Impact of secondhand smoke on air quality in partially enclosed outdoor hospitality venues: a review.

BACKGROUND: Smoking is a leading cause of premature mortality and morbidity globally. The pollutants generated from smoke are not only harmful to smokers, but also to those exposed to secondhand smoke. As a result of increasingly restrictive indoor smoke-free policies in many countries, there is a tendency for tobacco smoking to move outdoors into partially enclosed settings in hospitality venues. The aim of this systematic review was to evaluate the impact of secondhand smoke on air quality in outdoor hospitality venues. METHODS: Two electronic databases PubMed and Scopus were searched from 1 January 2010 to 30 June 2022 for studies of air quality impacts from tobacco smoking in outdoor hospitality venues. A total of 625 studies were screened and 13 studies were included in this review. RESULTS: The majority (9 studies) of reviewed studies monitored PM2.5 concentration as an indicator of secondhand smoke. PM2.5 was reported from 10.9 µg/m3 to 91.0 µg/m3 in outdoor smoking areas, compared to 4.0 µg/m3 to 20.4 µg/m3 in outdoor control sites unaffected by smoking. Secondhand smoke can also drift into adjacent outdoor areas or infiltrate into indoor environments thus affecting air quality in spaces where smoking is not permitted. CONCLUSIONS: The reviewed studies indicated that air quality within outdoor hospitality venues where smoking is permitted is unlikely to meet current World Health Organization (WHO) ambient air quality guidelines for PM2.5. Customers and staff in outdoor hospitality venues with active smoking, and in adjacent outdoor and indoor non-smoking areas, are potentially exposed to secondhand smoke at levels exceeding WHO guidelines. Stronger smoking control policies are recommended for outdoor hospitality venues to protect the health of customers and staff from harmful secondhand smoke exposure. PROSPERO REGISTRATION: CRD42022342417.

Morphology, aspect ratio, and surface elemental composition of primary aerosol particles at urban region of India.

The PM2.5 and PM10 particles were characterized in terms of morphology (size and shape) and surface elemental composition at two different (traffic and industrial) locations in urban region of India and further linked to different morphological defining parameters. The overall PM2.5 and PM10 showed significant daily variability indicating higher PM10 as compared to PM2.5. PM2.5/PM10 ratio was found to be 0.58 ± 0.10 indicating the abundance of PM2.5. Soot aggregates, aluminosilicates, and brochosomes particles were classified based on morphology, aspect ratio (AR), and surface elemental composition of single particles. The linear regression analysis indicates the significant correlation between area equivalent (Daeq) and feret diameter (Dfd) (R2 0.86-0.98). Higher aspect ratio (1.48 ± 0.87-1.43 ± 0.50) was noted at traffic site as compared to industrial site (1.33 ± 0.58-1.29 ± 0.30), while circularity showed the opposite trend. Fractal dimension (Df) of soot aggregates estimated by the soot parameters method (SPM) were found to be 1.70, 1.72, and 1.88, mainly attributed to vehicular emissions, biomass, and industrial emission/coal burning, respectively. This further inferred that freshly emitted soot particles exhibited lacey in nature with spherical shape (Df 1.70) at traffic site, while at industrial location, they were different with compact shapes (Df 1.88) due to particle aging processes. This study inferred the synoptic changes in mass, chemical characteristics, and morphology of aerosol particles which provide the new insights into individual atmospheric particle and their dynamic nature.

Indeno[1,2,3-cd]pyrene enhances the sensitivity of airway epithelial cells to ferroptosis and aggravates asthma.

Particulate matter of aerodynamic diameter ≤2.5 µm (PM2.5) exposure induces oxidative stress in lung tissues. Ferroptosis is a form of regulated cell death based on oxidative damage and lipid peroxidation. Whether PM2.5 exposure-induced oxidative stress can promote ferroptosis to aggravate asthma is not known. To investigate if PM2.5 exposure induces oxidative stress to promote ferroptosis and influence asthma development, a cockroach extract-induced asthma model in mice was used for in vivo studies. Airway epithelial cell (AEC) ferroptosis was detected by assays (CCK8, malonaldehyde, and 4-hydroxynonenal). Molecular mechanisms were investigated by real-time reverse transcription-quantitative polymerase chain reaction, western blotting, flow cytometry, liquid chromatography-tandem mass spectrometry, and chromatin immunoprecipitation. We found that exposure to PM2.5 and Indeno[1,2,3-cd] pyrene (IP; one of the prominent absorbed polycyclic aromatic hydrocarbons in PM2.5) enhanced the sensitivity of AECs to ferroptosis to aggravate asthma, whereas ferroptosis inhibitors and cytosolic phospholipase A2 (cPLA2) inhibitors reversed this augmented inflammatory response in mice suffering from asthma. IP treatment enhanced cPLA2 expression/activation through aryl hydrocarbon receptor (AhR) genomic and non-genomic pathways, resulting in arachidonic-acid release to promote the sensitivity of AECs to ferroptosis. IP exposure enhanced the release of leukotriene-B4 from lung macrophages, resulting in enhanced expression of acyl-coA synthetase long chain family member4(ACSL4) and the sensitivity of AECs to ferroptosis. This finding suggests that exposure to PM2.5 and IP promote ferroptosis sensitivity in AECs to aggravate asthma, which may provide new targets for the prevention and treatment of asthma.

Association of ambient PM2.5 and its components with in vitro fertilization outcomes: The modifying role of maternal dietary patterns.

Despite the associations of dietary patterns and air pollution with human reproductive health have been demonstrated, the interaction of maternal preconception diet and PM2.5 and its components exposure on in vitro fertilization (IVF) treatment outcomes has not been investigated. A total of 2688 couples from an ongoing prospective cohort were included. Principle component analysis with varimax rotation was performed to determine dietary patterns. One-year and 85-day average PM2.5 and its components exposure levels before oocyte retrieval were estimated. Generalized linear regression models were conducted to assess the association of dietary patterns and PM2.5 and its components exposure with IVF outcomes. Interactive effects of dietary patterns on the association between PM2.5 and its components and IVF outcomes were evaluated by stratified analyses based on different dietary patterns. A positive association between the "Fruits-Vegetables-Dairy" pattern and normal fertilization (p-trend = 0.009), Day 3 available embryos (p-trend = 0.048), and top-quality embryos (p-trend = 0.041) was detected. Conversely, women with higher adherence to the "Puffed food-Bakery-Candy" pattern were less likely to achieve Day 3 available embryos (p-trend = 0.042) and top-quality embryos (p-trend = 0.030), clinical pregnancy (p-trend = 0.049), and live birth (p-trend = 0.020). Additionally, increased intake of animal organs and seafood improved the odds of live birth (p-trend = 0.048). Exposure to PM2.5, SO42-, organic matter (OM), and black carbon (BC) had adverse effects on embryo development and pregnancy outcomes. Furthermore, our findings indicated that the effects of PM2.5 components exposure on normal fertilization and embryo quality were modified by the "Grains-Tubers-Legumes". Moreover, moderate intake of animal organs and seafood appeared to attenuate the effect of NO3- and NH4+ on the risk of early abortion. Our findings provide human evidence of the interaction between dietary patterns and PM2.5 exposure on IVF outcomes during preconception, implicating the potential for dietary interventions in infertile women to improve reproductive outcomes under conditions of unavoidable ambient air-pollutant exposure.

Temporal change and impact on air quality of an energy recovery plant using the M-BACI design in Gipuzkoa.

A significant concern in our society is the potential impact on both health and the environment of air pollutants released during the incineration of waste. Therefore, it is crucial to conduct thorough control and monitoring measures. In this context, the objective of this research was to study the evolution of particulate matter (PM2.5) and associated trace elements during the period before and after the installation of an Energy Recovery Plant (ERP). For that, a descriptive and temporal analysis of PM2.5 concentration and composition were performed on two similar areas (impact/control) using the Before-After/Control-Impact (BACI) design and two periods (before from January 01, 2018 to February 06, 2020 and after from December 10, 2020 to September 30, 2022). Results showed a decrease in the levels of PM2.5 and associated trace elements is observed in the impact zone (IZ) and in the control zone (CZ) throughout the study period. In the case of PM2.5, the most notable decrease occurred in the period of the start-up of the ERP, a period that coincides with the confinement and restrictions of COVID, with a subsequent increase in both zones, without reaching the levels observed in the period prior to the start-up of the ERP. Selenium is the only trace element that increases significantly in the IZ. In conclusion, a decrease is observed for all pollutants except selenium in both zones, although less pronounced in the IZ. Since selenium already showed an upward trend in the phase prior to the start of the ERP, it is necessary to investigate its evolution and find out the possible cause.

Residential radon decay products are associated with cough and phlegm in patients with COPD.

Radon decay products attach to particulate matter (referred to as particle radioactivity, PR) has been shown to be potential to promote airway damage after inhalation. In this study, we investigated associations between PR with respiratory symptoms and health-related quality of life (HRQL) in patients with COPD. 141 male patients with COPD, former smokers, completed the St. George's Respiratory Questionnaire (SGRQ) after up to four 1-week seasonal assessments (N=474) of indoor (home) and ambient (central site) particulate matter ≤ 2.5 µm in diameter (PM2.5) and black carbon (BC). Indoor PR was measured as α-activity (radiation) on PM2.5 filter samples. The ratio of indoor/ambient sulfur in PM2.5 (a ventilation surrogate) was used to estimate α-PR from indoor radon decay. SGRQ responses assessed frequent cough, phlegm, shortness of breath, wheeze, and chest attacks in the past 3 months. Multivariable linear regression with generalized estimating equations accounting for repeated measures was used to explore associations, adjusting for potential confounders. Median (IQR) indoor α-PR was 1.22 (0.62) mBq/m3. We found that there were positive associations between α-PR with cough and phlegm. The strongest associations were with estimated α-PR of indoor origin for cough (31.1 % increase/IQR, 95 %CI: 8.8 %, 57.8 %), and was suggestive for phlegm (13.0 % increase/IQR, 95 %CI: -2.5 %, 31.0 %), similar adjusting for indoor BC or PM2.5. α-PR of indoor origin was positively associated with an increase in SGRQ Symptoms score [1.2 units/IQR; 95 %CI: -0.3, 2.6] that did not meet conventional levels of statistical significance. Our results suggested that exposure to indoor radon decay products measured as particle radioactivity, a common indoor exposure, is associated with cough, and suggestively associated with phlegm and worse HRQL symptoms score in patients with COPD.

Air Quality Monitoring and the Safety of Farmworkers in Wildfire Mandatory Evacuation Zones.

The increasing frequency and severity of wildfires due to climate change pose health risks to migrant farm workers laboring in wildfire-prone regions. This study focuses on Sonoma County, California, investigating the effectiveness of air monitoring and safety protections for farmworkers. The analysis employs AirNow and PurpleAir PM2.5 data acquired during the 2020 wildfire season, comparing spatial variability in air pollution. Results show significant differences between the single Sonoma County AirNow station data and the PurpleAir data in the regions directly impacted by wildfire smoke. Three distinct wildfire pollution episodes with elevated PM2.5 levels are identified to examine the regional variations. This study also examines the system used to exempt farmworkers from wildfire mandatory evacuation orders, finding incomplete information, ad hoc decision-making, and scant enforcement. In response, we make policy recommendations that include stricter requirements for employers, real-time air quality monitoring, post-exposure health screenings, and hazard pay. Our findings underscore the need for significant consideration of localized air quality readings and the importance of equitable disaster policies for protecting the health of farmworkers (particularly those who are undocumented migrants) in the face of escalating wildfire risks.

Asbestos-Related lung Cancer: An underappreciated oncological issue.

Asbestos, a group of class I (WHO) carcinogenic fibers, is the main cause of mesothelioma. Asbestos inhalation also increases the risk to develop other solid tumours with lung cancer as the most prominent example [91]. The incidence of asbestos-related lung cancer (ARLC) is estimated to be to six times larger than the mesothelioma incidence thereby becoming an important health issue [86]. Although the pivotal role of asbestos in inducing lung cancer is well established, the precise causal relationships between exposures to asbestos, tobacco smoke, radon and 'particulate' (PM2.5) air pollution remain obscure and new knowledge is needed to establish appropriate preventive measures and to tailor existing screening practices[22,61,65]. We hypothesize that a part of the increasing numbers of lung cancer diagnoses in never-smokers can be explained by (historic and current) exposures to asbestos as well as combinations of different forms of air pollution (PM2.5, asbestos and silica).

A causal relationship between particulate matter 2.5 and obesity and its related indicators: a Mendelian randomization study of European ancestry.

Background: In recent years, the prevalence of obesity has continued to increase as a global health concern. Numerous epidemiological studies have confirmed the long-term effects of exposure to ambient air pollutant particulate matter 2.5 (PM2.5) on obesity, but their relationship remains ambiguous. Methods: Utilizing large-scale publicly available genome-wide association studies (GWAS), we conducted univariate and multivariate Mendelian randomization (MR) analyses to assess the causal effect of PM2.5 exposure on obesity and its related indicators. The primary outcome given for both univariate MR (UVMR) and multivariate MR (MVMR) is the estimation utilizing the inverse variance weighted (IVW) method. The weighted median, MR-Egger, and maximum likelihood techniques were employed for UVMR, while the MVMR-Lasso method was applied for MVMR in the supplementary analyses. In addition, we conducted a series of thorough sensitivity studies to determine the accuracy of our MR findings. Results: The UVMR analysis demonstrated a significant association between PM2.5 exposure and an increased risk of obesity, as indicated by the IVW model (odds ratio [OR]: 6.427; 95% confidence interval [CI]: 1.881-21.968; P FDR = 0.005). Additionally, PM2.5 concentrations were positively associated with fat distribution metrics, including visceral adipose tissue (VAT) (OR: 1.861; 95% CI: 1.244-2.776; P FDR = 0.004), particularly pancreatic fat (OR: 3.499; 95% CI: 2.092-5.855; PFDR =1.28E-05), and abdominal subcutaneous adipose tissue (ASAT) volume (OR: 1.773; 95% CI: 1.106-2.841; P FDR = 0.019). Furthermore, PM2.5 exposure correlated positively with markers of glucose and lipid metabolism, specifically triglycerides (TG) (OR: 19.959; 95% CI: 1.269-3.022; P FDR = 0.004) and glycated hemoglobin (HbA1c) (OR: 2.462; 95% CI: 1.34-4.649; P FDR = 0.007). Finally, a significant negative association was observed between PM2.5 concentrations and levels of the novel obesity-related biomarker fibroblast growth factor 21 (FGF-21) (OR: 0.148; 95% CI: 0.025-0.89; P FDR = 0.037). After adjusting for confounding factors, including external smoke exposure, physical activity, educational attainment (EA), participation in sports clubs or gym leisure activities, and Townsend deprivation index at recruitment (TDI), the MVMR analysis revealed that PM2.5 levels maintained significant associations with pancreatic fat, HbA1c, and FGF-21. Conclusion: Our MR study demonstrates conclusively that higher PM2.5 concentrations are associated with an increased risk of obesity-related indicators such as pancreatic fat content, HbA1c, and FGF-21. The potential mechanisms require additional investigation.

Air Pollution in Cardio-Oncology and Unraveling the Environmental Nexus: JACC: CardioOncology State-of-the-Art Review.

Although recent advancements in cancer therapies have extended the lifespan of patients with cancer, they have also introduced new challenges, including chronic health issues such as cardiovascular disease arising from pre-existing risk factors or cancer therapies. Consequently, cardiovascular disease has become a leading cause of non-cancer-related death among cancer patients, driving the rapid evolution of the cardio-oncology field. Environmental factors, particularly air pollution, significantly contribute to deaths associated with cardiovascular disease and specific cancers, such as lung cancer. Despite these statistics, the health impact of air pollution in the context of cardio-oncology has been largely overlooked in patient care and research. Notably, the impact of air pollution varies widely across geographic areas and among individuals, leading to diverse exposure consequences. This review aims to consolidate epidemiologic and preclinical evidence linking air pollution to cardio-oncology while also exploring associated health disparities and environmental justice issues.

Residential exposure to ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) and incident breast cancer among young women in Ontario, Canada.

BACKGROUND: Air pollution has been classified as a human carcinogen based largely on findings for respiratory cancers. Emerging, but limited, evidence suggests that it increases the risk of breast cancer, particularly among younger women. We characterized associations between residential exposure to ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) and breast cancer. Analyses were performed using data collected in the Ontario Environmental Health Study (OEHS). METHODS: The OEHS, a population-based case-control study, identified incident cases of breast cancer in Ontario, Canada among women aged 18-45 between 2013 and 2015. A total of 465 pathologically confirmed primary breast cancer cases were identified from the Ontario Cancer Registry, while 242 population-based controls were recruited using random-digit dialing. Self-reported questionnaires were used to collect risk factor data and residential histories. Land-use regression and remote-sensing estimates of NO2 and PM2.5, respectively, were assigned to the residential addresses at interview, five years earlier, and at menarche. Logistic regression was used to estimate odds ratios (OR) and their 95 % confidence intervals (CI) in relation to an interquartile range (IQR) increase in air pollution, adjusting for possible confounders. RESULTS: PM2.5 and NO2 were positively correlated with each other (r = 0.57). An IQR increase of PM2.5 (1.9 µg/m3) and NO2 (6.6 ppb) at interview residence were associated with higher odds of breast cancer and the adjusted ORs and 95 % CIs were 1.37 (95 % CI = 0.98-1.91) and 2.33 (95 % CI = 1.53-3.53), respectively. An increased odds of breast cancer was observed with an IQR increase in NO2 at residence five years earlier (OR = 2.16, 95 % CI: 1.41-3.31), while no association was observed with PM2.5 (OR = 0.96, 95 % CI 0.64-1.42). CONCLUSIONS: Our findings support the hypothesis that exposure to ambient air pollution, especially those from traffic sources (i.e., NO2), increases the risk of breast cancer in young women.

Spatiotemporal distribution of oxidative potential in PM2.5 and its key components across six Chinese cities.

Increasing evidence has supported that oxidative potential (OP) serves as a crucial indicator of health risk of exposure to PM2.5 over mass concentration. However, there is a lack of comparative studies across multiple cities, particularly on a fine temporal scale. In this study, we aim to investigate daily variation of ambient PM2.5 OP through simultaneous samplings in six Chinese cities for one year. Results showed that more than 60 % of the sampling days exhibited non-zero ranking difference between volume-normalized oxidative potential (OPv) and mass concentration among the six cities. Key components contributing to OPv inculde Mn, NO3-, and K+, followed by Ca2+, Al, SO42-, Cl-, Fe, and NH4+. Based on these chemical components, we developed a stepwise multivariable linear regression model (R2: 0.71) for OPv prediction. The performance of the model is comparable to both species- and sources-based ones in the literature. These findings suggest that a relatively lower daily-averaged mass concentration of PM2.5 does not necessarily indicate a lower oxidative risk. Future studies and policy developments on health benefits should also consider OPv rather than mass concentration alone. Priority could be given to sources/species that contribute significantly to oxidative potential of ambient PM2.5. SYNOPSIS: This study highlights inclusion of oxidative potential as a complementary metric for air pollution assessment and control.

Associations of insulin sensitivity and immune inflammatory responses with child blood lead (Pb) and PM2.5 exposure at an e-waste recycling area during the COVID-19 lockdown.

Fine particular matter (PM2.5) and lead (Pb) exposure can induce insulin resistance, elevating the likelihood of diabetes onset. Nonetheless, the underlying mechanism remains ambiguous. Consequently, we assessed the association of PM2.5 and Pb exposure with insulin resistance and inflammation biomarkers in children. A total of 235 children aged 3-7 years in a kindergarten in e-waste recycling areas were enrolled before and during the Corona Virus Disease 2019 (COVID-19) lockdown. Daily PM2.5 data was collected and used to calculate the individual PM2.5 daily exposure dose (DED-PM2.5). Concentrations of whole blood Pb, fasting blood glucose, serum insulin, and high mobility group box 1 (HMGB1) in serum were measured. Compared with that before COVID-19, the COVID-19 lockdown group had lower DED-PM2.5 and blood Pb, higher serum HMGB1, and lower blood glucose and homeostasis model assessment of insulin resistance (HOMA-IR) index. Decreased DED-PM2.5 and blood Pb levels were linked to decreased levels of fasting blood glucose and increased serum HMGB1 in all children. Increased serum HMGB1 levels were linked to reduced levels of blood glucose and HOMA-IR. Due to the implementation of COVID-19 prevention and control measures, e-waste dismantling activities and exposure levels of PM2.5 and Pb declined, which probably reduced the association of PM2.5 and Pb on insulin sensitivity and diabetes risk, but a high level of risk of chronic low-grade inflammation remained. Our findings add new evidence for the associations among PM2.5 and Pb exposure, systemic inflammation and insulin resistance, which could be a possible explanation for diabetes related to environmental exposure.

Air quality in a revitalized special economic zone at the center of an urban monocentric agglomeration.

In this study, we have examined the air quality within a revitalized, post-industrial urban area in Lódz, Poland. The use of Dron technology with mobile measurement equipment allowed for accurate assessment of air quality (particulate matter and gaseous pollutants) and factors influencing air quality (wind speed and direction) on a local scale in an area of 0.18 km2 and altitudes from 2 to 50 m. The results show that the revitalization carried out in the Lodz special economic zone area contributed to eliminate internal air pollution emitters through the use of ecological and effective heat sources. The exceedances permissible concentration values were local, and concerned mainly the higher measurement zones of the troposphere (more than 30 m above ground level). In the case of gaseous pollutants, higher wind speeds were associated with a decrease in the concentration of SO2 and an increase in H2S concentration. In both cases, the wind contributed to the occurrence of local areas of accumulation of these gaseous pollutants in the spaces between buildings or wooded areas.

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.

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.

Characterization of winter PM2.5 source contributions and impacts of meteorological conditions and anthropogenic emission changes in the Sichuan Basin, 2002-2020.

In this study, the Weather Research and Forecasting (WRF) model and Community Multiscale Air Quality-Integrated Source Apportionment Method (CMAQ-ISAM) were utilized, which were integrated with the Multiresolution Emission Inventory for China (MEIC) emission inventory, to simulate winter PM2.5 concentrations, regional transport, and changes in emission source contributions in the Sichuan basin (SCB) from 2002 to 2020, considering variations in meteorological conditions and anthropogenic emissions. The results indicated a gradual decrease in the basin's winter average PM2.5 concentration from 300 µg/m3 to 120 µg/m3, with the most significant decrease occurring after 2014, reflecting the actual impact of China's air pollution control measures. Spatially, the main pollution area shifted from Chongqing to Chengdu and the western basin. The sources of PM2.5 at the eastern and western margins of the basin have remained stable and have been dominated by local emissions for many years, while the sources of PM2.5 in the central part of the basin have evolved from a multiregional co-influenced source during the early period to a high proportion of local emissions; except for boundary condition sources, residential sources were the main PM2.5 sources in the basin (approximately 29.70 %), followed by industrial sources (approximately 14.11 %). Industrial sources exhibited higher contributions in Chengdu and Chongqing and gradually stabilized with residential sources over the years, while residential sources dominated in the eastern and western parts of the basin and exhibited a declining trend. Meteorological conditions exacerbated pollution in the whole basin from 2008 to 2014, especially in the west (21-40 µg/m3). The eastern basin and Chongqing exhibited more years with alleviated meteorological pollution, including a 40+ µg/m3 decrease in Chongqing from 2002 to 2005. Reduced anthropogenic emissions alleviated annual pollution levels, with a greater reduction (> -20 µg/m3) after 2011 due to pollution control measures.

Health-Oriented Emission Control Strategy of Energy Utilization and Its Co-CO2 Benefits: A Case Study of the Yangtze River Delta, China.

Reducing air pollutants and CO2 emissions from energy utilization is crucial for achieving the dual objectives of clean air and carbon neutrality in China. Thus, an optimized health-oriented strategy is urgently needed. Herein, by coupling a CO2 and air pollutants emission inventory with response surface models for PM2.5-associated mortality, we shed light on the effectiveness of protecting human health and co-CO2 benefit from reducing fuel-related emissions and generate a health-oriented strategy for the Yangtze River Delta (YRD). Results reveal that oil consumption is the primary contributor to fuel-related PM2.5 pollution and premature deaths in the YRD. Significantly, curtailing fuel consumption in transportation is the most effective measure to alleviate the fuel-related PM2.5 health impact, which also has the greatest cobenefits for CO2 emission reduction on a regional scale. Reducing fuel consumption will achieve substantial health improvements especially in eastern YRD, with nonroad vehicle emission reductions being particularly impactful for health protection, while on-road vehicles present the greatest potential for CO2 reductions. Scenario analysis confirms the importance of mitigating oil consumption in the transportation sector in addressing PM2.5 pollution and climate change.

Gut microbiota mediates ambient PM2.5 exposure-induced abnormal glucose metabolism via short-chain fatty acids.

PM2.5 exposure has been found to cause gut dysbiosis and impair glucose homeostasis in human and animals, yet their underlying biological connection remain unclear. In the present study, we aim to investigate the biological significance of gut microbiota in PM2.5-induced glucose metabolic abnormalities. Our results showed that microbiota depletion by antibiotics treatment significantly alleviated PM2.5-induced glucose intolerance and insulin resistance, as indicated by the intraperitoneal glucose tolerance test, glucose-induced insulin secretion, insulin tolerance test, insulin-induced phosphorylation levels of Akt and GSK-3ß in insulin sensitive tissues. In addition, faecal microbiota transplantation (FMT) from PM2.5-exposed donor mice successfully remodeled the glucose metabolism abnormalities in recipient mice, while the transplantation of autoclaved faecal materials did not. Faecal microbiota analysis demonstrated that the composition and alpha diversity of the gut bacterial community were altered by PM2.5 exposure and in FMT recipient mice. Furthermore, short-chain fatty acids levels analysis showed that the circulating acetate was significantly decreased in PM2.5-exposed donor and FMT recipient mice, and supplementation of sodium acetate for 3 months successfully improved the glucose metabolism abnormalities induced by PM2.5 exposure. These results indicate that manipulating gut microbiota or its metabolites could be a potential strategy for preventing the adverse health effects of ambient PM2.5.

Temporal variation characteristics of microbial aerosols in the goose house environment.

1. Preventing disease is important in poultry production systems, but this has mainly been studied in chickens. The aim of this study is to explore the impact of microbial aerosols in intensive goose house environments.2. To evaluate the environmental quality of geese housing, fine particulate matter (PM2.5) was collected using an ambient air particulate matter sampler. High-throughput sequencing was used to analyse bacterial diversity and relative abundance. Results showed that the number of general and operational taxonomic units (OTUs) were 1,578 and 19 112 in all PM2.5 samples. Firmicutes, Bacteroidota, Proteobacteria, Acidobacterota were the four most abundant phyla in PM2.5.3. Compared with bacterial phyla in the PM2.5 from chicken houses, those in the genus Acidobacterota were increased in goose housing. There are various genera of bacteria present in PM2.5, and their composition was similar across different samples. No significant change was observed in the diversity of microbiota in the PM2.5, although multiple pathogenic bacteria were detected.4. A prediction function showed that a variety of bacterial phyla correlated positively with the human diseases.5. In summary, the microbial aerosols in the goose shed pose significant risks to the health of the geese. Regular monitoring of the composition of microbial aerosols is important for the healthy growth of geese and disease prevention and control.