Effects Of Particulate Matter Exposure Research Articles

Double trouble: combined cardiovascular effects of particulate matter exposure and coronavirus disease 2019.

The coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has rapidly grown into a pandemic. According to initial reports, the lungs were thought to be the primary target, but recent case studies have shown its reach can extend to other organs including the heart and blood vessels. The severity of cardiac complications of COVID-19 depends on multiple underlying factors, with air pollutant exposure being one of them, as reported by several recent studies. Airborne particulate matter (PM) attracts heightened attention due to its implication in various diseases, especially respiratory and cardiovascular diseases. Inhaled PM not only carries microorganisms inside the body but also elicits local and systemic inflammatory responses resulting in altering the host’s immunity and increasing susceptibility to infection. Previous and recent studies have documented that PM acts as a ‘carrier’ for the virus and aids in spreading viral infections. This review presents the mechanisms and effects of viral entry and how pollution can potentially modulate pathophysiological processes in the heart. We aimed to concisely summarize studies examining cardiovascular outcomes in COVID-19 patients and postulate on how PM can influence these outcomes. We have also reviewed evidence on the use of renin–angiotensin system inhibitors, namely angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, in patients with COVID-19. The interplay of pollution and SARS-CoV-2 is essential to understanding the effects of accentuated cardiovascular effects of COVID-19 and deserves in-depth experimental investigations.

Effects of particulate matter exposure on the transmissibility and case fatality rate of COVID-19: A Nationwide Ecological Study in China.

Effects of particulate matter exposure on the transmissibility and case fatality rate of COVID-19: A Nationwide Ecological Study in China.

Integrated metabolomics and lipidomics reveals high accumulation of polyunsaturated lysoglycerophospholipids in human lung fibroblasts exposed to fine particulate matter

Exposure to fine particulate matter (PM) comprising toxic compounds arising from air pollution is a major human health concern. It is linked to increased mortality and incidence of various lung diseases. However, the mechanisms underlying the toxic effects of PM on lung fibroblasts have not been fully explored. We used targeted quantitative metabolomics and lipidomics analysis along with cytotoxicity studies to comprehensively characterize the alterations in the metabolite profiles of human lung fibroblasts (HEL 299) upon exposure to PM2.5 and PM10. This exposure at 50 μg/mL for 72 h induced an abnormally high apoptotic response via triggering intracellular reactive oxygen species (ROS) production and mitochondrial dysfunction through an imbalance between pro- and anti-apoptotic signaling pathways. The cytotoxic effects of PM2.5 were more severe than those of PM10. Metabolomics and lipidomics analyses revealed that PM exposure triggered substantial changes in the cellular metabolite profile, which involved reduced mitochondria-related metabolites such as tricarboxylic acid (TCA) cycle intermediates, amino acids, and free fatty acids as well as increased lysoglycerophospholipids (LPLs) containing polyunsaturated fatty acids. The decrease in mitochondria-related metabolites suggested that PM exposure led to reduced TCA cycle capacity and energy production. Apoptotic and inflammatory responses as well as mitochondrial dysfunction were likely to be accelerated because of excessive accumulation of LPLs, contributing to the disruption of membrane rafts and Ca2+ homeostasis and causing increased mitochondrial ROS formation. These results provide valuable insights regarding the toxic effects of PM exposure. Our study also provides a new direction for research on PM exposure-related health disorders using different cell lines.

Characterization and cytoprotective properties of Sargassum natans fucoidan against urban aerosol-induced keratinocyte damage

The escalation of fine particulate matter (PM) air pollution has recently become a global concern. Evidence is fast accumulating on PM exposure-related skin damage. The present study explored the therapeutic potentials of fucoidan purified from Sargassum natans against damaging effects of PM exposure on human HaCaT keratinocytes. Fucoidan (SNF7) was purified from S. natans by an enzyme-assisted extraction and purified by anion exchange chromatography. SNF7 (≈50 kDa) was identified as a fucoidan containing 70.97% fucose and 36.41 ± 0.59% of sulfate. Treatment of fine dust from Beijing, China (CFD) increased intracellular ROS levels in HaCaT cells triggering DNA damage and apoptosis. Treatment of SNF7 dose-dependently attenuated CFD-induced surge of intracellular ROS levels in keratinocytes by increasing antioxidant defense enzymes. Moreover, SNF7 chelated metal ions Pb2+, Ba2+, Sr2+, Cu2+, Fe2+, and Ca2+ coming from CFD. The results substantiated the potential therapeutic effects of SNF7 against CFD-induced oxidative stress. Further studies could promote SNF7's use as an active ingredient in cosmetics.

Effect of Particulate Matter Exposure on Respiratory Health of e-Waste Workers at Agbogbloshie, Accra, Ghana.

Background: Direct and continuous exposure to particulate matter (PM), especially in occupational settings is known to impact negatively on respiratory health and lung function. Objective: To determine the association between concentrations of PM (2.5, 2.5–10 and 10 µm) in breathing zone and lung function of informal e-waste workers at Agbogbloshie. Methods: To evaluate lung function responses to PM (2.5, 2.5–10 and 10 µm), we conducted a longitudinal cohort study with three repeated measures among 207 participants comprising 142 healthy e-waste workers from Agbogbloshie scrapyard and 65 control participants from Madina-Zongo in Accra, Ghana from 2017–2018. Lung function parameters (FVC, FEV1, FEV1/FVC, PEF, and FEF 25-75) and PM (2.5, 2.5–10 and 10 µm) concentrations were measured, corresponding to prevailing seasonal variations. Socio-demographic data, respiratory exposures and lifestyle habits were determined using questionnaires. Random effects models were then used to examine the effects of PM (2.5, 2.5–10 and 10 µm) on lung function. Results: The median concentrations of PM (2.5, 2.5–10 and 10 µm) were all consistently above the WHO ambient air standards across the study waves. Small effect estimates per IQR of PM (2.5, 2.5–10 and 10 µm) on lung function parameters were observed even after adjustment for potential confounders. However, a 10 µg increase in PM (2.5, 2.5–10 and 10 µm) was associated with decreases in PEF and FEF 25–75 by 13.3% % [β = −3.133; 95% CI: −0.243, −0.022) and 26.6% [β = −0.266; 95% CI: −0.437, 0.094]. E-waste burning and a history of asthma significantly predicted a decrease in PEF by 14.2% [β = −0.142; 95% CI: −0.278, −0.008) and FEV1 by 35.8% [β = −0.358; 95% CI: −0.590, 0.125] among e-waste burners. Conclusions: Direct exposure of e-waste workers to PM predisposes to decline in lung function and risk for small airway diseases such as asthma and COPD.

Associations between prenatal exposure to fine particulate matter and birth weight and modifying effects of birth order related to a new baby boom: A prospective birth cohort study in Guangzhou, China

Abstract Although studies have assessed the associations between prenatal exposure with fine particulate matter (PM) with birth weight, few have investigated the effect of PM1 exposure and identified the susceptible exposure window. Additionally, a baby boom occurred after China implemented the universal two-child policy, but whether the effects of PM are modified by birth order remains unknown. The objective of this study was to estimate the effects of prenatal exposure to PM (PM2.5 and PM1) on birth weight, identify the susceptible exposure windows, and assess the modifying effect of birth order on the effects of PM exposure. All participants were selected from the Prenatal Environment and Offspring Health (PEOH) cohort conducted since 2016 in Guangzhou, China. A spatiotemporal land–use-regression (STLUR) model was used to estimate a pregnant woman's weekly PM2.5 exposure, and a generalized additive model (GAM) was used to estimate each PM1 exposure. A distributed lag non-linear model (DLNM) was applied to assess the exposure–lag-response associations between weekly PM exposure and birth weight. The sample included 4086 pregnant women. The results showed that maternal exposure to PM2.5 and PM1 during the 15th to 24th and 16th to 24th gestational weeks were associated with lower birth weight, the strongest association was observed in the 19th week, during which each 10 μg/m3 increment in PM2.5 and PM1 was associated with a 1.47 g (95% CI: 2.49 g, 0.44 g) and 1.58 g (95%CI: 2.74 g, 0.41 g) decrease in birth weight, respectively. Compared with the first-born neonates, greater effects of PM2.5 and PM1 exposure on birth weight were observed among the second-born neonates in the 15th to 21st and 15 h to 22nd gestational weeks. Further studies tracking the health of the second-born children are warranted because they may be more sensitive to environmental factors than the first-born children.

Sargassum horneri extract containing mojabanchromanol attenuates the particulate matter exacerbated allergic asthma through reduction of Th2 and Th17 response in mice

Airborne particulate matter (PM) has become a serious health issue causing pulmonary diseases such as asthma. Due to the side effects and non-specificity of conventional drugs, there is a need to develop natural-product-based alternative treatments. Sargassum horneri is a brown alga shown to have anti-oxidant, anti-inflammatory, and anti-allergic effects. Thus, we sought to determine whether ethanol extract of Sargassum horneri (SHE) mitigates the effect of PM exposure on asthma development. To establish a mouse model of asthma, BALB/c mice were sensitized with ovalbumin (OVA, 10 μg) and challenged with PM (5 mg/m3) for 7 days consecutively. SHE (200, 400 mg/kg), Prednisone (5 mg/kg), or PBS was daily administrated orally before PM exposure. SHE mitigated PM exacerbated dendritic cell activation. More importantly, SHE restrained Th2 polarization by attenuating transcription factors GATA3 and STAT5, which further mitigated the expression of Th2 cytokines interleukin (IL)-4, IL-5, and IL-13 in the lung homogenates of PM-exacerbated asthmatic mice. SHE further attenuated PM-exacerbated eosinophil infiltration in the lung, trachea, and BALF. In addition, SHE markedly mitigated the activation of mast cells and the IgE level in serum. Concomitantly, SHE further restrained the Th17 cell response in PM-exposed allergic mice through attenuating expression of transcription factors RORγT, STAT3 and expression of relevant effector cytokines IL-17a. This resulted in mitigated neutrophil infiltration in the lung. Taken together, SHE significantly suppressed PM-exacerbated hypersecretion of mucus in asthmatic mice. These results suggest that SHE has therapeutic potential for treating PM-exacerbated allergic asthma through concomitantly inhibiting Th2/Th17 responses.

Effects of particulate matter exposure on semen quality: A retrospective cohort study.

Particulate matter (PM) exposure is closely associated with male infertility. Even though an association between poor semen quality and PM exposure has been widely accepted, which and when the semen parameter could be affected are still controversial. The purpose of this study is to estimate the effects of PM exposure on semen quality in Huai'an, China. The study included 1955 men with 2073 semen samples between 2015 and 2017 with moderate to high exposure to air pollution in Huai'an, China. Three multivariable linear regression models were used to conduct exposure-response analyses for PM exposure and semen quality and to estimate the influence during different exposure periods by every 15 days period before ejaculation in all participants group and normal semen quality participants group. The average age of the observations was 28.9±5.4 old years and the average abstinence period was 4.2±1.5 days. The results showed high correlations between both PM2.5 and PM10 exposures throughout entire spermatogenesis and the declines of sperm count (β: -0.93, p<2×10-16 and β: -1.00, p<2×10-16), and sperm concentration (β: -1.00, p<2×10-16 and β: -1.06, p<2×10-16), and PM10 exposure decreased sperm total motility (β: -0.60, p=2.56×10-7), but not sperm progressive motility. Furthermore, PM2.5 exposure decreased sperm count and concentration during 15-75 lag days, and PM10 exposure showed significant association with sperm count and concentration during 0-75 lag days. PM2.5 and PM10 exposures during 45-59 lag days were both inversely associated with sperm total motility (all p value<0.05). The present study revealed that ambient PM exposure throughout spermatogenesis during a long period, especially at early and middle stage were adversely associated with semen quality, sperm count and sperm concentration in particular.

Short-term effects of particulate matter exposure on emergency room visits for cardiovascular disease in Lanzhou, China: a time series analysis.

Cardiovascular disease (CVD) has been the leading cause of death in China. Identifying the relationship between particulate matter (PM) and CVD in China is a significant challenge. In this study, daily CVD emergency room visit, environmental monitoring, and weather data from January 1, 2017, to December 31, 2018, in Lanzhou were collected. Generalized additive models (GAMs) were constructed to estimate the short-term effects of daily PM2.5, PMC, and PM10 concentrations on CVD emergency room visits with different lag structures after controlling for the influence of meteorological elements and gaseous pollutants. Stratified analyses were conducted according to age (≥ 65years and < 65years), sex (male and female), cold season (from November to April), and warm season (from May to October). The results showed that each 10μg/m3 increase in PM2.5 was associated with a 1.93% (95% CI 0.12-3.78%) increase in CVD emergency room visits at lag03, and no single lag model was statistically significant. The excess relative risks (ERRs) of PM10 and PMC were not statistically significant at any lag pattern. The exposure-response curves demonstrated a nonlinear upward trend for these three PM pollutants. When adjusting for other gaseous pollutants, such as NO2, SO2, CO, and O3, in the two-pollutant models, the associations between PM10 and PMC and CVD emergency room visits did not change compared with the single-pollutant models. The ERRs of PM2.5 were 1.67% (95% CI 0.03-3.34%) at lag02 after adjustment for NO2 and 1.65% (95% CI 0.02-3.30%) at lag02 after adjustment for SO2. The ERRs of PM2.5 were still statistically significant at lag03 when we adjusted for any one of the gaseous pollutants. Susceptibility to PM2.5 was increased in people aged < 65years, in males, and in the warm season. The findings are very important for local governments to develop environmental policies and strategies to reduce ambient PM2.5 levels.

Nasal Microbiota Modifies the Effects of Particulate Air Pollution on Plasma Extracellular Vesicles

Air pollution exposure has been linked to modifications of both extracellular vesicle (EV) concentration and nasal microbiota structure (NMB), which might act as the respiratory health gatekeeper. This study aimed to assess whether an unbalanced NMB could modify the effect of particulate matter (PM) exposure on plasmatic EV levels. Due to two different NMB taxonomical profiles characterized by a widely different relative abundance of the Moraxella genus, the enrolled population was stratified into Mor− (balanced NMB) and Mor+ (unbalanced NMB) groups (Moraxella genus’s cut-off ≤25% and >25%, respectively). EV features were assessed by nanoparticle tracking analysis (NTA) and flow-cytometry (FC). Multivariable analyses were applied on EV outcomes to evaluate a possible association between PM10 and PM2.5 and plasmatic EV levels. The Mor− group revealed positive associations between PM levels and plasmatic CD105+ EVs (GMR = 4.39 p = 0.02) as for total EV count (GMR = 1.92 p = 0.02). Conversely, the Mor+ group showed a negative association between exposure and EV outcomes (CD66+ GMR = 0.004 p = 0.01; EpCAM+ GMR = 0.005 p = 0.01). Our findings provide an insight regarding how a balanced NMB may help to counteract PM exposure effects in terms of plasmatic EV concentration. Further research is necessary to understand the relationship between the host and the NMB to disentangle the mechanism exerted by inhaled pollutants in modulating EVs and NMB.

The Effect of Particulate Matter Exposure on the Inflammatory Airway Response of Street Runners and Sedentary People

Physical exercise promotes many health benefits. However, its effects are not well known in a polluted environment. Thus, this study aimed to compare upper airway inflammatory responses between street runners and sedentary individuals. Twenty-eight volunteers were recruited: runners (n = 14) and sedentary individuals (n = 14), who lived and worked in the same metropolitan area of São Paulo, Brazil. Particulate matter (PM) levels were monitored ten weeks before winter (low PM levels) and ten weeks after the beginning of winter (high PM levels) [PM10 (p &lt; 0.0001) and PM2.5 (p &lt; 0.0001)]. The cytokines (TNF-α, IL-6, IL-10, and IL-17A) levels in the nasal lavage and fractional exhaled nitric oxide (FeNO) were taken at the beginning of the winter (baseline) and ten weeks afterwards (after ten weeks of high PM exposure). IL-6 concentration increased in both runners (p = 0.037) and sedentary individuals (p = 0.027) after high PM exposure compared to the baseline. IL-10 concentration increased in sedentary individuals (p = 0.037) while IL-17A levels were increased in runners (p = 0.001) after high PM exposure compared to the baseline. FeNO levels decreased in runners (p = 0.025) after high PM exposure compared to the baseline. Outdoor endurance training acts as an inducer of a differentiated immune response in the upper airways of runners compared to individuals with a sedentary lifestyle from the same community after elevated PM exposure.

Particulate matter exposure aggravates osteoarthritis severity.

Several diseases have been linked to particulate matter (PM) exposure. Outdoor activities, such as road running or jogging, are popular aerobic exercises due to few participatory limitations. Osteoarthritis (OA) is a progressive degenerative joint disease, usually observed at age 40, and not noticed before pain or diagnosis. Although exercise has health benefits, it is unclear whether outdoor jogging in higher PM (standard reference material 1649b, SRM 1649b) concentration environments could affect OA development or severity. Hence, a PM exposure monosodium iodoacetate (MIA)-induced OA animal jogged model was established for investigation. Results showed that high doses of PM (5 mg) significantly increased pro-inflammatory factors such as tumor necrosis factor α (TNF-α), interleukin (IL)-1β, and IL-6, and M1 macrophages in the lung region, also obtained in systemic IL-6 and TNF-α expressions in this MIA-OA rat model. Moreover, levels of osteocalcin, cartilage oligomeric matrix protein (COMP), and N-telopeptides of type I collagen were especially influenced in MIA+PM groups. Morphological and structural changes of the knee joint were detected by micro-computed tomography images (micro-CT) and immunohistochemistry. MIA + PM rats exhibited severe bone density decrease, cartilage wear, and structure damages, accompanied by lower levels of physical activity, than the sham group and groups receiving MIA or PM alone. The findings suggest that the severity of OA could be promoted by PM exposure with a PM concentration effect via systemic inflammatory mechanisms. To the best of our knowledge, this is the first study to provide direct effects of PM exposure on OA severity.

Exposure Beyond Mass

PDS 76: Source specific outdoor air pollution studies, Exhibition Hall (PDS), Ground floor, August 26, 2019, 4:30 PM - 5:30 PM Background: Most epidemiological studies of health effects of atmospheric particulate matter use conventional filter measurements. These measurements quantify total mass concentration but may oversimplify air pollution exposure estimates as they are blind to many critical physiochemical properties of atmospheric particles. These properties likely have larger exposure variability than particulate matter mass. Objectives: This study is designed to measure and predict the spatial variations of particulate matter exposure using state-of-the-art single-particle mass spectrometry to resolve detailed physicochemical properties, namely number, size, source and chemical mixing state of individual particles in a populous urban area to study their population exposure variability and the contrasts with mass exposure. Methods: We performed mobile sampling using an advanced single-particle mass spectrometer to measure the within-city variability of number concentration of source-resolved 50 – 1000 nm particles and particle mixing state in Pittsburgh, PA, USA. We built land use regression (LUR) models to estimate their spatial patterns. We coupled demographic data to estimate population exposure. Results: Particle number concentration has a much larger spatial variability (factor of ~5) than mass concentration (factor of 2) within the city. Fresh primary particles emitted from traffic and cooking drive the exposure variability on the number concentration basis, but the mass exposure is dominated by aged background particles composed of secondary material. In addition, we show that people exposed to elevated number concentrations of atmospheric particles are also exposed to more externally mixed, primary particles. Conclusions: There is a large intra-city spatial heterogeneity of exposure to traffic and cooking particles on the number basis. Such heterogeneity is not captured by conventional mass exposure measurements. In addition, the resulting strong spatial patterns of particle chemical mixing state may potentially be significant when evaluating health effects of particulate matter exposure.

A keratinocyte and integrated fibroblast culture model for studying particulate matter-induced skin lesions and therapeutic intervention of fucosterol

Increased levels of particulate matter (PM) air pollutants in East Asia have resulted in detrimental health impacts increasing morbidity and mortality. Epidemiological studies suggest a possible relation between the cutaneous exposure of PM and increased oxidative stress and inflammation which lead to skin lesions. The present study utilizes an integrated cell culture model of keratinocytes and fibroblasts to mimic viable skin layers and investigate the possible effects of PM exposure after penetration through corneocytes. The skin perfection is upheld by homeostatic functionality of epidermal cells and the integrity of connective tissues. Exposure to xenobiotics could alter the skin cell homeostasis aggravating premature skin aging. Stimulation of HaCaT keratinocytes by PM collected from Beijing, China (CPM) increased the intracellular ROS levels triggering a cascade of events aggravating inflammatory responses and connective tissue degradation. In HDF fibroblasts, treatment with preconditioned keratinocyte culture media augmented inflammatory responses, cellular differentiation, and connective tissue degradation. Above events were marked by the increased intracellular ROS, inflammatory mediators, pro-inflammatory cytokines, matrix metalloproteinases (MMP)-1 and -2 levels, collagenase, and elastase activity. Fucosterol treatment of keratinocytes dose-dependently attenuated the detrimental effects both in keratinocytes and fibroblasts restoring the conditions near to physiological levels. Further evaluations could be advanced on developing fucosterol, in forms such as rejuvenating cosmeceuticals which could attenuate detrimental responses of CPM exposure.

Out-of-hospital cardiac arrests in a large metropolitan area: synergistic effect of exposure to air particulates and high temperature.

Air pollution and climate change are intrinsically linked to emerging hazards for global health. High air particulate matter (PM) levels may trigger out-of-hospital cardiac arrest (OHCA). High temperature could act synergistically with PM in determining OHCA. The aim of the present study was to investigate the effect of PM exposure alone, and in combination with temperature, on the risk of OHCA, in a large European metropolitan area with population >4 million. We evaluated the association between short-term PM exposure, temperature, and the risk of OHCA over a two-year study period, allowing us to investigate 5761 events using a time-stratified case-crossover design combined with a distributed lag non-linear model. Higher risk of OHCA was associated with short-term exposure to PM10. The strongest association was experienced three days before the cardiac event where the estimated change in risk was 1.70% (0.48-2.93%) per 10 µg/m3 of PM. The cumulative exposure risk over the lags 0-6 was 8.5% (0.0-17.9%). We observed a joint effect of PM and temperature in triggering cardiac arrests, with a maximum effect of 14.9% (10.0-20.0%) increase, for high levels of PM before the cardiac event, in the presence of high temperature. The present study helps to clarify the controversial role of PM as OHCA determinant. It also highlights the role of increased temperature as a key factor in triggering cardiac events. This evidence suggests that tackling both air pollution and climate change might have a relevant impact in terms of public health.

Carnosine Supplementation Mitigates the Deleterious Effects of Particulate Matter Exposure in Mice.

BackgroundExposure to fine airborne particulate matter (PM 2.5) induces quantitative and qualitative defects in bone marrow–derived endothelial progenitor cells of mice, and similar outcomes in humans may contribute to vascular dysfunction and the cardiovascular morbidity and mortality associated with PM 2.5 exposure. Nevertheless, mechanisms underlying the pervasive effects of PM 2.5 are unclear and effective interventional strategies to mitigate against PM 2.5 toxicity are lacking. Furthermore, whether PM 2.5 exposure affects other types of bone marrow stem cells leading to additional hematological or immunological dysfunction is not clear.Methods and ResultsMice given normal drinking water or that supplemented with carnosine, a naturally occurring, nucleophilic di‐peptide that binds reactive aldehydes, were exposed to filtered air or concentrated ambient particles. Mice drinking normal water and exposed to concentrated ambient particles demonstrated a depletion of bone marrow hematopoietic stem cells but no change in mesenchymal stem cells. However, HSC depletion was significantly attenuated when the mice were placed on drinking water containing carnosine. Carnosine supplementation also increased the levels of carnosine‐propanal conjugates in the urine of CAPs–exposed mice and prevented the concentrated ambient particles–induced dysfunction of endothelial progenitor cells as assessed by in vitro and in vivo assays.ConclusionsThese results suggest that exposure to PM 2.5 has pervasive effects on different bone marrow stem cell populations and that PM 2.5‐induced hematopoietic stem cells depletion, endothelial progenitor cell dysfunction, and defects in vascular repair can be mitigated by excess carnosine. Carnosine supplementation may be a viable approach for preventing PM 2.5‐induced immune dysfunction and cardiovascular injury in humans.

Effects of particulate matter (PM) on childhood asthma exacerbation and control in Xiamen, China

BackgroundThe short-term effects of particulate matter (PM) exposure on childhood asthma exacerbation and disease control rate is not thoroughly assessed in Chinese population yet. The previous toxic effects of PM exposure are either based on long-term survey or experimental data from cell lines or mouse models, which also needs to be validated by real-world evidences.MethodsWe evaluated the short-term effects of PM exposure on asthma exacerbation in a Chinese population of 3106 pediatric outpatientsand disease control rate (DCR) in a population of 3344 children using case-crossover design. All the subjects enrolled are non-hospitalized outpatients. All data for this study were collected from the electronic health record (EHR) in the period between January 1, 2016 and June 30, 2018 in Xiamen, China.ResultsWe found that exposure to PM2.5 and PM10 within the past two weeks was significantly associated with elevated risk of exacerbation (OR = 1.049, p < 0.001 for PM2.5and OR = 1.027, p < 0.001 for PM10). In addition, exposure to PM10 was associated with decreased DCR (OR = 0.976 for PM10, p < 0.001).ConclusionsOur results suggest that exposure to both PM10 and PM2.5 has significant short-term effects on childhood asthma exacerbation and DCR, which serves as useful epidemiological parameters for clinical management of asthma risk in the sensitive population.

Metabolic Syndrome and Air Pollution: A Narrative Review of Their Cardiopulmonary Effects.

Particulate matter (PM) exposure and metabolic syndrome (MetSyn) are both significant global health burdens. PM exposure has been implicated in the pathogenesis of MetSyn and cardiopulmonary diseases. Individuals with pre-existing MetSyn may be more susceptible to the detrimental effects of PM exposure. Our aim was to provide a narrative review of MetSyn/PM-induced systemic inflammation in cardiopulmonary disease, with a focus on prior studies of the World Trade Center (WTC)-exposed Fire Department of New York (FDNY). We included studies (1) published within the last 16-years; (2) described the epidemiology of MetSyn, obstructive airway disease (OAD), and vascular disease in PM-exposed individuals; (3) detailed the known mechanisms of PM-induced inflammation, MetSyn and cardiopulmonary disease; and (4) focused on the effects of PM exposure in WTC-exposed FDNY firefighters. Several investigations support that inhalation of PM elicits pulmonary and systemic inflammation resulting in MetSyn and cardiopulmonary disease. Furthermore, individuals with these preexisting conditions are more sensitive to PM exposure-related inflammation, which can exacerbate their conditions and increase their risk for hospitalization and chronic disease. Mechanistic research is required to elucidate biologically plausible therapeutic targets of MetSyn- and PM-induced cardiopulmonary disease.

Long-term exposure to air pollution raises circulating levels of proprotein convertase subtilisin/kexin type 9 in obese individuals.

Exposure to airborne particulate matter has been consistently associated with early death and increased morbidity, particularly raising the risk of cardiovascular disease. Obesity, one of the leading cardiovascular disease risk factors, increases susceptibility to the adverse effects of particulate matter exposure. Proprotein convertase subtilisin/kexin type 9 has been related to a large number of cardiovascular risk factors, e.g. atherogenic lipoproteins, arterial stiffness and platelet activation. Thus, the present study was aimed at evaluating, in a series of obese individuals, the effects of particulate matter less than 10 µm in diameter (PM10) on proprotein convertase subtilisin/kexin type 9 circulating levels. In 500 obese subjects, participating in the cross-sectional Susceptibility to Particle Health Effects, miRNAs and Exosomes (SPHERE) study, we evaluated the effects of long- and short-term PM10 exposure on circulating proprotein convertase subtilisin/kexin type 9 levels. In the studied individuals (body mass index: 33.3 ± 5.2 kg/m2) with an annual average PM10 exposure of 40.12 ± 4.71 µg/m3, proprotein convertase subtilisin/kexin type 9 levels were 248.7 ± 78.6 ng/mL. In univariate analysis, PM10 exposure (annual average) was associated with proprotein convertase subtilisin/kexin type 9 levels (β=1.83, standard error = 0.75, p = 0.014). Interestingly, in a multivariable linear regression model, this association was observed only for carriers of lower concentrations of interferon-γ, whereas it was lost in the presence of higher interferon-γ levels. Proprotein convertase subtilisin/kexin type 9 levels were positively associated with the Framingham Risk Score, which was raised by 15.8% for each 100 ng/ml rise of proprotein convertase subtilisin/kexin type 9. In obese individuals, more sensitive to the damaging effects of environmental air pollution, PM10 exposure positively associates with proprotein convertase subtilisin/kexin type 9 plasma levels especially in those with low levels of interferon-γ.

Particulate Matter Air Pollution: Effects on the Cardiovascular System.

Air pollution is a complex mixture of gaseous and particulate components, each of which has detrimental effects on human health. While the composition of air pollution varies greatly depending on the source, studies from across the world have consistently shown that air pollution is an important modifiable risk factor for significantly increased morbidity and mortality. Moreover, clinical studies have generally shown a greater impact of particulate matter (PM) air pollution on health than the gaseous components. PM has wide-ranging deleterious effects on human health, particularly on the cardiovascular system. Both acute and chronic exposure to PM air pollution is associated with increased risk of death from cardiovascular diseases including ischemic heart disease, heart failure, and ischemic/thrombotic stroke. Particulate matter has also been shown to be an important endocrine disrupter, contributing to the development of metabolic diseases such as obesity and diabetes mellitus, which themselves are risk factors for cardiovascular disease. While the epidemiological evidence for the deleterious effects of PM air pollution on health is increasingly accepted, newer studies are shedding light on the mechanisms by which PM exerts its toxic effects. A greater understanding of how PM exerts toxic effects on human health is required in order to prevent and minimize the deleterious health effects of this ubiquitous environmental hazard. Air pollution is a growing public health problem and mortality due to air pollution is expected to double by 2050. Here, we review the epidemiological evidence for the cardiovascular effects of PM exposure and discuss current understanding about the biological mechanisms, by which PM exerts toxic effects on cardiovascular system to induce cardiovascular disease.