Exacerbation Of Respiratory Diseases Research Articles

Yearly Assessment of Weather and Air Quality Impact on Respiratory Disease Hospitalizations: Faial Island (Azores) Study

Building upon our previous research conducted at weekly and monthly intervals, this study investigates the yearly dynamics of weather conditions and air quality on respiratory diseases, specifically tailored to Faial Island in the Azores. Expanding our analysis to a yearly basis allows for a more comprehensive understanding of long-term trends and seasonal variations in hospital admissions. Drawing upon extensive daily data spanning from 2008 to 2019, sourced from the Statistics Service of Hospital da Horta, the Meteorological Observatory Príncipe Alberto de Mónaco, and the Air Quality Monitoring Network of the Azores, we examined the differentiated relationships between yearly meteorological variables, such as temperature, dew point, and wind direction, and respiratory health outcomes. Additionally, we explored the persistent influence of air quality indicators, including suspended particulate matter with an aerodynamic diameter of 10 micrometers (µm) or less (PM10), sulfur dioxide (SO<sub>2)</sub>, nitrogen dioxide (NO<sub>2)</sub>, and ozone (O<sub>3</sub>), across different seasons and years. By incorporating yearly data into our analysis, this study aims to provide a comprehensive and nuanced understanding of the interplay between environmental factors and respiratory disease hospitalizations, thereby informing targeted interventions and public health strategies in insular regions. The principal component analysis (PCA) applied to the yearly data reveals interesting correlation patterns between meteorological variables and hospitalizations for respiratory diseases such as asthma, pneumonia, and rhinitis. Hospital admissions were found to increase during periods of lower temperatures and smaller temperature amplitudes, suggesting that prolonged cold conditions may exacerbate symptoms of these diseases. Additionally, atmospheric pollutant concentrations, such as suspended particles PM10, SO<sub>2</sub>, NO<sub>2</sub>, and O<sub>3</sub>, significantly varied across seasons, with a notable influence on the exacerbation of respiratory diseases. In insular regions like the Azores, these findings highlight the importance of targeted public health strategies to mitigate the impact of environmental factors on respiratory health.

The Association Between Periodontitis and Respiratory Diseases: A Comprehensive Review

Periodontal disease is a significant factor in periodontal destruction, primarily initiated by a multi-bacterial infection that progresses through a cascade of chronic inflammatory responses. This persistent inflammation not only affects periodontal tissues but also has systemic implications, heightening the risk of various systemic diseases. Among these, respiratory diseases—which are closely linked to inflammatory processes, are of particular concern. Conditions such as asthma, pneumonia, chronic obstructive pulmonary disease (COPD), and lung cancer have been increasingly associated with the chronic inflammatory state induced by periodontitis. The aim of this review was to elucidate the mechanisms underlying the association between periodontitis and respiratory diseases. Chronic periodontitis creates a state of systemic inflammation that can disseminate through the bloodstream, impacting distant organs, including the lungs. Emerging evidence from recent studies highlights the role of periodontitis in both the initiation and exacerbation of respiratory diseases. Microbial pathogens associated with periodontitis, such as Porphyromonas gingivalis, can be aspirated into the lower respiratory tract, leading to either direct infection or modulation of the local immune response. This can increase susceptibility to respiratory conditions such as pneumonia and exacerbate pre-existing diseases like COPD and asthma. In summary, the relationship between periodontitis and respiratory diseases is complex and multifaceted, involving direct microbial interactions, systemic inflammation, and immune modulation. Understanding these connections is crucial for developing integrated therapeutic strategies that address both oral and respiratory health.

Progranulin derivative attenuates lung neutrophilic infiltration from diesel exhaust particle exposure.

Air pollutants, such as diesel exhaust particles (DEPs), induce respiratory disease exacerbation with neutrophilic infiltration. Progranulin (PGRN), an epithelial cell and macrophage-derived secretory protein, is associated with neutrophilic inflammation. PGRN is digested into various derivatives at inflammatory sites and is involved in several inflammatory processes. PGRN and its derivatives likely regulate responses to DEP exposure in allergic airway inflammation. To investigate the role of PGRN and its derivatives in the regulation of responses to DEP exposure in allergic airway inflammation. A murine model of allergic airway inflammation was generated in PGRN-deficient mice, and they were simultaneously exposed to DEP followed by intranasal administration of full-length recombinant PGRN (PGRN-FL) and a PGRN-derived fragment (FBAC). Inflammatory status was evaluated by bronchoalveolar lavage fluid and histopathologic analyses. Human bronchial epithelial cells were stimulated with DEPs and house dust mites (HDMs), and the effect of FBAC treatment was evaluated by assessing various intracellular signaling molecules, autophagy markers, inflammatory cytokines, and intracellular oxidative stress. DEP exposure exaggerated neutrophilic inflammation, enhanced IL-6 and CXCL15 secretions, and increased oxidative stress in the murine model; this effect was greater in PGRN-deficient mice than in wild-type mice. The DEP-exposed mice with PGRN-FL treatment revealed no change in neutrophil infiltration and higher oxidative stress status in the lungs. On the contrary, FBAC administration inhibited neutrophilic infiltration and reduced oxidative stress. In human bronchial epithelial cells, DEP and HDM exposure increased intracellular oxidative stress and IL-6 and IL-8 secretion. Decreased nuclear factor erythroid 2-related factor 2 (Nrf2) expression and increased phosphor-p62 and LC3B expression were also observed. FBAC treatment attenuated oxidative stress from DEP and HDM exposure. FBAC reduced neutrophilic inflammation exaggerated by DEP exposure in a mouse model of allergic airway inflammation by reducing oxidative stress. PGRN and PGRN-derived proteins may be novel therapeutic agents in attenuating asthma exacerbation induced by air pollutant exposure.

The Interplay between Airway Cilia and Coronavirus Infection, Implications for Prevention and Control of Airway Viral Infections.

Coronaviruses (CoVs) are a class of respiratory viruses with the potential to cause severe respiratory diseases by infecting cells of the upper respiratory tract, bronchial epithelium, and lung. The airway cilia are distributed on the surface of respiratory epithelial cells, forming the first point of contact between the host and the inhaled coronaviruses. The function of the airway cilia is to oscillate and sense, thereby defending against and removing pathogens to maintain the cleanliness and patency of the respiratory tract. Following infection of the respiratory tract, coronaviruses exploit the cilia to invade and replicate in epithelial cells while also damaging the cilia to facilitate the spread and exacerbation of respiratory diseases. It is therefore imperative to investigate the interactions between coronaviruses and respiratory cilia, as well as to elucidate the functional mechanism of respiratory cilia following coronavirus invasion, in order to develop effective strategies for the prevention and treatment of respiratory viral infections. This review commences with an overview of the fundamental characteristics of airway cilia, and then, based on the interplay between airway cilia and coronavirus infection, we propose that ciliary protection and restoration may represent potential therapeutic approaches in emerging and re-emerging coronavirus pandemics.

Immunological Effects of Diesel Particles in a Murine Model of Healthy Mice.

Introduction: Exposure to environmental pollutants such as diesel exhaust particles (DEP) increases the risk of respiratory disease exacerbation. However, the possible effects of these particles on the general population remain poorly understood. The present study aimed to assess the immunomodulatory and inflammatory effects of the inhalation of DEP in a model of healthy mice undergoing short-, mid- and long-term exposure. Materials and Methods: BALB/c ByJ mice were randomly divided into five experimental groups. The control group received three intranasal instillations of saline over 8 days while the other four groups received intranasal instillations of 150 µg of DEP 3 days per week for 8, 17, 26, and 53 days. Lung function assessment and flow cytometry were performed. Results: In lung tissue, intranasal exposure to DEP decreased total monocytes (p < 0.015 in all groups). At 26 days, a reduction in inflammatory monocytes and an increase in resident monocytes were observed, p = 0.001 and 0.0001, respectively. Eosinophils and neutrophils decreased at 26 days (p = 0.017 and p = 0.041, respectively). The intranasal challenges of DEP increased the total population of dendritic cells (DC) at 26 and 53 days (p = 0.017 and p = 0.022, respectively) and decreased the total and alveolar populations of macrophages (p < 0.003 for all groups compared to control), while interstitial macrophage populations increased over the time period (p = 0.0001 for all groups compared to control). Conclusions: Continuous DEP exposure triggers immune mechanisms that predispose healthy individuals to a pro-inflammatory and hyper-reactive microenvironment. This mouse model provides evidence of the capacity of DEP to increase DC, interstitial macrophages, and resident monocytes.

Impact of indoor air pollution on DNA damage and chromosome stability: a systematic review.

Indoor air pollution is becoming a rising public health problem and is largely resulting from the burning of solid fuels and heating in households. Burning these fuels produces harmful compounds, such as particulate matter regarded as a major health risk, particularly affecting the onset and exacerbation of respiratory diseases. As exposure to polluted indoor air can cause DNA damage including DNA sd breaks as well as chromosomal damage, in this paper, we aim to provide an overview of the impact of indoor air pollution on DNA damage and genome stability by reviewing the scientific papers that have used the comet, micronucleus, and γ-H2AX assays. These methods are valuable tools in human biomonitoring and for studying the mechanisms of action of various pollutants, and are readily used for the assessment of primary DNA damage and genome instability induced by air pollutants by measuring different aspects of DNA and chromosomal damage. Based on our search, in selected studies (in vitro, animal models, and human biomonitoring), we found generally higher levels of DNA strand breaks and chromosomal damage due to indoor air pollutants compared to matched control or unexposed groups. In summary, our systematic review reveals the importance of the comet, micronucleus, and γ-H2AX assays as sensitive tools for the evaluation of DNA and genome damaging potential of different indoor air pollutants. Additionally, research in this particular direction is warranted since little is still known about the level of indoor air pollution in households or public buildings and its impact on genetic material. Future studies should focus on research investigating the possible impact of indoor air pollutants in complex mixtures on the genome and relate pollutants to possible health outcomes.

The Natural History of Severe Chronic Obstructive Pulmonary Disease: The SPOCCAT Study Protocol

IntroductionPatients with severe chronic obstructive pulmonary disease (COPD) are often underrepresented in cohorts, creating uncertainty about the natural history and prognostic factors of this subgroup. Our goal was to describe the SPOCCAT (Severe COPD: Prospective Observational study of COPD in Catalonia) study protocol. Material and methodsSPOCCAT is a non-interventional, multicenter, prospective cohort study of patients with severe COPD (FEV1% predicted<50%). The study aims to: (1) establish a five-year prospective cohort; (2) identify demographic and clinical characteristics; (3) describe treatment patterns; (4) better understand the natural history of severe COPD, including lung function decline, exacerbation rates, and mortality; and (5) identify prognostic factors for poor outcomes.Recruitment began in January 2024, and the cohort will be followed for a minimum of five years (or until death or lung transplant) with follow-up visits every 12 months. Baseline data include demographics, laboratory analyses, comorbidities, lung function, respiratory symptoms, respiratory disease exacerbations and etiology, quality of life, physical activity, chest computed tomography, and treatment. Annual follow-up visits will assess changes in treatment, exacerbation frequency and severity, microbiological outcomes, complementary tests, and mortality. Participation requires written informed consent from all patients, with data collected in an anonymized electronic Case Report Form. ResultsThe results of the SPOCCAT study will provide relevant information about the characteristics, treatment, and prognostic factors of severe COPD. ConclusionsSPOCCAT has the potential to enhance understanding of severe COPD, exploring innovative aspects and establishing a robust research framework for future COPD-related projects.

Preventive nasal administration of flagellin restores antimicrobial effect of gentamicin and protects against a multidrug-resistant strain of Pseudomonas aeruginosa.

The increasing prevalence of multidrug-resistant Pseudomonas aeruginosa (PA) is a significant concern for chronic respiratory disease exacerbations. Host-directed drugs, such as flagellin, an agonist of toll-like receptor 5 (TLR5), have emerged as a promising solution. In this study, we evaluated the prophylactic intranasal administration of flagellin against a multidrug-resistant strain of PA (PAMDR) in mice and assessed the possible synergy with the antibiotic gentamicin (GNT). The results indicated that flagellin treatment before infection decreased bacterial load in the lungs, likely due to an increase in neutrophil recruitment, and reduced signs of inflammation, including proinflammatory cytokines. The combination of flagellin and GNT showed a synergistic effect, decreasing even more the bacterial load and increasing mice survival rates, in comparison to mice pre-treated only with flagellin. These findings suggest that preventive nasal administration of flagellin could restore the effect of GNT against MDR strains of PA, paving the way for the use of flagellin in vulnerable patients with chronic respiratory diseases.

PCSK9 genetic variants and risk of vascular and non-vascular diseases in Chinese and UK populations.

Lowering low-density lipoprotein cholesterol (LDL-C) through PCSK9 inhibition represents a new therapeutic approach to preventing and treating cardiovascular disease (CVD). Phenome-wide analyses of PCSK9 genetic variants in large biobanks can help to identify unexpected effects of PCSK9 inhibition. In the prospective China Kadoorie Biobank, we constructed a genetic score using three variants at the PCSK9 locus associated with directly measured LDL-C [PCSK9 genetic score (PCSK9-GS)]. Logistic regression gave estimated odds ratios (ORs) for PCSK9-GS associations with CVD and non-CVD outcomes, scaled to 1 SD lower LDL-C. PCSK9-GS was associated with lower risks of carotid plaque [n = 8340 cases; OR = 0.61 (95% confidence interval: 0.45-0.83); P = 0.0015], major occlusive vascular events [n = 15 752; 0.80 (0.67-0.95); P = 0.011], and ischaemic stroke [n = 11 467; 0.80 (0.66-0.98); P = 0.029]. However, PCSK9-GS was also associated with higher risk of hospitalization with chronic obstructive pulmonary disease [COPD: n = 6836; 1.38 (1.08-1.76); P = 0.0089] and with even higher risk of fatal exacerbations amongst individuals with pre-existing COPD [n = 730; 3.61 (1.71-7.60); P = 7.3 × 10-4]. We also replicated associations for a PCSK9 variant, reported in UK Biobank, with increased risks of acute upper respiratory tract infection (URTI) [pooled OR after meta-analysis of 1.87 (1.38-2.54); P = 5.4 × 10-5] and self-reported asthma [pooled OR of 1.17 (1.04-1.30); P = 0.0071]. There was no association of a polygenic LDL-C score with COPD hospitalization, COPD exacerbation, or URTI. The LDL-C-lowering PCSK9 genetic variants are associated with lower risk of subclinical and clinical atherosclerotic vascular disease but higher risks of respiratory diseases. Pharmacovigilance studies may be required to monitor patients treated with therapeutic PCSK9 inhibitors for exacerbations of respiratory diseases or respiratory tract infections. Genetic analyses of over 100 000 participants of the China Kadoorie Biobank, mimicking the effect of new drugs intended to reduce cholesterol by targeting the PCSK9 protein, have identified potential severe effects of lower PCSK9 activity in patients with existing respiratory disease.PCSK9 genetic variants that are associated with lower cholesterol and reduced rates of cardiovascular disease are also associated with increased risk of a range of respiratory diseases, including asthma, upper respiratory tract infections, and hospitalization with chronic obstructive pulmonary disease (COPD).These genetic variants are not associated with whether or not individuals have COPD; instead, they are specifically associated with an increase in the chance of those who already have COPD being hospitalized and even dying, suggesting that careful monitoring of such patients should be considered during development of and treatment with anti-PCSK9 medication.

Effects of solvent extracted organic matter from outdoor air pollution on human type II pneumocytes: Molecular and proteomic analysis

Outdoor air pollution is responsible for the exacerbation of respiratory diseases in humans. Particulate matter with an aerodynamic diameter ≤2.5 μm (PM2.5) is one of the main components of outdoor air pollution, and solvent extracted organic matter (SEOM) is adsorbed to the main PM2.5 core. Some of the biological effects of black carbon and polycyclic aromatic hydrocarbons, which are components of PM2.5, are known, but the response of respiratory cell lineages to SEOM exposure has not been described until now. The aim of this study was to obtain SEOM from PM2.5 and analyze the molecular and proteomic effects on human type II pneumocytes. PM2.5 was collected from Mexico City in the wildfire season and the SEOM was characterized to be exposed on human type II pneumocytes. The effects were compared with benzo [a] pyrene (B[a]P) and hydrogen peroxide (H2O2). The results showed that SEOM induced a decrease in surfactant and deregulation in the molecular protein and lipid pattern analyzed by reflection-Fourier transform infrared (ATR-FTIR) spectroscopy on human type II pneumocytes after 24 h. The molecular alterations induced by SEOM were not shared by those induced by B[a]P nor H2O2, which highlights specific SEOM effects. In addition, proteomic patterns by quantitative MS analysis revealed a downregulation of 171 proteins and upregulation of 134 proteins analyzed in the STRING database. The deregulation was associated with positive regulation of apoptotic clearance, removal of superoxide radicals, and positive regulation of heterotypic cell-cell adhesion processes, while ATP metabolism, nucleotide process, and cellular metabolism were also affected. Through this study, we conclude that SEOM extracted from PM2.5 exerts alterations in molecular patterns of protein and lipids, surfactant expression, and deregulation of metabolic pathways of type II pneumocytes after 24 h of exposure in absence of cytotoxicity, which warns about apparent SEOM silent effects.

Variants in transient receptor potential channels and toll-like receptors modify airway responses to allergen and air pollution: a randomized controlled response human exposure study

BackgroundEnvironmental co-exposure to allergen and traffic-related air pollution is common globally and contributes to the exacerbation of respiratory diseases. Individual responses to environmental insults remain variable due to gene-environment interactions.ObjectiveThis study examined whether single nucleotide polymorphisms (SNPs) in lung cell surface receptor genes modifies lung function change and immune cell recruitment in allergen-sensitized individuals exposed to diesel exhaust (DE) and allergen.MethodsIn this randomized, double-blinded, four-arm, crossover study, 13 allergen-sensitized participants underwent allergen inhalation challenge following a 2-hour exposure to DE, particle-depleted diesel exhaust (PDDE) or filtered air (FA). Lung function tests and bronchoscopic sample collection were performed up to 48 h after exposures. Transient receptor potential channel (TRPA1 and TRPV1) and toll-like receptor (TLR2 and TLR4) risk alleles were used to construct an unweighted genetic risk score (GRS). Exposure-by-GRS interactions were tested using mixed-effects models.ResultsIn participants with high GRS, allergen exposure was associated with an increase in airway hyperresponsiveness (AHR) when co-exposed to PDDE (p = 0.03) but not FA or DE. FA and PDDE also were associated with a relative increase in macrophages and decrease in lymphocytes in bronchoalveolar lavage.ConclusionsTRPs and TLRs variants are associated with increased AHR and altered immune cellularity in allergen-exposed individuals. This effect is blunted by DE exposure, suggesting greater influence of unmeasured gene variants as primary meditators of a particulate-rich co-exposure.Trial registrationThe study was registered with ClinicalTrials.gov on December 20, 2013 (NCT02017431).

Airway and Oral microbiome profiling of SARS-CoV-2 infected asthma and non-asthma cases revealing alterations-A pulmonary microbial investigation.

New evidence strongly discloses the pathogenesis of host-associated microbiomes in respiratory diseases. The microbiome dysbiosis modulates the lung's behavior and deteriorates the respiratory system's effective functioning. Several exogenous and environmental factors influence the development of asthma and chronic lung disease. The relationship between asthma and microbes is reasonably understood and yet to be investigated for more substantiation. The comorbidities such as SARS-CoV-2 further exacerbate the health condition of the asthma-affected individuals. This study examines the raw 16S rRNA sequencing data collected from the saliva and nasopharyngeal regions of pre-existing asthma (23) and non-asthma patients (82) infected by SARS-CoV-2 acquired from the public database. The experiment is designed in a two-fold pattern, analyzing the associativity between the samples collected from the saliva and nasopharyngeal regions. Later, investigates the microbial pathogenesis, its role in exacerbations of respiratory disease, and deciphering the diagnostic biomarkers of the target condition. LEfSE analysis identified that Actinobacteriota and Pseudomonadota are enriched in the SARS-CoV-2-non-asthma group and SARS-CoV-2 asthma group of the salivary microbiome, respectively. Random forest algorithm is trained with amplicon sequence variants (ASVs) attained better classification accuracy, ROC scores on nasal (84% and 87%) and saliva datasets (93% and 97.5%). Rothia mucilaginosa is less abundant, and Corynebacterium tuberculostearicum showed higher abundance in the SARS-CoV-2 asthma group. The increase in Streptococcus at the genus level in the SARS-CoV-2-asthma group is evidence of discriminating the subgroups.

Effects of climate variability on respiratory diseases in the Western Region of Bahia, Brazil

ObjectivesThis study aimed to analyse hospitalisations for respiratory diseases in the Western Region of Bahia, Northeast Brazil, from 2010 to 2019, and to explore possible correlations with meteorological data. Study designThis descriptive, epidemiological, ecological study analysed data from 37 municipalities in the Western Bahia health macro-region, defined according to geographical, administrative, demographic, epidemiological, social and cultural criteria, and accounting for availability of health resources. MethodsHospitalisation data for respiratory diseases, including total admissions and disease frequency, mean and prevalence, were obtained from DATASUS (Ministry of Health). The data were evaluated by sex, age group and city. Statistical tests, such as the Chi-squared test and analysis of variance, were used for data analysis. Meteorological data were compared using the t-test and Mann–Whitney test. Correlations between health indicators and weather data were assessed using the Pearson and Spearman correlation coefficients. ResultsOver the investigated period, there were 536,195 hospitalisation records in the region, with respiratory diseases accounting for 17.1% of admissions. Notably, 40% of respiratory hospitalisations were among children aged 0–9 years. The most prevalent respiratory conditions were pneumonia and asthma, which together constituted 73% of all respiratory hospitalisations. A significant negative correlation was observed between respiratory diseases and rainfall (r = −0.70, P = 0.011). ConclusionsPneumonia and asthma remain important causes of hospitalisation among children in the Western Bahia Region. The study findings suggest that respiratory diseases are influenced by rainfall, possibly due to increased atmospheric pollutants during time of low rainfall. These findings emphasise the importance of environmental factors in the development and exacerbation of respiratory diseases.

Relative Humidity and Its Impact on the Immune System and Infections.

Relative humidity (RH) represents an underestimated outdoor and indoor environmental parameter. Conditions below and above the optimal range could facilitate infectious transmission as well as the exacerbation of respiratory diseases. The aim of this review is to outline the consequences for health of suboptimal RH in the environment and how to limit this negative impact. RH primarily affects the rheological properties of the mucus, modifying its osmolarity and thus the mucociliary clearance. The integrity of the physical barrier, maintained by mucus and tight junctions, is critical for protection from pathogens or irritants. Moreover, the control of RH seems to be a strategy to prevent and control the spread of viruses and bacteria. However, the imbalance of RH in the outdoor and indoor environments is frequently associated with the presence of other irritants, allergens, and pathogens, and therefore the burden of a single risk factor is not clearly defined in different situations. Nonetheless, RHmay have a synergistic negative effect with these risk factors, and its normalization, if possible, may have a positive impact on a healthier environment.

PM10 promotes an inflammatory cytokine response that may impact SARS-CoV-2 replication in vitro.

In the last decades, a decrease in air quality has been observed, mainly associated with anthropogenic activities. Air pollutants, including particulate matter (PM), have been associated with adverse effects on human health, such as exacerbation of respiratory diseases and infections. High levels of PM in the air have recently been associated with increased morbidity and mortality of COVID-19 in some regions of the world. To evaluate the effect of coarse particulate matter (PM10) on the inflammatory response and viral replication triggered by SARS-CoV-2 using in vitro models. Peripheral blood mononuclear cells (PBMC) from healthy donors were treated with PM10 and subsequently exposed to SARS-CoV-2 (D614G strain, MOI 0.1). The production of pro-inflammatory cytokines and antiviral factors was quantified by qPCR and ELISA. In addition, using the A549 cell line, previously exposed to PM, the viral replication was evaluated by qPCR and plaque assay. SARS-CoV-2 stimulation increased the production of pro-inflammatory cytokines in PBMC, such as IL-1β, IL-6 and IL-8, but not antiviral factors. Likewise, PM10 induced significant production of IL-6 in PBMCs stimulated with SARS-CoV-2 and decreased the expression of OAS and PKR. Additionally, PM10 induces the release of IL-1β in PBMC exposed to SARS-CoV-2 as well as in a co-culture of epithelial cells and PBMCs. Finally, increased viral replication of SARS-CoV-2 was shown in response to PM10. Exposure to coarse particulate matter increases the production of pro-inflammatory cytokines, such as IL-1β and IL-6, and may alter the expression of antiviral factors, which are relevant for the immune response to SARS-CoV-2. These results suggest that pre-exposure to air particulate matter could have a modest role in the higher production of cytokines and viral replication during COVID-19, which eventually could contribute to severe clinical outcomes.

The role of exposure to airborne pollutants in the workplace on the prevalence and severity of chronic respiratory disease in Italy

occupational exposure to vapours, gases, dusts and fumes (VGDF) plays an important role in the development and exacerbation of respiratory diseases. The aim of this study is to evaluate the possible association of occupational exposure to airborne pollutants and chronic respiratory diseases. multicase-control study. cases of chronic respiratory diseases and controls from the Italian multicentric study Gene Environment Interaction in Respiratory Diseases (GEIRD). the occurrence of rhinitis, asthma, chronic bronchitis/chronic obstructive pulmonary disease (COPD), asthma severity, spirometry data, exhaled nitric oxide (FeNO) were examined in relation to chronic and acute occupational exposures to airborne pollutants using multiple regression models. 2,943 subjects were enrolled in the study. Regularm exposure to VGDF was associated with a higher prevalence of chronic bronchitis/COPD (OR 1.40, 95%CI 0.98-1.99), especially in those also having asthma (OR 1.80, 95%CI 1.14-2.85), a lower prevalence of remittent asthma (OR 0.53, 95%CI 0.29-0.96) and, in those with asthma, an increased activity of the disease (severity score) (OR 1.77, 95%CI 1.20-2.60). No associations were observed between occupational exposure and prevalence of rhinitis, spirometry and FeNO data. Finally, an association was found between acute exposure to airborne pollutants (occupational and non-occupational) and the respiratory diseases investigated, in particular active asthma and asthma associated chronic bronchitis/BPCO. these data confirm a significant role of occupational exposure to airborne pollutants on respiratory health, underlying the importance of workplace exposure prevention, in particular for more susceptible subjects, as those with respiratory diseases.

Integrating network pharmacology and experimental verification to decipher the immunomodulatory effect of Bu-Zhong-Yi-Qi-Tang against poly (I:C)-induced pulmonary inflammation.

Pulmonary inflammation caused by respiratory tract viral infections is usually associated with acute exacerbation of respiratory diseases, such as asthma and chronic obstructive pulmonary disease (COPD). Therefore, maintaining the pulmonary immune homeostasis is particular important for prevention of the acute exacerbation. Bu-Zhong-Yi-Qi-Tang (BZYQT), a traditional Chinese medicine formula, has been broadly used to improve respiratory and gastrointestinal disorders in China for over 700years. Previously, we have found the regulatory activity of BZYQT on the lower respiratory immune system, while its potential effects during pulmonary inflammation remain unknown. Thus, the current study focused on deciphering its immunomodulatory effect and potential mechanism against pulmonary inflammation by using a viral RNA analogue, poly (I:C), induced murine pulmonary inflammation model and BEAS-2B cell model coupled with network pharmacology. Inflammatory cells in the bronchoalveolar lavage fluid were counted through microscope examination according to the cell's morphology and staining characteristics; protein and gene levels of inflammatory mediators were determined with Elisa and quantitative PCR, respectively; network pharmacology was conducted based on 46 BZYQT-related potential bioactive components, pulmonary inflammation and immune-related targets. Our results indicated that the recruitment of neutrophils and the expression of Adgre1 (encoding the F4/80, which is a macrophage marker) in the lung induced by poly (I:C) were significantly reduced after BZYQT treatment, and these effects were further demonstrated to be related to the interference of leukocyte transendothelial migration from the decreased levels of CXCL10, IL-6, TNF-α, CXCL2, ICAM-1, VCAM-1, and E/P-selectins. Furthermore, BZYQT inhibited the CXCL10, TNF-α, and IFN-β expression of poly (I:C)-challenged BEAS-2B cells in a dose-dependent manner. Through integrating results from network pharmacology, experiments, and the published literature, isoliquiritigenin, Z-ligustilide, atractylenolide I, atractylenolide III, formononetin, ferulic acid, hesperidin, and cimigenoside were presumed as the bioactive components of BZYQT against pulmonary inflammation. Overall, our findings demonstrated that BZYQT possesses a pronounced immunomodulatory effect on poly (I:C)-induced pulmonary inflammation, which provides a pharmacological basis for BZYQT in the treatment of respiratory disorders.

A Personalized Respiratory Disease Exacerbation Prediction Technique Based on a Novel Spatio-Temporal Machine Learning Architecture and Local Environmental Sensor Networks

Chronic respiratory diseases, such as the Chronic Obstructive Pulmonary Disease (COPD) and asthma, are a serious health crisis, affecting a large number of people globally and inflicting major costs on the economy. Current methods for assessing the progression of respiratory symptoms are either subjective and inaccurate, or complex and cumbersome, and do not incorporate environmental factors to track individualized risks. Lacking predictive assessments and early intervention, unexpected exacerbations often lead to hospitalizations and high medical costs. This work presents a multi-modal solution for predicting the exacerbation risks of respiratory diseases, such as COPD, based on a novel spatio-temporal machine learning architecture for real-time and accurate respiratory events detection, and tracking of local environmental and meteorological data and trends. The proposed new neural network model blends key attributes of both convolutional and recurrent neural architectures, allowing extraction of the salient spatial and temporal features encoded in respiratory sounds, thereby leading to accurate classification and tracking of symptoms. Combined with the data from environmental and meteorological sensors, and a predictive model based on retrospective medical studies, this solution can assess and provide early warnings of respiratory disease exacerbations, thereby potentially reducing hospitalization rates and medical costs.

Current status of herbal medicine research for respiratory diseases induced by particulate matter: a protocol for a scoping review

BackgroundParticulate matter (PM) is an important environmental risk factor for the initiation and exacerbation of respiratory disease. Various herbal medicines have exhibited a reduction in symptoms of respiratory diseases induced by PM in animal models. However, the types and characteristics of studies on herbal medicine for respiratory diseases by PM have not been reviewed. This scoping review will focus on the currents status and research gap of herbal medicines for respiratory diseases caused by PM.MethodsWe will follow the scoping review framework developed by Arksey and O’Malley. MEDLINE (via PubMed), EMBASE, and the Cochrane Central Register of Controlled Trials will be searched for relevant English-language publications, and only peer-reviewed, controlled comparative in vivo/in-vitro/human studies examining the effects of herbs on respiratory disease induced by PM will be included. The basic characteristics, research methods, detailed regimens, possible mechanisms, outcomes, and results will be extracted using a predefined standardized data extraction form. Outcomes will be presented in the following categories: pulmonary function, inflammatory markers, reactive oxygen species, histology and mechanisms, and adverse events. Two researchers will independently perform the study selection, data extraction, and quality assessment. We will also present the research map and implications for further study.Ethics and disseminationEthical approval is not required because individual patient data will not be included. The findings will be disseminated through peer-reviewed publications or conference presentations.Systematic review registrationThis review protocol has been registered with the Open Science Framework on February 12, 2021 (https://osf.io/s7uvk/)

Environmental pollution and allergy

Air pollution, climate change, and the decrease of biological diversity are major threats to human health. In the past decades, an increase in allergic diseases, including asthma and rhinoconjunctivitis, has been observed. Up to 40 % of the world population may have an allergic disease, which represents a significant impact on the quality of life of those who suffer from it, and environmental pollution is one of the causes of its presentation. Air pollution causes significant morbidity and mortality in patients with inflammatory airway diseases such as allergic rhinitis, chronic rhinosinusitis, asthma, and chronic obstructive pulmonary disease. Oxidative stress in patients with respiratory diseases can induce eosinophilic inflammation in the airways, increase atopic allergic sensitization, and rise susceptibility to infections. Climate change has influenced exposure to extramural allergens and it is associated with exacerbations of respiratory diseases in the upper and lower airway. The interaction of indoor and outdoor environmental exposure and host factors can affect the development and progression of lifelong allergic diseases. The decrease of exposure to air pollutants has been associated with a favorable response in respiratory health, which is why it is necessary to implement measures that contribute to an improvement in air quality.