any period.

The Impact of Ambient and Wildfire Air Pollution on Rhinosinusitis and Olfactory Dysfunction.

PURPOSE OF REVIEW: With increasing industrialization, exposure to ambient and wildfire air pollution is projected to increase, necessitating further research to elucidate the complex relationship between exposure and sinonasal disease. This review aims to summarize the role of ambient and wildfire air pollution in chronic rhinosinusitis (CRS) and olfactory dysfunction and provide a perspective on gaps in the literature. RECENT FINDINGS: Based on an emerging body of evidence, exposure to ambient air pollutants is correlated with the development of chronic rhinosinusitis in healthy individuals and increased symptom severity in CRS patients. Studies have also found a robust relationship between long-term exposure to ambient air pollutants and olfactory dysfunction. Ambient air pollution exposure is increasingly recognized to impact the development and sequelae of sinonasal pathophysiology. Given the rising number of wildfire events and worsening impacts of climate change, further study of the impact of wildfire-related air pollution is a crucial emerging field.

Profiling Microbiota from Multiple Sites in the Respiratory Tract to Identify a Biomarker for PM2.5 Nitrate Exposure-Induced Pulmonary Damages.

The microbiota present in the respiratory tract (RT) responds to environmental stimuli and engages in a continuous interaction with the host immune system to maintain homeostasis. A total of 40 C57BL/6 mice were divided into four groups and exposed to varying concentrations of PM2.5 nitrate aerosol and clean air. After 10 weeks of exposure, assessments were conducted on the lung and airway microbiome, lung functions, and pulmonary inflammation. Additionally, we analyzed data from both mouse and human respiratory tract (RT) microbiomes to identify possible biomarkers for PM2.5 exposure-induced pulmonary damages. On average, 1.5 and 13.5% inter-individual microbiome variations in the lung and airway were explained by exposure, respectively. In the airway, among the 60 bacterial OTUs (operational taxonomic units) > 0.05% proportion, 40 OTUs were significantly affected by PM2.5 exposure (FDR ≤ 10%). Further, the airway microbiome was associated with peak expiratory flow (PEF) (p = 0.003), pulmonary neutrophil counts (p = 0.01), and alveolar 8-OHdG oxidative lesions (p = 0.0078). The Clostridiales order bacteria showed the strongest signals. For example, the o_Clostridiales;f_;g_ OTU was elevated by PM2.5 nitrate exposure (p = 4.98 × 10-5) and negatively correlated with PEF (r = -0.585 and p = 2.4 × 10-4). It was also associated with the higher pulmonary neutrophil count (p = 8.47 × 10-5) and oxidative lesion (p = 7.17 × 10-3). In human data, we confirmed the association of airway Clostridiales order bacteria with PM2.5 exposure and lung function. For the first time, this study characterizes the impact of PM2.5 exposure on the microbiome of multiple sites in the respiratory tract (RT) and its relevance to airflow obstructive diseases. By analyzing data from both humans and mice, we have identified bacteria belonging to the Clostridiales order as a promising biomarker for PM2.5 exposure-induced decline in pulmonary function and inflammation.

The Exosome-Mediated Cascade Reactions for the Transfer and Inflammatory Responses of Fine Atmospheric Particulate Matter in Macrophages.

Exposure to atmospheric particulate matter (PM) is a frequent occurrence to humans, and their adverse outcomes have become a global concern. Although PM-induced inflammation is a common phenomenon, a clear picture of the mechanisms underlying exosome-mediated inflammation of PM has not yet emerged. Here, we show that exosomes can mediate the cascade reactions for the transfer of PM and inflammatory responses of macrophages. Specifically, two fine PM2.5, namely F1 (<0.49 µm) and F2 (0.95-1.5 µm), stimulated a substantial release of exosomes from macrophages (THP-1 cells) with the order of F1 > F2, via regulation of the P2X7 receptor (P2X7R). Inhibiting P2X7R with a specific inhibitor largely prevented the secretion of exosomes. In particular, we found that exosomes served as a mediator for the transfer of PM2.5 to the recipient macrophages and activated NF-κB signaling through toll-like receptor 4 (TLR-4), thereby stimulating inflammatory cytokine release and altering the inflammatory phenotype of recipients. Importantly, the exosomes derived from PM2.5-treated macrophages induced the inflammatory responses of lung in mice. Our results highlight that exosomes undergo a secretion-particle transfer-adverse outcome chain in macrophages treated with PM2.5. Given the ubiquitous atmospheric particulate matter, these new findings underscore an urgent need for assessing the secretion of exosomes and their impact on human health via exosome-centric physiological pathways.

Polar Nitrated Aromatic Compounds in Urban Fine Particulate Matter: A Focus on Formation via an Aqueous-Phase Radical Mechanism.

Polar nitrated aromatic compounds (pNACs) are key ambient brown carbon chromophores; however, their formation mechanisms, especially in the aqueous phase, remain unclear. We developed an advanced technique for pNACs and measured 1764 compounds in atmospheric fine particulate matter sampled in urban Beijing, China. Molecular formulas were derived for 433 compounds, of which 17 were confirmed using reference standards. Potential novel species with up to four aromatic rings and a maximum of five functional groups were found. Higher concentrations were detected in the heating season, with a median of 82.6 ng m-3 for Σ17pNACs. Non-negative matrix factorization analysis indicated that primary emissions particularly coal combustion were dominant in the heating season. While in the non-heating season, aqueous-phase nitration could generate abundant pNACs with the carboxyl group, which was confirmed by their significant association with the aerosol liquid water content. Aqueous-phase formation of 3- and 5-nitrosalicylic acids instead of their isomer of 4-hydroxy-3-nitrobenzoic acid suggests the existence of an intermediate where the intramolecular hydrogen bond favors kinetics-controlled NO2• nitration. This study provides not only a promising technique for the pNAC measurement but also evidence for their atmospheric aqueous-phase formation, facilitating further evaluation of pNACs' climatic effects.

The spread of the omicron variant: Identification of knowledge gaps, virus diffusion modelling, and future research needs.

The World Health Organization (WHO) recognised variant B.1.1.529 of the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) as a variant of concern, termed "Omicron", on November 26, 2021. Its diffusion was attributed to its several mutations, which allow promoting its ability to diffuse worldwide and its capability in immune evasion. As a consequence, some additional serious threats to public health posed the risk to undermine the global efforts made in the last two years to control the pandemic. In the past, several works were devoted to discussing a possible contribution of air pollution to the SARS-CoV-2 spread. However, to the best of the authors' knowledge, there are still no works dealing with the Omicron variant diffusion mechanisms. This work represents a snapshot of what we know right now, in the frame of an analysis of the Omicron variant spread. The paper proposes the use of a single indicator, commercial trade data, to model the virus spread. It is proposed as a surrogate of the interactions occurring between humans (the virus transmission mechanism due to human-to-human contacts) and could be considered for other diseases. It allows also to explain the unexpected increase in infection cases in China, detected at beginning of 2023. The air quality data are also analyzed to evaluate for the first time the role of air particulate matter (PM) as a carrier of the Omicron variant diffusion. Due to emerging concerns associated with other viruses (such as smallpox-like virus diffusion in Europe and America), the proposed approach seems to be promising to model the virus spreading.