Effects Of PM2 Research Articles

Research on the Influence of Haze Weather on Audible Noise of HVDC Transmission Line

In order to study the influence of haze weather on audible noise of HVDC transmission line, a calculation model of ion flow field of HVDC transmission line considering the influence of haze is established, and then the relationship between different haze levels, different haze particle concentrations and audible noise is analyzed by taking the maximum potential gradient on the conductor surface as the intermediary. Then a ± 800kV DC transmission line is simulated and the results show that the audible noise will be more prominent with the increase of haze concentration, and the increment is more obvious at higher haze concentration; The charging of haze particles is the principal origin for the increase of audible noise, and the effect of PM2.5 is the most significant.

Air Quality Forecast using Convolutional Neural Network for Sustainable Development in Urban Environments

The expansion of IT based technology has widely gathered and enhanced all the eras of applicable domain to maintain the sustainable transformation. In fact, the new evolving technology has broadened its scope for sustainable environment exploiting diverse technological advancement utilizing future prediction modelling. Moreover, smart cities are grounded on the concept of prioritizing development goal discussed among all the nations, the significance sustainable areas are subjected on air, water and energy. Hence, current study of approach relies specifically on atmospheric pollutants which arise due to industrial or high-powered transport emission. The aim of the study, was to utilize the CNN model on the air quality dataset to detect patterns for future prediction modelling. The proposed study, is implemented on two phases where the first phase focuses on preprocessing and data analysis, whereas the Second phase is used for the purpose of testing the model accuracy where the data has been classified on accurate models. The overall model is implemented using Python programming and scripting language. Further, the inclusive result analysis were implemented and gathered to discover the highest level of CO, SO2 and NO2 levels in past five years among the different cities of India from 2015-2020. The cities with highest level of air pollutants and PM2.5 and PM10 effects on the overall Indian cities. Nonetheless, the accuracy of the model is measured to determine the applicability of algorithm.

Particulate Matter (PM10) Promotes Cell Invasion through Epithelial–Mesenchymal Transition (EMT) by TGF-β Activation in A549 Lung Cells

Air pollution presents a major environmental problem, inducing harmful effects on human health. Particulate matter of 10 μm or less in diameter (PM10) is considered an important risk factor in lung carcinogenesis. Epithelial–mesenchymal transition (EMT) is a regulatory program capable of inducing invasion and metastasis in cancer. In this study, we demonstrated that PM10 treatment induced phosphorylation of SMAD2/3 and upregulation of SMAD4. We also reported that PM10 increased the expression and protein levels of TGFB1 (TGF-β), as well as EMT markers SNAI1 (Snail), SNAI2 (Slug), ZEB1 (ZEB1), CDH2 (N-cadherin), ACTA2 (α-SMA), and VIM (vimentin) in the lung A549 cell line. Cell exposed to PM10 also showed a decrease in the expression of CDH1 (E-cadherin). We also demonstrated that expression levels of these EMT markers were reduced when cells are transfected with small interfering RNAs (siRNAs) against TGFB1. Interestingly, phosphorylation of SMAD2/3 and upregulation of SMAD induced by PM10 were not affected by transfection of TGFB1 siRNAs. Finally, cells treated with PM10 exhibited an increase in the capacity of invasiveness because of EMT induction. Our results provide new evidence regarding the effect of PM10 in EMT and the acquisition of an invasive phenotype, a hallmark necessary for lung cancer progression.

PM2.5 exposure increases the risk of preterm birth in pre-pregnancy impaired fasting glucose women: A cohort study in a Southern province of China

Previous studies have indicated maternal exposure to particles with aerodynamic diameter <2.5 μm (PM2.5) is associated with preterm birth (PTB). However, no study has investigated this effect in pre-pregnancy impaired fasting glucose (IFG) women. This study aimed to differentiate the effects of maternal PM2.5 exposure on PTB between pre-pregnancy IFG and normoglycemia women, and to further identify the susceptible window. This cohort study was conducted between January 2014 and December 2017 in 21 Chinese cities. All the recruited women received pre-pregnancy fasting serum glucose (FSG) tests and were followed up for their delivery outcomes. The PM2.5 exposures were estimated by the daily air pollution concentrations of the nearby monitors. Women with FSG below 7.0 mmol/L were included in the analysis. We employed the Cox proportional hazards models to examine whether PM2.5 exposure was associated with PTB. 237957 women were included and 7055 (3.0%) of them were pre-pregnancy IFG. During the entire pregnancy, we found 24.1% (HR = 1.241; 95% CI: 1.069, 1.439), 61.8% (HR = 1.618; 95% CI: 1.311, 1.997) and 18.6% (HR = 1.186; 95% CI: 1.004, 1.402) of increases in risk for all PTB, early PTB (20–33 gestational weeks) and late PTB (34–36 gestational weeks) among the pre-pregnancy IFG women, and 15.9% (HR = 1.159; 95% CI: 1.127, 1.192), 33.9% (HR = 1.339; 95% CI: 1.255, 1.430) and 13.2% (HR = 1.132; 95% CI: 1.098, 1.168) of increases in risk for all PTB, early PTB and late PTB among the normoglycemia women, with each 10 μg/m3 increment of PM2.5 exposure, respectively. Furthermore, PM2.5 exposure had the strongest effect on all PTB during trimester 1 (0–12 gestational weeks) among the pre-pregnancy IFG women, compared with the less strong effect during trimester 1 among the normoglycemia women. In conclusion, pre-pregnancy IFG increases the risk of PTB attributed to PM2.5, especially during trimester 1. Moreover, the effects of PM2.5 are greater on early PTB than late PTB for both pre-pregnancy IFG and normoglycemia women.

The impacts of continuous improvements in air quality on mortality in Beijing: A longitudinal comparative study

There has been increasing concern about the health effects of air pollution in China, and many measures have been implemented to control air pollution. To investigate the impacts of air quality improvement on mortality from non-accidental causes (NAD), cardiovascular disease (CD), and respiratory disease (RD), a longitudinal comparative study was conducted in Beijing. This study investigated the effects of air pollutants on outcomes across five periods (stages 1–5). Health effect data from stage1–5 (1990–2013) were obtained through a systematic literature search of studies published before 2021. Daily atmospheric pollutant, meteorological, and cause-specific death data were collected to determine the effects in stage 5 (2015–2017). Poisson generalized additive models were used to analyze the associations between short-term exposure to air pollutants and mortality. Random-effects meta-analysis models were used to estimate the pooled effects at each stage. The effects of changes in air quality were analyzed through a difference-in-differences approach. Our results indicate that the absolute change of concentrations of sulfur dioxide (SO2), nitrogen dioxide (NO2), and particulate matter with aerodynamic diameter≤ 10 μm (PM10) and≤ 2.5 μm (PM2.5) decreased by up to 42%, 10%, 33%, and 15% (stage 5), respectively. The effects of SO2 on deaths from CD and RD decreased by up to 2.76% and 1.43% (stage 3). The effects of NO2 on mortality from NAD, CD, and RD decreased by up to 0.39%, 0.74%, and 0.37% (stage 5). The effects of PM10 on death decreased by up to 0.11% (stage 3). The effects of PM2.5 on deaths from CD and RD decreased by up to 0.33% and 0.13% (stage 5). The results indicate that continued improvements in air quality have reduced the acute impact of air pollutants on population health.

Association between exposure to air pollutants and the risk of hospitalization for pulmonary embolism in Beijing, China: A case-crossover design using a distributed lag nonlinear model

BackgroundPulmonary embolism (PE) is a life-threatening condition. Few studies have evaluated the relationship between air pollution and PE, and these results have been inconsistent. Therefore, our study aimed to investigate the association between air pollutant exposure and the risk of hospitalization due to PE. Materials and methodsDaily PE admissions, meteorological data, and ambient pollution data from January 1, 2015, to December 31, 2018, were collected in Beijing. A quasi-Poisson regression model combined with time-stratified case-crossover design and a distributed lag nonlinear model was used to determine the effect of air pollutant exposure on PE admission. To examine the stability of air pollutants' effects, multi-pollutant analyses were performed. Stratified analyses by age and sex were further conducted. ResultsThere were 5060 PE admissions during the study period, with an estimated incidence of 6.5 per 100,000. PM2.5, PM10, SO2, O3 and CO exposures were significantly associated with elevated risk of PE hospitalization. The highest cumulative risks were observed at a lag of 0–28 days for PM2.5 (relative risk [RR] = 1.056, 95% confidence intervals [CI]: 1.015–1.098), PM10 (RR = 1.042, 95%CI: 1.010–1.075), and CO (RR = 1.466, 95%CI: 1.127–1.906), at a lag of 0–27 days for SO2 (RR = 1.674, 95%CI: 1.200–2.335), and at a lag of 0–4 days for O3 (RR = 1.019, 95%CI: 1.001–1.038). All associations mentioned above except O3 remained significant in multi-pollutant models. Stratified analyses showed that women and those aged ≥65 years people were more sensitive to PM10 and CO exposure than men and those aged <65 years. The effect of PM2.5 exposure was statistically significant in all subgroups. ConclusionsExposure to PM2.5, PM10, SO2, and CO showed a positive association with PE hospitalization. High-risk PE groups should take special precautions on days with poor air quality.

Long-term exposure to PM2.5 and cardiovascular disease incidence and mortality in an Eastern Mediterranean country: findings based on a 15-year cohort study

BackgroundEvidence concerning the impact of long-term exposure to fine Particulate Matter ≤2.5 μm (PM2.5) on Cardio-Vascular Diseases (CVDs) for those people subject to ambient air pollution in developing countries remains relatively scant. This study assessed the relationship of 15-year PM2.5 exposure with cardiovascular incidence and mortality rate in Isfahan province, Iran.MethodsThe cohort comprised 3081 participants over 35 years old who were free of CVDs. They were selected through multi-stage cluster sampling in Isfahan, Iran. PM2.5 exposure was determined separately for each individual via satellite-based spatiotemporal estimates according to their residential addresses. In this context, CVD is defined as either fatal and non-fatal Acute Myocardial Infarctions (AMI) or stroke and sudden cardiac death. The incidence risk for CVD and the ensuing mortality was calculated based on the average PM2.5 exposure within a study period of 15 years using the Cox proportional hazards frailty model upon adjusting individual risk factors. The mean annual rate of PM2.5 and the follow-up data of each residential area were combined.ResultsMean three-year PM2·5 exposure for the cohort was measured at 45.28 μg/m3, ranging from 20.01 to 69.80 μg/m3. The median time period for conducting necessary follow-ups was 12.3 years for the whole population. Notably, 105 cardiovascular and 241 all-cause deaths occurred among 393,786 person-months (27 and 61 per 100,000 person-months, respectively). In well-adjusted models, 10 μg/m3 increase in PM2.5 corresponded to a 3% increase in the incidence rate of CVDs [0.95 CI = 1.016, 1.036] (in case of p = 0.000001 per 10 μg/m3 increase in PM2.5, the Hazard Ratio (HR) for AMI and Ischemic Heart Disease (IHD) was 1.031 [0.95 CI = 1.005, 1.057] and 1.028 [0.95 CI = 1.017, 1.039]), respectively. No consistent association was observed between PM2.5 concentration and fatal CVD (fatal AMI, fatal stroke, SCD (Sudden Cardiac Death)) and all-cause mortality.ConclusionsResults from analyses suggest that the effect of PM2.5 on cardiovascular disease occurrence was stronger in the case of older people, smokers, and those with high blood pressure and diabetes. The final results revealed that long-term exposure to ambient PM2.5 with high concentrations positively correlated with IHD incidence and its major subtypes, except for mortality. The outcome accentuates the need for better air quality in many countries.

Seasonal impact of air particulate matter on morbidity: Interaction effect assessment in a time-stratified case-crossover design

The present study aimed to explore the interaction effect between PM10 and season as well as temperature on hospital admissions (HAs) in a region in North East of Iran. Distributed lag non-linear model in a time-stratified case-crossover design with a fixed and disjointed window was used in order to assess the impact of PM10 on HAs. Two approaches were applied to assess the interaction effect between season and the pollutant named stratification and interaction term in the regression model. In addition, a bivariate response surface model in Generalized Additive Model (GAM) was used to explore the interaction effect between PM10 and weather parameters, in order to see whether the seasonal variation of the PM10 effect is explained by weather conditions or not. The existence of interaction effect between PM10 and season was supported by both approaches; it was evident that spring significantly shared a large proportion of the adverse impact of PM10 on HAs. However, the interactive effects of PM10 and mean temperature were less obvious in this study. The results showed that all people were at risk of HAs due to high levels of PM10, with a particularly more immediate impact on elderlies. The results of the interaction effect can help policymakers to address spring when any preventive interventions are developed in the region.

Ambient particulate matter exposure interacts with abdominal obesity to increase blood triglycerides

Abstract Background Blood lipids levels dysregulation represent potential mechanism intermediating the adverse cardiovascular effects of ambient particulate matter (PM) exposure. The present study aims to estimate the effect of particulate matter (PM10) exposure on blood lipid levels (TC, Total Cholesterol; HDL-C, High-Density Lipoprotein Cholesterol; LDL-C, Low-Density Lipoprotein Cholesterol; TG, Triglycerides) in the adult Portuguese mainland population and to assess the potential mediation and/or modification action of abdominal obesity on this effect. Methods We used data from 2390 participants of the 1st Portuguese Health Examination Survey (INSEF, 2015) with available data on blood lipids parameters and living within a 30km radius of an air quality monitoring station with available PM10 measurements. PM10 concentrations were acquired from the air quality monitoring network of the Portuguese Environment Agency. Generalized linear models were used to assess the effect of 1-year PM10 exposure on blood lipids values. An interaction term was introduced in the models to test the modification action of abdominal obesity. Results We found an association between long-term exposure to PM10 and non-fasting blood TG levels after adjustment for age, sex, education, occupation, lifestyles related variables and temperature but only in participants with abdominal obesity (1.84% TG increase per each 1 µg/m3 PM10 increment, 95% CI: 0.02%; 3.69%) which is well supported by the sensitivity analysis. Conclusions Our study demonstrate that even at low levels of exposure, long-term PM10 exposure interacts with abdominal obesity to increase blood TG levels. To the best of our knowledge, this is the first study showing the modification action of abdominal obesity regarding the PM10 effect on a blood lipid parameter. Our findings suggest that reducing both abdominal obesity prevalence and PM10 below current standards would result in additional health benefits for the population. Key messages Long-term PM10 exposure interacts with abdominal obesity to increase non-fasting blood triglycerides levels by about 2% per each 1 µg/m3 PM10 increase. Reducing both abdominal obesity prevalence and PM10 below current standards would result in additional health benefits for the population.

Exposure of particulate matter (PM10) induces neurodevelopmental toxicity in zebrafish embryos

Particulate matter with 10 μm or less in diameter (PM10) exposure is a major threat to health and environment around the world. Even though a number of clinical and experimental studies have focused on the cardiopulmonary effects of PM10, its impact on neurovascular development and the underlying toxicity is relatively less studied. The present study is therefore undertaken to evaluate the potential toxic effects of PM10 on neurodevelopment and the associated gene expression profiles in the zebrafish embryo/larvae. During 2017–2018, PM10 samples (24 h sampling, 180 sampling days) were collected in an urban downtown site of Jinan, Shandong province, China. To delineate the potential toxic effects of PM10 during neurodevelopment, zebrafish embryos/larvae were exposed to different concentrations viz., 25, 50, 100, 200, and 400 μg/mL of PM10 solution for 24–120 h post-fertilization (hpf) and the effects on the mortality, morphology, swimming behavior, electroencephalogram discharges, growth of dopaminergic neurons, neurovasculature development and gene expression profiles of dopaminergic and neurodevelopment-related genes using qRT-PCR were studied.A significant increase in the mortality rate and morphological abnormalities were observed in 200 μg/mL of the PM10 treated group at 120 hpf. High concentrations (≥100 μg/mL) of PM10 exposure reduced locomotor behavior, caused abnormal electroencephalogram discharges, degeneration of dopaminergic neurons, inhibition of neurovascular development, cerebral hemorrhage, and significant changes in the expression pattern of genes involved in dopaminergic pathway and neurodevelopment such as (th1, dat, drd1, drd2a, drd3, drd4b, syn2a, gap43, α1-tubulin, gfap, map2, elavl3, eno2, neurog1, sox2, shha, and mbp). Taken together, all these parameters collectively imply developmental neurotoxicity and dysfunction of the dopaminergic neurons which provides the first evidence of PM10-induced neurodevelopmental toxicity in the zebrafish embryo/larvae.

Time series analysis of short-term effects of particulate matter pollution on the circulatory system disease mortality risk in Lishui District, China.

Epidemiological evidence has shown a significant association between short-term exposure to air pollution and mortality risk for circulatory system diseases (CSD). However, informative insights on the significance and magnitude of its relationship in the process of government interventions on abating air pollution are still lacking, particularly in a burgeoning Chinese city. In this study, we conducted a time series study in Lishui District, Nanjing, to examine the effect of ambient particulate matter (PM), e.g., PM2.5 and PM10, on daily death counts of CSD which included cardiovascular disease (CVD), cerebrovascular disease (CEVD), and arteriosclerotic heart disease (ASHD) mortality from January 1, 2015, to December 31, 2019. The results revealed that each 10μg/m3 increase in PM2.5 and PM10 concentration at lag0 day was associated with an increase of 1.33% (95% confidence interval, 0.08%, 2.60%) and 1.12% (0.43%, 1.82%) in CSD mortality; 2.42% (0.44%, 4.43%) and 1.43% (0.32%, 2.55%) in CVD mortality; 1.20% (- 0.31%, 2.73%) and 1.21% (0.38%, 2.05%) in CEVD mortality; and 2.78% (0.00%, 5.62%) and 1.66% (0.14%, 3.21%) in ASHD mortality, respectively. For cumulative risk, the corresponding increase in daily mortality for the same change in PM2.5 concentration at lag03 day was significantly associated with 1.94% (0.23%, 3.68%), 3.17% (0.58%, 5.84%), 2.38% (0.17%, 4.63%), and 4.92% (1.18%, 8.81%) for CSD, CVD, CEVD, and ASHD, respectively. The exposure-response curves were approximately nonlinear over the entire exposure range of the PM concentrations. We also analyzed the effect modifications by season (warm or cold), age group (0-64years, 65-74years, or ≥ 75years), and sex (male or female). Although not statistically significant, stratified analysis showed greater vulnerability to PM exposure for cold season, population over 65years of age, and female group.

A nationwide study of air pollution from particulate matter and daily hospitalizations for respiratory diseases in Italy

Background/aimThe relationship between air pollution and respiratory morbidity has been widely addressed in urban and metropolitan areas but little is known about the effects in non-urban settings. Our aim was to assess the short-term effects of PM10 and PM2.5 on respiratory admissions in the whole country of Italy during 2006–2015. MethodsWe estimated daily PM concentrations at the municipality level using satellite data and spatiotemporal predictors. We collected daily counts of respiratory hospital admissions for each Italian municipality. We considered five different outcomes: all respiratory diseases, asthma, chronic obstructive pulmonary disease (COPD), lower and upper respiratory tract infections (LRTI and URTI). Meta-analysis of province-specific estimates obtained by time-series models, adjusting for temperature, humidity and other confounders, was applied to extrapolate national estimates for each outcome. At last, we tested for effect modification by sex, age, period, and urbanization score. Analyses for PM2.5 were restricted to 2013–2015 cause the goodness of fit of exposure estimation. ResultsA total of 4,154,887 respiratory admission were registered during 2006–2015, of which 29% for LRTI, 12% for COPD, 6% for URTI, and 3% for asthma. Daily mean PM10 and PM2.5 concentrations over the study period were 23.3 and 17 μg/m3, respectively. For each 10 μg/m3 increases in PM10 and PM2.5 at lag 0–5 days, we found excess risks of total respiratory diseases equal to 1.20% (95% confidence intervals, 0.92, 1.49) and 1.22% (0.76, 1.68), respectively. The effects for the specific diseases were similar, with the strongest ones for asthma and COPD. Higher effects were found in the elderly and in less urbanized areas. ConclusionsShort-term exposure to PM is harmful for the respiratory system throughout an entire country, especially in elderly patients. Strong effects can be found also in less urbanized areas.

A STUDY ON AMBIENT AIR POLLUTION AND HOSPITAL VISITS OF PATIENTS IN TERTIARY HOSPITAL AT NORTH CHENNAI – AN OBSERVATIONAL STUDY

BACKGROUND: Air pollution is an important environmental risk factor for human health. Evidence is mounting that ambient air pollution exposure is signicantly associated with respiratory diseases. Ambient air pollution, such as nitrogen dioxide (NO2), sulfur dioxide (SO2), and particulate matter (PM), is associated with mortality and morbidity induced by respiratory diseases. The relationship between air pollutants and respiratory hospital admissions has been reported both in developed countries and in developing countries. Other studies have shown an adverse effect of ambient air pollution exposure on morbidity and mortality, as well as on healthcare costs. AIM OF THE STUDY: To investigate the association between ambient air pollutant exposure and daily hospital admissions for respiratory diseases in both childrens and Adults. METHODOLOGY: The daily emergency hospital admissions for respiratory conditions in the north part of Chennai during 2019- 2020 were recorded. Daily counts of hospital admissions for total respiratory conditions (43 admissions day(-1)), acute respiratory infections including pneumonia (18 day(-1)), chronic obstructive pulmonary disease (COPD) (13 day(-1)), and asthma (4.5 day(-1)) among residents of all ages and among children (0-14 yrs) were analysed. The generalized additive models included spline smooth functions of the day of study, mean temperature, mean humidity, inuenza epidemics, and indicator variables for days of the week and holidays. Total respiratory admissions were signicantly associated with the same-day level of NO2 (2.5% increase per interquartile range (IQR) change, 22.3 microg x m(-3)) and CO (2.8% increase per IQR, 1.5 mg x m(-3)). RESULTS: The daily mean concentrations of pollutants across all studies were 65.2 µg/m3 for PM10, 45.8 µg/m3 for PM2.5, 27.7 µg/m3 for SO2, 35.0 µg/m3 forNO2and1698µg/m3for CO, and 81.1µg/m3for O3. For the single variable models, the linear effect of PM10, PM2.5, and PM1 was evaluated by adjusting for the inuence of temperature. The association between hospital admissions for respiratory disease and the level of particulate matter was statistically signicant at 0-3 daylag in females and overall. In males, no statistically signicant effect was found at lag 3 for PM10 or at lag2-3 for PM2.5 and PM1.The associations between PM2.5 and PM1, and risk of admission were no longer signicant at some lags after adjusting for NO2, SO2, CO, and O3 separately. No associations were found at lag 3 after adjusting for NO2 or at lag 2 and 3 after adjusting for O3. The effects of PM2.5 and PM1 were not changed after adjusting for CO but were weaker after adjusting for other air pollutants (NO2, SO2,and O3). CONCLUSION: The ndings of this study demonstrated that O3 was associated with an increased risk of respiratory-related admissions, especially for children &lt;5years old. The effect was stronger in the winter than in the summer with each increase of 10 µg/m3 of O3 in winter, the risk of admissions for respiratory diseases after 5 days of exposure increased by 6.2% (95% CI3.7% - 8.8%). No signicant association between O3 and hospital admissions for wheeze-associated disorders specically was observed in children.

Effect of PM2.5 on circulating inflammatory cells and microRNA expression in acute coronary syndrome

Abstract Background Air pollutants increase the risk of myocardial infarction. Air pollution-induced atherosclerotic plaque destabilization may be related to inflammation, but the specific inflammatory alterations remain unclear. Purpose The aim of this prospective study was to assess the inflammatory changes in circulating immune cells and microRNAs in patients with acute coronary syndrome related to short-term exposure to PM2.5. Methods We prospectively included all consecutive patients admitted between March 2017 and July 2018 with the diagnosis of acute coronary syndrome (STEMI, NSTEMI, unstable angina) and coronary angiography in the acute phase of the disease. We also included a control group of patients with stable angina. For each patient we collected air concentrations of PM2.5 from the closest meteorological station to the patient residence obtaining the previous 24-hour average before hospital admission. All patients underwent systematic circulating inflammatory cell analysis. A selection of patients underwent miRNAs analysis. Results A total of 261 patients were included. According to PM2.5 exposure, 31 patients were selected for miRNA analyses. STEMI patients exposed to PM2.5 showed a reduction of CD4+ regulatory T (Treg) cells (Figure 1A). In the microRNA assessment, PM2.5 exposure was associated with higher circulating levels of let-7f-5p, miR-223-3p, miR-423-3p, miR-197-3p, miR-335–5, miR-376c-3p and miR-501-3p. Regarding clinical presentation, PM2.5 exposure in STEMI and NSTEMI patients was associated with an increase of miR-let-7f-5p, whereas miR-423-3p and miR-146a-5p were increased only in STEMI patients (Figure 1B). Conclusions STEMI related to PM2.5 short-term exposure is associated to specific changes involving CD4+CD25+Foxp3+ Treg cells and miR-146a-5p. Funding Acknowledgement Type of funding sources: Other. Main funding source(s): Ministerio de Ciencia e Innovaciόn; Fundaciόn BBVA Equipos de Investigaciόn Científica 2018 and from Caixa Banking Foundation; Sociedad Espanola de Cardiologia; Ministerio de Ciencia, Innovaciόn y Universidades, Carlos III Institute of Health-Fondo de Investigaciόn Sanitaria; Comunidad de Madrid; Fondo Europeo de Desarrollo Regional

Particulate Matter Exposure and Allergic Rhinitis: The Role of Plasmatic Extracellular Vesicles and Bacterial Nasal Microbiome.

Particulate matter (PM) exposure is linked to the worsening of respiratory conditions, including allergic rhinitis (AR), as it can trigger nasal and systemic inflammation. To unveil the underlying molecular mechanisms, we investigated the effects of PM exposure on the release of plasmatic extracellular vesicles (EV) and on the complex cross-talk between the host and the nasal microbiome. To this aim, we evaluated the effects of PM10 and PM2.5 exposures on both the bacteria-derived-EV portion (bEV) and the host-derived EVs (hEV), as well as on bacterial nasal microbiome (bNM) features in 26 AR patients and 24 matched healthy subjects (HS). In addition, we assessed the role exerted by the bNM as a modifier of PM effects on the complex EV signaling network in the paradigmatic context of AR. We observed that PM exposure differently affected EV release and bNM composition in HS compared to AR, thus potentially contributing to the molecular mechanisms underlying AR. The obtained results represent the first step towards the understanding of the complex signaling network linking external stimuli, bNM composition, and the immune risponse.

Effects of ambient particulate matter (PM10) on prevalence of diabetes and fasting plasma glucose

Objective: To explore the effect of long-term exposure to ambient particulate matter (PM10) on the prevalence of diabetes and fasting plasma glucose (FPG). Methods: The subjects of the study were from the baseline population of "Jinchang Cohort", and 24 285 subjects were finally included after excluding incomplete home address information and diabetic diagnosis information. The demographic characteristics, lifestyle and health status of the survey subjects were collected through questionnaire, physical examination and laboratory tests. ArcGIS software was used to match the nearest environmental monitoring stations for each subject according to residential address. Two-year average concentrations of PM10 were calculated to estimate exposure level. The logistic regression and the multiple linear regression were conducted to assess the effects of ambient PM10 on the prevalence of diabetes and FPG. The restricted cubic spline was used to quantify the dose-response relationship. Stratified analysis and effect modification analysis were also performed. Results: The age of 24 285 participants was (49.32±8.60) years, and the BMI was (24.22±6.09) kg/m2. There were 13 950 (57.44%) males and 2 066 (8.51%) diabetic patients. After adjusting for confounders, for every 10 μg/m3 increase in the average PM10 concentration in the first two years of the survey, the prevalence of diabetes increased [OR (95%CI) =1.05 (1.01-1.09)]and the FPG level elevated [β (95%CI) = 0.061 (0.047-0.076) mmol/L]. The results of the restricted cubic spline analysis showed a nonlinear relationship between PM10 concentration and FPG level (P<0.001). Further subgroup analysis showed that female [OR (95%CI) =1.10 (1.03-1.18)], people over 50 years old [OR (95%CI) =1.06 (1.02-1.11) ], subjects with family history of diabetes [OR (95%CI) = 1.13 (1.04-1.23) ], and with hypertension [OR (95%CI) = 1.07 (1.02-1.12) ] had a stronger association between the prevalence of diabetes and PM10 exposure (all P interaction values were<0.05). The effects of PM10 on FPG were more significant in people older than 50 years[β (95%CI) = 0.080 (0.050-0.109) mmol/L], with family history of diabetes [β (95%CI) = 0.087 (0.036-0.137) mmol/L], and hypertension [β (95%CI) = 0.077 (0.046-0.108) mmol/L] (all P interaction values were<0.05). Conclusions: Long-term exposure to ambient PM10 increases the diabetes prevalence and FPG. People older than 50 years old, with family history of diabetes and hypertension could be more sensitive to the effects of PM10 exposure.

Incidence of osteoporosis and ambient air pollution in South Korea: a population-based retrospective cohort study

BackgroundThis study investigated the associations between exposure to ambient air pollutants and the incidence of osteoporosis using the Korean National Insurance Service–National Sample Cohort.MethodsThis nationwide, population-based, retrospective cohort study included 237,149 adults aged ≥40 years that did not have a diagnosis of osteoporosis at baseline between January 1, 2003, and December 31, 2015. Osteoporosis was defined as claim codes and prescriptions of bisphosphonates or selective estrogen receptor modulators at least twice annually. After matching values for PM10, NO2, CO, and SO2 during the 2002–2015 time period and PM2.5 in 2015 with residential areas, the incidence of osteoporosis was analyzed using a Cox proportional hazards regression model according to the quartile of average yearly concentrations of pollutants.ResultsOverall 22.2% of the study subjects, 52,601 (male: 5.6%, female: 37.6%) adults in total, were newly diagnosed with osteoporosis and treated. Exposure to PM10 was positively associated with incidence of osteoporosis (Q4: 1798 per 100,000 person-years vs. Q1: 1655 per 100,000 person-years). The adjusted hazard ratio (HR) with 95% confidence interval (CI) of Q4 in PM10 was 1.034 (1.009–1.062). The effect of PM10 on osteoporosis incidence was distinct in females (adjusted sub-HR: 1.065, 95% CI: 1.003–1.129), subjects aged < 65 years (adjusted sub-HR: 1.040, 95% CI: 1.010–1.072), and for residents in areas with low urbanization (adjusted sub-HR: 1.052, 95% CI: 1.019–1.087). However, there was no increase in osteoporosis based on exposure to NO2, CO, SO2, or PM2.5.ConclusionsLong-term exposure to PM10 was associated with newly diagnosed osteoporosis in Korean adults aged ≥40 years. This finding can aid in policy-making that is directed to control air pollution as a risk factor for bone health.

PM2.5 mediated alterations in the in vitro human granuloma and its effect on reactivation of mycobacteria.

Exposure to particulate matter pollutant PM2.5 diminishes the immune response to mycobacterial antigens relevant to contain the infection in the granuloma, thus leading to reactivation of latent bacilli. The present study was therefore designed based on the hypothesis that exposure to PM2.5 affects the granuloma formation and reactivation of latent mycobacterial bacilli contained in the granuloma. For the sampling of PM2.5, based on initial standardisations, Teflon filter was selected over the quartz filter. Two different approaches were used to study the effect of PM2.5 on the human PBMC granuloma formed by Mycobacterium bovis BCG at multiplicity of infection (MOI) 0.1. In the first approach, granuloma formed in the presence of PM2.5 was loosely packed and ill-defined with significant downregulation of dormancy-associated mycobacterial genes, upregulation of reactivation-associated rpfB gene along with a significant increase in TNFα level without any change in the bacterial load in terms of CFUs. In the second approach, preformed human PBMC granuloma using M. bovis BCG was treated with PM2.5 that resulted in the disruption of granuloma architecture along with downregulation of not only dormancy-associated genes but also reactivation-associated rpfB gene of mycobacterial bacilli recovered from granuloma. However, there was no significant change in the host cytokine levels. Therefore, it can be inferred that PM2.5 can modulate the granuloma formation in vitro as well as mycobacterial gene expression in the granuloma with a possible role in the reactivation of latent bacilli.

Particular matter influences the incidence of acute otitis media in children

Particulate matter (PM) is the main component of air pollution. Children are vulnerable to PM and acute otitis media (AOM), which is one of the most common diseases in children. However, studies on the relationship between AOM in children and PM are rare and their results are inconsistent. The aim of this study is to investigate the effect of PM on AOM in children on the basis of the Korea National Health Insurance service (NHIS) claims data. NHIS claim data from 2008 to 2015 was used to identify outpatient visits, antibiotic use to treat AOM, and demographic data. This data was combined with the data on PM2.5 (≤ 2.5 μm) and PM10 (≤ 10 μm according to its aerodynamic diameter) level extracted from air pollution data from Korean National Institute of Environmental Research for 16 administrative regions. The children with AOM were divided into three age groups (< 2, 2–4, 5–10 years). Generalized linear Poisson regression model was used to estimate the association between AOM and PM using daily counts of AOM and daily mean PM concentrations. It was adjusted to temperature, wind, humidity, season, year, age, and region. With an increase in PM2.5 of 10 μg/m3, the relative risk of OM increased by 4.5% in children under 2 years of age. The effect of PM2.5 was strongest influence on the day of exposure. The exposure to PM10 was related to the incidence of AOM on the day of exposure and the following seven days in all three age groups. The PM concentrations did not strongly affect either AOM duration or the use of antibiotics to cure AOM. The RR in the each lag day after exposure to PM10 was diverse according to the age groups. Regardless of PM size and children’s age, the PM levels are positively related to the incidence of AOM. Both PM2.5 and PM10 have the most adverse effects on children under 2 years of age and on the day of exposure.

MiR-582-3p participates in the regulation of biological behaviors of A549 cells by ambient PM2.5 exposure.

Ambient fine particulate matter (PM2.5) is one of the main environmental air pollutants that is closely related to the development of lung cancer, but the mechanisms are unclear. In this study, A549 cells were exposed to ambient PM2.5 to investigate the alterations of biological behaviors, and the possible role of miR-582-3p in the effects was further explored. The findings showed that PM2.5 exposure could significantly enhance the biological behaviors of A549 cells, and promote their epithelial-mesenchymal transition (EMT) transformation, especially at relatively low doses. Over-activation of Wnt/β-catenin signaling pathway and increased expression of miR-582-3p were also found in A549 cells after PM2.5 exposure. After the knockdown of miR-582-3p in A549 cells, the effects of PM2.5 on malignant biological behavior changes, EMT, and the activation of Wnt/β-catenin signaling pathway were all significantly alleviated. Furthermore, the inhibition of Wnt/β-catenin signaling pathway also inhibited the EMT process of A549 cells, which was rescued by the overexpression of miR-582-3p. Therefore, this study showed that ambient PM2.5 can upregulate the expression of miR-582-3p, consequently activate the Wnt/β-catenin signaling pathway, and thereby enhance EMT transformation and promote the malignant biological behaviors of A549 cells. These findings provide evidence for further research into the mechanisms by which exposure to PM2.5 in the environment promotes lung cancer.