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Innate lymphoid cells (ILCs) are a heterogeneous population that play diverse roles in airway inflammation after exposure to allergens and infections. However, how ILCs respond after exposure to environmental toxins is not well understood. Here we show a novel method for studying the heterogeneity of rare lung ILC populations by magnetic enrichment for lung ILCs followed by particle-templated instant partition sequencing (PIP-seq). Using this method, we were able to identify novel group 1 and group 2 ILC subsets that exist after exposure to both fungal allergen and burn pit-related constituents (BPC) that include dioxin, aromatic hydrocarbon, and particulate matter. Toxin exposure in combination with fungal allergen induced activation of specific ILC1/NK and ILC2 populations as well as promoted neutrophilic lung inflammation. Oxidative stress pathways and downregulation of specific ribosomal protein genes (Rpl41 and Rps19) implicated in anti-inflammatory responses were present after BPC exposure. Increased IFNγ expression and other pro-neutrophilic mediator transcripts were increased in BPC-stimulated lung innate lymphoid cells. Further, the addition of BPC induced Hspa8 (encodes HSC70) and aryl hydrocarbon transcription factor activity across multiple lung ILC subsets. Overall, using an airway disease model that develops after occupational and environmental exposures, we demonstrate an effective method to better understand heterogenous ILC subset activation.

Environmentally persistent free radicals (EPFRs) play an important role in aerosol effects on air quality and public health, but their atmospheric abundance and sources are poorly understood. We measured EPFRs contained in PM2.5 collected in Fairbanks, Alaska, in winter 2022. We find that EPFR concentrations were enhanced during surface-based inversion and correlate strongly with incomplete combustion markers, including carbon monoxide and elemental carbon (R2 > 0.75). EPFRs exhibit moderately good correlations with PAHs, biomass burning organic aerosols, and potassium (R2 > 0.4). We also observe strong correlations of EPFRs with hydrocarbon-like organic aerosols, Fe and Ti (R2 > 0.6), and single-particle mass spectrometry measurements reveal internal mixing of PAHs, with potassium and iron. These results suggest that residential wood burning and vehicle tailpipes are major sources of EPFRs and nontailpipe emissions, such as brake wear and road dust, may contribute to the stabilization of EPFRs. Exposure to the observed EPFR concentrations (18 ± 12 pmol m-3) would be equivalent to smoking ∼0.4-1 cigarette daily. Very strong correlations (R2 > 0.8) of EPFR with hydroxyl radical formation in surrogate lung fluid indicate that exposure to EPFRs may induce oxidative stress in the human respiratory tract.

Indonesia faces significant air quality issues due to multiple emissions sources, including rapid urbanization and peatland fires associated with agricultural land management. Limited prior research has estimated the episodic shock of intense fires on morbidity and mortality in Indonesia but has largely ignored the impact of poor air quality throughout the year on biomarkers of cardiovascular disease risk. We conducted a cross-sectional study of the association between particulate matter less than 2.5 microns in diameter (PM2.5) and blood pressure. Blood pressure measurements were obtained from the fifth wave of the Indonesian Family Life Survey (IFLS5), an ongoing population-based socioeconomic and health survey. We used the GEOS-Chem chemical transport model to simulate daily PM2.5 concentrations at 0.5° × 0.625° resolution across the IFLS domain. We assessed the association between PM2.5 and diastolic and systolic blood pressure, using mixed effects models with random intercepts for regency/municipality and household and adjusted for individual covariates. An interquartile range increase in monthly PM2.5 exposure was associated with a 0.234 (95% CI: 0.003, 0.464) higher diastolic blood pressure, with a greater association seen in participants age 65 and over (1.16 [95% CI: 0.24, 2.08]). For the same exposure metric, there was a 1.90 (95% CI: 0.43, 3.37) higher systolic blood pressure in participants 65 and older. Our assessment of fire-specific PM2.5 yielded null results, potentially due to the timing and locations of health data collection. To our knowledge, this is the first study to provide evidence for an association between PM2.5 and blood pressure in Indonesia.

First-ever measurements of particulate matter (PM2.5, PM10, and TSP) along with gaseous pollutants (CO, NO2, and SO2) were performed from June 2019 to April 2020 in Faisalabad, Metropolitan, Pakistan, to assess their seasonal variations; Summer 2019, Autumn 2019, Winter 2019-2020, and Spring 2020. Pollutant measurements were carried out at 30 locations with a 3-km grid distance from the Sitara Chemical Industry in District Faisalabad to Bhianwala, Sargodha Road, Tehsil Lalian, District Chiniot. ArcGIS 10.8 was used to interpolate pollutant concentrations using the inverse distance weightage method. PM2.5, PM10, and TSP concentrations were highest in summer, and lowest in autumn or winter. CO, NO2, and SO2 concentrations were highest in summer or spring and lowest in winter. Seasonal average NO2 and SO2 concentrations exceeded WHO annual air quality guide values. For all 4 seasons, some sites had better air quality than others. Even in these cleaner sites air quality index (AQI) was unhealthy for sensitive groups and the less good sites showed Very critical AQI (> 500). Dust-bound carbon and sulfur contents were higher in spring (64 mg g-1) and summer (1.17 mg g-1) and lower in autumn (55 mg g-1) and winter (1.08 mg g-1). Venous blood analysis of 20 individuals showed cadmium and lead concentrations higher than WHO permissible limits. Those individuals exposed to direct roadside pollution for longer periods because of their occupation tended to show higher Pb and Cd blood concentrations. It is concluded that air quality along the roadside is extremely poor and potentially damaging to the health of exposed workers.

Exposure to ambient air pollution has significant adverse health effects; however, whether air pollution is associated with urological cancer is largely unknown. We conduct a systematic review and meta-analysis with epidemiological studies, showing that a 5 μg/m3 increase in PM2.5 exposure is associated with a 6%, 7%, and 9%, increased risk of overall urological, bladder, and kidney cancer, respectively; and a 10 μg/m3 increase in NO2 is linked to a 3%, 4%, and 4% higher risk of overall urological, bladder, and prostate cancer, respectively. Were these associations to reflect causal relationships, lowering PM2.5 levels to 5.8 μg/m3 could reduce the age-standardized rate of urological cancer by 1.5 ~ 27/100,000 across the 15 countries with the highest PM2.5 level from the top 30 countries with the highest urological cancer burden. Implementing global health policies that can improve air quality could potentially reduce the risk of urologic cancer and alleviate its burden.

BACKGROUND: Numerous studies have linked fine particulate matter (PM2.5) to increased cardiovascular mortality. Less is known how the PM2.5-cardiovascular mortality association varies by use of cardiovascular medications. This study sought to quantify effect modification by statin use status on the associations between long-term exposure to PM2.5 and mortality from any cardiovascular cause, coronary heart disease (CHD), and stroke. METHODS: In this nested case-control study, we followed 1.2 million community-dwelling adults aged ≥66 years who lived in Ontario, Canada from 2000 through 2018. Cases were patients who died from the three causes. Each case was individually matched to up to 30 randomly selected controls using incidence density sampling. Conditional logistic regression models were used to estimate odds ratios (ORs) for the associations between PM2.5 and mortality. We evaluated the presence of effect modification considering both multiplicative (ratio of ORs) and additive scales (the relative excess risk due to interaction, RERI). RESULTS: Exposure to PM2.5 increased the risks for cardiovascular, CHD, and stroke mortality. For all three causes of death, compared with statin users, stronger PM2.5-mortality associations were observed among non-users [e.g. for cardiovascular mortality corresponding to each interquartile range increase in PM2.5, OR = 1.042 (95% CI, 1.032-1.053) vs OR = 1.009 (95% CI, 0.996-1.022) in users, ratio of ORs = 1.033 (95% CI, 1.019-1.047), RERI = 0.039 (95% CI, 0.025-0.050)]. Among users, partially adherent users exhibited a higher risk of PM2.5-associated mortality than fully adherent users. CONCLUSIONS: The associations of chronic exposure to PM2.5 with cardiovascular and CHD mortality were stronger among statin non-users compared to users.

In California, wildfire risk and severity have grown substantially in the last several decades. Research has characterized extensive adverse health impacts from exposure to wildfire-attributable fine particulate matter (PM2.5), but few studies have quantified long-term outcomes, and none have used a wildfire-specific chronic dose-response mortality coefficient. Here, we quantified the mortality burden for PM2.5 exposure from California fires from 2008 to 2018 using Community Multiscale Air Quality modeling system wildland fire PM2.5 estimates. We used a concentration-response function for PM2.5, applying ZIP code-level mortality data and an estimated wildfire-specific dose-response coefficient accounting for the likely toxicity of wildfire smoke. We estimate a total of 52,480 to 55,710 premature deaths are attributable to wildland fire PM2.5 over the 11-year period with respect to two exposure scenarios, equating to an economic impact of $432 to $456 billion. These findings extend evidence on climate-related health impacts, suggesting that wildfires account for a greater mortality and economic burden than indicated by earlier studies.

Wildfires are increasing in duration and intensity across the United States' Pacific West region, resulting in heightened particulate matter from smoke in the atmosphere. Levels of peak particulate matter are concurrent to peak visitor attendance at National Parks, given seasonal alignment with summer vacation travel and heightened forest fire conditions. Particulate matter threatens visitor health and safety and contributes to poor visibility and a deteriorated visitor experience. To assess visitation response to diminished air quality, we utilized wildfire-generated particulate matter (PM2.5) data in conjunction with monthly attendance records for three ecoregions containing eight national parks in Washington, Oregon, and California from 2009 to 2019. We analyzed daily PM2.5 levels from data gridded at the 10 km scale for National Park Service units by Level III forest ecoregions within the National Park Service's Pacific West Unit. Data were then compared to normalized monthly visitation trends for each of the ecoregions using two statistical methods Kendall's Tau and Analysis of Variance (ANOVA) with post-hoc Tukey tests. Results demonstrate that attendance at these national parks does not decrease in response to increased PM2.5 levels. Instead, we see several statistically significant increases in attendance across these ecoregions during periods of reduced air quality. Of 115 shifts between air quality categories during the busy season of July to September, there are no significant decreases in attendance as air quality worsens. These findings suggest that visitors are willing to tolerate reduced air quality compared to other factors such as temperature or precipitation. Given that park units within each ecoregion feature diverse historical contexts, varied built environments, and unique ecological systems, our discussion specifically addresses managerial concerns associated with maintained high levels of visitation during suboptimal, and potentially dangerous, conditions. There is substantial need for specific, scalable approaches to mitigate adverse health and experiential impacts as visitors are exposed to increased risks during a range of exertional activities associated with diverse settings.

We examined associations between prenatal fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) exposures and child respiratory outcomes through age 8-9 years in 1279 ECHO-PATHWAYS Consortium mother-child dyads. We averaged spatiotemporally modeled air pollutant exposures during four fetal lung development phases: pseudoglandular (5-16 weeks), canalicular (16-24 weeks), saccular (24-36 weeks), and alveolar (36+ weeks). We estimated adjusted relative risks (RR) for current asthma at age 8-9 and asthma with recent exacerbation or atopic disease, and odds ratios (OR) for wheezing trajectories using modified Poisson and multinomial logistic regression, respectively. Effect modification by child sex, maternal asthma, and prenatal environmental tobacco smoke was explored. Across all outcomes, 95% confidence intervals (CI) included the null for all estimates of associations between prenatal air pollution exposures and respiratory outcomes. Pseudoglandular PM2.5 exposure modestly increased risk of current asthma (RRadj = 1.15, 95% CI: 0.88-1.51); canalicular PM2.5 exposure modestly increased risk of asthma with recent exacerbation (RRadj = 1.26, 95% CI: 0.86-1.86) and persistent wheezing (ORadj = 1.28, 95% CI: 0.86-1.89). Similar findings were observed for O3, but not NO2, and associations were strengthened among mothers without asthma. While not statistically distinguishable from the null, trends in effect estimates suggest some adverse associations of early pregnancy air pollution exposures with child respiratory conditions, warranting confirmation in larger samples.

BACKGROUND: Epidemiological findings regarding the association of particulate matter ≤2.5 μm (PM2.5) exposure with hypertensive disorders in pregnancy (HDP) are inconsistent; evidence for HDP risk related to PM2.5 components, mixture effects, and windows of susceptibility is limited. We aimed to investigate the relationships between HDP and exposure to PM2.5 during pregnancy. METHODS AND FINDINGS: A large retrospective cohort study was conducted among mothers with singleton pregnancies in Kaiser Permanente Southern California from 2008 to 2017. HDP were defined by International Classification of Diseases-9/10 (ICD-9/10) diagnostic codes and were classified into 2 subcategories based on the severity of HDP: gestational hypertension (GH) and preeclampsia and eclampsia (PE-E). Monthly averages of PM2.5 total mass and its constituents (i.e., sulfate, nitrate, ammonium, organic matter, and black carbon) were estimated using outputs from a fine-resolution geoscience-derived model. Multilevel Cox proportional hazard models were used to fit single-pollutant models; quantile g-computation approach was applied to estimate the joint effect of PM2.5 constituents. The distributed lag model was applied to estimate the association between monthly PM2.5 exposure and HDP risk. This study included 386,361 participants (30.3 ± 6.1 years) with 4.8% (17,977/373,905) GH and 5.0% (19,381/386,361) PE-E cases, respectively. In single-pollutant models, we observed increased relative risks for PE-E associated with exposures to PM2.5 total mass [adjusted hazard ratio (HR) per interquartile range: 1.07, 95% confidence interval (CI) [1.04, 1.10] p < 0.001], black carbon [HR = 1.12 (95% CI [1.08, 1.16] p < 0.001)] and organic matter [HR = 1.06 (95% CI [1.03, 1.09] p < 0.001)], but not for GH. The population attributable fraction for PE-E corresponding to the standards of the US Environmental Protection Agency (9 μg/m3) was 6.37%. In multi-pollutant models, the PM2.5 mixture was associated with an increased relative risk of PE-E ([HR = 1.05 (95% CI [1.03, 1.07] p < 0.001)], simultaneous increase in PM2.5 constituents of interest by a quartile) and PM2.5 black carbon gave the greatest contribution of the overall mixture effects (71%) among all individual constituents. The susceptible window is the late first trimester and second trimester. Furthermore, the risks of PE-E associated with PM2.5 exposure were significantly higher among Hispanic and African American mothers and mothers who live in low- to middle-income neighborhoods (p < 0.05 for Cochrans Q test). Study limitations include potential exposure misclassification solely based on residential outdoor air pollution, misclassification of disease status defined by ICD codes, the date of diagnosis not reflecting the actual time of onset, and lack of information on potential covariates and unmeasured factors for HDP. CONCLUSIONS: Our findings add to the literature on associations between air pollution exposure and HDP. To our knowledge, this is the first study reporting that specific air pollution components, mixture effects, and susceptible windows of PM2.5 may affect GH and PE-E differently.

We investigated the relationship between porosity and flexoelectricity for aluminum (Al)/polyvinylidene fluoride (PVDF) composites. Neat PVDF, composites of micron aluminum (μAl)/PVDF, and composites of nano aluminum (nAl)/PVDF were 3D printed, and the flexoelectric response was measured using a cantilever beam test setup. Voids (up to 72.4 mm3) were incorporated into the samples by decreasing the infill percent of the 3D printed material. We found that increasing the porosity via millimeter scale voids incorporated into the infill pattern decreased the average effective flexoelectric coefficient relative to the near full-density (100% infill) control samples. This contrasts with other studies that have shown increasing micron scale porosity increases the flexoelectric coefficient. In addition, we measured higher flexoelectric responses for nAl/PVDF than μAl/PVDF as well as for samples printed by the Hyrel 3D SR printer as opposed to the Ender 3 V2 printer. These results indicate that charge generation due to flexoelectricity can be altered by changing parameters such as porosity, particle size of inclusions, or manufacturing method. Smaller voids and fine particles can induce larger strain gradients than larger inhomogeneities, leading to increased flexoelectric coefficients. A competing effect is that more porosity leads to less materials, which can decrease the flexoelectric coefficient. [ABSTRACT FROM AUTHOR]

Wildfires are a significant threat to human health, in part through degraded air quality. Prescribed burning can reduce wildfire severity but can also lead to an increase in air pollution. The complexities of fires and atmospheric processes lead to uncertainties when predicting the air quality impacts of fire and make it difficult to fully assess the costs and benefits of an expansion of prescribed fire. By modeling differences in emissions, surface conditions, and meteorology between wildfire and prescribed burns, we present a novel comparison of the air quality impacts of these fire types under specific scenarios. One wildfire and two prescribed burn scenarios were considered, with one prescribed burn scenario optimized for potential smoke exposure. We found that PM2.5 emissions were reduced by 52%, from 0.27 to 0.14 Tg, when fires burned under prescribed burn conditions, considerably reducing PM2.5 concentrations. Excess short-term mortality from PM2.5 exposure was 40 deaths for fires under wildfire conditions and 39 and 15 deaths for fires under the default and optimized prescribed burn scenarios, respectively. Our findings suggest prescribed burns, particularly when planned during conditions that minimize smoke exposure, could be a net benefit for the impacts of wildfires on air quality and health.

Wildfires have become more frequent and intense due to climate change and outdoor wildfire fine particulate matter (PM2.5) concentrations differ from relatively smoothly varying total PM2.5. Thus, we introduced a conceptual model for computing long-term wildfire PM2.5 and assessed disproportionate exposures among marginalized communities. We used monitoring data and statistical techniques to characterize annual wildfire PM2.5 exposure based on intermittent and extreme daily wildfire PM2.5 concentrations in California census tracts (2006 to 2020). Metrics included: 1) weeks with wildfire PM2.5 < 5 μg/m3; 2) days with non-zero wildfire PM2.5; 3) mean wildfire PM2.5 during peak exposure week; 4) smoke waves (≥2 consecutive days with

BACKGROUND: In contrast to fine particles, less is known of the inflammatory and coagulation impacts of coarse particulate matter (PM10-2.5, particulate matter with aerodynamic diameter ≤10μm and>2.5μm). Toxicological research suggests that these pathways might be important processes by which PM10-2.5 impacts health, but there are relatively few epidemiological studies due to a lack of a national PM10-2.5 monitoring network. OBJECTIVES: We used new spatiotemporal exposure models to examine associations of both 1-y and 1-month average PM10-2.5 concentrations with markers of inflammation and coagulation. METHODS: We leveraged data from 7,071 Multi-Ethnic Study of Atherosclerosis and ancillary study participants 45-84 y of age who had repeated plasma measures of inflammatory and coagulation biomarkers. We estimated PM10-2.5 at participant addresses 1 y and 1 month before each of up to four exams (2000-2012) using spatiotemporal models that incorporated satellite, regulatory monitoring, and local geographic data and accounted for spatial correlation. We used random effects models to estimate associations with interleukin-6 (IL-6), C-reactive protein (CRP), fibrinogen, and D-dimer, controlling for potential confounders. RESULTS: Increases in PM10-2.5 were not associated with greater levels of inflammation or coagulation. A 10-μg/m3 increase in annual average PM10-2.5 was associated with a 2.5% decrease in CRP [95% confidence interval (CI): -5.5, 0.6]. We saw no association between annual average PM10-2.5 and the other markers (IL-6: -0.7%, 95% CI: -2.6, 1.2; fibrinogen: -0.3%, 95% CI: -0.9, 0.3; D-dimer: -0.2%, 95% CI: -2.6, 2.4). Associations consistently showed that a 10-μg/m3 increase in 1-month average PM10-2.5 was associated with reduced inflammation and coagulation, though none were distinguishable from no association (IL-6: -1.2%, 95% CI: -3.0 , 0.5; CRP: -2.5%, 95% CI: -5.3, 0.4; fibrinogen: -0.4%, 95% CI: -1.0, 0.1; D-dimer: -2.0%, 95% CI: -4.3, 0.3). DISCUSSION: We found no evidence that PM10-2.5 is associated with higher inflammation or coagulation levels. More research is needed to determine whether the inflammation and coagulation pathways are as important in explaining observed PM10-2.5 health impacts in humans as they have been shown to be in toxicology studies or whether PM10-2.5 might impact human health through alternative biological mechanisms. https://doi.org/10.1289/EHP12972.

Future climate change can cause more days with poor air quality. This could trigger more alerts telling people to stay inside to protect themselves, with potential consequences for health and health equity. Here, we study the change in US air quality alerts over this century due to fine particulate matter (PM2.5), who they may affect, and how they may respond. We find air quality alerts increase by over 1 mo per year in the eastern United States by 2100 and quadruple on average. They predominantly affect areas with high Black populations and leakier homes, exacerbating existing inequalities and impacting those less able to adapt. Reducing emissions can offer significant annual health benefits ($5,400 per person) by mitigating the effect of climate change on air pollution and its associated risks of early death. Relying on people to adapt, instead, would require them to stay inside, with doors and windows closed, for an extra 142 d per year, at an average cost of $11,000 per person. It appears likelier, however, that people will achieve minimal protection without policy to increase adaptation rates. Boosting adaptation can offer net benefits, even alongside deep emission cuts. New adaptation policies could, for example: reduce adaptation costs; reduce infiltration and improve indoor air quality; increase awareness of alerts and adaptation; and provide measures for those working or living outdoors. Reducing emissions, conversely, lowers everyones need to adapt, and protects those who cannot adapt. Equitably protecting human health from air pollution under climate change requires both mitigation and adaptation.

Wildfires are a global natural phenomenon. In North America, wildfires have not only become more frequent, but also more severe and longer in duration, a trend ascribed to climate change combined with large fuel stores left from modern fire suppression. The intensification of wildfire activity has significant implications for planetary health and public health, as exposure to fine particulate matter (PM2.5) in wildfire smoke is linked to adverse health effects. This review focuses on respiratory morbidity from wildfire smoke exposure. Inhalation of wildfire PM2.5 causes lung injury via oxidative stress, local and systemic inflammation, airway epithelium compromise, and increased vulnerability to infection. Wildfire PM2.5 exposure results in exacerbations of pre-existing asthma and chronic obstructive pulmonary disease, with an escalation in healthcare utilization, including emergency department visits and hospitalizations. Wildfire smoke exposure may be associated with asthma onset, long-term impairment of lung function, and increased all-cause mortality. Children, older adults, occupationally-exposed groups, and possibly women are the most at risk from wildfire smoke. Future research is needed to clarify best practices for risk mitigation and wildfire management.

BackgroundPrior studies suggested that air pollution exposure may increase the risk of Parkinson's Disease (PD). We investigated the long-term impacts of traffic-related and multiple sources of particulate air pollution on PD in central California.MethodsOur case-control analysis included 761 PD patients and 910 population controls. We assessed exposure at residential and occupational locations from 1981 to 2016, estimating annual average carbon monoxide (CO) concentrations - a traffic pollution marker - based on the California Line Source Dispersion Model, version 4. Additionally, particulate matter (PM2.5) concentrations were based on a nationwide geospatial chemical transport model. Exposures were assessed as 10-year averages with a 5-year lag time prior to a PD diagnosis for cases and an interview date for controls, subsequently categorized into tertiles. Logistic regression models were used, adjusting for various factors.ResultsTraffic-related CO was associated with an increased odds ratio for PD at residences (OR for T3 vs. T1: 1.58; 95% CI: 1.20, 2.10; p-trend = 0.02) and workplaces (OR for T3 vs. T1: 1.91; 95% CI: 1.22, 3.00; p-trend

Detection sensitivity of aquatic species using environmental DNA (eDNA) generally decreases in turbid water but is poorly characterized. In this study, eDNA detection targeted delta smelt (Hypomesus transpacificus), a critically endangered estuarine fish associated with turbid water. eDNA sampling in the field was first paired with a trawl survey. Species-specific detection using a Taqman qPCR assay showed concordance between the methods, but a weak eDNA signal. Informed by the results of field sampling, an experiment was designed to assess how turbidity and filtration methods influence detection of a rare target. Water from non-turbid (5 NTU) and turbid (50 NTU) estuarine sites was spiked with small volumes (0.5 and 1 mL) of water from a delta smelt tank to generate low eDNA concentrations. Samples were filtered using four filter types: cartridge filters (pore size 0.45 μm) and 47 mm filters (glass fiber, pore size 1.6 μm and polycarbonate, pore sizes 5 and 10 μm). Prefiltration was also tested as an addition to the filtration protocol for turbid water samples. eDNA copy numbers were analyzed using a censored data method for qPCR data. The assay limits and lack of PCR inhibition indicated an optimized assay. Glass fiber filters yielded the highest detection rates and eDNA copies in non-turbid and turbid water. Prefiltration improved detection in turbid water only when used with cartridge and polycarbonate filters. Statistical analysis identified turbidity as a significant effect on detection probability and eDNA copies detected; filter type and an interaction between filter type and prefilter were significant effects on eDNA copies detected, suggesting that particulate-filter interactions can affect detection sensitivity. Pilot experiments and transparent criteria for positive detection could improve eDNA surveys of rare species in turbid environments.

Fine particulate matter (PM 2.5) has been implicated in various health concerns. However, a comprehensive understanding of the specific PM 2.5 components affecting depression remains limited. This study conducted a Cox proportional-hazards model to assess the effect of PM 2.5 components on the incidence of depression based on the China Health and Retirement Longitudinal Study (CHARLS). Participants with 10-item Center for Epidemiologic Studies Depression Scale (CESD-10) score of 10 or higher were classified as exhibiting depression. Our findings demonstrated a significant positive correlation between long-term exposure to black carbon (BC), sulfate (SO 4 2−), and organic matter (OM) components of PM 2.5 and the prevalence of depression. Per 1 Interquartile Range (IQR) increment in 3-year average concentrations of BC, OM, and SO 4 2− were associated with the hazard ratio (HR) of 1.54 (95 % confidence intervals (CI): 1.44, 1.64), 1.24 (95% CI : 1.16, 1.34) and 1.25 (95% CI : 1.16, 1.35). Notably, females, younger individuals, those with lower educational levels, urban residents, individuals who were single, widowed, or divorced, and those living in multi-story houses exhibited heightened vulnerability to the adverse effects of PM 2.5 components on depression. Firstly, pollutant data is confined to subjects' fixed addresses, overlooking travel and international residence history. Secondly, the analysis only incorporates five fine particulate components, leaving room for further investigation into the remaining fine particulate components in future studies. This study provides robust evidence supporting the detrimental impact of PM 2.5 components on depression. The identification of specific vulnerable populations contributes to a deeper understanding of the underlying mechanisms involved in the relationship between PM 2.5 components and depression. • This study explore the association between PM 2.5 components and depression. • Black carbon, sulfate, and organic matter have significant impacts on depression. • Females, who living in multi-story house were susceptible to the PM 2.5 components. [ABSTRACT FROM AUTHOR]

The short-term adverse effects of ambient fine particulate matter (PM 2.5) and ozone (O 3) on anxiety disorders (ADs) remained inconclusive. We applied an individual-level time-stratified case-crossover study, which including 126,112 outpatient visits for ADs during 2019–2021 in Guangdong province, China, to investigate the association of short-term exposure to PM 2.5 and O 3 with outpatient visits for ADs, and estimate excess outpatient visits in South China. Daily residential air pollutant exposure assessments were performed by extracting grid data (spatial resolution: 1 km × 1 km) from validated datasets. We employed the conditional logistic regression model to quantify the associations and excess outpatient visits. The results of the single-pollutant models showed that each 10 μg/m3 increase of PM 2.5 and O 3 exposures was significantly associated with a 3.14 % (95 % confidence interval: 2.47 %, 3.81 %) and 0.88 % (0.49 %, 1.26 %) increase in odds of outpatient visits for ADs, respectively. These associations remained robust in 2-pollutant models. The proportion of outpatient visits attributable to PM 2.5 and O 3 exposures was up to 7.20 % and 8.93 %, respectively. Older adults appeared to be more susceptible to PM 2.5 exposure, especially in cool season, and subjects with recurrent outpatient visits were more susceptible to O 3 exposure. As our study subjects were from one single hospital in China, it should be cautious when generalizing our findings to other regions. Short-term exposure to ambient PM 2.5 and O 3 was significantly associated with a higher odds of outpatient visits for ADs, which can contribute to considerable excess outpatient visits. • Exposure to ambient PM 2.5 and O 3 was associated with an increased odds of outpatient visits for anxiety disorders. • PM 2.5 and O 3 exposures were attributable to considerable excess outpatient visits. • Older adults were more susceptible to PM 2.5 exposure, especially in cool season. • Subjects with recurrent outpatient visits were more susceptible to O 3 exposure. [ABSTRACT FROM AUTHOR]

Microplastics (MPs) in the air are one of the major concerns due to their possible health risks. In addition, airborne microplastics act as a carrier for several toxic air pollutants and cause carcinogenic, mutagenic and teratogenic effects. Nylon 66 is one of the most abundant MPs in the microenvironments. In this study, we report an optimized method for the quantification of nylon 66 MPs present in the fine particulate matter (PM2.5) using high-performance liquid chromatography coupled to tandem mass spectrometry (HPLC-MS/MS). The optimized method exhibited excellent linearity, recovery rates, intraday and interday precision and sensitivity. The optimized method was deployed to carry out a pilot study to measure the mass concentrations of nylon 66 microplastics present in the inhalable fraction of particulate matter collected in a shopping complex. The observed mass concentrations of nylon 66 MPs in this study are in the range from 0.30 ng m−3 to 4.37 ng m−3. This study demonstrates the presence of inhalable fraction of nylon 66 MPs in the indoor environment and their mass concentrations were determined using HPLC-MS/MS. [ABSTRACT FROM AUTHOR]

The emissions from South Asia and Southeast Asia significantly impact air quality and meteorological conditions in China. However, the individual or joint contributions of anthropogenic emissions and/or biomass burning from outside China to surface particulate matter with aerodynamic diameters less than 2.5 μm (PM2.5) and aerosol optical depth (AOD) over southern China have not been fully investigated. Here, five experiments were designed to investigate the impacts of these emissions in January (winter), March (pre‐monsoon), and October (post‐monsoon) for 2017. Aerosols from South Asia and Southeast Asia contributed less to southern China during winter and post‐monsoon seasons, whereas the wind patterns and emission intensity during the pre‐monsoon season were conducive to the transport of aerosols. During pre‐monsoon season, the total emissions contributed approximately 5.0 μg m−3 to surface PM2.5 in Xizang Province. Biomass burning in Southeast Asia increased PM2.5 in Yunnan Province by 37.9 μg m−3, while anthropogenic emissions increased it by 8.9 μg m−3. Transboundary aerosols can be transported to Xizang Province and Yunnan Province, primarily influencing PM2.5 below 2 km height. It mainly affected PM2.5 levels above the planetary boundary layer over southeast China. Aerosols from outside China can account for 79.5% and 54.8% AOD in Yunnan Province and southeast China, respectively. These aerosols reduced surface incident solar radiation by approximately 6%, leading to decreases in air temperature, wind speed, and boundary layer height. The findings are only applicable to the pre‐monsoon season. Plain Language Summary: Air pollution in South Asia and Southeast Asia is closely related to anthropogenic emissions and biomass burning. Under the influence of prevailing winds, these emissions can affect air quality over southern China during different seasons. This study combines ground observations, satellite data, and chemical transport models to investigate the impacts of anthropogenic emissions and/or biomass burning from South Asia and Southeast Asia on air quality and meteorological conditions over southern China in January, March, and October for 2017. Key Points: Transportation from South Asia and Southeast Asia account for up to 50% PM2.5 concentrations over Xizang Province in ChinaAerosols transported from South Asia and Southeast Asia can impact PM2.5 at heights up to 6 km over southern China in pre‐monsoon seasonImpacts on the surface solar radiation, air temperature, relative humidity, wind speed and planetary boundary layer height are quantified [ABSTRACT FROM AUTHOR]

Mobilization of in situ fine particles in geothermal reservoirs is a key contributor to permeability damage and clogging of the reservoir rock, leading to a decline in well productivity during enhanced geothermal operations. This phenomenon is a result of disturbance in the mechanical equilibrium of the forces acting on a given fine particle, most significant of which are electrostatic and drag forces. These forces are affected by changes in fluid flow velocities, in situ temperatures, or ionic strength of in situ fluids. Theoretical formulation of migration of fine particles in porous media driven by non-isothermal flow remains challenging, and requires a considerable number of parameters to quantify the characteristics of a given colloidal particle-pore fluid–solid grain system. The identification of all the involved parameters often necessitates costly, intricate, and time-consuming physical experiments. Moreover, implementing the complete form of the Derjaguin-Landau-Verwey-Overbeek (DLVO) theory, commonly adopted to evaluate changes in electrostatic forces, is complicated, computationally demanding, and impractical, particularly when applied to evaluate fines migration at a reservoir scale. This study presents a theoretical framework for accurate and practical prediction of fine particle migration driven by non-isothermal flow in a clay-NaCl-quartz system. The novel contributions of this study are twofold. Firstly, a new numerical model is developed based on the complete DLVO theory, which integrates for the first time the effects of both thermal and hydraulic loads on all underlying parameters including both the static dielectric constant and the refractive index of the pore fluid. Secondly, an innovative simplified DLVO-based model has been introduced, requiring notably fewer parameters compared to existing models, thus offering a practical and efficient solution. The proposed models are utilized to conduct a comprehensive assessment of the fundamental mechanisms involved in fine particle liberation. Findings are key to predict fines-migration-induced permeability damage in geothermal reservoirs to achieve a sustainable design of energy storage/production operations as well as to develop effective strategies to prevent or mitigate the decline in well productivity in time. [ABSTRACT FROM AUTHOR]

Abstract\nNOVELTY STATEMENTEnvironmental pollution, especially from coal-based thermal power plants, poses significant risks to human respiratory health and the environment. This study evaluates the diversity of lichens in the areas. Physiological and bioaccumulation responses of two crustose lichens (Bacidia incongruens and Rindoina sophodes) and one foliose lichen (Pyxine cocoes) in the vicinity of the Feroz Gandhi Unchahar National Thermal Power Corporation, Raebareli, Uttar Pradesh, India were also assessed. These lichens, exposed to emissions including fly ash, greenhouse gases, metals, and particulate matter were analyzed for metal accumulation and physiological responses. Changes in physiological parameters and metal profiles concerning distance from the coal-based thermal power plant to the outskirts were analyzed for B. incongruens, R. sophodes and P. cocoes by utilizing Inductively Coupled Plasma Mass Spectrometry (ICP-MS). The study identified 18 lichen species from 12 genera and 10 families in the area, with Pyxine sorediata newly recorded in Uttar Pradesh. The dominant species, B. incongruens, P. cocoes, and R. sophodes, preferred substrates like Mangifera indica, Acacia nilotica, and Azadirachta indica bark. Physiological analyses revealed variations in pigment concentrations, with significant differences in chlorophyll a, chlorophyll b, total chlorophyll, carotenoids, and chlorophyll degradation, while protein content remained stable. Metal accumulation studies showed nine metals with distinct patterns, B. incongruens had higher concentrations in the west (52730.61 µg g-1) and P. cocoes in the east (23628.32 µg g-1). Correlation analyses indicated significant relationships between paired elements, suggesting specific sources of environmental contamination. This research highlights the significance of integrating physiological and environmental factors to understand lichen responses to coal based thermal power plant.This study contributes significantly to lichenological and environmental monitoring by documenting the occurrence and physiological responses of lichen species in the vicinity of a thermal power plant. The study reports the Pyxine sorediata as a new addition to the lichen flora of Uttar Pradesh, India. Furthermore, the research comprehensively analyzes photosynthetic pigments and metal accumulation in Bacidia incongruens, Pyxine cocoes, and Rinodina sophodes. This study marks the first time these three lichen species have been compared based on their physiological characteristics and metal profiles, highlighting the difference between crustose and foliose lichen. The study uniquely correlated the physiological parameters and metal accumulation pattern of these lichen species with their spatial distribution around the coal-based Feroze Gandhi Unchahar National Thermal Power Plant. The detailed PCA analysis offers new insights into the distinct sources and distribution patterns of various metals in the environment. The novelty of the work also lies in the revival and focused study of lichen species to explore their responses to environmental stressors. By investigating the physiological, elemental distribution and bioaccumulation characteristics of both crustose and foliose lichens in the vicinity of thermal power plant, the research highlights the unique potential of these lichens as bioindicators. The approach not only provides critical insights into pollution levels and ecosystem health but also underscores the importance of lichens in environmental monitoring and conservation efforts. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the mechanism underlying particulate matter (PM) exposure-induced oxidative stress and potential rescue strategies against pulmonary damage in this context. Methods: A combination of omics technology and bioinformatic analysis were used to uncover mechanisms underlying cellular responses to PM exposure in human bronchial epithelia (HBE) cells and imply the potential rescue. Results: Our results implicated that oxidative stress, metal ion homeostasis, and apoptosis were the major cellular responses to PM exposure in HBE cells. PM exposure disrupted oxidative phosphorylation (OXPHOS)-related gene expressions in HBE cells. Rescuing the expression of these genes with supplemental coenzyme Q10 (Co Q10) inhibited reactive oxygen species (ROS) generation; however, it only partially protected HBEs against PM exposure-induced apoptosis. Further, metallothionein (MT)-encoding genes associated with metal ion homeostasis were significantly induced in HBE cells, which was transcriptionally regulated by specificity protein 1 (SP1). SP1 knock-down (KD) aggravated PM-induced apoptosis in HBE cells, suggesting it plays a role in MT induction. Subsequent studies corroborated the protective role of MT by showing that exogenous MT supplement demonstrated effective protection against PM-induced oxidative stress and apoptosis in HBE cells. Importantly, exogenous MT supplement was shown to reduce ROS generation and apoptosis in airway epithelia in both HBE cells and a PM-inhaled murine model. Conclusion: This study demonstrates that the impact of MT on airway epithelia by suppressing oxidative stress and maintaining metal ion homeostasis is beneficial in attenuating damage to pulmonary cells undergoing PM exposure. [ABSTRACT FROM AUTHOR]

Four hundred and sixty-six references with 625 data reports were included in our study. The high frequency of ratio OC/EC for PM0.1 was observed in 3.92–5.93; PM1 in 1.08–3.08; PM2.5, 2.08–4.08; PM10 in 2.70–4.70 and TSP in 2.66–4.66. The rank order of areas based on the pooled concentration of OC bound to PM2.5 was traffic (17.893 µg/m3) > industrial (10.58 µg/m3) > urban (7.696 µg/m3) > rural (4.08 µg/m3). The rank order of areas based on the pooled (mean) concentration of EC in PM2.5 was traffic (17.893 µg/m3) > industrial (2.65 µg/m3) > Urban (1.48 µg/m3) > rural (1.06 µg/m3). The pooled concentrations of OC and EC bound to PM2.5 in traffic areas were higher than in other areas. Therefore, it is recommended that monitoring and effectively reducing concentration plans are carried out, especially in traffic areas. [ABSTRACT FROM AUTHOR]

Background: Particulate matter with a diameter of < 2.5 μm (PM2.5) influences gene regulation via DNA methylation; however, its precise mechanism of action remains unclear. Thus, this study aimed to examine the connection between personal PM2.5 exposure and DNA methylation in CpG islands as well as explore the associated gene pathways. Methods: A total of 95 male patients with chronic obstructive pulmonary disease (COPD) were enrolled in this study. PM2.5 concentrations were measured for 12 months, with individual exposure recorded for 24 h every 3 months. Mean indoor and estimated individual PM2.5 exposure levels were calculated for short-term (7 days), mid-term (35 days), and long-term (90 days). DNA methylation analysis was performed on the blood samples, which, after PCR amplification and hybridization, were finally sequenced using an Illumina NovaSeq 6000 system. Correlation between PM2.5 exposure and CpG methylation sites was confirmed via a mixed-effects model. Functional enrichment analysis was performed on unique CpG methylation sites associated with PM2.5 exposure to identify the relevant biological functions or pathways. Results: The number of CpG sites showing differential methylation was 36, 381, and 182 for the short-, mid-, and long-term indoor models, respectively, and 3, 98, and 28 for the short-, mid-, and long-term estimated exposure models, respectively. The representative genes were TMTC2 (p = 1.63 × 10-3, R2 = 0.656), GLRX3 (p = 1.46 × 10-3, R2 = 0.623), DCAF15 (p = 2.43 × 10-4, R2 = 0.623), CNOT6L (p = 1.46 × 10-4, R2 = 0.609), BSN (p = 2.21 × 10-5, R2 = 0.606), and SENP6 (p = 1.59 × 10-4, R2 = 0.604). Functional enrichment analysis demonstrated that the related genes were mostly associated with pathways related to synaptic transmission in neurodegenerative diseases and cancer. Conclusion: A significant association was observed between PM2.5 exposure and DNA methylation upon short-term exposure, and the extent of DNA methylation was the highest upon mid-term exposure. Additionally, various pathways related to neurodegenerative diseases and cancer were associated with patients with COPD. ClinicalTrials.gov identifier: NCT04878367. [ABSTRACT FROM AUTHOR]

Epidemiology has shown a strong relationship between fine particulate matter (PM) exposure and cardiovascular disease. However, it remains unknown whether PM aggravates myocardial ischemia-reperfusion (I/R) injury, and the related mechanisms are unclear. Our previous study has shown that adipose stem cell-derived exosomes (ADSC-Exos) contain high levels of Mir221 and Mir222. The present study investigated the effects of PM exposure on I/R-induced cardiac injury through mitophagy and apoptosis, as well as the potential role of Mir221 and Mir222 in ADSC-Exos. Wild-type, mir221- and mir222-knockout (KO), and Mir221- and Mir222-overexpressing transgenic (TG) mice were intratracheally injected with PM (10 mg/kg). After 24 h, mice underwent left coronary artery ligation for 30 min, followed by 3 h of reperfusion (I/R). H9c2 cardiomyocytes were cultured under 1% O2 for 6 h, then reoxygenated for 12 h (hypoxia-reoxygenation [H/R]). PM aggravated I/R (or H/R) cardiac injury by increasing ROS levels and causing mitochondrial dysfunction, which increased the expression of mitochondrial fission-related proteins (DNM1L/Drp1 and MFF) and mitophagy-related proteins (BNIP3 and MAP1LC3B/LC3B) in vivo and in vitro. Treatment with ADSC-Exos or Mir221- and Mir222-mimics significantly reduced PM+I/R-induced cardiac injury. Importantly, ADSC-Exos contain Mir221 and Mir222, which directly targets BNIP3, MAP1LC3B/LC3B, and BBC3/PUMA, decreasing their expression and ultimately reducing cardiomyocyte mitophagy and apoptosis. The present data showed that ADSC-Exos treatment regulated mitophagy and apoptosis through the Mir221 and Mir222-BNIP3-MAP1LC3B-BBC3/PUMA pathway and significantly reduced the cardiac damage caused by PM+I/R. The present study revealed the novel therapeutic potential of ADSC-Exos in alleviating PM-induced exacerbation of myocardial I/R injury.Abbreviation: ADSC-Exos: adipose-derived stem cell exosomes; AL: autolysosome; ATP: adenosine triphosphate; BBC3/PUMA: BCL2 binding component 3; BNIP3: BCL2/adenovirus E1B interacting protein 3; CASP3: caspase 3; CASP9: caspase 9; CDKN1B/p27: cyclin dependent kinase inhibitor 1B; CVD: cardiovascular disease; DCFH-DA: 2‘,7’-dichlorodihydrofluorescein diacetate; DHE: dihydroethidium; DNM1L/Drp1: dynamin 1-like; EF: ejection fraction; FS: fractional shortening; H/R: hypoxia-reoxygenation; I/R: ischemia-reperfusion; LDH: lactate dehydrogenase; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MFF: mitochondrial fission factor; miRNA: microRNA; NAC: N-acetylcysteine; OCR: oxygen consumption rate; PIK3C3/Vps34: phosphatidylinositol 3-kinase catalytic subunit type 3; PM: particulate matter; PRKAA1/AMPK: protein kinase AMP-activated catalytic subunit alpha 1; ROS: reactive oxygen species; SQSTM1/p62: sequestosome 1; TEM: transmission electron microscopy; TRP53/p53: transformation related protein 53; TUNEL: terminal deoxynucleotidyl transferase dUTP nick end labeling. [ABSTRACT FROM AUTHOR]

Gold has been one of the most valued metals throughout human history. Traditionally, gravity plants primarily utilized equipment designed to recover only coarse-grained free gold, including jigs, spiral separators, cone concentrators, shaking tables, sluices, and hydrocyclones. The introduction of centrifugal concentrators in the 1980s initiated a trend toward more compact, simplified, and low-maintenance circuits. The use of centrifugal concentrators such as Knelson, Falcon, Multi-gravity separator (MGS), Kelsey, and Itomak has significantly enhanced the recovery of fine gold particles. A review of studies comparing centrifugal equipment, highlighting their main technological advantages, and disadvantages is presented. Depending on their mineral composition, the concentrates obtained can be processed by various methods. Due to increasingly stringent environmental regulations, there is a growing trend to abandon pyrometallurgical methods in favor of developing hydrometallurgical methods for processing gravity concentrates. Particular attention is given to the intensive cyanidation of concentrates. The main technological advantages and disadvantages of intensive cyanidation reactors, specifically Consep Acacia, ILR Gekko, and August Irgiredmet are discussed. Additionally, examples of intensifying chemical reagents used as additives in the intensive cyanidation of concentrates, along with their main characteristics are provided [ABSTRACT FROM AUTHOR]

Background: Operators in the obituary and necropsy sectors are exposed to various environmental hazards during specific tasks. Despite this exposure, occupational risks have often been underestimated, resulting in a lack of substantial evidence. The primary objectives of this study were to identify sources of chemical risk, establish procedures for monitoring and quantifying exposure during necropsy activities, and recommend adjustments to regulatory guidelines to protect the health of the operators. The study was conducted at the Legal Medicine Unit of the Umberto I General Hospital in Rome, focusing on the quantitative measurement of particulate matter (PM) exposure among at-risk operators during necropsy activities. Environmental levels of total suspended particles, PM10, PM4, PM2.5, and PM1 were assessed by evaluating the average, minimum, and maximum instantaneous indoor concentrations using an airborne analyzer. Results: The monitoring activities revealed that the PM concentrations were significantly lower than the recognized reference values. However, bone sawing, body removal, and cleaning were identified as high-risk maneuvers for dust suspension. Conclusions: Our study highlighted specific risks associated with necropsy activities, particularly concerning timing and certain maneuvers. These results may lead to interventions for improving current prevention procedures, implementing good practices, and developing specific guidelines to enhance operator safety. [ABSTRACT FROM AUTHOR]

Background: Atmospheric particulate matter (PM) exposure-induced neuroinflammation is critical in mediating nervous system impairment. However, effective intervention is yet to be developed. Results: In this study, we examine the effect of β-nicotinamide mononucleotide (NMN) supplementation on nervous system damage upon PM exposure and the mechanism of spatial regulation of lipid metabolism. 120 C57BL/6 male mice were exposed to real ambient PM for 11 days (subacute) or 16 weeks (sub-chronic). NMN supplementation boosted the level of nicotinamide adenine dinucleotide (NAD+) in the mouse brain by 2.04 times. This augmentation effectively reduced neuroinflammation, as evidenced by a marked decrease in activated microglia levels across various brain regions, ranging from 29.29 to 85.96%. Whole brain lipidomics analysis revealed that NMN intervention resulted in an less increased levels of ceramide (Cer) and lysophospholipid in the brain following subacute PM exposure, and reversed triglyceride (TG) and glycerophospholipids (GP) following sub-chronic PM exposure, which conferred mice with anti-neuroinflammation response, improved immune function, and enhanced membrane stability. In addition, we demonstrated that the hippocampus and hypothalamus might be the most sensitive brain regions in response to PM exposure and NMN supplementation. Particularly, the alteration of TG (60:10, 56:2, 60:7), diacylglycerol (DG, 42:6), and lysophosphatidylcholine (LPC, 18:3) are the most profound, which correlated with the changes in functional annotation and perturbation of pathways including oxidative stress, inflammation, and membrane instability unveiled by spatial transcriptomic analysis. Conclusions: This study demonstrates that NMN intervention effectively reduces neuroinflammation in the hippocampus and hypothalamus after PM exposure by modulating spatial lipid metabolism. Strategies targeting the improvement of lipid homeostasis may provide significant protection against brain injury associated with air pollutant exposure. [ABSTRACT FROM AUTHOR]

Background: Epidemiological and toxicological studies indicate that increased exposure to air pollutants can lead to neurodegenerative diseases. To further confirm this relationship, we evaluated the association between exposure to ambient air pollutants and corneal nerve measures as a surrogate for neurodegeneration, using corneal confocal microscopy. Methods: We used population-based observational cross-sectional data from The Maastricht Study including N = 3635 participants (mean age 59.3 years, 51.6% were women, and 19.9% had type 2 diabetes) living in the Maastricht area. Using the Geoscience and hEalth Cohort COnsortium (GECCO) data we linked the yearly average exposure levels of ambient air pollutants at home address-level [particulate matter with diameters of ≤ 2.5 µm (PM2.5), and ≤ 10.0 µm (PM10), nitrogen dioxide (NO2), and elemental carbon (EC)]. We used linear regression analysis to study the associations between Z-score for ambient air pollutants concentrations (PM2.5, PM10, NO2, and EC) and Z-score for individual corneal nerve measures (corneal nerve bifurcation density, corneal nerve density, corneal nerve length, and fractal dimension). Results: After adjustment for potential confounders (age, sex, level of education, glucose metabolism status, corneal confocal microscopy lag time, inclusion year of participants, smoking status, and alcohol consumption), higher Z-scores for PM2.5 and PM10 were associated with lower Z-scores for corneal nerve bifurcation density, nerve density, nerve length, and nerve fractal dimension [stβ (95% CI): PM2.5 -0.10 (-0.14; -0.05), -0.04 (-0.09; 0.01), -0.11 (-0.16; -0.06), -0.20 (-0.24; -0.15); and PM10 -0.08 (-0.13; -0.03), -0.04 (-0.09; 0.01), -0.08 (-0.13; -0.04), -0.17 (-0.21; -0.12)], respectively. No associations were found between NO2 and EC and corneal nerve measures. Conclusions: Our population-based study demonstrated that exposure to higher levels of PM2.5 and PM10 are associated with higher levels of corneal neurodegeneration, estimated from lower corneal nerve measures. Our results suggest that air pollution may be a determinant for neurodegeneration assessed in the cornea and may impact the ocular surface health as well. [ABSTRACT FROM AUTHOR]

Air quality is of large concern in the city of Krakow, southern Poland. A comprehensive study was launched by us in which two PM fractions (PM1 and PM10) were sampled during 1-year campaign, lasting from April 21, 2018 to March 19, 2019. A suite of modern analytical methods was used to characterize the chemical composition of the collected samples. The contents of 14 sugars, sugar alcohols and anhydrosugars, 16 polycyclic aromatic hydrocarbons, selected metals and non-metals and ions were analyzed, in addition to organic and elemental carbon content. The carbon isotope composition in both analysed PM fractions, combined with an isotope-mass balance method, allowed to distinguish three main components of carbonaceous emissions in the city: (1) emissions related to combustion of hard coal, (2) emissions related to road transport, and (3) biogenic emissions. The heating season emissions from coal combustion had the biggest contribution to the reservoir of carbonaceous aerosols in the PM10 fraction (44%) and, together with the biogenic emission, they were the biggest contributors to the PM1 fraction (41% and 44%, respectively). In the non-heating season, the dominant source of carbon in PM10 and PM1 fraction were the biogenic emissions (48 and 54%, respectively). [ABSTRACT FROM AUTHOR]

Heavy metals mainly exist on the surface of sediment particles and are transported using particulate matter as carriers. Therefore, the particle size of sediment particles can affect the adsorption, release, and migration of heavy metals. This study aim to investigate the distribution characteristics and chemical fraction of Cd, Pb, and As contents in sediments of different particle sizes using the BCR method, and to determine the key factors affecting the distribution of heavy metals through mineralogical methods such as XRD and EDS. The results revealed that the overall content of various forms of heavy metals increases with the decrease of particle size, mainly presents in fine particles. The mineralogical analysis results indicated that fine particles predominantly contained clay minerals such as chlorite and illite and coarse particles mainly include primary minerals. Due to the mining areas in the middle-upstream, Cd, Pb and As were primarily associated with galena, sphalerite and pyrite, respectively. The distribution of heavy metals is jointly influenced by sediment particle size and sediment material composition. [ABSTRACT FROM AUTHOR]

This study investigates the association between maternal exposure to particulate matter (PM 10) and nitric dioxide (NO 2) during the first, second and third trimester and placental weight and birth weight/placental weight (BW/PW) ratio in twins at birth. Cross-sectional data of 3340 twins from the East Flanders Prospective Twin Survey was used. Air pollutant exposure was estimated via spatial temporal interpolation. Univariable and multivariable mixed model analyses with a random intercept to account for the relatedness of newborns were conducted for twins with separate placentas. Twin pairs with one placental mass were studied with linear and logistic regression. In the third trimester, for each 10 μm/m3 increase in PM 10 or NO 2 placental weight decreased −19.7 g (95%-C.I. −35.1; −4.3) and −17.7 g (95%-C.I. −30.4; −0.5) respectively, in moderate to late preterm twins with separate placentas. Consequently, BW/PW ratio increased with higher air pollution exposure. PM 10 exposure in the last week of pregnancy was associated with a higher odds ratio (OR) of 1.20 (95%-C.I. 1.00; 1.44) for a "small for gestational age placenta" (placental weight <10th percentile). Conversely, first trimester air pollutant exposure was associated with lower ORs of 0.55 (95%-C.I. 0.35; 0.88) and 0.60 (95%-C.I. 0.42; 0.84). The association of PM 10 and NO 2 on placental weight is trimester-specific, differs for twins with one versus two placentas and is most pronounced in moderate to late preterm twins. Longitudinal studies are needed to better understand the relationship between air pollutant exposure and placental weight evolution across different trimesters. • Effects of NO 2 /PM 10 on placental weight differ for twins with one or two placentas. • The effects of air pollutants are most pronounced in twins born between 32 and 36 weeks. • Higher NO 2 /PM 10 exposure in the last trimester is linked to lower placental weight. • NO 2 /PM 10 exposure in early pregnancy is linked to a lower odds for "SGA-placenta". • NO 2 /PM 10 exposure in late pregnancy is linked to a higher odds for "SGA-placenta". [ABSTRACT FROM AUTHOR]

Global and South African populations continue to increase exponentially, with large flows of persons into urban centres. Urban air quality and bioaerosol are therefore becoming an increasingly important consideration in the face of a growing burden of allergic respiratory diseases. More than 20% of South Africans have asthma, with morbidity being disproportionately high compared to high-income countries (HICs). Air pollutants (particularly particulate matter and ozone), pollen and fungal spores are known triggers and exacerbating factors in asthma and, alarmingly, the levels of air pollutants remain high in hotspot areas despite robust air-quality legislation in South Africa. The concern is that genetically and environmentally vulnerable children in low- and middle-income countries (LMICs) such as South Africa will have asthma triggered and exacerbated disproportionately by poor air quality. Urban green areas are increasingly being recognised by many stakeholders as important possible mitigation tools. However, multiple factors must be considered for having an optimal green space design. In this review, we bring together experts across the fields of health, air quality and aerobiology to outline the intersection between asthma and air quality and/or aerobiology in South Africa. We highlight the importance of careful multidisciplinary green space design as a possible healing tonic. We conclude that detailed studies combining air quality, pollen dispersal and health issues are needed to derive more precise exposure--response functions of the green spaces in South Africa and other LMICs. [ABSTRACT FROM AUTHOR]

It is of great significance to explore the causality between regional integration (RI) and PM2.5 pollution within urban agglomerations in the current pursuit of ecological civilization construction and high‐quality development. Using panel data of 285 prefecture‐level cities in China from 2003 to 2016, this study considers the expansion of the city economic coordination committee in Yangtze River Delta (YRDECC) as a quasi‐natural experiment of RI, and use a difference‐in difference method to explore the effect and inner mechanisms of RI on PM2.5 concentration. After a descriptive analysis of the spatial‐temporal variation trend of the PM2.5 concentration in the Yangtze River Delta urban agglomeration, the empirical results show that RI helps to alleviate 4.8% of the PM2.5 concentration overall. For the original cities, the reduction effect on the PM2.5 concentration is 5.2%, for the new cities, however, RI exacerbates 2.1% of the local PM2.5 concentration. A series of robustness tests confirm the validity of the baseline results, and further indicate that the effect of RI remains significant in the long term and starts to increase from the third year. Furthermore, the reduction effect of RI on PM2.5 concentration is more pronounced in cities with larger scales, more developed economies, and higher degrees of marketization. The mechanism analysis shows that industrial transfer, population migration and technological innovation are significant channels of RI that affect PM2.5 concentrations. The conclusions of this paper provide a new path to alleviate PM2.5 pollution and achieve ecological conservation and high‐quality development in the city cluster area. [ABSTRACT FROM AUTHOR]

Background Recent evidence has linked air pollution with frailty, yet little is known about the role of NO2 in this association. Our aim was to assess the association between frailty and NO2 air concentrations in Mexican older adults. Methods We used georeferenced data from the population-based Nutrition and Health Survey in Mexico (NHNS) 2021, representative of national and subnational regions, to measure a frailty index based on 31 health deficits in adults aged 50 and older. Air pollution due to NO2 concentrations was estimated from satellite images validated with data from surface-level stations. Maps were produced using Jensen's Natural break method. The association of frailty and NO2 concentrations was measured using the frailty index (multivariate fractional response logit regression) and a frailty binary variable (frailty index [FI] ≥0.36, multivariate logit regression). Results There was a positive and significant association of the frailty index with the NO2 concentrations, adjusting for age, sex, urban and rural area, years of education, socioeconomic status, living arrangement, particulate matter smaller than 2.5 microns, and indoor pollution. For each standard deviation increase in NO2 concentrations measured 10 years before the survey, the odds of being frail were 15% higher, and the frailty index was 14.5% higher. The fraction of frailty attributable to NO2 exposure ranged from 1.8% to 23.5% according to different scenarios. Conclusions Frailty was positively associated with exposure to NO2 concentrations. Mapping frailty and its associated factors like NO2 air concentrations can contribute to the design of targeted pro-healthy aging policies. [ABSTRACT FROM AUTHOR]

Objective: PM2.5 is closed linked to asthma exacerbation. The Notch1 pathway acts as an important pathway, ultimately inducing T-helper cells that express GATA3 and its corresponding Th2 cytokines. The regulatory effects of miR-139-5p on the Notch1 pathway have been indicated in cancer. However, studies on miR-139-5p have not applied asthma-related models. The role of miR-139-5p and its regulatory effects on the Notch1-GATA3 pathway in asthma exacerbation induced by acute PM2.5 exposure has not been elucidated. We hypothesize that acute PM2.5 exposure induces asthma exacerbation by regulating the expression of miR-139-5p and activating the Notch1-GATA3 pathway. Methods: We first employed Diseased Human Bronchial Epithelial Cells-Asthma cells to establish an in vitro model of acute exposure to PM2.5, and explored the relationship between the different concentrations and durations of acute PM2.5 exposure and the activation of Notch1-GATA3 pathway. We investigated the protein and mRNA expression changes of Notch1, upstream Jagged1, downstream GATA3, as well as the regulatory effect of miR-139-5p involved in it. Results: The miR-139-5p expression increased within 24 h of PM2.5 exposure. However, if PM2.5 exposure was sustained, miR-139-5p expression turned to decrease, accompanied by upregulations of the mRNA and protein expression of Notch1-GATA3 pathway. Overexpression of miR-139-5p blocked Notch1-GATA3 pathway activation induced by acute PM2.5 exposure. Conclusion: Acute PM2.5 exposure can activate Notch1-GATA3 pathway in asthma bronchial epithelial cells model, which might be involved in PM2.5-induced asthma exacerbation. miR-139-5p has a potential protective role of inhibiting PM2.5-induced asthma airway inflammation by targeting Notch1. [ABSTRACT FROM AUTHOR]

It has been hypothesized that air pollution can increase an individual's susceptibility to COVID-19. Our study sought to investigate if short-term exposure to a high average level of Air Quality Index (AQI), ozone (O3), particulate matter (PM2.5, PM10), sulfur dioxide (SO2), carbon monoxide (CO), and nitrogen dioxide (NO2) are risk factors for death from COVID-19. We conducted an unmatched case-control study to compare the risk of mortality among reported COVID-19 cases within metropolitan statistical areas in Indiana from March 31, 2020, to December 31, 2020 (N = 53,459). Air pollution concentration data at the county level were retrieved from the U.S. Environmental Protection Agency. Pollutant concentrations for the 90 days before disease development were averaged. Data were analyzed using stepwise logistic regression accounting for median air temperature, race, ethnicity, and preexisting conditions as confounders. At the population level, individuals who were exposed to a greater average of PM2.5 in the 90 days before the development of COVID-19 had an increased risk of death: OR = 2.16, 95% confidence interval (CI) [1.12, 18.57]. Individuals with chronic lung disease had an increased risk of death in relation to PM10: OR = 2.72, 95% CI [1.15, 6.43]. Short-term exposure to particulate matter may serve as a risk factor for COVID-19 mortality. [ABSTRACT FROM AUTHOR]

Introduction The effects of smoking on lung function among post-9/11 Veterans deployed to environments with high levels of ambient particulate matter are incompletely understood. Materials and Methods We analyzed interim data (04/2018-03/2020) from the Veterans Affairs (VA) Cooperative Studies Program #595, "Service and Health Among Deployed Veterans". Veterans with ≥1 land-based deployments enrolled at 1 of 6 regional Veterans Affairs sites completed questionnaires and spirometry. Multivariable linear regression models assessed associations between cigarette smoking (cumulative, deployment-related and non-deployment-related) with pulmonary function. Results Among 1,836 participants (mean age 40.7 ± 9.6, 88.6% male), 44.8% (n  = 822) were ever-smokers (mean age 39.5 ± 9.5; 91.2% male). Among ever-smokers, 86% (n  = 710) initiated smoking before deployment, while 11% (n  = 90) initiated smoking during deployment(s). Smoking intensity was 50% greater during deployment than other periods (0.75 versus 0.50 packs-per-day; P  < .05), and those with multiple deployments (40.4%) were more likely to smoke during deployment relative to those with single deployments (82% versus 74%). Total cumulative pack-years (median [IQR] = 3.8 [1, 10]) was inversely associated with post-bronchodilator FEV1%-predicted (−0.82; [95% CI] = [−1.25, −0.50] %-predicted per 4 pack-years) and FEV1/FVC%-predicted (−0.54; [95% CI] = [−0.78, −0.43] %-predicted per 4 pack-years). Deployment-related pack-years demonstrated similar point estimates of associations with FEV1%-predicted (−0.61; [95% CI] = [−2.28, 1.09]) and FEV1/FVC%-predicted (−1.09; [95% CI] = [−2.52, 0.50]) as non-deployment-related pack-years (−0.83; [95% CI] = [−1.26, −0.50] for FEV1%-predicted; −0.52; [95% CI] = [−0.73, −0.36] for FEV1/FVC%-predicted). Conclusions Although cumulative pack-years smoking was modest in this cohort, an inverse association with pulmonary function was detectable. Deployment-related pack-years had a similar association with pulmonary function compared to non-deployment-related pack-years. [ABSTRACT FROM AUTHOR]

A study was carried out to evaluate phytodiversity along with the metal accumulation potential of native plants growing in the vicinity of a thermal power plant (TPP). We documented 26 tree species, six shrubs, and 35 herbs. Importance value index (IVI), which measures the extent to which a species dominates in an area, was found highest for Senna siamea (95.7) followed by Tectona grandis (56.5), and Pithecellobium dulce (19.6). Soil was acidic (pH 5.4) in nature with higher concentrations of Al and Fe. The pH of ground water was found acidic while pH of nearby river was found slightly alkaline. Values of PM2.5 and PM10 were slightly higher than NAAQS standards for industrial areas. The concentration of metals was found higher in aquatic plants than in terrestrial plants. In general, herbs and shrubs showed more metal accumulation potential than trees. Our results suggest that Senna siamea could be used for revegetation purposes in FA landfills. Further, terrestrial and aquatic plants such as Ageratina adenophora and Stuckenia pectinata could be used for reclamation of Mn, Zn, Al, and Fe from contaminated soils. Hydrilla verticillata (Ni and Mn), Nelumbo nucifera, and Ipomoea aquatica (Cr) can be used for metal removal from contaminated water. Novelty statement: The study focuses on the assessment of phytodiversity, soil and water analysis, ambient air quality, and bioaccumulation of heavy metals in plants growing in and around a thermal power plant. The study assumes significance as more than 65% of India's electricity generation is still by coal-fired power plants, having major implications for air, soil, and water pollution. By selecting native plant species adapted to the region, we can enhance biodiversity, restore habitats, and contribute to the overall ecological health of the area surrounding the power plant. [ABSTRACT FROM AUTHOR]

In this study, the possibility of using rubber waste particles (RWP) as a substitute for fine aggregate type in mortar, which can provide valuable results in reducing both natural resource consumption and environmental pollution, was evaluated in terms of engineering properties. Due to the dimensional proximity of RWP and fine aggregate and the physical properties of RWP, substitution of these two materials was used in this study. In the mortar produced in this study, 4 different mixtures were produced in which RWP was substituted with fine aggregate and sand at 0%, 5%, 7.5%, and 10% by volume. The binder dosage was kept constant at 550 kg/m3 and the water/cement ratio was 0.532. The changes in the mechanical properties (flexural tensile strength, compressive strength, and stress-strain) of the mixtures were evaluated after freeze-thaw cycles, a natural environmental effect. Prism specimens were subjected to compressive and tensile strength tests after 25, 50, 100, and 200 freeze-thaw (FT)-cycles, while the change in stress-strain behavior was studied on cube specimens after FT-cycles. The results showed that the losses in compressive and flexural tensile strength were in the range of 8%–27% and 5%–49%, respectively. Moreover, the load-displacement behavior varies with varying compressive strengths after different number of cycles. [ABSTRACT FROM AUTHOR]

A milled recycled asphalt pavement (RAP) particle can be a cluster of one or more aggregates coated with an aged RAP binder. While RAP material is added to virgin aggregates and binder in a pugmill, the RAP cluster undergoes dissociation or agglomeration, depending on the cluster size and thermo-physical conditions inside the pugmill. The degree of dissociation or agglomeration of RAP material has an important relation with the degree of RAP binder availability. The RAP binder availability in mix design depends on the exposed surface area of dissociated coarse RAP particles and also on the agglomeration tendency of fine RAP particles. In the present study, the degree of RAP binder availability (DoAv), cluster dissociation of course RAP, and agglomeration tendency of fine RAP particles were examined at different mixing durations inside an asphalt pugmill—60 s, 120 s, and 180 s. The study examined whether the RAP cluster dissociation and postmixing agglomeration has any effect on the RAP binder availability. The degree of RAP binder availability of RAP mix was found by determining the virgin binder requirement of RAP mixes in excess of optimum binder content determined for the control mix prepared using virgin aggregates. Cluster dissociation and agglomeration was studied by hot mixing of RAP fractions in a pugmill with abrasive charges, followed by sieving. The statistical analysis of data found that RAP mixes incorporating fractionated fine RAP material exhibited higher DoAv at every mixing duration. For mixes incorporating fractionated coarse RAP, cluster dissociation index was positively correlated with DoAv, which implied that RAP cluster dissociation is a possible reason for RAP binder availability. In mixes incorporating fractionated fine RAP fractions, the RAP particles got agglomerated. The agglomeration index was found to correlate well with RAP binder availability, thereby establishing that agglomeration tendency in fine RAP fractions can be considered as an indicator of RAP binder availability. [ABSTRACT FROM AUTHOR]

As a result of firing pulverized coal in thermal power plants, enormous amounts of fly ash (FA) are produced as industrial waste. The release into the atmosphere and storage of this industrial waste remains one of the major environmental problems that threaten human health by contributing to air, water, and soil pollution. The recovery and reuse of FA in the construction industry is the only economic solution to the existing problem. In this study, the potential radiological risk caused by the usage of FA in concrete and cement production as a main component and its storage in landfill sites was evaluated for people and works by estimating radiological parameters (activity concentration and alpha index, annual effective doses, and the corresponding excess lifetime cancer risks) based on activity concentrations of terrestrial radionuclides in FA. Also, the radiological risk to the workers working in the FA landfill site was evaluated using the Residual Radioactivity Onsite 7.2 code. The average activity concentrations of terrestrial radionuclides in FA samples from the Tunçbilek lignite coal-fired thermal power plant at Kütahya province of Turkey were measured as 417, 156 and 454 Bq kg−1 for 226Ra, 232Th and 40K, respectively. When using up to 35% by mass of FA in cement and concrete, the average values of the radiological parameters revealed that they were within the recommended safety limits. However, code estimations showed that a regular worker in FA storage would be exposed to a total effective dose rate greater than 3 mSv y−1. [ABSTRACT FROM AUTHOR]

Respiratory virus infections are related to over 80% of childhood asthma exacerbations. They enhance pro-inflammatory mediator release, especially for sensitized individuals exposed to pollens/molds. Using a time-series study design, we investigated possible effect modification by respiratory virus infections of the associations between aeroallergens/PM2.5 and asthma exacerbation rates. Outpatient, emergency department (ED), and inpatient visits for asthma exacerbation among children with asthma (28,540/24,444 [warm/cold season]), as well as viral infection counts were obtained from electronic health records of the Children's Hospital of Philadelphia from 2011 to 2016. Rate ratios (RRs, 90th percentile vs. 0) for late-season grass pollen were 1.00 (0.85–1.17), 1.04 (0.95–1.15), and 1.12 (0.96–1.32), respectively, for respiratory syncytial virus (RSV) counts within each tertile. However, similar trends were not observed for weed pollens/molds or PM2.5. Overall, our study provides little evidence supporting effect modification by respiratory viral infections. [ABSTRACT FROM AUTHOR]