The detrimental effects of particulate matter (PM) on human health have been widely corroborated. We aimed to examine the association between outdoor PM and the drug resistance risk among workers and farmers with pulmonary tuberculosis (PTB).

We performed a population-based time-series study using routinely collected meteorological and TB surveillance data.

We selected Suzhou City, China, as the study area. Data on patients with PTB and meteorological factors were extracted from the National Tuberculosis Online Registration System and the China Meteorological Data Sharing Center.

This study included 7868 patients with PTB diagnosed from January 2017 to December 2021 in Suzhou.

The generalised additive model was used to estimate the effects of outdoor PM on the drug resistance risk of TB among workers and farmers who typically work outdoors. Moreover, subgroup analyses were carried out to evaluate the associations in different populations and seasons.

Although there was no significant association between PM with an aerodynamic diameter≤10 µm (PM10) and drug-resistant risk in the overall analysis, subgroup analysis revealed a significant positive association in the winter season. Similarly, PM with an aerodynamic diameter≤2.5 µm (PM2.5) was significantly associated with drug resistance risk among males with a lag of 0-3 days, people ≤60 years with a lag of 0-7 days and in the winter season with a lag of 0-7 days, 0-15 days, 0-90 days or 0-180 days.

Outdoor PM10 and PM2.5 were positively related to the drug resistance risk of workers and farmers with PTB. Reducing ambient PM pollution might reduce the burden of TB. Further research is required to verify the association through in vitro experiments and extensive cohort studies.

Chronic obstructive pulmonary disease (COPD) is a common chronic incurable disease. Treatment of COPD often focuses on symptom management and progression prevention using pharmacological and nonpharmacological therapies (eg, medication, inhaler use, and smoking cessation). Self-management is an important aspect of managing COPD. Self-management interventions are increasingly delivered through eHealth, which may help people with COPD engage in self-management. However, little is known about the actual content of these eHealth interventions.

This literature review aimed to investigate the state-of-the-art eHealth self-management technologies for COPD. More specifically, we aimed to investigate the functionality, modality, technology readiness level, underlying theories of the technology, the positive health dimensions addressed, the target population characteristics (ie, the intended population, the included population, and the actual population), the self-management processes, and behavior change techniques.

A scoping review was performed to answer the proposed research questions. The databases PubMed, Scopus, PsycINFO (via EBSCO), and Wiley were searched for relevant articles. We identified articles published between January 1, 2012, and June 1, 2022, that described eHealth self-management interventions for COPD. Identified articles were screened for eligibility using the web-based software Rayyan.ai. Eligible articles were identified, assessed, and categorized by the reviewers, either directly or through a combination of methods, using Atlas.ti version 9.1.7.0. Thereafter, data were charted accordingly and presented with the purpose of giving an overview of currently available literature while highlighting existing gaps.

A total of 101 eligible articles were included. This review found that most eHealth technologies (91/101, 90.1%) enable patients to self-monitor their symptoms using (smart) measuring devices (39/91, 43%), smartphones (27/91, 30%), or tablets (25/91, 27%). The self-management process of "taking ownership of health needs" (94/101, 93.1%), the behavior change technique of "feedback and monitoring" (88/101, 87%), and the positive health dimension of "bodily functioning" (101/101, 100%) were most often addressed. The inclusion criteria of studies and the actual populations reached show that a subset of people with COPD participate in eHealth studies.

The current body of literature related to eHealth interventions has a strong tendency toward managing the physical aspect of COPD self-management. The necessity to specify inclusion criteria to control variables, combined with the practical challenges of recruiting diverse participants, leads to people with COPD being included in eHealth studies that only represent a subgroup of the whole population. Therefore, future research should be aware of this unintentional blind spot, make efforts to reach the underrepresented population, and address multiple dimensions of the positive health paradigm.

The miR-125a-5p has been reported influence the development of lung cancer, however, the link between it and chronic obstructive pulmonary disease (COPD) is still not well understood. Hence, this study was designed to investigate the molecular pathway by which miR-125a-5p related biomarkers were involved in COPD.

The differentially expressed genes (DEGs) and module genes related to COPD in GSE100153 were screened out by differential analysis and weighted gene co-expression network analysis, respectively. Then, the target genes of miR-125a-5p obtained from miRWalk database were intersected with DEGs and module genes, followed by identification of biomarkers through SVM-RFE algorithms. Moreover, the gene set enrichment analysis, immune infiltration analysis, construction of regulatory network, single-cell analysis and Mendelian randomization (MR) analysis were performed. At last, the expression levels of the biomarkers were further validated in GSE100153 and GSE146560 as well as in qRT-PCR.

A total of 10 genes were acquired by intersecting the 126 DEGs, the 3989 module genes, and 2329 target genes, of which PITHD1, CNTNAP2 and GUCD1 were identified as biomarkers. Enrichment analysis showed their roles in various cellular functions. In addition, significant associations were identified between 9 distinct cells and biomarkers. Subsequently, 5 TFs and 63 therapeutic agents were predicted as biomarkers. Moreover, GUCD1 and PITHD1 were significantly different between case and control in T cells and Alveolar cells. In COPD, GUCD1 and PITHD1 were significantly down-regulated in GSE100153 and GSE146560 datasets and confirmed by qRT-PCR.

In our study, PITHD1, CNTNAP2, and GUCD1 were recognized as biomarkers related to miR-125a-5p-related genes in COPD, providing new references for treatment of COPD.

Long-term exposure to air pollutants and diabetes are both linked to cancer development. However, their combined effect remains unclear. This study examined the relationship between air pollutants and cancer incidence, with diabetes as a potential mediator. Data from 10,590 participants in the 2015 China Health and Retirement Longitudinal Study (CHARLS) were analyzed. Participants were grouped based on cancer diagnosis, and air pollutant exposure levels were estimated using satellite-based spatiotemporal models. Generalized linear regression and restricted cubic spline (RCS) analysis were used to assess the impact of air pollutants and diabetes in covariates-adjusted models. Further analyses, including conditional independence test, mediation effect and sensitivity analysis based on Bayesian networks, were performed to further analyze specific air pollutants. After adjusting for covariates, particulate matter (PM) (PM ≤ 1 μm in aerodynamic diameter [PM1], PM2.5, ammonium (NH4), nitrate (NO3) and diabetes showed significant associations with cancer incidence. RCS analysis confirmed significant direct effects of PM2.5 and PM10 on cancer and the mediated effects of diabetes. The interaction between diabetes and both PM2.5 and PM10 was further supported by conditional independence tests, highlighting diabetes as a significant mediator in the PM2.5-cancer relationship. This study offers a novel perspective by identifying diabetes as a key intermediary in the association between PM2.5 exposure and cancer risk, providing evidence that diabetes plays a significant mediating role in air pollutant-related cancer development.

Allergic asthma is a significant international concern in respiratory health, which can be exacerbated by the increasing levels of non-allergenic pollutants. This rise in airborne pollutants is a primary driver behind the growing prevalence of asthma, posing a health emergency. Additionally, climatic risk factors can contribute to the onset and progression of asthma. Understanding the complex interplay between pollution, climate, and asthma induction is crucial to elucidate how environmental changes intensify asthma. In this study, we investigated the proteomic and metabolomic changes in the lungs of a mouse asthma model following co-exposure to carbon black nanoparticles and high humidity, which represent airborne and climatic factors, respectively. An asthma model was established using ovalbumin, and mice were intratracheally instilled with 15 or 30 μg/kg of carbon black and simultaneously exposed to either 70% or 90% relative humidity. Protein and metabolite profiles from the lung were used to analyze the most significantly changed clusters, and potential biomarkers and enriched pathways were identified to dissect the adverse effects of the two risk factors. The lung proteome and metabolome are significantly altered by the co-exposure, with the effects modulated by carbon black concentration and humidity level. This study proposes 10 proteins and 18 metabolites as candidate biomarkers. The significantly enriched KEGG pathways include one protein pathway (primary immunodeficiency) and six metabolic pathways (ABC transporters, nucleotide metabolism, Parkinson's disease, purine metabolism, choline metabolism in cancer, and biosynthesis of cofactors). A joint proteomic and metabolomic analysis identifies five common pathways across both omics, namely, ABC transporters, central carbon metabolism in cancer, EGFR tyrosine kinase inhibitor resistance, glioma, and NF-kappa B signaling pathway, disturbed by the co-exposure. We provide a multi-omic basis for the health risk assessment and management of co-exposures to environmental risk factors.

The acute health effects of air pollution on the risk of chronic obstructive pulmonary disease (COPD) have not been adequately studied and results remain inconsistent. Furthermore, fewer studies have explored the impact of air pollution on the cost of treating patients with COPD. Generalized additive models (GAM) based on Poisson distribution and gamma were applied to evaluate the association between short-term exposure to air pollution and daily COPD outpatient visits and daily COPD treatment costs. A total of 14,611 outpatient in Xinxiang from 2016 to 2021 were included for analysis. We found that short-term exposure to PM2.5, PM10, NO2 and CO were positively associated with COPD outpatient visits, and gaseous pollutants appeared to have greater effects on outpatient visits than particulate matter. For the largest effect, per 10 μg/m3 increment in (per 1 mg/m3 increment in CO concentration) CO (lag 01), NO2 (lag 01), PM2.5 (lag 02) and PM10 (lag 06) were significantly associated with 7.859 % (95 % CI:3.421,12.488), 4.894 % (95 % CI:3.422,6.386), 0.627 % (95 % CI:0.010, 1.248) and 0.531 % (95 % CI:0.050,1.014) increase in daily COPD outpatient visits, respectively. Short-term exposure to air pollutants (PM10, CO and NO2) was positively associated with COPD treatment costs. No significant sex or age differences were found in the stratified analysis of outpatient visits. The effect of gaseous pollutants (NO2) on COPD outpatient visits was greater in the cold season (October to March) (P < 0.05), whereas the effect of particulate matter (PM2.5 and PM10) was greater in the warm season (April to September) (P < 0.05). Greater health benefits could be obtained when pollutant concentrations meet WHO standards. In conclusion, short-term exposure to PM2.5, PM10, NO2 and CO was significantly associated with increased COPD outpatient visits, and gaseous pollutants appeared to have greater effects on outpatient visits than particulate matter. Further larger-scale studies are needed to validate our findings.

Tracheal, bronchus, and lung (TBL) cancer attributable to ambient particulate matter pollution (APMP) is a growing global health concern, particularly in individuals aged 70 and above. This study aims to evaluate past trends, identify key drivers, and project future disease burden.

Data from the Global Burden of Disease Study 2021 was analyzed for TBL cancer-related disability-adjusted life years (DALYs) and mortality from 1990 to 2021, stratified by SDI regions. Statistical methods, including Joinpoint regression, age-period-cohort modeling, and decomposition analysis, were used to identify temporal trends and drivers of DALYs. Future projections were made using the Nordpred model.

From 1990 to 2021, global DALYs of TBL cancer due to APMP increased steadily (AAPC 0.75%). Population growth was the main driver, accounting for 79.37% of the increase, with epidemiological factors playing a varying role across regions. The highest DALY growth was observed in middle SDI regions (AAPC 2.99%), while high SDI regions saw a decline (AAPC -1.76%). Projections up to 2044 suggest a substantial increase in DALYs across all SDI regions, with the fastest growth expected among individuals aged 70-74, but DALY rates are projected to decline steadily.

Population growth is the primary factor driving the increase in DALYs associated with TBL cancer, with significant regional disparities. Projections suggest a continued rise in disease burden, particularly in lower SDI regions, underlining the urgency for targeted public health interventions and strategies to mitigate exposure and improve healthcare outcomes for at-risk populations.

Exposure to air pollution, especially fine particulate matter (PM2.5), is closely linked to various adverse health effects, particularly in the respiratory system. The present study was designed to investigate the lncRNA-mRNA interactions in PM2.5-induced lung cell injury using weighted gene co-expression network analysis (WGCNA). We downloaded the gene expression data of GSE138870 from the Gene Expression Omnibus (GEO) database and screened for differentially expressed lncRNAs and mRNAs. We constructed co-expression modules with WGCNA. Furthermore, functional enrichment analysis was also performed. We also constructed lncRNA-mRNA co-expression networks and lncRNA-mRNA-pathway networks to identify key regulatory relationships. The results revealed several modules significantly correlated with PM2.5-induced lung injury, such as the turquoise and blue modules. Genes within these modules were enriched in pathways related to signal transduction, metabolism, and cancer. Hub lncRNAs in the turquoise module, including LOC100129034 and CROCCP2, were found to be co-expressed with mRNAs involved in apoptosis and proliferation regulation. In the blue module, lnc-CLVS2-2 and GARS1-DT were connected to genes related to cell migration, invasion, and lung injury. These findings contribute novel perspectives to the molecular mechanisms involved in PM2.5-induced lung injury and suggest that WGCNA could be a valuable tool for predicting and understanding this disease process.

Epidemiological studies have consistently demonstrated a robust association between long-term exposure to air pollutants and respiratory diseases. However, establishing causal relationships remains challenging due to residual confounding in observational studies. In this study, Mendelian randomization (MR) analysis was used to explore the causal and epigenetic relationships between various air pollutants and common respiratory diseases.

We utilized a two-sample Mendelian randomization (TSMR) approach to explore the impact of PM2.5, PM2.5-10, PM10, NO2, and NOX on the incidence of nine respiratory diseases using data from large-scale European GWAS datasets (N = 423,796-456,380 for exposures; N = 162,962-486,484 for outcomes). The primary analytical method was inverse variance weighting (IVW), which explored the exposure-outcome relationship using single nucleotide polymorphisms (SNPs) associated with air pollution. Sensitivity analyses, including MR-Egger regression and leave-one-out analyses, were employed to ensure result consistency. Multivariate MR (MVMR) was performed to adjust for potential smoking-related confounders, such as cigarettes per day, household smoking, exposure to tobacco smoke at home, ever smoked, second-hand smoke, smoking initiation, and age at smoking initiation, as well as the independent effects of each air pollutant. Additionally, methylation and enrichment analyses were conducted to further elucidate the potential effects of air pollution on respiratory diseases.

TSMR analysis revealed that exposure to PM2.5 increased the risk of early-onset chronic obstructive pulmonary disease (COPD), pneumonia, pulmonary embolism and lung cancer. PM2.5-10 exposure was associated with an increased risk of lung cancer, while PM10 exposure increased the risk of pneumonia and bronchiectasis. NO2 exposure was associated with increased risks of lung cancer and adult asthma. Importantly, these associations remained robust even after controlling for potential tobacco-related confounders in the MVMR analyses. In the MVMR analysis adjusting for other pollutants, significant associations persisted between PM2.5 and early-onset COPD, and between PM10 and pneumonia. Genetic co-localization analyses confirmed that methylation of PM2.5-associated CpG loci (cg11386376 near c1orf175, cg11846064 near rfx2, cg18612040 near rptor, and cg19765378 near c7orf50) was associated with an increased risk of early-onset COPD. Finally, SNPs significantly associated with exposure and outcome were selected for enrichment analysis.

Our findings suggest that exposure to air pollutants may play a causal role in the development of respiratory diseases, with a potential role of epigenomic modifications emphasized. Strengthening comprehensive air pollution regulations by relevant authorities could potentially mitigate the risk of these diseases.

Chronic obstructive pulmonary disease (COPD) patients commonly exhibit significant morbidity and experience a diminished quality of life. Since there has been no prior research on pneumonia in our study population, we carried out this study to learn more about the situation.

A retrospective analysis of 912 COPD patients with CAP who were receiving ICS treatment at the DHQ Hospital in Muzaffargarh, Punjab, Pakistan was conducted. Study began in February 2022 and ended in February 2023. Using multinomial logistic regression, the odds ratio and relative risk and Kaplan-Meier curves showed time-to-death and recovery by COPD status.

Patients with COPD having a smoking history from 25 pack years and above had 22.791 higher odds of CAP (95% CI: 20.413-31.515), 21.527 higher odds of HTN (95% CI: 12.323-57.103), 16.955 higher odds of diabetes (95% CI: 22.954-29.331), and 13.964 higher odds of death in severity without COVID-19 vaccination (95% CI: 5.988-32.561) compared to patients with COPD having a smoking history from 10 to 15 pack years.

COPD patients with a shorter ICS duration had a lower CAP risk, and vice versa, while vaccinated patients had a less severe disease as compared to non-vaccinated patients.

Chronic obstructive pulmonary disease (COPD) is a common chronic lung disease that impacts hundreds of millions of individuals worldwide. It is principally characterized by irreversible and progressive airflow limitation. Environmental pollutants, including cigarette smoke, air pollution, occupational pollutants, remain predominant risk factors for COPD and play remarkable roles in COPD progression. Despite the availability of treatments to alleviate symptoms of COPD, it continues to exert a serious health and socioeconomic burden. Ferroptosis, a unique form of iron-dependent cell death distinguished by lipid peroxidation, is implicated in various diseases. Recent studies, utilizing COPD patients samples, animal models, and Gene Expression Omnibus (GEO) database, have revealed that ferroptosis is involved in pathogenesis of COPD. Inhibiting ferroptosis signaling pathways halts the progression of COPD. This review consolidates current insights into the mechanisms of ferroptosis in environmental pollutants-induced COPD, which might offer a novel therapeutic strategy for COPD.

Ambient humidity has a significant impact on respiratory health and influences disease and symptoms. However, large-scale studies are required to clarify its specific effects on lung function and respiratory symptoms. We examined the relationship between relative humidity (RH), lung function, and respiratory symptoms using data from the Korea National Health and Nutrition Examination Survey (KNHANES).

In this cross-sectional study, we analyzed data from KNHANES participants aged ≥ 40 years, collected between 2016 and 2018. Pulmonary function tests (PFTs) and health questionnaires were used to assess lung function and respiratory symptoms. Individual environmental data, including RH, were obtained from the Community Multiscale Air Quality model and linked to the participants' addresses. Short-term (0-14 days), mid-term (30-180 days), and long-term (1-5 years) RH exposures were examined. Linear regression models were used to evaluate the associations between RH and PFTs. Univariate and multivariable logistic regression models were applied to assess the risk of lung function abnormalities and respiratory symptoms.

In total, 10,396 participants were included (mean age: 58.3 years, male: 43.6%). In multiple regression analysis, higher RH was negatively associated with the forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) ratio across various time lags, while FVC was positively correlated with long-term RH exposure. In multiple logistic analysis adjusted for clinical and environmental covariates, long-term higher RH exposure was associated with a lower risk of restrictive lung disease (odds ratio [OR] at 4-year moving average [MA]: 0.978, 95% confidence interval [CI]: 0.959-0.997), while mid-term RH exposure decreased the risk of chronic cough (OR at 90-day MA: 0.968, 95% CI: 0.948-0.987) and sputum production (OR at 90-day MA: 0.985, 95% CI: 0.969-1.001).

Higher RH was negatively associated with lung function and increased the risk of obstructive lung disease, whereas mid-term RH exposure reduced the risk of chronic cough and sputum production.

Ambient pollution and non-optimal temperature are major risk factors for respiratory health. However, the relationships between short-term exposure to these factors and bronchiectasis mortality remain unknown.

A nationwide, time-stratified case-crossover study across Mainland China was conducted from 2013 to 2019. Records of bronchiectasis deaths were extracted from the National Death Registration Reporting Information System. Daily concentrations of fine particulate matter (PM2.5), coarse particulate matter (PM2.5-10), nitrogen dioxide (NO2), ozone (O3), and daily temperature were obtained from high-resolution prediction models. We utilized conditional logistic regression model and distributed lag nonlinear model to explore the associations of these exposures with bronchiectasis mortality.

We included a total of 19,320 bronchiectasis deaths. Air pollutant was associated with bronchiectasis mortality within the first 3 days after exposure and the exposure-response relationships were almost linear. An interquartile range increase in PM2.5, PM2.5-10, and O3 was associated with increments of 3.18%, 4.14%, and 4.36% in bronchiectasis mortality at lag 02 d, respectively. Additionally, lower temperature was associated with higher odds of bronchiectasis mortality. Compared to referent temperature (23.6 °C), the odds ratio for bronchiectasis mortality associated with extremely low temperature (P1: -13.4 °C) was 1.54 (95% CI: 1.05, 2.25).

This national study provides compelling evidence, and highlights the necessity and importance of reducing air pollution exposures and keeping warm for susceptible populations.

National Natural Science Foundation of China (81925001; 82330070); Innovation Program of Shanghai Municipal Education Commission (202101070007-E00097); Program of Shanghai Municipal Science and Technology Commission (21DZ2201800); Program of Shanghai Shenkang Development Center (SHDC12023110); and Major Project of National Health Commission of China.

The concurrence of chronic obstructive pulmonary disease (COPD) and lung cancer has been widely reported and extensively addressed by pulmonologists and oncologists. However, most studies have focused on shared risk factors, DNA damage pathways, immune microenvironments, inflammation, and imbalanced proteases/antiproteases. In the present review, we explore the association between COPD and lung cancer in terms of airway pluripotent cell fate determination and discuss the various cell types and signaling pathways involved in the maintenance of lung epithelium homeostasis and their involvement in the pathogenesis of co-occurring COPD and lung cancer.

Rationale: Growing evidence suggests that air pollution exposure is a major risk factor in chronic obstructive pulmonary disease (COPD) that is associated with an increased prothrombotic state and adverse cardiovascular outcomes. However, much of this work is based on observational data or human exposure studies involving younger participants. The biological causality and mechanism of air pollution-induced prothrombotic response in patients with COPD remain to be explored. Objectives: The main aim of this work was to investigate the impact of short-term diesel exhaust (DE) exposure on circulating prothrombotic markers-fibrinogen and plasminogen activator inhibitor-1 (PAI-1)-and urinary eicosanoids in patients with COPD. Methods: Twenty-nine research participants were recruited in this randomized, double-blind, crossover, controlled human exposure study to DE. Participants included former smokers with and without mild or moderate COPD (ex-smokers [ES] and COPD group) and healthy never-smokers without COPD (nonsmoker [NS] group). Each participant was exposed to DE (300 μg/m3 of particulate matter with an aerodynamic diameter ≤2.5 μm) and filtered air for 2 hours on different occasions, in randomized order, separated by a 4-week washout. Blood and urine samples were collected before and 24 hours after each exposure. Plasma fibrinogen and serum PAI-1 concentrations were quantified using enzyme-linked immunosorbent assays. Urinary eicosanoid concentrations were quantified using ultraperformance liquid chromatography coupled to tandem mass spectrometry. Linear mixed-effects models were used for statistical comparisons. Results: Participants with COPD showed an increase in plasma fibrinogen (effect estimate, 1.27 [1.06-1.53]; P = 0.01) after DE relative to filtered air, but no significant DE-associated change in serum PAI-1 (0.95 [0.87-1.04]; P = 0.26). In never-smokers and ex-smokers without COPD, fibrinogen (NS group, 1.10 [0.99-1.23]; P = 0.08; ES group, 0.86 [0.68-1.09]; P = 0.08] and PAI-1 (NS group, 1.12 [0.96-1.32]; P = 0.15; ES group, 0.90 [0.79-1.03]; P = 0.13) were not changed after DE exposure. Participants with COPD showed a DE-attributable increase in urinary thromboxane B2 (TXB2) metabolite concentrations as follows: 11-dehydro-TXB2 (1.45 [1.02-2.08]; P = 0.04) and 2,3-dinor-TXB2 (1.45 [1.05-2.00]; P = 0.03). Conclusions: Participants with COPD had increased plasma fibrinogen and urinary TXB2 metabolites after short-term DE exposure, suggesting they may be more susceptible to a pollution-attributable prothrombotic response than healthy control subjects or ex-smokers without COPD. Clinical trial registered with www.clinicaltrials.gov (NCT02236039).

Ambient air pollution has become a challenging global health issue since industrialization, especially affecting respiratory diseases. However, the causal link between air pollution and allergic respiratory diseases (ARDs) remains unclear due to confounding factors in conventional epidemiological studies across different populations. Thus, we aimed to clarify the causal associations between air pollution and ARDs in European and East Asian populations using Mendelian randomization (MR).

MR utilizes genetic variants and provides a satisfactory level of causal evidence. Genetic data for exposures (PM2.5, PM2.5 absorbance, PM10, PMcoarse, NO2 and NOx) and outcomes (allergic rhinitis, chronic rhinosinusitis, asthma, and obesity related asthma) were obtained from genome-wide association studies. Instrumental variables were strictly filtered based on core assumptions. Two-sample MR and sensitivity analyses were conducted separately for European and East Asian populations.

PMcoarse was causally associated with an increased risk of chronic rhinosinusitis (OR = 1.588 [1.002-2.518]; p = 0.049) and obesity related asthma (OR = 1.956 [1.012-3.780]; p = 0.046) in European population, and PM10 was associated with a decreased risk of allergic rhinitis in East Asian population (OR = 0.882 [0.798-0.974]; p = 0.013). No heterogeneity or pleiotropy was detected in any significant causal association.

Our findings indicate that ambient air pollution has opposite impacts on the etiology of ARDs in European and East Asian populations, which provides evidence for decisions on public policies and suggests that different responses to environmental factors such as air pollution may contribute to racial heterogeneity of ARDs.

Sarcoidosis is a chronic granulomatous disease predominantly affecting the lungs and inducing significant morbidity and elevated mortality rate. The etiology of the disease is unknown but may involve exposure to an antigenic agent and subsequent inflammatory response resulting in granuloma formation. Various environmental and occupational risk factors have been suggested by previous observations, such as moldy environments, insecticides, and bird breeding. Our study investigated the association of air pollution with diagnosis of sarcoidosis using a case-control design. Penn State Health electronic medical records from 2005 to 2018 were examined for adult patients with (cases) and without (controls) an International Classification of Disease (ICD)-9 or -10 code for sarcoidosis. Patient addresses were geocoded and 24-hr residential-level air pollution concentrations were estimated using spatio-temporal models of particulate matter <2.5 μm (PM2.5), ozone, and PM2.5 elemental carbon (EC) and moving averages calculated. In total, 877 cases and 34,510 controls were identified. Logistic regression analysis did not identify significant associations between sarcoidosis incidence and air pollution exposure estimates. However, the odds ratio (OR) for EC for exposures occurring 7-10 years prior did approach statistical significance, and ORs exhibited an increasing trend for longer averaging periods. Data suggested a latency period of more than 6 years for PM2.5 and EC for reasons that are unclear. Overall, results for PM2.5 and EC suggest that long-term exposure to traffic-related air pollution may contribute to the development of sarcoidosis and emphasize the need for additional research and, if the present findings are substantiated, for public health interventions addressing air quality as well as increasing disease surveillance in areas with a large burden of PM2.5 and EC.

Chronic obstructive pulmonary disease (COPD) currently ranks among the top three causes of mortality worldwide, presenting as a prevalent and complex respiratory ailment. Ongoing research has underscored the pivotal role of immune function in the onset and progression of COPD. The immune response in COPD patients exhibits abnormalities, characterized by diminished anti-infection capacity due to immune senescence, heightened activation of neutrophils and macrophages, T cell infiltration, and aberrant B cell activity, collectively contributing to airway inflammation and lung injury in COPD.

This review aimed to explore the pivotal role of the immune system in COPD and its therapeutic potential.

We conducted a review of immunity and COPD published within the past decade in the Web of Science and PubMed databases, sorting through and summarizing relevant literature.

This article examines the pivotal roles of the immune system in COPD. Understanding the specific functions and interactions of these immune cells could facilitate the development of novel therapeutic strategies and interventions aimed at controlling inflammation, enhancing immune function, and mitigating the impact of respiratory infections in COPD patients.

Lanzhou is the largest heavy industrial city in northwest China and it is a typical geographical valley-like city. However, there are few studies on the relationship between air pollutants and COPD, and their respective sample sizes are small, resulting in inconsistent results. The aim of this study is to analyze the effects of air pollutants on COPD hospitalizations in Lanzhou, China.

An ecological time series study with distributed lag non-linear model (DLNM) was used for analysis. Daily COPD hospitalization data in Lanzhou from 1 January 2015 to 31 December 2019 were collected from 25 hospitals, as well as air pollutant data and meteorological data.

A total of 18,275 COPD hospitalizations were enrolled. For 10 μg/m3 increase in PM2.5, PM10, SO2, NO2, and 1 mg/m3 increase in CO at lag 07 day, the RR95%CI of COPD hospitalizations were 1.048 (1.030, 1.067), 1.008 (1.004, 1.013), 1.091 (1.048, 1.135), 1.043 (1.018, 1.068), and 1.160 (1.084, 1.242), respectively. The exposure-response curves between air pollutants (except O3-8h) and COPD hospitalizations were approximately linear with no thresholds. Female, and the harmful effect of PM on aged <65 years, the effect of gaseous pollutant on those aged ≥65 years, were stronger, particularly in the cold season. Exposure to air pollutants (except O3-8h) might increase the risk of COPD hospitalizations. O3-8h has a weak and unstable effect on COPD.

Exposure to air pollutants (except O3-8h) increases the risk of COPD hospitalizations. O3-8h has a weak and unstable effect on COPD hospital admissions. The harmful effect of gaseous pollutants (except O3-8h) on COPD-hospitalized patients was stronger than that of PM.

Exposure to particulate matter (PM) can cause airway inflammation and worsen various airway diseases. However, the underlying molecular mechanism by which PM triggers airway inflammation has not been completely elucidated, and effective interventions are lacking. Our study revealed that PM exposure increased the expression of histone deacetylase 9 (HDAC9) in human bronchial epithelial cells and mouse airway epithelium through the METTL3/m6A methylation/IGF2BP3 pathway. Functional assays showed that HDAC9 upregulation promoted PM-induced airway inflammation and activation of MAPK signaling pathway in vitro and in vivo. Mechanistically, HDAC9 modulated the deacetylation of histone 4 acetylation at K12 (H4K12) in the promoter region of dual specificity phosphatase 9 (DUSP9) to repress the expression of DUSP9 and resulting in the activation of MAPK signaling pathway, thereby promoting PM-induced airway inflammation. Additionally, HDAC9 bound to MEF2A to weaken its anti-inflammatory effect on PM-induced airway inflammation. Then, we developed a novel inhaled lipid nanoparticle system for delivering HDAC9 siRNA to the airway, offering an effective treatment for PM-induced airway inflammation. Collectively, we elucidated the crucial regulatory mechanism of HDAC9 in PM-induced airway inflammation and introduced an inhaled therapeutic approach targeting HDAC9. These findings contribute to alleviating the burden of various airway diseases caused by PM exposure.

Chronic respiratory diseases (CRDs) are among the top three causes of human mortality. The relationship between modifiable environmental risk factor of noise and risk of mortality in CRDs is unclear. We investigated the longitudinal association between environmental noise exposure and cause-specific mortality in individuals with CRDs, considering the modifying effect of air pollution.

Residential noise exposure was modelled using Common Noise Assessment Methods in Europe. Information on death causes were acquired from death registry data. Cox proportional-hazards models were used to estimate effect sizes.

Among 41,222 participants selected from UK Biobank with CRDs in baseline, a total of 3618 death cases occurred during an average follow-up of 12 years with mortality density of 7.16 per 1000 person years. Exposure with highest noise level (> percentile 90) were associated with 22 % (Hazard ratio [HR] = 1.22, 95 % confidence interval [CI]: 1.05, 1.42), 71 % (HR = 1.71, 95 % CI: 1.14, 2.56), and 84 % (HR = 1.84, 95 % CI: 1.10, 3.07) increased risks for all-cause, respiratory disease (RD)-cause, and COPD-cause mortalities, separately. Both multiplicative and additive interactions was found between air pollution and noise with the risk of RD-cause mortality. Participants with high air pollution and noise exposure were associated with a 101 % (HR = 2.01, 95 % CI: 1.10, 3.66) increased risk of RD-cause mortality.

It is imperative to mitigate noise exposure as a preventive measure against incident mortality in individuals with CRDs.

Short-term exposure to particulate matter air pollution has been associated with the exacerbations of COPD, but its association with COPD mortality was not fully elucidated. We aimed to assess the association between short-term particulate matter exposure and the risk of COPD mortality in China using individual-level data.

We derived 2.26 million COPD deaths from a national death registry database in Chinese mainland between 2013 and 2019. Exposures to fine particulate matter (PM2.5) and coarse particulate matter (PM2.5-10) were assessed by satellite-based models of a 1 × 1 km resolution and assigned to each individual based on residential address. The associations of PM2.5 and PM2.5-10 with COPD mortality were examined using a time-stratified case-crossover design and conditional logistic regressions with distributed lag models. We further conducted stratified analyses by age, sex, education level, and season.

Short-term exposures to both PM2.5 and PM2.5-10 were associated with increased risks of COPD mortality. These associations appeared and peaked on the concurrent day, attenuated and became nonsignificant after 5 or 7 days, respectively. The exposure-response curves were approximately linear without discernible thresholds. An interquartile range increase in PM2.5 and PM2.5-10 concentrations was associated with 4.23% (95% CI: 3.75%, 4.72%) and 2.67% (95% CI: 2.18%, 3.16%) higher risks of COPD mortality over lag 0-7 d, respectively. The associations of PM2.5 and PM2.5-10 attenuated slightly but were still significant in the mutual-adjustment models. A larger association of PM2.5-10 was observed in the warm season.

This individual-level, nationwide, case-crossover study suggests that short-term exposure to PM2.5 and PM2.5-10 might act as one of the environmental risk factors for COPD mortality.

This study is supported by the National Key Research and Development Program of China (2023YFC3708304 and 2022YFC3702701), the National Natural Science Foundation of China (82304090 and 82030103), the 3-year Action Plan for Strengthening the Construction of the Public Health System in Shanghai (GWVI-11.2-YQ31), and the Science and Technology Commission of Shanghai Municipality (21TQ015).

Cobalt (Co) is a metal which is widely used in the industrial production. The previous studies found the toxic effects of environmental Co exposure on multiple organs. However, the correlation of blood Co concentration with lung function was inconsistent in patients with chronic obstructive pulmonary disease (COPD).

All 771 stable COPD patients were recruited. Peripheral blood and clinical information were collected. The levels of blood Co and serum CC16 were measured.

Cross-sectional study suggested that the level of blood Co was inversely and dose-dependently related to lung function parameters. Each 1 ppm elevation of blood Co was related to 0.598 L decline in FVC, 0.465 L decline in FEV1, 6.540% decline in FEV1/FVC%, and 14.013% decline in FEV1%, respectively. Moreover, higher age, enrolled in winter, current-smoking, higher smoking amount, and inhaled corticosteroids prominently exacerbated the negative correlation between blood Co and lung function. Besides, serum CC16 content was gradually reduced with blood Co elevation in COPD patients. Besides, serum CC16 was positively correlated with lung function, and inversely related to blood Co. Additionally, decreased CC16 substantially mediated 11.45% and 6.37% Co-triggered downregulations in FEV1 and FEV1%, respectively.

Blood Co elevation is closely related to the reductions of pulmonary function and serum CC16. CC16 exerts a significantly mediating role of Co-related to pulmonary function decrease among COPD patients.

Chronic obstructive pulmonary disease (COPD) and lung cancer represent formidable challenges in global health, characterized by intricate pathophysiological mechanisms and multifaceted disease progression. This comprehensive review integrates insights from diverse perspectives to elucidate the intricate roles of long non-coding RNAs (lncRNAs) in the pathogenesis of COPD and lung cancer, focusing on their diagnostic, prognostic, and therapeutic implications. In the context of COPD, dysregulated lncRNAs, such as NEAT1, TUG1, MALAT1, HOTAIR, and GAS5, emerge as pivotal regulators of genes involved in the disease pathogenesis and progression. Their identification, profiling, and correlation with the disease severity present promising avenues for prognostic and diagnostic applications, thereby shaping personalized disease interventions. These lncRNAs are also implicated in lung cancer, underscoring their multifaceted roles and therapeutic potential across both diseases. In the domain of lung cancer, lncRNAs play intricate modulatory roles in disease progression, offering avenues for innovative therapeutic approaches and prognostic indicators. LncRNA-mediated immune responses have been shown to drive lung cancer progression by modulating the tumor microenvironment, influencing immune cell infiltration, and altering cytokine production. Their dysregulation significantly contributes to tumor growth, metastasis, and chemo-resistance, thereby emphasizing their significance as therapeutic targets and prognostic markers. This review summarizes the transformative potential of lncRNA-based diagnostics and therapeutics for COPD and lung cancer, offering valuable insights into future research directions for clinical translation and therapeutic development.

Chronic obstructive pulmonary disease (COPD) is a complex syndrome with poorly understood mechanisms driving its early progression (GOLD stages 1-2). Elucidating the genetic factors that influence early-stage COPD, particularly those related to airway inflammation and remodeling, is crucial. This study analyzed lung tissue sequencing data from patients with early-stage COPD (GSE47460) and smoke-exposed mice. We employed Weighted Gene Co-Expression Network Analysis (WGCNA) and machine learning to identify potentially pathogenic genes. Further analyses included single-cell sequencing from both mice and COPD patients to pinpoint gene expression in specific cell types. Cell-cell communication and pseudotemporal analyses were conducted, with findings validated in smoke-exposed mice. Additionally, Mendelian randomization (MR) was used to confirm the association between candidate genes and lung function/COPD. Finally, functional validation was performed in vitro using cell cultures. Machine learning analysis of 30 differentially expressed genes identified 8 key genes, with CLEC5A emerging as a potential pathogenic factor in early-stage COPD. Bioinformatics analyses suggested a role for CLEC5A in macrophage-mediated inflammation during COPD. Two-sample Mendelian randomization linked CLEC5A single nucleotide polymorphisms (SNPs) with Forced Expiratory Volume in One Second (FEV1), FEV1/Forced Vital Capacity (FVC) and early/later on COPD. In vitro, the knockdown of CLEC5A led to a reduction in inflammatory markers within macrophages. Our study identifies CLEC5A as a critical gene in early-stage COPD, contributing to its pathogenesis through pro-inflammatory mechanisms. This discovery offers valuable insights for developing early diagnosis and treatment strategies for COPD and highlights CLEC5A as a promising target for further investigation.

Some occupational and environmental exposures could increase the risk of chronic obstructive pulmonary disease (COPD) and hypertension in various work and living environments. However, the effect of exposure to multiple exogenous harmful substances on COPD and hypertension co-morbidities remains unclear.

Participants were selected from eight hospitals in five provinces in China using a multistage cluster sampling procedure. Participants' demographic, exposure, and disease information were collected through questionnaires, spirometry, and blood pressure examinations. Demographic data were used as matching factors, and 1:1 matching between the exposed and non-exposed groups was performed by employing propensity score matching (PSM) to minimize the influence on the results. A one-way chi-squared analysis and multifactorial logistic regression were used to analyze the association between the exposure to exogenous harmful substances (metals and their compound dust, inorganic mineral dust, organic chemicals, and livestock by-products) and the co-morbidity of COPD and hypertension.

There were 6,610 eligible participants in the final analysis, of whom 2,045 (30.9%) were exposed to exogenous harmful substances. The prevalence of co-morbidities of COPD and hypertension (6.0%) in the exposure group was higher than their prevalence in the total population (4.6%). After PSM, exogenous harmful substance exposure was found to be a risk factor for the co-morbidity of COPD and hypertension [odds ratio (OR) = 1.347, 95% confidence interval (CI): 1.011-1.794], which was not statistically significant before PSM (OR = 1.094, 95% CI: 0.852-1.405). Meanwhile, the results of different outcomes showed that the association between hypertension and exogenous harmful substance exposure was not statistically significant (OR = 0.965, 95% CI: 0.846-1.101). Smoking (OR = 4.702, 95% CI: 3.321-6.656), history of a respiratory disease during childhood (OR = 2.830, 95% CI: 1.600-5.006), and history of respiratory symptoms (OR = 1.897, 95% CI: 1.331-2.704) were also identified as risk factors for the co-morbidity of COPD and hypertension.

The distribution of exogenous harmful substance exposure varies in the population, and the prevalence of co-morbidities is generally higher in susceptible populations. Exposure to exogenous harmful substances was found to be a key risk factor after adjusting for demographic confounders.

Chronic obstructive pulmonary disease (COPD) affecting 334 million people in the world remains a major cause of morbidity and mortality. Proper diagnosis of COPD is still a challenge and largely solely based on spirometric criteria. We aimed to investigate the potential of nitrosative/oxidative stress and related metabolic biomarkers in exhaled breath condensate (EBC) to discriminate COPD patients.

Three hundred three participants were randomly selected from a 15,000-transit worker cohort within the Respiratory disease Occupational Biomonitoring Collaborative Project (ROBoCoP). COPD was defined using the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria as post-bronchodilator ratio of Forced Expiratory Volume in 1st second to Forced Vital Capacity < 0.7 in spirometry validated by an experienced pulmonologist. Discriminative power of biomarker profiles in EBC was analyzed using linear discriminant analyses.

Amongst 300 participants with validated spirometry, 50.3% were female, 52.3 years old in average, 36.0% were current smokers, 12.7% ex-smokers with mean tobacco exposure of 15.4 pack-years. Twenty-one participants (7.0%) were diagnosed as COPD, including 19 new diagnoses, 12 of which with a mild COPD stage (GOLD 1). Amongst 8 biomarkers measured in EBC, combination of 2 biomarkers, Lactate and Malondialdehyde (MDA) significantly discriminated COPD subjects from non-COPD, with a 71%-accuracy, area under the receiver curve of 0.78 (p-value < 0.001), and a negative predictive value of 96%.

These findings support the potential of biomarkers in EBC, in particular lactate and MDA, to discriminate COPD patients even at a mild or moderate stage. These EBC biomarkers present a non-invasive and drugless technique, which can improve COPD diagnosis in the future.

Air pollution poses a risk to the respiratory health of individuals with COPD. Long- and short-term exposures to higher levels of particulate-rich air pollution are associated with increased COPD exacerbation, hospitalization, and mortality, collectively implicating air pollution as a cause of adverse COPD-related outcomes.

This review summarizes the evidence for COPD as a phenotype that confers susceptibility for adverse health outcomes in the face of common air pollution. We highlight how typical contributors to compromised urban air quality, including that from traffic, wildfire smoke, and indoor biomass combustion, adversely affect the COPD patient population. Evidence underscoring the burden of ongoing air pollution exposure on patients with COPD is discussed. We then detail the detrimental impact of that exposure on COPD pathophysiology, which in turn increases the patient's susceptibility. We specifically propose that indoor air is a particularly rational target for increased monitoring and remediation to protect patients with COPD. Because COPD is a heterogeneous disease with several endotypes, future intervention studies need to better include control populations, to highlight COPD-specific risks and identify subpopulations within patients with COPD who will benefit the most from improved indoor air quality.

Regulatory efforts must continue to broadly lower emission standards to protect this susceptible population from the negative health impacts of air pollution.

Pollution and climate change constitute a combined, grave and pervasive threat to humans and to the life-support systems on which they depend. Evidence shows a strong association between pollution and climate change on cardiovascular and respiratory diseases, and pulmonary vascular disease (PVD) is no exception. An increasing number of studies has documented the impact of environmental pollution and extreme temperatures on pulmonary circulation and the right heart, on the severity and outcomes of patients with pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension (PH), on the incidence of pulmonary embolism, and the prevalence and severity of diseases associated with PH. Furthermore, the downstream consequences of climate change impair health care systems' accessibility, which could pose unique obstacles in the case of PVD patients, who require a complex and sophisticated network of health interventions. Patients, caretakers and health care professionals should thus be included in the design of policies aimed at adaptation to and mitigation of current challenges, and prevention of further climate change. The purpose of this review is to summarize the available evidence concerning the impact of environmental pollution and climate change on the pulmonary circulation, and to propose measures at the individual, healthcare and community levels directed at protecting patients with PVD.

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

Most patients with chronic obstructive pulmonary disease (COPD) have at least one additional, clinically relevant chronic disease. Those with the most severe airflow obstruction will die from respiratory failure, but most patients with COPD die from non-respiratory disorders, particularly cardiovascular diseases and cancer. As many chronic diseases have shared risk factors (eg, ageing, smoking, pollution, inactivity, and poverty), we argue that a shift from the current paradigm in which COPD is considered as a single disease with comorbidities, to one in which COPD is considered as part of a multimorbid state-with co-occurring diseases potentially sharing pathobiological mechanisms-is needed to advance disease prevention, diagnosis, and management. The term syndemics is used to describe the co-occurrence of diseases with shared mechanisms and risk factors, a novel concept that we propose helps to explain the clustering of certain morbidities in patients diagnosed with COPD. A syndemics approach to understanding COPD could have important clinical implications, in which the complex disease presentations in these patients are addressed through proactive diagnosis, assessment of severity, and integrated management of the COPD multimorbid state, with a patient-centred rather than a single-disease approach.

Chronic obstructive pulmonary disease (COPD) is a common, irreversible but preventable disease characterized by persistent respiratory symptoms. The mortality rate of COPD is predicted to reach 5.4 million by the year 2060. Despite its heavy burden on healthcare expenditure worldwide, only 15% of cases are medically identified. The potential benefits of facemask-wearing for COPD patients remain a topic of debate.

We will conduct a systematic review of all randomized trials and non-randomized controlled trials to evaluate the impact of facemasks on COPD patients. Our review will be based on literature obtained through a comprehensive search strategy across multiple electronic databases, including the Cochrane Library, Embase, PubMed, Web of Science, the Chinese Biomedical Database (SinoMed), and China National Knowledge Infrastructure (CNKI), with no restrictions on language or date of publication. Two independent researchers will extract and assess all relevant data using pre-designed data extraction forms. The included studies will be assessed using the Cochrane RoB2 tool and the suggested risk of bias criteria proposed by the Effective Practice and Organization of Care reviews group of the Cochrane collaboration. The quality of evidence will be assessed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. We will use Review Manager 5.4 software for statistical analysis.

In the context of COVID-19, it is important for COPD patients to wear facemasks. This study aims to conduct a comprehensive and systematic assessment of the impact of facemasks on the physiology and activity of COPD patients.

PROSPERO registration number CRD42022326265.