Accumulating animal studies have demonstrated associations between ambient air pollution (AP) and metabolic dysfunction-associated fatty liver disease (MAFLD), but relevant epidemiological evidence is limited. We evaluated the association of long-term exposure to AP with the risk of incident MAFLD in Northwest China. The average AP concentration between baseline and follow-up was used to assess individual exposure levels. Cox proportional hazard models and restricted cubic spline functions (RCS) were used to estimate the association of PM2.5 and its constituents with the risk of MAFLD and the dose-response relationship. Quantile g-computation was used to assess the joint effects of mixed exposure to air pollutants on MAFLD and the weights of the various pollutants. We observed 1516 cases of new-onset MAFLD, with an incidence of 10.89%. Increased exposure to pollutants was significantly associated with increased odds of MAFLD, with hazard ratios (HRs) of 2.93 (95% CI: 1.22, 7.00), 2.86 (1.44, 5.66), 7.55 (3.39, 16.84), 4.83 (1.89, 12.38), 3.35 (1.35, 8.34), 1.89 (1.02, 1.62) for each interquartile range increase in PM2.5, SO42-, NO3-, NH4+, OM, and BC, respectively. Stratified analyses suggested that females, frequent exercisers and never-drinkers were more susceptible to MAFLD associated with ambient PM2.5 and its constituents. Mixed exposure to SO42-, NO3-, NH4+, OM and BC was associated with an increased risk of MAFLD, and the weight of BC had the strongest effect on MAFLD. Exposure to ambient PM2.5 and its constituents increased the risk of MAFLD.

Addressing environmental factors has recently been recommended to curb the growing trend of anemia in low- and middle-income countries (LMICs). Fine particulate matter (PM2.5) generated by dust storms were concentrated in place with a high prevalence of anemia. In a multicounty, multicenter study, we analyzed the association between anemia and life-course averaged exposure to dust PM2.5 among children aged <5 years based on 0.65 million records from 47 LMICs. In the fully adjusted mixed effects model, each 10 μg/m3 increase in life-course averaged exposure to dust PM2.5 was associated with a 9.3% increase in the odds of anemia. The estimated exposure-response association was nonlinear, with a greater effect of dust PM2.5 exposure seen at low concentrations. Applying this association, we found that, in 2017, among all children aged <5 years in the 125 LMICs, dust PM2.5 contributed to 37.98 million cases of anemia. Results indicated that dust PM2.5 contributed a heavier burden than all of the well-identified risk factors did, except for iron deficiency. Our study revealed that long-term exposure to dust PM2.5 can be a novel risk factor, pronouncedly contributed to the burden of child anemia in LMICs, affected by land degradations or arid climate.

Short-term exposure to PM2.5 or O3 can increase mortality risk; however, limited studies have evaluated their interaction. A multicity time series study was conducted to investigate the synergistic effect of PM2.5 and O3 on mortality in China, using mortality data and high-resolution pollutant predictions from 272 cities in 2013-2015. Generalized additive models were applied to estimate associations of PM2.5 and O3 with mortality. Modification and interaction effects were explored by stratified analyses and synergistic indexes. Deaths attributable to PM2.5 and O3 were evaluated with or without modification of the other pollutant. The risk of total nonaccidental mortality increased by 0.70% for each 10 μg/m3 increase in PM2.5 when O3 levels were high, compared to 0.12% at low O3 levels. The effect of O3 on total nonaccidental mortality at high PM2.5 levels (1.26%) was also significantly higher than that at low PM2.5 levels (0.59%). Similar patterns were observed for cardiovascular or respiratory diseases. The relative excess risk of interaction and synergy index of PM2.5 and O3 on nonaccidental mortality were 0.69% and 1.31 with statistical significance, respectively. Nonaccidental deaths attributable to short-term exposure of PM2.5 or O3 when considering modification of the other pollutant were 28% and 31% higher than those without considering modification, respectively. Our results found synergistic effects of short-term coexposure to PM2.5 and O3 on mortality and suggested underestimations of attributable risks without considering their synergistic effects.

Air pollution induced by fine particulate matter with diameter ≤ 2.5 μm (PM2.5) poses a significant challenge for global air quality management. Understanding how factors such as climate change, land use and land cover change (LULCC), and changing emissions interact to impact PM2.5 remains limited. To address this gap, we employed the Community Earth System Model and examined both the individual and combined effects of these factors on global surface PM2.5 in 2010 and projected scenarios for 2050 under different Shared Socioeconomic Pathways (SSPs). Our results reveal biomass-burning and anthropogenic emissions as the primary drivers of surface PM2.5 across all SSPs. Less polluted regions like the US and Europe are expected to experience substantial PM2.5 reduction in all future scenarios, reaching up to ~5 μg m-3 (70 %) in SSP1. However, heavily polluted regions like India and China may experience varied outcomes, with a potential decrease in SSP1 and increase under SSP3. Eastern China witness ~20 % rise in PM2.5 under SSP3, while northern India may experience ~70 % increase under same scenario. Depending on the region, climate change alone is expected to change PM2.5 up to ±5 μg m-3, while the influence of LULCC appears even weaker. The modest changes in PM2.5 attributable to LULCC and climate change are associated with aerosol chemistry and meteorological effects, including biogenic volatile organic compound emissions, SO2 oxidation, and NH4NO3 formation. Despite their comparatively minor role, LULCC and climate change can still significantly shape future air quality in specific regions, potentially counteracting the benefits of emission control initiatives. This study underscores the pivotal role of changes in anthropogenic emissions in shaping future PM2.5 across all SSP scenarios. Thus, addressing all contributing factors, with a primary focus on reducing anthropogenic emissions, is crucial for achieving sustainable reduction in surface PM2.5 levels and meeting sustainable pollution mitigation goals.

Although industrial activities are significant contributors to atmospheric releases of particulate matter (PM) and associated toxic substances that lead to adverse human health effects, a knowledge gap exists concerning the human health risk resulting from such activities owing to lack of evaluation of industrial emissions. Here, we comprehensively characterized and quantified PM from 118 full-scale industrial plants. The dominant (97.9 %) PM showed diameters of <2.5 μm; 79.0 % had diameters below 1 μm. Annual atmospheric releases of Fe and heavy metals (As, Cd, Cr, Cu, Ni, Pb, Zn) contained in fine PM from these global industrial activities are estimated to be 51,161 t and 69,591 t, respectively. Emissions of heavy metals from these industries cause increased cancer risk, estimated to range from 1461 % to 50,752 %. Five crystalline compounds (ZnO, PbSO4, Mn3O4, Fe3O4, Fe2O3) that can indicate specific industrial sources are identified. Global annual emissions of these toxic compounds in fine PM from the industrial sources are estimated to be 78,635 t. The Global South displayed higher emissions than the Global North. These results are significant for recognizing regional health risks of industrial emissions.

China\'s swift socioeconomic development has led to extremely severe ambient PM2.5 levels, the associated negative health outcomes of which include premature death. However, a comprehensive explanation of the socioeconomic mechanism contributing to PM2.5-related premature deaths has not yet to be fully elucidated through long-term spatial panel data. Here, we employed a global exposure mortality model (GEMM) and the system generalized method of moments (Sys-GMM) to examine the primary determinants contributing to premature deaths in Chinese provinces from 2000 to 2021. We found that in the research period, premature deaths in China increased by 46 %, reaching 1.87 million, a figure that decreased somewhat after the COVID-19 outbreak. 62 thousand premature deaths were avoided in 2020 and 2021 compared to 2019, primarily due to the decline in PM2.5 concentrations. Premature deaths have increased across all provinces, particularly in North China, and a discernible spatial agglomeration effect was observed, highlighting effects on nearby provinces. The findings also underscored the significance of determinants such as urbanization, import and export trade, and energy consumption in exacerbating premature deaths, while energy intensity exerted a mitigating influence. Importantly, a U-shaped relationship between premature deaths and economic development was unveiled for the first time, implying the need for vigilance regarding potential health impact deterioration and the implementation of countermeasures as the per capita GDP increases in China. Our findings deserve attention from policymakers as they shed fresh insights into atmospheric control and Health China action.

Fine particulate matters-PM2.5 in the air can have considerable negative effects on human health and the environment. Various human cell-based studies examined the effect of PM2.5 on human health in different cities of the world using various chemical parameters. Unfortunately, limited information is available regarding the relationship between toxicity and chemical characteristics of PM2.5 collected in Istanbul, Türkiye, located in one of the most populated cities in the world. To investigate the chemical characteristics and cytotoxicity of PM2.5 in Istanbul, samples were collected for 12 months, then potentially toxic metals, oxidative potential, and particle indicators (e.g., functional groups and elements) were determined, and the cytotoxicity of PM2.5 on human A549 lung alveolar epithelial cells was examined. The mean PM2.5 mass concentration was 24.0 ± 17.4 µg m-3 and higher in cold months compared to other seasons. Moreover, the results of the metals, elemental, and functional groups indicated that seasonal and monthly characteristics were influenced by the regional anthropogenic sources and photochemistry input. The cytotoxicity results also showed that the viability of A549 cells was reduced with the exposure of PM2.5 (30-53%) and higher cytotoxicity was obtained in summer compared to the other seasons due to the impact of the metals, elements, and oxidative characteristics of PM2.5.

Airborne fine particulate matter (PM2.5) in air pollution has become a significant global public health concern related to allergic diseases. Previous research indicates that PM2.5 not only affects the respiratory system but may also induce systemic inflammation in various tissues. Moreover, its impact may vary among different populations, with potential consequences during pregnancy and in newborns. However, the precise mechanisms through which PM2.5 induces inflammatory reactions remain unclear. This study aims to explore potential pathways of inflammatory responses induced by PM2.5 through animal models and zebrafish embryo experiments. In this study, zebrafish embryo experiments were conducted to analyze the effects of PM2.5 on embryo development and survival, and mouse experimental models were employed to assess the impact of PM2.5 stimulation on various aspects of mice. Wild-type zebrafish embryos were exposed to a PM2.5 environment of 25-400 μg/mL starting at 6 h after fertilization (6 hpf). At 6 days post-fertilization, the survival rates of the 25, 50, 100, and 200 µg/mL groups were 100%, 80, 40%, and 40%, respectively. Zebrafish embryos stimulated with 25 μg/mL of PM2.5 still exhibited successful development and hatching. Additionally, zebrafish subjected to doses of 25-200 μg/mL displayed abnormalities such as spinal curvature and internal swelling after hatching, indicating a significant impact of PM2.5 stimulation on embryo development. In the mouse model, mice exposed to PM2.5 exhibited apparent respiratory overreaction, infiltration of inflammatory cells into the lungs, elevated levels of inflammatory response-related cytokines, and inflammation in various organs, including the liver, lungs, and uterus. Blood tests on experimental mice revealed increased expression of inflammatory and chemotactic cytokines, and GSEA indicated the induction of various inflammatory responses and an upregulation of the TNF-α/NFκB pathway by PM2.5. Our results provide insights into the harmful effects of PM2.5 on embryos and organs. The induced inflammatory responses by PM2.5 may be mediated through the TNF-α/NFκB pathway, leading to systemic organ inflammation. However, whether PM2.5-induced inflammatory responses in various organs and abnormal embryo development are generated through different pathways requires further study to comprehensively clarify and identify potential treatment and prevention methods.

Pyroptosis represents a type of cell death mechanism notable for its cell membrane disruption and the subsequent release of proinflammatory cytokines. The Nod-like receptor family pyrin domain containing inflammasome 3 (NLRP3) plays a critical role in the pyroptosis mechanism associated with various diseases resulting from particulate matter (PM) exposure. Tert-butylhydroquinone (tBHQ) is a synthetic antioxidant commonly used in a variety of foods and products. The aim of this study is to examine the potential of tBHQ as a therapeutic agent for managing sinonasal diseases induced by PM exposure. The occurrence of NLRP3 inflammasome-dependent pyroptosis in RPMI 2650 cells treated with PM < 4 µm in size was confirmed using Western blot analysis and enzyme-linked immunosorbent assay results for the pyroptosis metabolites IL-1β and IL-18. In addition, the inhibitory effect of tBHQ on PM-induced pyroptosis was confirmed using Western blot and immunofluorescence techniques. The inhibition of tBHQ-mediated pyroptosis was abolished upon nuclear factor erythroid 2-related factor 2 (Nrf2) knockdown, indicating its involvement in the antioxidant mechanism. tBHQ showed potential as a therapeutic agent for sinonasal diseases induced by PM because NLRP3 inflammasome activation was effectively suppressed via the Nrf2 pathway.

Air pollution is one of the major global public health challenges. Using annual fine particulate matter (PM2.5) concentration data from 2016 to 2021, along with the global exposure mortality model (GEMM), we estimated the multi-year PM2.5-pollution-related deaths divided by different age groups and diseases. Then, using the VSL (value of statistical life) method, we assessed corresponding economic losses and values. The number of deaths attributed to PM2.5 in Beijing in 2021 fell by 33.74 percent from 2016, while health economic losses would increase by USD 4.4 billion as per capita disposable income increases year by year. In 2021, the average annual concentration of PM2.5 in half of Beijing\'s municipal administrative districts is less than China\'s secondary ambient air quality standard (35 μg/m3), but it can still cause 48,969 deaths and corresponding health and economic losses of USD 16.31 billion, equivalent to 7.9 percent of Beijing\'s GDP. Therefore, it is suggested that more stringent local air quality standards should be designated to protect public health in Beijing.