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Journal articleNamporn T, Manopwisedjaroen S, Ngodngamthaweesuk M, et al., 2025,
Evidence of Mpox clade IIb infection in primary human alveolar epithelium
, EMERGING MICROBES & INFECTIONS, Vol: 14 -
Journal articleSousa-Pinto B, Louis R, Anto JM, et al., 2025,
Adherence to inhaled corticosteroids and long-acting β2-agonists in asthma: A MASK-air study
, PULMONOLOGY, Vol: 31, ISSN: 2531-0437- Cite
- Citations: 11
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Journal articleWilliams P, Buttery S, Perkins A, et al., 2025,
Exploring the predictors and barriers to accepting smoking cessation support within a targeted lung health check setting
, BMJ Open Respiratory Research, ISSN: 2052-4439Background: The Quit Smoking Lung Health Intervention Trials (QuLIT-1 and -2) and other studies show that providing immediate smoking cessation within lung cancer screening services substantially improves quit rates. However, in the QuLIT2 trial only around half of those offered smoking cessation support actually accepted it. Understanding what underpins this and how to facilitate higher smoking cessation rates would enhance the health impact of the Targeted Lung Health Check programme.Method: We compared characteristics of participants in the intervention arm of the QuLIT-2 study who accepted or declined the offer of smoking cessation support and conducted thematic analysis of interviews with 15 smokers who had declined it. Results: Of 152 randomised to smoking cessation support (61.3±4.8 years, 42% female), 80 declined the offer and 15 dropped out after the initial session leaving 57 “accepters”. Accepters were more likely to be female [53% vs 40% AOR: 3.30, 95%CI 1.47-7.48], younger [AOR: 0.90(0.80-0.98)] and were more likely to live in areas of medium or low deprivation, [AOR: 5.30(1.86-22.85)]. Thematic analysis of the interviews revealed four main barriers to acceptance: concerns about mental health, beliefs about quitting smoking and about the effectiveness of interventions, and negative past experiences of smoking cessation support.Discussion: Cessation services embedded in lung screening clinics need to anticipate barriers such as mental health concerns, past experiences and personal beliefs. Efforts should be made to design and offer equitable services that meet the needs of this population. Trial registration: This study is registered online: ISRCTN12455871.What is already known on this topic- Intensive smoking cessation support embedded within lung cancer screening services significantly increases 3 and 12 month quit rates among this high-risk population. What this study adds- Despite the success of cessation embedded into screening, a
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Journal articleAli N, Katsouli J, Auyang E, et al., 2025,
Microplastic and nanoplastic pollution and associated potential disease risks
, The Lancet Planetary Health, ISSN: 2542-5196 -
Journal articleAntão J, Rodrigues G, Zounemat-Kermani N, et al., 2025,
Proteomic and Transcriptomic Signatures of Poor Asthma Symptom Control in the U-BIOPRED Cohort.
, AllergyBACKGROUND: Controlling asthma symptoms remains challenging. Understanding its molecular mechanisms may provide new insights into asthma pathophysiology. We explored the associations between the transcriptome and proteome in blood and sputum and asthma symptom control. METHODS: This cross-sectional study included asthmatic and healthy adults from the U-BIOPRED cohort. Uncontrolled symptoms were defined as a mean ≥ 1.5 points on the 5-item asthma control questionnaire. Stability selection using LASSO logistic regression identified genes/proteins associated with symptom control, followed by logistic regression. Analyses were adjusted for age, sex, age of asthma onset, smoking status, body mass index (BMI), FEV1% predicted, exacerbation history, anti-IgE therapy and urinary steroid levels. The selected variables were compared with healthy controls using linear regression, adjusted for age, sex, BMI, smoking status and urinary steroid levels. RESULTS: Four serum proteins were selected based on data from 415 asthmatics (median age 52 [41, 61] years; 59% female; 64% uncontrolled). Higher TWEAKR/TNFRSF12A [OR 2.25 (95% CI 1.15, 4.77)] and MBL/MBP-C [1.6 (1.07, 2.42)] levels increased the odds of uncontrolled symptoms, whereas higher MK08/MAPK8 [0.48 (0.29, 0.76)] and CD5L [0.59 (0.41, 0.82)] levels decreased the odds. CD5L levels were significantly lower in severe asthma than in healthy controls [estimate -0.23 (95% CI -0.41, -0.04)]. No associations were found between symptom control and the sputum proteome (N = 90) or the sputum (N = 96) and blood (N = 360) transcriptomes. CONCLUSION: Four serum proteins distinguished asthmatics with uncontrolled from controlled symptoms. CD5L levels were also lower in asthmatics with severe disease than in healthy controls, warranting further investigation into its potential therapeutic value.
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Journal articleTahmasebi S, Amani D, Adcock IM, et al., 2025,
Harnessing miR-145 in NSCLC: mechanistic roles, diagnostic-prognostic utility, and therapeutic potential
, Cancer Cell International, ISSN: 1475-2867Non-small cell lung cancer (NSCLC) is responsible for most lung cancer diagnoses and causes elevated worldwide mortality rates, mostly due to late detection and the development of resistance against medicines. This review summarizes evidence regarding miR-145, a downregulated NSCLC microRNA, and emphasizes the multifaceted tumor-suppressor activity of miR-145 involving the repression of oncogenes such as c-Myc, epidermal growth factor receptor (EGFR), and octamer-binding transcription factor 4 (OCT4) to restrict cell growth, stemness, epithelial-to-mesenchymal-transition (EMT), metastasis via Phosphoinositide 3-kinases (PI3Ks)/ activation of protein kinase B (AKT, Mitogen‑activated protein kinase (MAPK), and transforming growth factor beta (TGF-β)/Smad signaling. miR-145 also exhibits potential diagnostic specificity in distinguishing NSCLC cases from controls through serum/plasma testing, with greater sensitivity/specificity in multi-miRNA sets, and prognostic value predicting resistance, survival, and disease advancement. Therapeutically, miR-145 enhances responses to chemotherapies, targeted therapies, radiotherapy, and immunotherapies by counteracting resistance networks. Utilizing novel delivery platforms, such as nanoparticles, exosomes, and chemical modifications, may overcome stability and targeting issues that exist with miRNA therapies. Through the integration of preclinical and clinical information, this review helps identify crucial research gaps, such as incompletely defined regulatory networks and the need for large-scale studies, and calls for the application of advanced techniques to expedite the integration of miR-145-based treatments with personalized NSCLC therapy for improved outcomes.
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Journal articlede Santana MBR, Cruz ÁA, de Araújo JLF, et al., 2025,
Variants in the Glucocorticoid Receptor gene (NR3C1), asthma control and serum cytokine levels.
, Respir MedINTRODUCTION: Asthma is a heterogeneous disease usually treated with inhaled corticosteroids (ICS) and long-acting beta2 agonists. However, not all individuals achieve adequate control with ICS. AIM: To identify genetic variants in the glucocorticoid receptor gene (NR3C1) associated with asthma endophenotypes, bronchodilator reversibility, and asthma control under medium-to-high ICS doses. METHODS: Association analyses were performed in 365 patients with moderate-to-severe asthma, 383 with mild asthma, and 330 non-asthmatic individuals. Asthma severity was defined by the need for regular treatment with medium-to-high ICS doses. Bronchodilator reversibility was defined as an increase of ≥200 ml and ≥12% in FEV1 from baseline. Asthma control was assessed using the ACQ6 score. Serum cytokine concentrations were measured with Luminex. RESULTS: The A allele of rs2918417 was associated with reduced risk of moderate-to-severe asthma (OR: 0.50; 95% CI: 0.26-0.98) and fewer exacerbations (OR: 0.54; 95% CI: 0.30-0.96); GA/AA genotypes showed lower IL-8 and IL-13 levels compared to GG. The G allele of rs6877893 decreased the risk of uncontrolled asthma in the recessive model (OR: 0.53; 95% CI: 0.29-0.98), with GG carriers showing reduced IL-17A. Conversely, the A allele of rs4585488 increased risk of uncontrolled asthma (OR: 4.42; 95% CI: 1.06-18.48), and the C allele of rs4912650 was linked to poor control (OR: 1.64; 95% CI: 1.01-2.69). The G allele of rs4607376 was associated with lack of bronchodilator reversibility (OR: 1.51; 95% CI: 1.05-2.17) and asthma exacerbations (OR: 1.37; 95% CI: 1.01-1.87). CONCLUSIONS: NR3C1 variants are associated with moderate-to-severe asthma, poor control, lack of bronchodilator reversibility, and differential cytokine profiles.
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Journal articleSousa-Pinto B, Schleich F, Louis G, et al., 2025,
Daily digital biomarkers in the follow-up and clustering of patients with asthma
, Pulmonology, Vol: 31, ISSN: 2531-0429Background and Research questionWe aimed to assess whether levels of digital biomarkers can reflect monthly patterns of asthma controlStudy design and methodsWe performed a longitudinal study on patients with asthma and comorbid rhinitis who filled ≥26 days of data in a month in the MASK-air® app and who reported at least 1 day of treatment with an inhaled corticosteroid with or without a long-acting β2-agonist (ICS ± LABA). We applied k-means cluster analysis to define clusters of months according to daily asthma control and medication use. Clusters were compared using digital biomarkers (visual analogue scale [VAS] on asthma symptoms and electronic daily asthma control score [e-DASTHMA]). We compared patients who did not switch with patients who switched their ICS ± LABA.ResultsWe assessed 243 patients and 1358 months. We identified three clusters of poor asthma control despite high ICS ± LABA adherence, one cluster of poor asthma control and poor ICS ± LABA adherence, one cluster of good asthma control and high ICS ± LABA adherence and one cluster of good asthma control despite poor ICS ± LABA adherence. These clusters displayed relevant differences in VAS asthma and e-DASTHMA levels. Similar clusters were found in ‘non-switchers’ versus ‘switchers’.ConclusionLevels of digital biomarkers reflect asthma control patterns and might be used to monitor patients with asthma.
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Journal articleAlimohammadi M, Amani D, Adcock IM, et al., 2025,
Dual role of mir-146a in non-small cell lung cancer progression: molecular mechanisms and clinical potential
, Cellular Signalling, Vol: 136, ISSN: 0898-6568Non-small cell lung cancer (NSCLC) remains a leading cause of cancer mortality. 2.48 million new cases were reported globally in 2022, driven by rising adenocarcinoma rates linked to environmental factors such as air pollution. MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression by targeting messenger RNA for degradation or translational repression. Emerging studies highlight miR-146a as a molecular pivot with dual functionality that acts as a tumor suppressor by inhibiting NF-κB signaling to reduce inflammation and chemoresistance while paradoxically exhibiting oncogenic potential through immune modulation in specific microenvironments. The expression of miR-146a has been associated with numerous pathological and physiological alterations in cancer cells, including the modulation of various signaling pathways such as TNF-α, NF-κB, MEK-1/2, and JNK-1/2. miR-146a can act exogenously through extracellular vesicles and thereby reprogram tumor-associated macrophages to either promote or inhibit metastasis depending on cellular context. The diagnostic potential of miR-146a is underscored by expression patterns correlating with disease progression and treatment response in NSCLC, whilst preclinical studies suggest therapeutic promise when combined with checkpoint inhibitors. In this review, we first discuss the biogenesis and function of miR-146a in NSCLC development, with emphasis on recent findings that underscore the dual role of miR-146a in the regulation of cell proliferation, invasion, inflammation, immune responses, and chemoresistance in NSCLC. We also describe the possible function of miR-146a as a biomarker for cancer diagnosis, prognosis, and therapeutic target.
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Journal articleFeng Y, Weng J, Li C, et al., 2025,
FUNDC1 promoted ferroptosis via JNK pathway in cigarette smoking-induced chronic obstructive pulmonary disease
, Lung, Vol: 203, ISSN: 0341-2040BackgroundCigarette smoking (CS), the major risk factor for chronic obstructive pulmonary disease (COPD), induces oxidative stress, mitophagy, and ferroptosis. Because FUN14 domain-containing protein 1 (FUNDC1), a mitophagy receptor, may drive the onset and progression of COPD, we investigated its role in CS-induced ferroptosis in COPD and to explore the underlying cellular signaling mechanisms.MethodsWild-type (C57BL/6J background) and FUNDC1-knockdown (KD) mice were exposed to CS for 12 weeks. FUNDC1-KD and FUNDC1-overexpressing (OE) alveolar epithelial A549 cells were exposed to CS extracts (CSE) in the presence and absence of the JNK inhibitor, SP6001 (10 mM). Oxidative stress, inflammation, mitochondrial function, and ferroptosis were measured.ResultsFUNDC1 expression was increased in lung tissues from COPD patients and CS-exposed mice. CS exposure induced airway inflammation, reduced lung function, and enhanced ferroptosis in mice. FUNDC1-KD prevented CS-induced lung injury in mice. Similarly, CSE exposure up-regulated FUNDC1 expression, promoted ferroptosis, inflammation, oxidative stress, lipid peroxidation, and mitochondrial damage in A549 cells. FUNDC1-KD prevented CSE-induced cellular damage. Transcriptomic data indicated that FUNDC1 mediated ferroptosis through the JNK pathway. These in vitro results were further confirmed by pretreatment with the JNK inhibitor SP6001.ConclusionFUNDC1 plays an important role in CS-exposed alveolar epithelial cells and in a mouse model of COPD through the JNK-ferroptosis pathway.
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Journal articleRoofchayee ND, Heshmatnia J, Jamatti H, et al., 2025,
Transcription Factor and Cytokine Profiles in Peripheral Blood T Helper Cells in Patients with Idiopathic Pulmonary Fibrosis
, IRANIAN JOURNAL OF ALLERGY ASTHMA AND IMMUNOLOGY, Vol: 24, Pages: 786-798, ISSN: 1735-1502 -
Journal articleHopkinson NS, 2025,
A lesson from Nye Bevan on the roots of fascism
, The BMJ, Vol: 391, ISSN: 0959-8146 -
Journal articleUsmani OS, Toumpanakis D, Meah S, et al., 2025,
Whole lung directed anti-muscarinic therapy improves small airway dysfunction in COPD patients
, European Respiratory Journal, ISSN: 0903-1936 -
Journal articleBloom C, Yang F, Mcclean M, et al., 2025,
Global prevalence of eligibility for biologic therapy in ATS/ERS-defined severe asthma: A Systematic Review
, World Allergy Organization Journal, ISSN: 1939-4551 -
Journal articleZimmer AJ, Das R, Lopez PE, et al., 2025,
Objective cough counting in clinical practice and public health: a scoping review.
, Lancet Digit HealthQuantifying cough can offer value for respiratory disease assessment and monitoring. Traditionally, patient-reported outcomes have provided subjective insights into symptoms. Novel digital cough counting tools now enable objective assessments; however, their integration into clinical practice is limited. The aim of this scoping review was to address this gap in the literature by examining the use of automated and semiautomated cough counting tools in patient care and public health. A systematic search of six databases and preprint servers identified studies published up to Feb 12, 2025. From 6968 records found, 618 full-text articles were assessed for eligibility, and 77 were included. Five clinical use cases were identified-disease diagnosis, severity assessment, treatment monitoring, health outcome prediction, and syndromic surveillance-with scarce available evidence supporting each use case. Moderate correlations were found between objective cough frequency and patient-reported cough severity (median correlation coefficient of 0.42, IQR 0·38 to 0·59) and quality of life (median correlation coefficient of -0·49, -0·63 to -0·44), indicating a complex relationship between quantifiable measures and perceived symptoms. Feasibility challenges include device obtrusiveness, monitoring adherence, and addressing patient privacy concerns. Comprehensive studies are needed to validate these technologies in real-world settings and show their clinical value. Early feasibility and acceptability assessments are essential for successful integration.
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Journal articleManeechotesuwan K, Kanokkantapong C, Boonpromkul C, et al., 2025,
The association of defective pleural sRAGE production with the recurrence of malignant pleural effusion after Talc pleurodesis
, Scientific Reports, Vol: 15, ISSN: 2045-2322Symptomatic malignant pleural effusions (MPE) are treated with chemical pleurodesis to prevent recurrence. The serum soluble receptor for advanced glycation end products (sRAGE) has been linked to lung cancer progression but its role in predicting talc pleurodesis failure is unclear. A prospective cohort study was conducted from November 2023 to December 2024, encompassing subjects with confirmed MPE. Pleural fluid samples were collected prior to intercostal drainage (ICD) insertion for the measurement of sRAGE, ADAM10, MMP9, and HMGB1 levels. Participants were monitored for 90-day post-pleurodesis failure, pleural interventions, and survival. Among seventy-three adults (median age 66 [IQR 53–74 years]) with MPE who received pleurodesis, lung adenocarcinoma was the most common. Talc pleurodesis failure (24.7%) was associated with greater pleural fluid output, multiple pleurodesis attempts, longer ICD retention, and lower pH and lymphocyte fraction. Pleural sRAGE and MMP9 levels were significantly diminished (p = 0.0033 and p = 0.029, respectively), whereas HMGB1 levels were substantially elevated (p = 0.019) in the failure cases. Among biomarkers, pleural sRAGE had the most predictive value for talc pleurodesis failure, followed by HMGB1 and MMP9. However, pleural sRAGE and MMP-9 lacked prognostic significance for 90-day mortality. The present study demonstrated that lower pleural sRAGE is a potential predictive biomarker for talc pleurodesis failure despite inferiority to pleural acidity. Imbalance between sRAGE and HMGB1 in MPE may be associated with the underlying mechanism for talc pleurodesis failure.
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Journal articleLaverty A, Parnham J, Filippos T F, et al., 2025,
Social media use and child cigarette smoking and e-cigarette use: a cohort study 2015-2023
, Tobacco Induced Diseases, ISSN: 1617-9625IntroductionThere are growing concerns that advertising and promotion on social media are driving youth use of tobacco and e-cigarettes. The UK provides an instructive example as it has high levels of e-cigarette use, high levels of social media use and a restrictive tobacco control environment. Existing evidence in the UK however, has not focused on children, has not been updated to reflect changes in patterns of social media use and in the use of these products. The aim of this study is to assess the associations of social media use with smoking and vaping.MethodsUsing data from the United Kingdom Household Longitudinal Study on 10–17-year-olds between 2015-2023, Generalised Estimating Equation (GEE) models estimated relationships between time spent on social media and likelihood of smoking tobacco and using e-cigarettes. Models were controlled for possible confounders including socio-demographics and whether children lived in a home with e-cigarette use or tobacco smoking. ResultsWe included data from 9,359 participants with 25,704 observations. Current cigarette smoking was reported by 4.9% of the sample and current e-cigarette use by 3.1% of the sample. Our adjusted models found strong relationships between time spent on social media and both smoking and vaping (p value for trend <0.001). For example, use of social media for ≥7 hours/day was linked to greater odds of tobacco (Adjusted Odds Ratio (AOR) 5.13, 95% Confidence Interval (CI) 3.32-7.95) and e-cigarette use (AOR 4.26, CI 2.25-8.08). ConclusionsThis study finds associations between time spent on social media and both smoking and vaping among children. Enforcing regulations on content and restricting the duration of social media use may be warranted to protect children’s health.
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Journal articleUwagboe I, Mumby S, Dunlop IE, et al., 2025,
Does mechanobiology drive respiratory disease? Biomechanical induction of mucus hypersecretion in human bronchial organoids using a photocontrolled biomaterial gel
, Biomaterials Science, ISSN: 2047-4830Respiratory diseases such as COPD, IPF and severe asthma are major causes of death globally, characterized by chronic inflammation and by fibrotic biomechanical remodelling of the lung ECM. However, present treatments focus on relieving inflammation and symptoms and do not address the mechanobiological aspect. This is in great part because the role of mechanobiology in disease progression and aetiology is not well-understood, indicating a need for new investigatory models. Here we introduce a combined biomaterial and 3D-organoid model, based on a hybrid biomaterial-matrix double-network gel, whose mechanical properties are dynamically photocontrolled by the application of light. This combines basement membrane extract (Matrigel) with biocompatible polymer (poly(ethylene glycol) diacrylate), and a low-toxicity photoinitation system. We achieve rapid (<5 mins) photoinduced stiffening over the range of remodelled lung tissue (up to ~140 kPa). Bronchosphere organoids from primary human bronchial epithelial cells, embedded within the hybrid gel, replicate airway physiology and exhibit a dynamic biological response to matrix stiffening. We show that the expression of mucus proteins Muc5AC and Muc5B is biomechanically enhanced over a period of 24 – 72 h, with in particular Muc5B showing a substantial response at 48 h after matrix stiffening. Mucus hypersecretion is a symptom of respiratory disease, and these results support the hypothesis that biomechanics is a driver of disease aetiology. We combine the photostiffened hybrid matrix gel with organoids from COPD donors, generating an advanced disease model including both cellular and biomechanical aspects. We propose this technology platform for evaluating mechanomodulatory therapeutics in respiratory disease.
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Journal articleSanchez-Burgos I, Tejedor AR, Collepardo-Guevara R, et al., 2025,
Molecular insights on the mechanism of α1-antitrypsin condensate formation and maturation
, PLoS Computational Biology, Vol: 21, ISSN: 1553-734XThe deficiency of -antitrypsin protein is a genetic disorder characterized by the accumulation of misfolded protein aggregates within hepatocytes, leading to liver dysfunction. In the lung, it is found in macrophages, bronchial and epithelial alveolar cells type 2, leading to pulmonary emphysema. Despite extensive research, the precise mechanism underlying the formation of -antitrypsin inclusion bodies remain elusive. In this study, we combine equilibrium and non-equilibrium molecular dynamics simulations to elucidate the intricate process of -antitrypsin condensate formation and maturation. Our mechanistic model explains cluster accumulation—specifically the onset of this pathogenesis—through the emergence of phase-separated liquid-like protein droplets, which subsequently undergo inter-protein β-sheet transitions between misfolded variants, resulting in solid-like clusters. We find that this mechanism only applies to the misfolded variant, Z--antitrypsin, which phase-separates driven by its disordered C-terminus. In contrast, the native protein, M--antitrypsin, shows much lower propensity to phase-separate and later form kinetically trapped aggregates. Furthermore, we explore how Z--antitrypsin exhibits an increased capacity to form condensates near external walls with different types of interactions. Such conditions can be similar to those found within the endoplasmic reticulum membrane, where phase separation and hardening take place. Overall, our results shed light on the molecular basis of -antitrypsin-related disorders and provide valuable microscopic insights for the development of therapeutic strategies targeting protein misfolding and aggregation-related disorders.
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Journal articleAdesibikan A, Williams P, Cumella A, et al., 2025,
The relationship of material deprivation with emergency or unplanned healthcare utilisation in adults with Chronic Obstructive Pulmonary Disease: analysis from an Asthma + Lung UK survey
, BMJ Open Respiratory Research, ISSN: 2052-4439Background Various forms of deprivation have been linked to poor health. Emergency and unplanned healthcare utilisation (EUHU) is inefficient and represents suboptimal chronic disease management. Understanding the relationship between material deprivation – the inability to afford certain basic items of living – and EUHU in COPD may identify intervention targets. However, research is limited. This study investigates the relationship between material deprivation and the frequency of EUHU.MethodsData were analysed from 3472 individuals with COPD who completed an online Asthma + Lung UK survey (January-March2024). The relationship was assessed between material deprivation (nine-item European Union Statistics on Income and Living Conditions survey) and self-reported frequency of EUHU in the preceding year in 5 categories. ResultsPeople experiencing material deprivation had higher odds of reporting a higher frequency of emergency and unplanned healthcare utilisation compared to those who were not (OR:1.27, 95%CI:1.08-1.49, p=0.005), independent of identified confounders. Associations were also seen with six of the nine individual items including not being able to afford mortgage/rent/utility bills, cars, unexpected expenses, heating, decent meal, or a holiday. Living in cold/or damp housing was associated with increased emergency and unplanned healthcare utilisation.Discussion and ConclusionMaterial deprivation is associated with more frequent emergency and unplanned healthcare utilisation in COPD. Interventions targeting material deprivation may improve health outcomes and reduce emergency and unplanned healthcare utilisation.
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