Studies have found that ambient particulate matter (PM) affects fasting blood glucose. However, the results are not consistent. We conducted a systematic review and meta-analysis to determine the relationship between PM with an aerodynamic diameter of 10 μm or less (PM₁₀) and PM with an aerodynamic diameter of 2.5 μm or less (PM₂.₅) and fasting blood glucose. We searched PubMed, Web of Science, the Wanfang Database and the China National Knowledge Infrastructure up to April 1, 2019. A total of 24 papers were included in the review, and 17 studies with complete or convertible quantitative information were included in the meta-analysis. The studies were divided into groups by PM size fractions (PM₁₀ and PM₂.₅) and length of exposure. Long-term exposures were based on annual average concentrations, and short-term exposures were those lasting less than 28 days. In the long-term exposure group, fasting blood glucose increased 0.10 mmol/L (95% CI: 0.02, 0.17) per 10 μg/m³ of increased PM₁₀ and 0.23 mmol/L (95% CI: 0.01, 0.45) per 10 μg/m³ of increased PM₂.₅. In the short-term exposure group, fasting blood glucose increased 0.02 mmol/L (95% CI: −0.01, 0.04) per 10 μg/m³ of increased PM₁₀ and 0.08 mmol/L (95% CI: 0.04, 0.11) per 10 μg/m³ of increased PM₂.₅. Further prospective studies are needed to explore the relationship between ambient PM exposure and fasting blood glucose.

This study aims to examine the association between short-term exposures to PM₁, PM₂.₅ and PM₁₀ (particulate matter with aerodynamic diameters ≤1 μm, ≤2.5 μm and ≤10 μm, respectively) and hospital admission for ischemic stroke in China. Daily counts of hospital admission for ischemic stroke were collected in 5 hospitals in China during November 2013 to October 2015. Daily concentrations of PM₁, PM₂.₅ and PM₁₀ were collected in 5 cities where the hospitals were located. A time-stratified case-crossover design was used to examine the hospital-specific PM-ischemic stroke association after controlling for potential confounders. Then the effect estimates were pooled using a random-effect meta-analysis. A total of 68,122 hospital admissions for ischemic stroke were identified from 5 hospitals during the study period. The pooled results showed that exposures to PM₁, PM₂.₅ and PM₁₀ were significantly associated with increased hospital admission for ischemic stroke on the current day and previous 1 day. The RRs (relative risk associated with per 10 μg/m³ increase in each pollutant) and 95%CIs (confidence intervals) for the cumulative effects of PM₁, PM₂.₅ and PM₁₀ on ischemic stroke during lag 0–1 days were 1.014 (1.005, 1.0023), 1.007 (1.000, 1.014) and 1.005 (1.001, 1.009), respectively. In total, 3.5%, 3.6% and 4.1% of hospital admissions for ischemic stroke could be attributable to PM₁, PM₂.₅ and PM₁₀, respectively. Exposures to ambient PM₁, PM₂.₅ and PM₁₀ pollution showed acute adverse effects on hospital admission for ischemic stroke. The health effects of PM₁ should be considered by policy-makers.

This study examined the long-term trends in chemical components in PM₂.₅ (particulate matter with aerodynamic diameter ≤2.5 μm) samples collected at Lulin Atmospheric Background Station (LABS) located on the summit of Mt. Lulin (2862 m above mean sea level) in Taiwan in the western North Pacific during 2003–2018. High ambient concentrations of PM₂.₅ and its chemical components were observed during March and April every year. This enhancement was primarily associated with the long-range transport of biomass burning (BB) smoke emissions from Indochina, as revealed from cluster analysis of backward air mass trajectories. The decreasing trends in ambient concentrations of organic carbon (−0.67% yr⁻¹; p = 0.01), elemental carbon (−0.48% yr⁻¹; p = 0.18), and non–sea-salt (nss) K⁺ (−0.71% yr⁻¹; p = 0.04) during 2003–2018 indicated a declining effect of transported BB aerosol over the western North Pacific. These findings were supported by the decreasing trend in levoglucosan (−0.26% yr⁻¹; p = 0.20) during the period affected by the long-range transport of BB aerosol. However, NO₃⁻ displayed an increasing trend (0.71% yr⁻¹; p = 0.003) with considerable enhancement resulting from the air masses transported from the Asian continent. Given that the decreasing trends were for the majority of the chemical components, the columnar aerosol optical depth (AOD) also demonstrated a decreasing trend (−1.04% yr⁻¹; p = 0.0001) during 2006–2018. Overall decreasing trends in ambient (carbonaceous aerosol and nss-K⁺) as well as columnar (e.g., AOD) aerosol loadings at the LABS may influence the regional climate, which warrants further investigations. This study provides an improved understanding of the long-term trends in PM₂.₅ chemical components over the western North Pacific, and the results would be highly useful in model simulations for evaluating the effects of BB transport on an area.

Particulate matter (PM) is an air pollutant which poses a considerable risk to human health. The agricultural sector is responsible of the 15% of the total anthropogenic emissions of PM₁₀ (PM fraction with aerodynamic diameter below 10 μm) and soil preparation activities have been recognized as one of the main drivers of this contribution. The emission factors (EF) proposed by European environmental agency (EEA) for tilling operations are based on very few studies, none of which has been made in Italy. Moreover, few studies have considered the influence of operative parameters on PM₁₀ emissions during tilling. The aim of this work was to assess PM₁₀ emission and dispersion during rotary harrowing and to understand how operative parameters, such as forward speed and implement choice may affect PM release. A further objective was to assess the near field dispersion of PM₁₀ to address exposure risks. Emission factors (EFs) were determined during two different trials (T1 and T2). During T1, the effect of tractor speeds (0.6, 1.1 and 1.7 m s⁻¹) on PM₁₀ emissions was investigated, while in T2 a comparative essay was made to study the influence of levelling bar height on emissions. The average ground level downwind concentrations of PM₁₀ during harrowing operation was estimated through dispersion modelling. The observed PM₁₀ EFs for rotary harrowing were 8.9 ± 2.0 mg m⁻² and 9.5 ± 2.5 mg m⁻² on T1 and T2, respectively. The heavy metal content of soil-generated PM₁₀ was also assessed. In the generated PM, the elemental concentrations were higher than ones in soil. As, Cd and Ni concentration levels, determined in PM₁₀ near to the tractor path, were also high, being several times higher than the annual average regulatory threshold levels in ambient air, as defined by the European regulation.

Inflammation and the coagulation cascade are considered to be the potential mechanisms of ambient particulate matter (PM) exposure-induced adverse cardiovascular events. Tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-8 (IL-8), and fibrinogen are arguably the four most commonly assayed markers to reflect the relationships of PM with inflammation and blood coagulation. This review summarized and quantitatively analyzed the existing studies reporting short- and long-term associations of PM₂.₅(PM with an aerodynamic diameter ≤2.5 μm)/PM₁₀ (PM with an aerodynamic diameter≤10 μm) with important inflammation and blood coagulation markers (TNF-α, IL-6, IL-8, fibrinogen). We reviewed relevant studies published up to July 2020, using three English databases (PubMed, Web of Science, Embase) and two Chinese databases (Wang-Fang, China National Knowledge Infrastructure). The OHAT tool, with some modification, was applied to evaluate risk of bias. Meta-analyses were conducted with random-effects models for calculating the pooled estimate of markers. To assess the potential effect modifiers and the source of heterogeneity, we conducted subgroup analyses and meta-regression analyses where appropriate. The assessment and correction of publication bias were based on Begg’s and Egger’s test and “trim-and-fill” analysis. We identified 44 eligible studies. For short-term PM exposure, the percent change of a 10 μg/m³ PM₂.₅ increase on TNF-α and fibrinogen was 3.51% (95% confidence interval (CI): 1.21%, 5.81%) and 0.54% (95% confidence interval (CI): 0.21%, 0.86%) respectively. We also found a significant short-term association between PM₁₀ and fibrinogen (percent change = 0.17%, 95% CI: 0.04%, 0.29%). Overall analysis showed that long-term associations of fibrinogen with PM₂.₅ and PM₁₀ were not significant. Subgroup analysis showed that long-term associations of fibrinogen with PM₂.₅ and PM₁₀ were significant only found in studies conducted in Asia. Our findings support significant short-term associations of PM with TNF-α and fibrinogen. Future epidemiological studies should address the role long-term PM exposure plays in inflammation and blood coagulation markers level change.

To characterise the mass concentration, size-distribution, and respiratory deposition of selected trace metals (Cr, Mn, Fe, Ni, Cu, Zn, Ba, and Pb) in size-segregated PM₂.₅, a long-term monitoring campaign was undertaken at an urban background site in Como (Northern Italy). 96-h aerosol samples were collected weekly, from May 2015 to March 2016, using a 13-stage low pressure impactor and analysed via laser ablation-inductively coupled plasma-mass spectrometry. Significantly higher levels of trace metals were generally found during the heating season (two to more than four times) compared to the non-heating period at all size ranges, especially for concentrations in PM₀.₁–₁. Distinct distribution profiles characterised the different elements, even though the corresponding heating and non-heating shapes always exhibited similar features, with negligible seasonal shifts in the average mass median aerodynamic diameters. Fe, Ba, and Cu had >70% of their mass in PM₁–₂.₅, whereas Pb, Zn, and Ni showed higher contributions in the accumulation mode (>60%). Finally, broad size-distributions were found for Cr and Mn. The multiple-path particle dosimetry model estimated the overall deposition fractions in human airways varying between 27% (Pb) and 48% (Ba). The greatest deposition variability was always registered in the head region of the respiratory system, with the highest contributions for those metals predominantly accumulated in the PM₂.₅ coarse modes. In contrast, the deposition in the deepest respiratory tract maintained nearly constant proportions over time, becoming notably important for Pb, Ni, and Zn (∼13%) with respect to their total deposition. The comparison with national limits established for Pb and Ni suggested the absence of significant risks for the local population, as expected, with average concentrations two orders of magnitude lower than the corresponding annual limit and objective value. Similar findings were reported for all the other metals, for which the estimated hazard quotients were always well <1.

Little information exists on interaction effects between air pollution and influenza vaccination on allergic respiratory diseases. We conducted a large population-based study to evaluate the interaction effects between influenza vaccination and long-term exposure to ambient air pollution on allergic respiratory diseases in children and adolescents.A cross-sectional study was investigated during 2012–2013 in 94 schools from Seven Northeastern Cities (SNEC) in China. Questionnaires surveys were obtained from 56 137 children and adolescents aged 2–17 years. Influenza vaccination was defined as receipt of the influenza vaccine. We estimated air pollutants exposure [nitrogen dioxide (NO2) and particulate matter with aerodynamic diameters ≤1 μm (PM1), ≤2.5 μm (PM2.5) and ≤10 μm (PM10)] using machine learning methods. We employed two-level generalized linear mix effects model to examine interactive effects between influenza vaccination and air pollution exposure on allergic respiratory diseases (asthma, asthma-related symptoms and allergic rhinitis), after controlling for important covariates.We found statistically significant interactions between influenza vaccination and air pollutants on allergic respiratory diseases and related symptoms (doctor-diagnosed asthma, current wheeze, wheeze, persistent phlegm and allergic rhinitis). The adjusted ORs for doctor-diagnosed asthma, current wheeze and allergic rhinitis among the unvaccinated group per interquartile range (IQR) increase in PM1 and PM2.5 were significantly higher than the corresponding ORs among the vaccinated group [For PM1, doctor-diagnosed asthma: OR: 1.89 (95%CI: 1.57–2.27) vs 1.65 (95%CI: 1.36–2.00); current wheeze: OR: 1.50 (95%CI: 1.22–1.85) vs 1.10 (95%CI: 0.89–1.37); allergic rhinitis: OR: 1.38 (95%CI: 1.15–1.66) vs 1.21 (95%CI: 1.00–1.46). For PM2.5, doctor-diagnosed asthma: OR: 1.81 (95%CI: 1.52–2.14) vs 1.57 (95%CI: 1.32–1.88); current wheeze: OR: 1.46 (95%CI: 1.21–1.76) vs 1.11 (95%CI: 0.91–1.35); allergic rhinitis: OR: 1.35 (95%CI: 1.14–1.60) vs 1.19 (95%CI: 1.00–1.42)]. The similar patterns were observed for wheeze and persistent phlegm. The corresponding p values for interactions were less than 0.05, respectively. We assessed the risks of PM1-related and PM2.5-related current wheeze were decreased by 26.67% (95%CI: 1.04%–45.66%) and 23.97% (95%CI: 0.21%–42.08%) respectively, which was attributable to influenza vaccination (both p for efficiency <0.05).Influenza vaccination may play an important role in mitigating the detrimental effects of long-term exposure to ambient air pollution on childhood allergic respiratory diseases. Policy targeted at increasing influenza vaccination may yield co-benefits in terms of reduced allergic respiratory diseases.

Emerging evidence has showed that exposure to airborne particulate matter (PM) with an aerodynamic diameter less than 2.5 μm (PM₂.₅) is associated with neurodegeneration. Our previous studies in vitro found that PM₂.₅ exposure causes primary neurons damage through activating microglia. However, the molecular mechanism of microglia-mediated neurotoxicity remains to elucidate. In this study, five groups (N = 13 or 10) of six-week-old male C57BL/6 mice were daily exposed to PM₂.₅ (0.1 or 1 mg/kg/day body weight), Chelex-treated PM₂.₅ (1 mg/kg/day body weight), PM₂.₅ (1 mg/kg/day body weight) plus CB-839 (glutaminase inhibitor), or deionized water by intranasal instillation for 28 days, respectively. Compared with the control groups, We found that PM₂.₅ triggered reactive oxygen species (ROS) generation and microglia activation evidenced by significant increase of ionized calcium binding adaptor molecule-1 (IBa-1) staining in the mouse olfactory bulbs (OB). Data from transmission electron microscope (TEM) images and Western blot analysis showed that PM₂.₅ significantly increased extracellular vesicles (EVs) release from OB or murine microglial line BV2 cells, and glutaminase C (GAC) expression and glutamate generation in isolated OB and BV2 cells. However, treatment with N-acetylcysteine (NAC) or CB-839 significantly diminished the number of EVs and the expression of GAC and abolished PM₂.₅-induced neurotoxicity. These findings provide new insights that PM₂.₅ induces oxidative stress and microglia activation through its metal contents and glutaminase-containing EVs in OBs, which may serve as a potential pathway/mechanism of excessive glutamate generation in PM₂.₅-induced neurotoxicity.

We report on commuters’ exposure to black carbon (BC), PM₂.₅ and particle number (PN, with aerodynamic diameter, dₐ, in the range 0.01 <dₐ< 1.0 μm) collected on-board diesel- and biodiesel-fuelled buses of the Bus Rapid Transit (BRT) system of the city of Curitiba, Brazil. Particulate concentrations measured at high sampling rates allowed the capture of fine gradients along the route and the comparison of in-cabin air pollution on buses of different technologies.Of all metrics, BC showed the largest discrepancies, with mean concentrations of 20.1 ± 20.0 μg m⁻³ and 3.9 ± 26.0 μg m⁻³ on diesel- and biodiesel-fuelled buses, respectively. Mean PM₂.₅ concentrations were similar (31.6 ± 28.5 μg m⁻³ and 29.0 ± 17.8 μg m⁻³), whilst mean PN concentrations were larger on the biodiesel buses (56,697 ± 26,800 # cm⁻³vs. 43,322 ± 32,243 # cm⁻³). The results are in line with studies on biodiesel emission factors that reported lower BC mass but more particles with smaller diameters. Our hypothesis is that different emission factors of diesel and biodiesel engines reflected in differences of in-cabin particulate concentrations. We found that the passenger exposure during the bus commutes was affected not only by the fuel used but also by the street geometry along the route, with segments with canyon configurations resulting in peak exposure to particulates. The results suggest that i) switching from diesel to biodiesel may help abate commuters’ exposure to BC particles on-board buses of the BRT system, whilst it would need to be complemented with after-treatment technologies to reduce emissions; ii) further reductions in exposure (to peaks in particular) could be achieved by changing bus routes to ones that avoid passing through narrow urban street canyons.

Sensing of pathogens by specialized receptors is the hallmark of the innate immunity. Innate immune response also mounts a defense response against various allergens and pollutants including particulate matter present in the atmosphere. Air pollution has been included as the top threat to global health declared by WHO which aims to cover more than three billion people against health emergencies from 2019 to 2023. Particulate matter (PM), one of the major components of air pollution, is a significant risk factor for many human diseases and its adverse effects include morbidity and premature deaths throughout the world. Several clinical and epidemiological studies have identified a key link between the PM existence and the prevalence of respiratory and inflammatory disorders. However, the underlying molecular mechanism is not well understood. Here, we investigated the influence of air pollutant, PM₁₀ (particles with aerodynamic diameter less than 10 μm) during RNA virus infections using Highly Pathogenic Avian Influenza (HPAI) – H5N1 virus. We thus characterized the transcriptomic profile of lung epithelial cell line, A549 treated with PM₁₀ prior to H5N1infection, which is known to cause severe lung damage and respiratory disease. We found that PM₁₀ enhances vulnerability (by cellular damage) and regulates virus infectivity to enhance overall pathogenic burden in the lung cells. Additionally, the transcriptomic profile highlights the connection of host factors related to various metabolic pathways and immune responses which were dysregulated during virus infection. Collectively, our findings suggest a strong link between the prevalence of respiratory illness and its association with the air quality.