Long-term exposure to fine particulate matters (PM2.5) has been associated with respiratory and cardiovascular diseases and the burden are potentially higher in China experiencing heavy air pollution. In this study, we established the exposure-response association between long-term exposures to PM2.5 and lung function and blood pressure in Chinese middle-aged and older adults using linear mixed-effects and generalized additive mixed models based on 3 waves longitudinal health outcomes data by enrolling 19,988 participants from 121 cities across the mainland of China. We also assessed the effect of Clean Air Policy (CAP) based on a quasi-experimental difference-in-differences (DID) design. A 10 µg/m3 increase in PM2.5 concentration was associated with a 7.18 (95 % confidence interval [CI]: -8.35, -6.02) L/min decrease in PEF (peak expiratory flow) and a 0.72 (95 % [CI]: 0.53, 0.90) and a 0.30 (95 % [CI]: 0.18, 0.42) mmHg increase in systolic and diastolic blood pressure, respectively. The associations were more pronounced in males and rural areas for PEF, but similar across subgroups for blood pressure. DID results suggested that the effect of CAP on health outcomes were sensitive to magnitudes of reduction in PM2.5. A 5 µg/m3 reduction in PM2.5 or more generally led to 18.70 (95 % [CI]: 0.79, 36.61) higher PEF and -2.05 (95 % [CI]: -3.87, -0.23) lower diastolic blood pressure, respectively, compared to no reduction or increase in exposure. However, the effects were significant only in rural areas. Our analysis support CAP aiming to benefit public health and provides insights to inform future control policy for efficiently decreasing air pollution exposure burden.

Particulate matter (PM) with diameter ≤ 2.5 μm (PM2.5) and ≤ 10 μm (PM10), including from bushfire smoke, is associated with cardiovascular disease (CVD) morbidity and mortality. This systematic review assesses how CVD morbidity and mortality is affected by type, duration, and level of air pollution exposure.

A search was conducted on Ovid Medline, Embase and Scopus, spanning across 1 January 2012 to 30 July 2022. Primary quantitative studies exploring the effect of PM2.5, PM10 or bushfire smoke on CVD were included. Studies without adjustment for confounding factors were excluded. The Newcastle-Ottawa Scale was used to assess the risk of bias (ROB) in the studies, and meta-analysis was conducted on relevant outcomes.

A total 275 studies were obtained, and 80 studies were analysed with diseases ranging from ICD-10 I00-I99. For CVD morbidity, increased PM2.5 and PM10 was associated with 1.92 (95 % CI: 0.58,3.26) years of life lost per 10 μg/m3 increase in exposure. Increased PM2.5 and PM10 was associated with a 0.52 % (95 % CI: 0.37,0.68) increase in mortality per 10 μg/m3 increase in exposure. Bushfire smoke also presented similar trends. Two studies had high ROB, 42 had medium ROB, and 36 had low ROB. There was high heterogeneity between the studies, with I2 values ranging between 88.09 % and 94.25 %.

Air pollution including bushfire smoke is associated with increased CVD morbidity and mortality. This effect ranges across different types, durations, and levels of air pollution exposure, making stringent climate change and air pollution mitigation strategies imperative.

Particulate matter with an aerodynamic diameter of less than 2.5 µm (PM2.5) is one of the criteria air pollutants that (1) serve as an essential carrier of airborne toxicants arising from combustion-related events including emissions from industries, automobiles, and wildfires and (2) play an important role in transient to long-lasting cognitive dysfunction as well as several other neurological disorders. A systematic review was conducted to address differences in study design and various biochemical and molecular markers employed to elucidate neurological disorders in PM2.5 -exposed humans and animal models. Out of 340,068 scientific publications screened from 7 databases, 312 studies were identified that targeted the relationship between exposure to PM2.5 and cognitive dysfunction. Equivocal evidence was identified from pre-clinical (animal model) and human studies that PM2.5 exposure contributes to dementia, Parkinson disease, multiple sclerosis, stroke, depression, autism spectrum disorder, attention deficit hyperactivity disorder, and neurodevelopment. In addition, there was substantial evidence from human studies that PM2.5 also was associated with Alzheimer's disease, anxiety, neuropathy, and brain tumors. The role of exposome in characterizing neurobehavioral anomalies and opportunities available to leverage the neuroexposome initiative for conducting longitudinal studies is discussed. Our review also provided some areas that warrant consideration, one of which is unraveling the role of microbiome, and the other role of climate change in PM2.5 exposure-induced neurological disorders.

Airborne particulate matter (PM) pollution comprises various air-colloidal particles including gases, organic and inorganic particles. Over the past few years, a growing number of studies have shown that PM has a disastrous effect on the human cardiovascular system, particularly in relation to cardiac arrhythmias. However, the mechanisms underlying these observed effects have not yet been clearly defined. In this review, the electronic database PubMed was used as the source of selected peer-reviewed research articles published in English. Both pre-clinical studies and clinical trials were obtained using "particulate matter", "cardiac arrhythmias", "ion channel" and "cardiomyocytes" as keywords. We present evidence pertinent to the potential mechanisms underlying PM-induced cardiac arrhythmias, drawing from results spanning in vitro to clinical studies, with a particular focus on the profile of vulnerable cardiac ion channels. At a cellular level, PM has been shown to up-regulate the expression of myocardial Ca2+ ion channel proteins, increase Ca2+ release from ryanodine 2 (RyR2) and decrease sarcoplasmic reticulum (SR) re-uptake of Ca2+, leading to intracellular Ca2+ overload. Additionally, the disruption of myocardial Ca2+ homeostasis has been shown to aggravate the production of mitochondrial ROS, inflammatory cytokines, and apoptotic cascades, which may potentially contribute to arrhythmic substrates, especially in high-risk patients. The upregulation of genes encoding sodium (Na+) and potassium (K+) channels caused by PM has been implicated in the induction of QT prolongation and alterations in action potentials related to cardiac arrhythmias. Finally, we discuss potential interventions to mitigate PM-induced cardiac pathology and propose future directions for these therapeutic strategies.

Cardiovascular disease is a leading cause of mortality globally, with air pollution, particularly fine particulate matter (PM2.5), recognized as a significant risk factor. While long-term accumulated exposure to PM2.5 has been extensively studied, the impact of PM2.5 peaks on cardiovascular events remains unexplored.

This prospective cohort study analyzed data from 26,723 male participants aged 65 to 74 years from the Danish DANCAVAS and VIVA screening trials. We assessed the association between long-term cumulated repeated PM2.5 peak exposure and major adverse cardiovascular events (MACE), including non-fatal acute myocardial infarction, non-fatal stroke, cardiovascular mortality, and revascularization procedures, using Cox proportional hazards models. PM2.5 peak exposure was treated as a time-varying variable, and models were adjusted for potential confounders, including individual-level demographic, clinical, and socioeconomic factors. PM2.5 peaks were defined as monthly average concentrations exceeding the long-term mean by more than two standard deviations.

The fully adjusted model showed no significant elevation in the risk of MACE associated with increased PM2.5 peak exposure (HR = 0.9991, 95 % CI: 0.9974-1.0008). This lack of association was consistent across sensitivity analyses and different peak definitions, including shorter-term peaks in the five and one years preceding an event.

Our findings suggest that PM2.5 peak exposure does not significantly increase the risk of MACE in this Danish population. These results challenge the hypothesis that PM2.5 peaks over a long period are a determinant of cardiovascular risk. Further research is warranted to explore these relationships in different populations and to investigate potential mechanisms underlying the effects of air pollution peaks on cardiovascular health.

Air pollutants have been associated with multiple cardiovascular diseases, but evidence on the long-term and combined effects of air pollutants on the incidence of ischaemic heart disease (IHD) remains limited.

Prospective cohort study.

A total of 398,547 participants from the UK Biobank were included in this prospective cohort study. Concentrations of air pollutants were calculated using the Land Use Regression (LUR) model, including particulate matter (PM) [PM2.5, PM10-2.5, PM10] and nitrogen oxides (NOx and NO2). Cox proportional hazards models and restricted cubic spline models were utilised to detect associations between air pollutants and IHD incidence. A novel air pollution score was proposed to indicate the synergistic effect of five air pollutants by combining variance contribution and eigenvalue of each pollutant in principal components analysis (PCA).

In a median follow-up of 12.5 years, 23,721 of 398,547 participants were diagnosed with IHD. For every 1-μg/m3 increase, the risk of IHD was 1.026 (95 % confidence interval [CI]: 1.012-1.040) and 1.002 (95 % CI: 1.001-1.003) for PM2.5 and NOx, respectively. This study found that for every increase in quartile of PM2.5 level, the hazard ratios (HRs) for IHD were 1.035 (95 % CI: 0.998-1.073), 1.043 (95 % CI: 1.005-1.082) and 1. 063 (95 % CI: 1.022-1.106) compared with the lowest quartile. Long-term estimated exposure to multiple air pollutants showed a significant association with elevated risk of IHD (HRs = 1.029, 95 % CI: 1.007-1.051) and the exposure-response curve was linear.

Among UK adults, long-term and synchronous exposure to multiple air contaminants was associated with an increased risk of IHD.

To evaluate the relationship between short-term exposure to ambient air pollutants and cardiovascular disease (CVD) hospitalizations.

A time-series analysis was conducted using data from the Tehran Lipid and Glucose Study cohort of 3454 residents (1880 women) aged 50-70 from District 13 of Tehran. Follow-up data from January 1999 to March 2018 were analyzed. Daily mean temperatures and air pollution levels (CO, O3, PM10, NO2, and SO2) were recorded, and distributed lag non-linear models (DLNMs) assessed the lagged effects on outcome.

Over a median follow-up of 14.7 years, 2200 CVD hospitalizations occurred among 3454 participants (mean age 58.7 years, women = 1880). Among the general population, the DLNM models indicated that PM10 concentrations at 73 μg/m3 was associated with a 12 % increased risk of the outcome, with an RR of 1.12 (95 % CI: 1.01-1.24), and higher PM10 levels corresponded to increasing RRs. PM10 indicated a short-term exposure effect at 1-day lag on the outcome risk. SO2 concentrations reached significance at 24 μg/m3, with an RR of 1.06 (95 % CI: 1.04-1.07); the effect persisted up to 65 μg/m3, with an increased risk of the outcome observed at a 6-day lag. CO showed the highest RR of 1.92 (95 % CI: 1.65-2.23) for the concentration of 5 mg/m3. Exposure to CO was linked to an increased risk of the outcome with a 1-day lag. Sex as well as presence of metabolic syndrome and CKD did not modify the association between air pollutants with the outcome.

Short-term exposure to PM10, SO2 and CO significantly increased risk of CVD hospitalization.

Heart failure (HF) is a growing public health concern, with an increasing incidence among younger populations. Traditionally, HF was considered a condition primarily affecting the elderly, but of late, emerging evidence hints at a rapidly rising HF incidence in youth in the past 2 decades. HF in youth has been linked to a complex interaction between emerging risk factors, such as metabolic syndrome, environmental exposures, genetic predispositions, and lifestyle behaviors. This review examines these evolving determinants, including substance abuse, autoimmune diseases, and the long-term cardiovascular effects of coronavirus disease 2019, which disproportionately affect younger individuals. Through a comprehensive analysis, the study highlights the importance of early detection, targeted prevention strategies, and multidisciplinary management approaches to address this alarming trend. Promoting awareness and integrating age-specific interventions could significantly reduce the burden of HF and improve long-term outcomes among younger populations.

Coronary heart disease (CHD) is a leading cause of cardiovascular mortality, with air pollution serving as a significant risk factor. Henan Province, characterized by both a high incidence of CHD and severe air pollution, faces substantial health and economic challenges. However, limited research has explored the relationship between air pollution and CHD in this region.

This study employs a case-crossover design combined with a distributed lag non-linear model (DLNM) to examine the short-term effects of extreme concentrations of air pollutants (PM₂.₅, PM₁₀, NO₂, SO₂, CO, and O₃) on CHD hospitalizations in Henan. Data on 133,294 confirmed CHD patients from seven large hospitals across five cities (2016-2021) were collected, with patients' addresses linked to nearby air quality monitoring stations to assess exposure to air pollutants and meteorological factors. The time-stratified case-crossover design and DLNM were used to calculate relative risks (RRs) for pollutant exposure on CHD hospitalizations, and subgroup analyses were conducted to identify sensitive groups.

Significant increases in CHD hospitalizations were associated with extremely high concentrations of NO₂, SO₂, and PM₁₀, with maximum RRs of 1.768 for NO₂, 2.821 for SO₂, and 1.728 for PM₁₀ on the 7th cumulative day, while high O₃ levels showed a protective effect. Younger individuals (≤64y) and males were more sensitive to these effects, and high CO concentrations only increase the risk of CHD incidence in the younger (≤64y) subgroup. Synergistic interactions were observed between certain pollutants, such as CO and NO₂/SO₂/PM₁₀, suggesting that the negative impact of CO on CHD is amplified in a multi-pollutant environment due to interactions with other pollutants.

These findings highlight the significant public health impact of air pollution on CHD in Henan Province.

There is increasing evidence that air pollutants significantly increase the risk of cardiovascular disease (CVD). Nevertheless, less research has been conducted to date to reveal protective factors. Therefore, this study aims to indicate whether a healthy lifestyle can modify the effects of environmental pollution on CVD. This study screened 3010 participants from the China Health and Retirement Longitudinal Study (CHARLS) Wave 3 (2015). The study aimed to systematically demonstrate the impact of environmental pollution on CVD and elucidate the role of a healthy lifestyle. Air pollutant data were obtained from the China High Air Pollutant (CHAP) datasets. We analyzed the relationship between these pollutants and cardiovascular disease risk using generalized linear mixed models. In addition, healthy lifestyles were categorized as low, medium, and high; stratified analyses were conducted to estimate the effect of healthy lifestyles on the risk of CVD due to air pollutants. 607 had CVD among 3010 participants, and the three-year mean concentrations of the pollutants chloride ion (Cl-), nitrate ion (NO3-), particulate matter with a diameter of 10 micrometers or less (PM10), particulate matter with a diameter of 10 micrometers or less (PM1), particulate matter with a diameter of 10 micrometers or less (PM2.5) were each linked 1.37 (95%CI:1.22,1.54), 1.03 (95%CI:1.00,1.06), 1.02 (95%CI:1.01,1.03), 1.01 (95%CI:1.00,1.01), and 1.01 (95%CI:1.00,1.01) fold risk of CVD, respectively. For the subgroups of low, medium, and high according to the healthy lifestyle score in model 2, the average concentration of Cl- pollutant was each associated with 1.34 (1.12,1.62), 1.34 (1.12,1.61), and 1.32 (1.03,1.71) times risk with CVD, respectively. The NO3 - was each associated with 1.06 (1.02,1.11), 1.01 (0.97,1.05), and 0.98 (0.93,1.04) times risk with CVD, respectively. The PM1 was each associated with 1.03 (1.01,1.05), 1.01 (0.99,1.02), and 1.00 (0.97,1.02) times risk with CVD, respectively. The PM10 was each associated with 1.01 (1.00,1.01), 1.01 (0.99,1.01), and 1.00 (0.99,1.01) times risk with CVD, respectively. PM2.5 was each associated with 1.02 (1.01,1.03), 1.00 (0.99,1.01), and 1.00 (0.99,1.01) times risk with CVD, respectively. Exposure to these pollutants(Cl-, NO3-, PM10, PM1, PM2.5)is associated with higher risk of CVD, and healthier lifestyles can reduce the risk of CVD due to overall air pollutants.

The association of individual metals in PM2.5 with cardiovascular damage has been established in previous studies, but there are fewer studies on co-exposure to multiple metals and potential metabolic alterations in cardiovascular damage. To investigate the early cardiovascular effects of multiple metals and the mediating effects of metabolites, we conducted a panel study on young adults from 2017 Winter to 2018 Autumn in Caofeidian, China. A total of 180 serum samples were analyzed for metabolomic profiles using liquid chromatography-mass spectrometry. The associations between personal metal exposure, metabolite levels, and indicators of cardiovascular injury were analyzed by linear mixed-effects modeling (LME) and Bayesian kernel machine regression (BKMR). Metabolomic analyses showed 79 metabolites in the serum of healthy adults changed significantly between seasons and all metabolites were strongly associated with toxic metals. Additionally, differential metabolites were enriched in seven metabolic pathways and activated by metal exposure, such as Butanoate metabolism and Linoleic acid metabolism. BKMR model interpreted that the overall effect of metals mixture was negatively associated with Capryloyl glycine and Sphinganine and Sb mainly contributed to the effect. The results of mediation analysis revealed that the association between V and VEGF was mediated by Diethylhexyl with a partial proportion of 13.4%. Furthermore, the result also found the association between CerP(d18:1/26:1(17Z)) and ET-1 was mediated by TGFβ1 with a proportion of 53.4%. Our findings suggested that multiple metal exposure was associated with metabolomic changes of cardiovascular damage in young adults, and may simultaneously affect the metabolomic changes by inducing oxidative stress and inflammation.

PM2.5, recognized as a potential pathogenic factor for nervous system diseases, remains an area with many unknowns, particularly regarding its effects on human health. After five-month real-ambient PM2.5 exposure, we observed no significant pathological damage to the lung, liver, spleen, or kidney tissues. However, PM2.5 exposure led to neuronal degeneration in the hippocampal CA1 region of Brown Norway (BN) rats. The level of IL-6, IL-13, IL-1β, IL-12, IL-4, GRO/KC, MIP-1α, CM-CSF significantly increased in lung lavage fluid (P < 0.05 for all). Notably, we detected a slight impairment in spatial learning ability, as evidenced by the Barnes maze training outcomes. There were no significant changes in the bacterial community in lung lavage fluid (P = 0.621), but the bacterial community in the gut significantly changed (P < 0.001), with more species identified (P < 0.05). The metabolomic analysis revealed 147 and 149 significantly changed metabolites in the pulmonary system and serum, respectively (P < 0.05). PM2.5 exposure caused a decrease in Nervonic acid (NA) in both the lung and serum, which likely contributed to spatial learning impairment (P < 0.01). The correlation between lung metabolites, gut bacterial species, and serum metabolites indicated that PM2.5 exposure likely impaired spatial learning through the lung-gut-brain axis pathway. Lung and serum metabolic disorders and intestinal microbial imbalance occurred in BN rats post-five-month real-ambient PM2.5 exposure. There were two potential ways that PM2.5 exposure caused the decline of spatial learning ability in wild-type BN rats: (1) PM2.5 exposure led to a significant decrease of neuroprotective Nervonic acid in lung and serum metabolites. (2) PM2.5 exposure likely led to reduced spatial learning ability through the lung-gut-brain axis.

Particulate matter 2.5 (PM2.5) exposure is responsible for skin inflammation, aging, and disruption of skin homeostasis. The objective of this investigation was to assess the potential of myricetin in protecting against skin damage caused by PM2.5. Human keratinocytes (HaCaT) were pretreated with myricetin and subsequently exposed to PM2.5. Cell viability, reactive oxygen species (ROS) generation, oxidized cellular components, mitochondrial damage, cellular apoptosis, and endoplasmic reticulum (ER) stress were assessed. A mitogen-activated protein kinase (MAPK) signaling network was constructed, and the action site of myricetin was explored through docking analysis. PM2.5 induced oxidative stress, resulting in DNA damage, lipid peroxidation, protein carbonylation, and cellular apoptosis. Myricetin counteracted these effects by reducing the PM2.5-induced ROS levels. Additionally, myricetin mitigated the PM2.5-induced cytochrome c release into the cytoplasm and caspase activation, thereby ameliorating cellular apoptosis. Myricetin reduced PM2.5-induced cytosolic Ca2+ level and ER-related signaling molecules. Furthermore, myricetin inhibited cellular cytotoxicity by downregulating the MAPK signaling pathway. Docking and network analyses identified 12 major MAPK proteins targeted by myricetin, and these proteins primarily affected the classical MAPK pathway. These findings suggest that myricetin mitigates skin impairments caused by PM2.5 exposure by reducing ROS, mitochondrial damage, ER stress, and apoptosis via downregulating the MAPK signaling pathway.

Understanding the evolving patterns of cardiovascular disease (CVD) burden attributable to ambient particulate matter pollution (APMP) is essential. Furthermore, research on the underlying mechanisms has mostly been limited to laboratory and animal models, with few large-scale population-based studies.

Using data from the Global Burden of Disease Study (GBD) 2021, we analyzed disability-adjusted life years and mortality for CVD attributable to APMP (measured as particulate matter [PM]2.5) from 1990 to 2021. We examined shifts in burden between APMP and household air pollution (HAP), regional disparities by socio-demographic index (SDI), and predicted trends using a Bayesian age-period-cohort model. Additionally, we used UK Biobank (UKB) data (metabolomics: 230,000 + participants; proteomics: 50,000 +) to identify biomarkers mediating the association between PM2.5 exposure and CVD outcomes, and further analyzed their biological roles. Metabolic and proteomic signatures were constructed using regression and elastic net models, with predictive performance assessed via time-dependent receiver operating characteristic analysis. Life expectancy was evaluated using flexible parametric survival models. Subgroup analysis was conducted by age, sex, lifestyle, socioeconomic status, and genetic susceptibility.

In 2021, the global CVD absolute burden attributable to APMP was more than double that of 1990, with significant regional disparities. The burden shifted from HAP to APMP, with 15% of CVD cases globally attributed to APMP. The CVD burden attributable to APMP increased with age and is projected to rise through 2030. In the UKB, approximately 30 metabolites, including albumin, mediated the association between PM2.5 exposure and CVD outcomes, primarily involving lipid and fatty acids metabolism. Over 60 proteins, including growth differentiation factor-15 and trefoil factor 2, mediated the association with CVD outcomes, enriched in cytokine-receptor interaction and leukocyte migration pathways. Metabolic and proteomic signatures outperformed PM2.5 alone in predicting 1-, 5-, and 10-year CVD outcomes. Participants in the lowest decile of PM2.5 exposure, metabolic, and proteomic signatures had longer life expectancy than those in the highest decile.

The CVD burden attributable to APMP remains a critical public health concern. This study presents a novel approach for identifying and managing susceptible populations through metabolomic and proteomic perspectives.

In driving a transition in environmental governance, China's low-carbon city pilot (LCCP) policy has exerted a dichotomous impact on public health expenditure that is characterized by both a decline in relative proportion and expansion of absolute scale. Research to date is insufficient for understanding the transmission mechanisms and policy coordination pathways underlying this contradiction, which has hindered the sustainable realization of environmental health benefits. This study thus investigates the impact of China's LCCP policy on public health expenditure and the underlying mechanisms involved.

Based on panel data of 285 Chinese cities at the prefecture level and above from 2003 to 2019, a quasi-natural experiment was conducted using China's LCCP policy. The time-varying difference-in-differences simulation method and hierarchical regression method were used to analyze the effect and mechanism of the LCCP policy on China's public health expenditure.

The results demonstrate the inherently paradoxical nature of the effects of the LCCP policy on public health expenditure: although the LCCP policy produces a significant relative reduction in public health expenditure (β = -0.331, p < 0.001), it simultaneously produces a pronounced expansion in terms of absolute expenditure (β = 0.409, p < 0.001). These impacts are spatially heterogeneous across regions and exhibit supply-demand divergence in healthcare infrastructure readiness and environmental threshold effects that are contingent upon pollution severity gradients. Further analysis of the underlying mechanism reveals that public low-carbon behaviors serve as dual negative mediators in both expenditure dimensions, whereas household medical burdens exert a significant positive mediating effect on absolute expenditure but a statistically insignificant mediating effect on relative expenditure.

This study reveals the complex synergistic mechanisms linking environmental governance to health investment allocation. The internal contradictory effects of the LCCP policy on public health expenditures must be resolved by striking a balance between environmental governance and health investment, implementing regional differentiation strategies, optimizing the structure of preventive expenditures, and guiding the public to collaborative participation. China's environmental quality and public health should be promoted simultaneously.

The growing impact of climate change and escalating wildfire seasons has led to heightened ambient air pollution, potentially affecting children's sleep health. However, current epidemiological research often relies on outdoor weather data to model the environmental impacts on sleep health, potentially mischaracterizing the actual bedroom environment. To address these challenges, we conducted experiments to investigate the relationships among ambient, indoor, and personal exposure to PM2.5 concentrations and obstructive sleep apnea (OSA) in children. We employed computational fluid dynamics (CFD) simulations to assess how personal exposures are influenced by factors such as air distribution design, supply air temperature (Tsa), body shape, and sleep position. Our statistical analysis revealed notable associations between OSA severity as measured by obstructive apnea-hypopnea index (OAHI) and indoor PM2.5 concentrations (β: 11.52; 95% CI: 5.07 to 17.96; p < 0.01) and personal PM2.5 exposures (β: 18.92; 95% CI: 9.80 to 28.04; p < 0.001), with personal exposure demonstrating a stronger relationship. Our findings highlighted the critical role of Tsa and body shape in exacerbating personal exposure, as they could modify the bedding microenvironment around children's breathing zone during sleep. We assessed the effect of air filtration interventions on mitigating personal PM2.5 exposure and modulating OSA severity in children. Higher air filter efficiencies such as MERV14 or above can modulate severe OSA for more than 80% of the year. However, during wildfire episodes, because air filtration interventions alone may be insufficient, comprehensive strategies, including the potential use of air cleaners and personal protective equipment (PPE), are necessary to ensure children's health. Our research demonstrated that quantifying personal exposure is a more informative predictor than solely relying on ambient or indoor measures for estimating OSA in children.

Environmental pollutants can adversely impact various physiological processes, affecting systems such as the respiratory and immune systems. Immune responses are influenced by various factors including age, hormonal status, genetic background, and notably, sex, with effects extending to both innate and adaptive immunity. External factors, like environmental pollutants, can also disrupt innate and/or adaptive immunity and compromise pathogen recognition and memory against future infections. Furthermore, environmental pollutants can play a pivotal role in the development and exacerbation of many chronic respiratory diseases. It is becoming increasingly evident that environmental pollutants elicit sex-specific effects across different species. This review highlights recent findings on the intricate interplay between sex differences and immune-related effects induced by environmental pollutants, with a particular focus on the dysregulation of pulmonary immune responses.

Dietary polysaccharides, recognised as significant natural bioactive compounds, have demonstrated promising potential for the prevention and treatment of cardiovascular disease (CVD). This review provides an overview of the biological properties and classification of polysaccharides, with particular emphasis on their extraction and purification methods. The paper then explores the diverse mechanisms by which polysaccharides exert their effects in CVD, including their antioxidant activity, protection against ischemia-reperfusion injury, anti-apoptotic properties, protection against diabetic cardiomyopathy, anticoagulant and antithrombotic effects, prevention of ventricular remodeling, and protection against vascular injury. Furthermore, this paper summarises the current status of clinical trials involving polysaccharides in CVD and analyzes the support and challenges posed by these studies for the practical application of polysaccharides. Finally, the major challenges facing the therapeutic use of polysaccharides in CVD are discussed, particularly the issues of low bioavailability and lack of standardized quality control. Through this review, we aimed to provide a reference and guidance for further research on and application of dietary polysaccharides in CVD.

Cardiovascular diseases (CVD) are the main cause of death globally, especially in low- and middle-income countries (LMICs), where the largest number of inhabitants on the planet are concentrated. Air pollution inside and outside the home by microparticles 2 5 (PM2·5) has become an important risk factor for the presence of CVD and other chronic non-communicable diseases, particularly in LMICs. The use of solid fuels as an energy source for cooking food and heating inside the home has negative effects not only on human health but also on the health of the planet, as it contributes to deforestation and the consequent effect on climate change. In this narrative review we update how air pollution inside the home from cooking food with firewood and charcoal impacts the risk of CVD, the factors that determine the use of these polluting fuels, and the actions necessary for the massive transition toward the use of non-polluting energy, highlighting the development of university research to offer a stove that uses green hydrogen as a non-polluting energy source.

During the last decades, there has been a great interest on the link between macroeconomic conditions and health. More precisely, many studies had studied as health outcome cardiovascular disease mortality, focusing in different countries, determinants, and using numerous econometric techniques. Due to its importance, in this paper, we analyse cardiovascular disease mortality across the 17 Spanish regions over the period 2002-2019.

In doing so, we estimated several panel data models considering differences by sub-periods of time while also considering gender differences. That is, we transmit a difference on previous evidence by considering a longer period of time and different explanatory factors, so we provide new highlights for Spain.

Our empirical results show that: (i) both socioeconomic and environmental factors have a significant importance; (ii) political factors appear not to be significant; and (iii) there exists a Mediterranean (macro-region) cardiovascular disease mortality pattern.

These results may have usefulness for cardiovascular disease mortality prevention in Spain.

Fine particulate matter (PM2.5) is one of the major threats to human health, and may partly responsible for intentional self-harm deaths, while the limited results seemed contradictory. Further analysis on PM2.5 constituents may provide more reliable evidence. Heavy metals are crucial toxic components of PM2.5 that may induce suicide behavior. What role do PM2.5-bound heavy metals play in a threat to intentional self-harm death is still unclear. Two-year data of daily PM2.5-bound heavy metals (including metalloids) and daily intentional self-harm deaths were collected in Guangzhou. Bayesian kernel machine regression, weighted quantile sum, and quantile-based g-computation models were employed to depict the relationships between heavy metals and intentional self-harm deaths. The number of intentional self-harm deaths was 217 and 283 for 2015 and 2016, respectively. A positive correlation was found between the combined effect of the 13 heavy metals and intentional self-harm deaths. Nickel, cadmium, and iron were the primary contributors to this positive correlation. Heavy metal components play significant roles in PM2.5-related intentional self-harm deaths, and targeted source control measures are warranted to protect residents from suicide.

PAHs pollutants, as the key toxic components in PM2.5, have been proved to be closely related to the morbidity and mortality of people with cardiovascular diseases, however, their effects on organs and tissues other than cardiovascular/lung systems have not been deeply discussed. Here we collected PM2.5 samples from 2017 to 2020 in Xi'an, the city with one of the highest PM2.5 level in China, investigated the effects of PM2.5-bound PAHs on lung, spleen, liver and kidney by using the ApoE-/- mice model with high-fat diet. Firstly, six key toxic components in PAHs were screened to determine their relative importance in pollutants. The results showed that PAHs had the most significant toxicity in lung, followed by liver, kidney and spleen. In addition, PAHs activated systemic inflammation by enhancing the production of IL-6, particularly through strong protein interactions, mainly via van der Waals forces. This process exacerbated cardiovascular damage and led to elevated levels of pro-inflammatory cytokines circulating in the bloodstream, thereby increasing multi-organ toxicity. The results of this study deepened the understanding of comprehensive impacts of PAHs on cardiovascular patients, and suggest more strict emission source-control strategies on PAHs prevention especially for the susceptible population with cardiovascular diseases.

Gasoline exhaust particles (GEP) are risk factors for cardiovascular disease. Activating transcription factor 3 (ATF3) is a transcription factor known to form a heterodimer with AP-1 transcription factors for its target gene expression. However, the involvement of ATF3 in GEP-induced gene expression in human umbilical vein endothelial cells (HUVECs) has not been investigated. In this study, we found that GEP, at IC50 value of 59 μg/ml, induced the expression of ATF3, which led to the expression of matrix metalloproteinase 1 (MMP1) in HUVECs. GEP induce an interaction between c-Jun and ATF3, and c-Jun depletion attenuates GEP-induced MMP1 expression. Depletion of NADPH oxidase 4 (Nox4) suppressed GEP-induced reactive oxygen species (ROS) generation and the subsequent upregulation of ATF3 and MMP1, suggesting that Nox4-derived ROS play a role as upstream regulators of GEP-induced ATF3 expression and MMP1 upregulation. Furthermore, Nox4 depletion attenuated the interaction between ATF3 and c-Jun and their binding to the AP-1 binding site of the MMP1 promoter. Taken together, these findings demonstrate that GEP induce the expression of MMP1 by generating Nox4-dependent ROS, which subsequently increase ATF3 expression and its interaction with c-Jun. This leads to their binding to the promoter region of MMP1 and its transcription. These findings suggest that Nox4-derived ROS and ATF3 are critical for GEP-induced MMP1 expression.

Although climate change is increasing wildfire and smoke events globally, public health messaging and individual access to resources for protection are limited. Individual interventions can be highly effective at reducing wildfire smoke exposure. However, studies related to individual responses to wildfire smoke are limited and demonstrate mixed protective behaviors and risk perception. Our research helps fill this gap by assessing the self-reported behavior of 20 participants during wildfire season in Western Montana from 28 June through 1 November, 2022. We also measured continuous outdoor and indoor fine particulate matter (PM2.5) concentrations at participant residencies during this time period using PurpleAir sensors (PAII-SD, PurpleAir, Inc, USA) while participants took up to 16 self-reported online weekly activity surveys. Mixed-effect Poisson regression models were used to assess associations between exposure variables and participant reported behaviors. These results were compared with end-of-study interview findings. Wildfire smoke impacted days and increased concentrations of PM2.5 were associated with decreased outdoor exercise and opening of windows for ventilation. Interview themes were congruent with the regression analysis, with the additional finding of high portable air cleaner (PAC) use among participants. Additionally, these interviews gave context to both the tradeoffs participants face when making protective decisions and the importance of personal air quality data in increasing awareness about wildfire smoke risks. Future wildfire smoke studies can build off this research by providing personally relevant air quality data and PACs to participants and by improving public health messaging to address the compounding risks of wildfire smoke exposure and heat.

PM2.5 is an important environmental risk factor for cardiovascular disease (CVD) and poses a threat to global health. This study combines bibliometric analysis, Mendelian randomization (MR), and Global Burden of Disease (GBD) data to comprehensively explore the relationship between PM2.5 exposure and CVD. MR analyses provided strong evidence for causality, reinforcing findings from traditional observational studies. The estimated global burden of PM2.5-related CVD indicated, that there exist significant impacts on the elderly, men, and populations in low and medium socio-demographic index (SDI) areas. This study further found that population growth and aging are the main drivers of this burden with large inequities, although medical advances have mitigated some of the effects. Overall, the opportunity to reduce the burden of CVD remains significant, particularly in medium SDI countries. Projections to 2045 suggested that the absolute burden will increase, while age-standardized rates will decline due to improvements in air quality and health care. These findings emphasized the urgent need for targeted interventions to mitigate the deleterious effects of PM2.5 on global cardiovascular health and to address health inequalities between regions.

Evidence from megacity registry data regarding the independent association between ambient temperature and cardiovascular disease (CVD) mortality, after accounting for Particulate Matter 2.5 (PM2.5), remains scarce. In this study, we collected 308,116 CVD mortality cases in Shanghai from 2015 to 2020. The distributed lag non-linear model (DLNM) was utilized. The daily PM2.5 concentration was transformed using a natural spline (ns) function and integrated into the model for adjustment. The DLNM analysis revealed that the exposure-response curve between daily temperature and CVD mortality approximated an inverted "J" shape, consistent for both women and men. The minimum mortality temperature (MMT) for total CVD mortality was 25 °C, with an MMT of 26 °C for females and 24 °C for males. The highest relative risk (RR) of CVD mortality was 2.424 [95% confidence interval (95% CI): 2.035, 2.887] at the lowest temperature of -6.1 °C, with 2.244 (95% CI: 1.787, 2.818) for female and 2.642 (95% CI: 2.100, 3.326) for male. High temperatures exert acute and short-term effects, with the peak risk occurring on the day of exposure. In contrast, the risk from low temperature peaks on day 3 of the lag time and subsequently declines until days 16-21. This study offers evidence-based support for the prevention of temperature-induced CVD mortality.

Previous studies have typically explored daily lagged relationships between hemorrhagic fever with renal syndrome (HFRS) and meteorology, with a limited seasonal exploration of monthly lagged relationships, interactions, and the role of pollutants in multiple predictions of hemorrhagic fever.

Our researchers collected data on HFRS cases from 2005 to 2018 and meteorological and contaminative factors from 2015 to 2018 for the northeastern region. First, we applied the moving epidemic method (MEM) to estimate the epidemic threshold and intensity level. Then, we used a distributed lag non-linear model (DLNM) and a generalized additive model (GAM) with a maximum lag of 6 months to evaluate the lagged and interaction effects of meteorological and pollution factors on the HFRS cases. Multiple machine learning models were then applied after Spearman's rank correlation coefficient analysis was performed to screen for environmental factors in the Northeastern region.

There was a yearly downward trend in the incidence of HFRS in the northeastern region. High prevalence threshold years occurred from 2005 to 2007 and from 2012 to 2014, and the epidemic months were mainly concentrated in November. During the low prevalence threshold period, the main lag factor was low wind direction. In addition, the meteorological lag effect was pronounced during the high prevalence threshold period, where the main lag factors were cold air and hot dew point. Low levels of the AQI and PM10 and high levels of PM2.5 showed a dangerous lag effect on the onset of HFRS, while extremely high levels of PM2.5 appeared to have a protective effect. High levels of the AQI and PM10, as well as low levels of PM2.5, showed a protective lag effect. The model of PM2.5 and the AQI interaction pollution is better. The support vector machine (SVM)-radial algorithm outperformed other algorithms when pollutants are used as predictor variables.

This is the first mathematically based study of the seasonal threshold of HFRS in northeastern China, allowing for accurate estimation of the epidemic level. Our findings suggest that long-term exposure to air pollution is a risk factor for HFRS. Therefore, we should focus on monitoring pollutants in cold conditions and developing HFRS prediction models.

Zangsiwei(ZSW) is a traditional Tibetan medicine from China consisting of extracts of Rhododendron anthopogonoides Maxim, Gentiana Tourn, Corydalis hendersonii Hemsl and Berberis kansuensis C.K.Schneid. Traditionally, ZSW has been used by Tibetan physicians to treat chronic respiratory diseases. The role of ZSW in particulate matter-induced lung inflammation and fibrosis remains unclear.

Combining non-targeted metabolomics, network pharmacology, and molecular docking to explore the mechanism of ZSW in the treatment of particulate matter-induced lung inflammation and fibrosis, and validated by in vivo and in vitro experiments.

The serum metabolite profile post-ZSW administration was first identified utilizing non-targeted metabolomics. Network pharmacology and molecular docking were employed to predict potential bioactive components and their corresponding targets. The in silico predictions were subsequently validated through in vivo studies in mice exposed to PM2.5 and silica dust, as well as in vitro studies utilizing human lung epithelial cells (A549) and lung fibroblasts (MRC5).

Metabolomic analysis identified specific serum metabolites that were associated with ZSW treatment. Network pharmacology and molecular docking identified key targets involved in the Transforming growth factor-β (TGF-β)/SMAD pathway, which were subsequently validated through in vivo experiments demonstrating a reduction in lung inflammation and fibrosis in ZSW-treated mice. In vitro studies demonstrated that ZSW exerts protective effects against PM2.5-induced cytotoxicity and modulates fibrotic markers in a dose-dependent manner. This is consistent with the inhibition of the TGF-β/SMAD pathway.

Our integrated approach, which combines non-targeted metabolomics, network pharmacology, and molecular docking, followed by rigorous in vivo and in vitro validation, establishes ZSW as a potential therapeutic agent for particulate matter-induced lung inflammation and fibrosis.

Malnutrition and PM2.5 pollution remain a pressing global public health concern, especially to vulnerable populations like children under five years old. This study aimed to investigate the correlation between undernutrition in children under five years old and air pollution (exposure to PM2.5) on a global scale. This ecological study evaluated the correlation between undernutrition (wasting and stunting) and air pollution in 123 countries. A multiple linear regression analysis was used to identify the factors significantly related to the wasting and stunting. The scatter plots were utilized to depict the prevalence of wasting and stunting in children under five years old across studied countries concerning air pollution, Human Development Index (HDI), and Socio-Demographic Index (SDI). The prevalence of wasting was higher in countries with higher exposure to PM2.5 (R2 = 0.13, p < 0.001), less HDI (R2 = 0.20, p < 0.001), and less SDI (R2 = 0.16, p = 0.005). Also, the prevalence of stunting was higher in countries with higher exposure to PM2.5 (R2 = 0.07, p = 0.003), less HDI (R2 = 0.54, p < 0.003), and less SDI (R2 = 0.52, p = 0.005). The results of multivariable linear regression indicated a direct and positive correlation between the prevalence of wasting in children under five years old and exposure to PM2.5 (β = 0.06, p = 0.003) and an indirect and negative correlation with HDI (β =-10.3, p < 0.001). Also, there was a significant association between the prevalence of stunting and HDI (β =-44, p < 0.003). There was a significant relationship between the prevalence of wasting in children under five years old and exposure to PM2.5 and HDI. Further research is required to confirm this association.

Previous studies have suggested that neighborhoods characterized by higher walkability are related to a reduced risk of ischemic heart disease (IHD), whereas exposure to PM2.5 is positively associated with risk of IHD. Nevertheless, their joint impact on IHD warrants further investigation.

This prospective cohort study was performed in Yinzhou, Ningbo, China, comprising 47,516 participants. Individual-level walkability and PM2.5 were evaluated using a commercial walkability database and a land use regression (LUR) model, respectively. Hazard ratios (HRs) and 95 % confidence intervals (95 % CIs) were calculated using two Cox proportional hazards models: one based on two-year average PM2.5 levels prior to baseline, and the other incorporating time-varying PM2.5 assessed on a monthly scale. Dose-response relationships were explored using restricted cubic spline (RCS) functions. Interactions on both additive and multiplicative scales were assessed via relative excess risk due to interaction (RERI) and likelihood-ratio tests. Joint effects were explored and visualized using a 3D wireframe plot.

Over a median follow-up of 5.14 years, 1735 incident cases of IHD were identified. Adjusted HRs (95 % CIs) were 1.56 (1.34-1.81) per 10 μg/m3 increase in PM2.5 and 0.96 (0.94-0.98) per 10-unit increase in walkability, with both exposures exhibiting non-linear dose-response relationships. Walkability and PM2.5 were positively correlated (rs = 0.12, P < 0.001), and a multiplicative interaction was detected (Pinteraction = 0.019).

Walkability was inversely associated with risk of IHD, whereas exposure to PM2.5 was positively associated with IHD. Notably, the pernicious effects of PM2.5 could be attenuated in areas with higher levels of walkability. Our findings underscore the significance of walkable urban design, air quality improvement, as preventive strategies for IHD.

Facing Mount Tai in the south and the Yellow River in the north, Zibo District is an important petrochemical base in China. The effect of air pollution on cardiovascular diseases (CVDs) in Zibo was unclear.

Daily outpatient visits of common CVDs including coronary heart disease (CHD), stroke, and arrhythmia were obtained from 2019 to 2022 in Zibo. Air pollutants contained fine particulate matter (PM2.5), inhalable particulate matter (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and carbon monoxide (CO). Distributed lag non-linear models (DLNM) including single-pollutant model in single-day (lag0-lag7) and cumulative-days (lag01-lag07), concentration-response curve, subgroup analysis, and double-pollutant model were utilized to examine the relationships of daily air pollutants on CHD, stroke, and arrhythmia. Meteorological factors were incorporated to control confounding.

In single-pollutant model, NO2 was positively associated with CHD, stroke and arrhythmia, with the strongest excess risks (ERs) of 4.97% (lag07), 4.71% (lag07) and 2.16% (lag02), respectively. The highest ERs of PM2.5 on CHD, stroke and arrhythmia were 0.85% (lag01), 0.59% (lag0) and 0.84% (lag01), and for PM10, the ERs were 0.37% (lag01), 0.35% (lag0) and 0.39% (lag01). SO2 on CHD was 0.92% (lag6), O3 on stroke was 0.16% (lag6), and CO on CHD, stroke, and arrhythmia were 8.77% (lag07), 5.38% (lag01), 4.30% (lag0). No threshold was found between air pollutants and CVDs. The effects of ambient pollutants on CVDs (NO2&CVDs, PM2.5&stroke, PM10&stroke, CO&stroke, CO&arrhythmia) were greater in cold season than warm season. In double-pollutant model, NO2 was positively associated with CHD and stroke, and CO was also positively related with CHD.

Ambient pollutants, especially NO2 and CO were associated with CVDs in Zibo, China. And there were strong relationships between NO2, PM2.5, PM10, CO and CVDs in cold season.

Evidence from extensive cohort studies about the individual and combined associations of air pollution and air temperature with cardiovascular disease (CVD) morbidity is limited. This study aimed to examine the long-term effects of PM2.5 exposure and air temperature on CVD based on a cohort study of middle-aged and older populations in China.

A total of 9,316 non-CVD adults (≥40 years old) who joined the China Health and Retirement Longitudinal Study between 2011 and 2018 were included in our analysis. The two-year average PM2.5 concentration and air temperature of the city where participants lived were calculated. The Cox proportional hazards model was conducted to analyze the associations of PM2.5 exposure and air temperature with CVD morbidity.

In the multivariable-adjusted model, each 10 μg/m3 rise in 2-y PM2.5 concentration was associated with an increased risk of developing CVD (hazard ratio [HR]: 1.30; 95% confidence interval [CI]: 1.27-1.32). Compared with individuals in the bearable temperature group, those with low temperatures had a higher risk of CVD (HR: 1.77; 95% CI: 1.53-2.04). Stratified analyses found that cardiovascular metabolic risk factors could not change these associations. Compared with individuals in the low-level PM2.5 exposure and bearable temperature group, those in the high-level PM2.5 exposure and low-temperature group had a 7.08 times higher risk of CVD (95% CI: 5.55-9.03).

Long-term PM2.5 exposure and low air temperature are associated with a higher risk of CVD. Consequently, efforts to reduce air pollution and enhance protection against cold temperatures are vital for mitigating CVD risk.

The adverse effects of fine particulate matter (PM2.5), including cardiovascular outcomes, are well established. This review and meta-analysis investigates the association between long-term exposure to low concentration PM2.5 (<12 µg/m3) and CVD mortality in U.S. and Canadian populations.

We conducted a literature search and completed random effect meta-analyses.

Twenty-four studies were reviewed, with 12 from each of the U.S. and Canada. Fifteen of eighteen studies that reported hazard ratios (HRs) for total CVD mortality reported statistically significant positive associations with low concentration PM2.5. For cause-specific CVD mortality, more consistent results were shown for ischemic heart disease (IHD) mortality, with all eleven studies reporting statistically significant associations (HR = 1.09 to 2.48). Only three of 12 studies evaluating cerebrovascular mortality reported statistically significant associations (HR = 1.10 to 1.27). Studies that restricted analyses to participants with mean exposures <12 µg/m3 found statistically significant associations between PM2.5 and at least some of the CVD mortality outcomes of interest. However, the shape of the concentration-response functions varied widely. Only six studies controlled for at least one additional air pollutant, and multi-pollutant models generally showed an attenuated impact of PM2.5. Despite existing gaps in understanding the association between low concentrations of PM2.5 and cardiovascular mortality, this review highlights the critical importance of ongoing efforts to improve air quality for public health benefits.

Continued focus on understanding the shape of the concentration-response function for PM2.5, the impact of co-pollutants on observed effects, and how particle composition may impact effect estimates, is recommended.

Depression is a leading mental health disorder worldwide, contributing substantially to the global disease burden. While emerging evidence suggests links between specific air pollutants and depression, the potential interactions among multiple pollutants remain underexplored. Here we show the influence of six common air pollutants on depressive symptoms among middle-aged and older Chinese adults. In single-pollutant models, a 10 μg m-3 increase in SO2, CO, PM10, and PM2.5 is associated with increased risks of depressive symptoms, with odds ratios (95% confidence intervals) of 1.276 (1.238-1.315), 1.007 (1.006-1.008), 1.066 (1.055-1.078), and 1.130 (1.108-1.153), respectively. In two-pollutant models, SO2 remains significantly associated with depressive symptoms after adjusting for other pollutants. Multi-pollutant models uncover synergistic effects, with SO2, CO, NO2, PM10, and PM2.5 exhibiting significant interactions, identifying SO2 as the primary driver of these associations. Mediation analyses further indicate that cognitive and physical impairments partially mediate the relationship between air pollution and depressive symptoms. These findings underscore the critical mental health impacts of air pollution and highlight the need for integrated air quality management strategies. Targeted mitigation of specific pollutants, particularly SO2, is expected to significantly enhance public mental health outcomes.

The recently introduced concept of 'exposome' emphasizes the impact of non-traditional threats onto cardiovascular health. Among these, air pollutants - particularly fine particulate matter < 2.5 μm (PM2.5) - have emerged as significant environmental risk factors for cardiovascular disease and mortality. PM2.5 exposure has been shown to induce endothelial dysfunction, chronic low-grade inflammation, and cardiometabolic impairment, contributing to the development and destabilization of atherosclerotic plaques. Both short- and long-term exposure to air pollution considerably increase the incidence of ischemic heart disease (IHD)-related events, with clinical evidence linking pollution to higher mortality and adverse prognosis, especially in vulnerable populations. In this review, we explore the mechanistic pathways through which air pollutants exacerbate atherosclerotic cardiovascular disease (ASCVD) and discuss their clinical impact.Furthermore, special attention will be directed to the outcomes and prognosis of patients with pollution-aggravated coronary atherosclerosis, as well as the potential role of targeted public health interventions.

Due to the adverse health effects of PM2.5 (particles with a diameter less than 2.5 μm), the national ambient air quality standards (NAAQS) for PM2.5 have been established in many countries. Ambient PM2.5 concentrations are monitored to determine compliance with the NAAQS, where beta attenuation monitors (BAMs) are widely used as a reference method. However, the high costs of installation and maintenance of BAMs result in difficulties in enhancing the spatial resolution of PM2.5 monitoring. In this context, low-cost PM2.5 sensors (LCSs) have been widely deployed for PM2.5 measurements. Despite their low cost and ease of installation, concerns regarding the data reliability of LCSs remain unresolved, necessitating further field research under various environmental conditions. In this study, we conducted a data comparability assessment between 125 LCSs and two BAMs over 12 months. Daily average PM2.5 concentrations measured by LCSs generally agreed with those from BAMs. However, when comparing hourly PM2.5 data, we found that the data comparability of LCSs against BAMs was lower than that of the daily average data, primarily influenced by ambient PM2.5 levels. Additionally, we found statistical differences in PM2.5 concentrations among six regions within the study area. This indicates that ambient PM2.5 levels can vary within a small area, supporting the necessity of monitoring PM2.5 on a small scale. Overall, the results of this study suggest that the sensors demonstrate both potential and limitations in PM2.5 monitoring. Therefore, to use LCSs for PM2.5 monitoring, it is necessary to appropriately select the averaging time and PM2.5 concentration ranges, considering local environmental conditions and the inherent characteristics of LCSs.

Air pollution is a major risk factor for cardiovascular diseases and contributes to health disparities, particularly among minority ethnic groups, who often face higher exposure levels. Knowledge on whether the effect of air pollution on cardiovascular diseases differs between ethnic groups is crucial for identifying mechanisms underlying health disparities, ultimately informing targeted public health strategies and interventions. We explored differences in associations between air pollution and ischemic stroke and ischemic heart disease (IHD) for the six largest ethnic groups in the Netherlands.

This nationwide analysis (2014-2019), linked residential-address concentrations of NO2 and PM2.5 to individual-level hospital and mortality data. To evaluate incident ischemic stroke, we created a cohort of residents ≥30 years and free of ischemic stroke at baseline and for incident IHD we created a cohort free of IHD. We performed Cox proportional hazard survival analyses in each cohort with 2014 average concentrations of PM2.5 or NO2 as determinants, stratified by ethnicity (Dutch, German, Indonesian, Surinamese, Moroccan, Turkish) and adjusted for age, sex, socioeconomic indicators and region.

Both cohorts included > 9.5 million people. During follow-up, 127,673 (1.3%) developed ischemic stroke and 156,517 (1.6%) developed IHD. For ischemic stroke, the p-values for the interaction between air pollution and ethnicity were 0.057 for NO2 and 0.055 for PM2.5. The HR of 1 IQR increase (6.42 µg/m3) of NO2 for ischemic stroke was lowest for Moroccans (0.92 [0.84-1.02], p-value = 0.032 difference with Dutch) and highest for Turks (1.09 [1.00-1.18], p-value = 0.157 difference with Dutch). PM2.5 results were similar. For IHD, higher exposure was unexpectedly associated with lower incidence. The p-values for the interaction with ethnicity were 1.75*10- 5 for NO2 and 1.06*10- 3 for PM2.5. The HRs for IHD were lowest for Turks (NO2: 0.88 [0.83-0.92], p-value = 2.0*10- 4 difference with Dutch, PM2.5: 0.86 [0.82-0.91], p-value = 1.3*10- 4 difference with Dutch) and highest for Surinamese (NO2: 1.02 [0.97-1.07], p-value = 0.014 difference with Dutch) and Dutch (PM2.5: 0.96 [0.94-0.98]).

Associations between air pollutants and ischemic stroke or IHD differ notably between ethnic groups in the Netherlands. Policies to reduce air pollution and prevent ischemic stroke should target populations vulnerable to air pollution with a high cardiovascular disease risk.

Urban air quality stands as a pressing concern in cities globally, with airborne particulate matter (PM) emerging as a significant threat to human health. An investigation was carried out to examine the potential of four prevalent evergreen roadside tree species grown at different locations in Dhaka to capture PM using their leaves. The distribution of PM by mass and quantity in Dhaka are presented for the first time for Bangladesh and these results will also be applicable to countries with similar climates and tree species. Separate gravimetric analyses were carried out to quantify PM in three different size ranges (0.2-2.5 μm, 2.5-10 μm, and 10-100 μm) accumulated on surfaces and trapped within waxes by using the rinse and weigh method. The method is validated for the first time through SEM-EDX analysis, which confirmed that the increase in weight from chloroform-rinsed leaves was exclusively attributable to particle deposition on the filter. The chemical composition of the deposited PM2.5 was analyzed quantitatively by determining the concentration of twenty-five trace elements employing ICP-MS. SEM-EDX analysis revealed the significance of leaf microstructural traits in effectively capturing PM. Significant variations in the deposition of PM were found among different species for two PM categories (surface PM and wax-embedded PM) and three size fractions (large, coarse, and fine) (one-way ANOVA; p < 0.05). The quantity of wax retained on the foliage of trees documented in these locations also varied (p < 0.05). Among the species studied, Ficus benghalensis demonstrated a greater ability to retain PM. Mangifera indica was identified to be the most efficient collector of wax-related PM and appears to be the ideal species for traffic-heavy areas distinguished by high concentrations of organic compounds from vehicle emissions.

Considerable evidence has been accumulated on serious acute health outcomes associated with short-term exposure to ambient fine particulate matter (PM2.5). Modifying factors of those associations, however, have been less explored and need further analyses. In this national study, we investigated whether short-term effects of PM2.5 are modified according to region, cause of mortality/hospitalization, season, age, and sex. PM2.5-related adverse health effects were estimated by an ecological time-series study, covering about 80 % of the Canadian population for 18 years (2001-2018). We estimated city-specific associations using daily averages of PM2.5 and temperature, and daily counts of hospitalizations and mortality (non-accidental all-cause, circulatory, and respiratory). National and regional associations were then estimated with a 2-stage model. We considered potential modifying factors of PM2.5-related adverse health effects, and examined linear trends in the annual associations. Nationally, PM2.5 exposure was associated with both hospitalizations and mortality, and there was evidence of differences by the modifying factors. Of the various causes, circulatory mortality and respiratory hospitalization were more attributable to PM2.5 exposure. We found regional differences for both all-cause hospitalization and all-cause mortality, and seasonal differences for respiratory hospitalization (warm season) and circulatory hospitalization (cold season). Circulatory mortality risk was significant for seniors and females. All-cause hospitalizations appeared to gradually decrease over time, but annual all-cause mortality remained constant at 0.6 % of the population. Adverse health effects of PM2.5 exposures may depend on not only PM2.5 concentration, but also other factors (region, cause, season, age, sex). National estimates for the baseline (age ≥ 1 year, both sexes) risk cannot be interpreted without consideration of the differences by modifying factors. Study findings can be used by seniors, women, and those who have pre-existing health conditions to make informed decisions regarding their health risks from daily exposure to ambient PM2.5.

The effects of ultrafine particle (UFP) inhalation on neurodevelopment, especially during critical windows of early life, remain largely unexplored. The specific time windows during which exposure to UFP might be the most detrimental remain poorly understood. Here, we studied early-life exposure to clean ultrafine carbonaceous particles (UFPC) and neurodevelopment and central nervous system function in offspring.Pregnant wild-type C57BL/6J mice were either sham-exposed (HEPA-filtered air) or exposed to clean ultrafine carbonaceous particles at a concentration of 438 ± 72 μg/m³ (mean ± SD) and a count median diameter of 49 ± 2 nm (CMD ± GSD) via whole-body exposure for four hours per day. For prenatal exposure, mice were exposed for two consecutive days in two exposure periods, while the postnatal exposure was conducted for four consecutive days in two exposure periods. The mice were divided into four groups: (i) sham, (ii) only prenatal exposure, (iii) only postnatal exposure, and (iv) both prenatal and postnatal exposure. Neurodevelopmental behaviour was assessed throughout the life of the offspring using a functional observation battery.Early-life UFPC-exposed offspring exhibited altered anxiety-related behaviour in the open field test, with exclusively postnatally exposed offspring (567 ± 120 s) spending significantly more time within the border zone of the arena compared to the sham group (402 ± 73 s), corresponding to an increase of approximately 41% (p < 0.05). The behavioural alterations remained unaffected by olfactory function or maternal behaviour. Mice with both prenatal and postnatal exposure did not show this effect. No discernible impact on developmental behavioural reflexes was evident.Early life exposure to UFPC, particularly during the early postnatal period, may lead to developmental neurotoxicity, potentially resulting in complications for the central nervous system later in life. The current data will support future studies investigating the possible effects and characteristics of nanoparticle-based toxicity.

Exposure to airborne fine particulate matter (PM2.5) is strongly associated with poor fertility and ovarian damage. However, the mechanism underlying this remains largely unclear. Here, we found that PM2.5 markedly impaired murine ovarian reserve, decreased hormone levels, and aggravated ovarian inflammation. Circulating interleukin-6 (IL-6) was elevated in PM2.5-exposed mice and was further confirmed to mediate this damage by IL-6 recombinant protein intervention. PM2.5 exposure led to increased alveolar macrophage infiltration in the lungs. However, alveolar macrophage clearance with clodronate liposomes could not fully reverse the elevated IL-6 levels and ovarian injury, suggesting that alveolar macrophages were probably not the only source of circulating IL-6. Further experiments indicated that IL-6 mainly targeted ovarian theca-interstitial cells and impaired testosterone synthesis via suppressing the peroxisome proliferator-activated receptor γ (PPARγ) pathway. In addition, apoptosis of granulosa cells and restriction of follicular growth were observed in co-cultures with IL-6-treated theca-interstitial cells, which could be further reversed by the PPARγ agonist. Moreover, IL-6-neutralizing antibodies ameliorated PM2.5-induced ovarian damage. Notably, increased levels of circulating IL-6 were observed in premature ovarian aging patients and were inversely associated with their ovarian function. In summary, our findings offer a mechanistic explanation for PM2.5-induced ovarian dysfunction and verify IL-6 as a biomarker and potential therapeutic target.