Imperial College London

ProfessorFanChung

Faculty of MedicineNational Heart & Lung Institute

Professor of Respiratory Medicine
 
 
 
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Contact

 

+44 (0)20 7594 7954f.chung Website

 
 
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Assistant

 

Miss Carolyn Green +44 (0)20 7594 7959

 
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Location

 

227BGuy Scadding BuildingRoyal Brompton Campus

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Summary

 

Publications

Publication Type
Year
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1578 results found

Weng J, Liu Q, Li C, Feng Y, Chang Q, Xie M, Wang X, Li M, Zhang H, Mao R, Zhang N, Yang X, Chung KF, Adcock IM, Huang Y, Li Fet al., 2024, TRPA1-PI3K/Akt-OPA1-ferroptosis axis in ozone-induced bronchial epithelial cell and lung injury., Sci Total Environ, Vol: 918

BACKGROUND: Transient receptor potential (TRP) ankyrin 1 (TRPA1) could mediate ozone-induced lung injury. Optic Atrophy 1 (OPA1) is one of the significant mitochondrial fusion proteins. Impaired mitochondrial fusion, resulting in mitochondrial dysfunction and ferroptosis, may drive the onset and progression of lung injury. In this study, we examined whether TRPA1 mediated ozone-induced bronchial epithelial cell and lung injury by activating PI3K/Akt with the involvement of OPA1, leading to ferroptosis. METHODS: Wild-type, TRPA1-knockout (KO) mice (C57BL/6 J background) and ferrostatin-1 (Fer-1)-pretreated mice were exposed to 2.5 ppm ozone for 3 h. Human bronchial epithelial (BEAS-2B) cells were treated with 1 ppm ozone for 3 h in the presence of TRPA1 inhibitor A967079 or TRPA1-knockdown (KD) as well as pharmacological modulators of PI3K/Akt-OPA1-ferroptosis. Transcriptome was used to screen and decipher the differential gene expressions and pathways. Oxidative stress, inflammation and ferroptosis were measured together with mitochondrial morphology, function and dynamics. RESULTS: Acute ozone exposure induced airway inflammation and airway hyperresponsiveness (AHR), reduced mitochondrial fusion, and enhanced ferroptosis in mice. Similarly, acute ozone exposure induced inflammatory responses, altered redox responses, abnormal mitochondrial structure and function, reduced mitochondrial fusion and enhanced ferroptosis in BEAS-2B cells. There were increased mitochondrial fusion, reduced inflammatory responses, decreased redox responses and ferroptosis in ozone-exposed TRPA1-KO mice and Fer-1-pretreated ozone-exposed mice. A967079 and TRPA1-KD enhanced OPA1 and prevented ferroptosis through the PI3K/Akt pathway in BEAS-2B cells. These in vitro results were further confirmed in pharmacological modulator experiments. CONCLUSION: Exposure to ozone induces mitochondrial dysfunction in human bronchial epithelial cells and mouse lungs by activating T

Journal article

Weng C-M, Wu W-C, Lee M-J, Chen M-C, Chou C-L, Lin C-Y, Chung KF, Kuo H-Pet al., 2024, Influence of Staphylococcal enterotoxin-specific IgE sensitization on therapeutic efficacy of omalizumab therapy in severe asthma., Respirology, Vol: 29, Pages: 252-255

Journal article

Li J, Xu J, Yang L, Xu Y, Zhang X, Bai C, Kang J, Ran P, Shen H, Wen F, Huang K, Yao W, Sun T, Shan G, Yang T, Lin Y, Zhu J, Wang R, Shi Z, Zhao J, Ye X, Song Y, Wang Q, Hou G, Zhou Y, Li W, Ding L, Wang H, Chen Y, Guo Y, Xiao F, Lu Y, Peng X, Zhang B, Wang Z, Zhang H, Bu X, Zhang X, An L, Zhang S, Cao Z, Zhan Q, Yang Y, Liang L, Cao B, Dai H, Chung KF, Chen Z, He J, Wu S, Xiao D, Wang C, China Pulmonary Health Study Groupet al., 2024, Mediating Effect of Tobacco Dependence on the Association Between Maternal Smoking During Pregnancy and Chronic Obstructive Pulmonary Disease: Case-Control Study., JMIR Public Health Surveill, Vol: 10

BACKGROUND: Maternal smoking during pregnancy (MSDP) is a known risk factor for offspring developing chronic obstructive pulmonary disease (COPD), but the underlying mechanism remains unclear. OBJECTIVE: This study aimed to explore whether the increased COPD risk associated with MSDP could be attributed to tobacco dependence (TD). METHODS: This case-control study used data from the nationwide cross-sectional China Pulmonary Health study, with controls matched for age, sex, and smoking status. TD was defined as smoking within 30 minutes of waking, and the severity of TD was assessed using the Fagerstrom Test for Nicotine Dependence. COPD was diagnosed when the ratio of forced expiratory volume in 1 second to forced vital capacity was <0.7 in a postbronchodilator pulmonary function test according to the 2017 Global Initiative for Chronic Obstructive Lung Disease criteria. Logistic regression was used to examine the correlation between MSDP and COPD, adjusting for age, sex, BMI, educational attainment, place of residence, ethnic background, occupation, childhood passive smoking, residential fine particulate matter, history of childhood pneumonia or bronchitis, average annual household income, and medical history (coronary heart disease, hypertension, and diabetes). Mediation analysis examined TD as a potential mediator in the link between MSDP and COPD risk. The significance of the indirect effect was assessed through 1000 iterations of the "bootstrap" method. RESULTS: The study included 5943 participants (2991 with COPD and 2952 controls). Mothers of the COPD group had higher pregnancy smoking rates (COPD: n=305, 10.20%; controls: n=211, 7.10%; P<.001). TD was more prevalent in the COPD group (COPD: n=582, 40.40%; controls: n=478, 33.90%; P<.001). After adjusting for covariates, MSDP had a significant effect on COPD (β=.097; P<.001). There was an association between MSDP and TD (β=.074; P<.001) as well as between TD and COPD (β=

Journal article

Agache I, Canelo-Aybar C, Annesi-Maesano I, Cecchi L, Biagioni B, Chung F, D'Amato G, Damialis A, Del Giacco S, De Las Vecillas L, Dominguez-Ortega J, Galàn C, Gilles S, Giovannini M, Holgate S, Jeebhay M, Nadeau K, Papadopoulos N, Quirce S, Sastre J, Traidl-Hoffmann C, Walusiak-Skorupa J, Sousa-Pinto B, Salazar J, Rodríguez-Tanta LY, Cantero Y, Montesinos-Guevara C, Song Y, Alvarado-Gamarra G, Sola I, Alonso-Coello P, Nieto-Gutierrez W, Jutel M, Akdis CAet al., 2024, The impact of indoor pollution on asthma-related outcomes: A systematic review for the EAACI guidelines on environmental science for allergic diseases and asthma., Allergy

Systematic review using GRADE of the impact of exposure to volatile organic compounds (VOCs), cleaning agents, mould/damp, pesticides on the risk of (i) new-onset asthma (incidence) and (ii) adverse asthma-related outcomes (impact). MEDLINE, EMBASE and Web of Science were searched for indoor pollutant exposure studies reporting on new-onset asthma and critical and important asthma-related outcomes. Ninety four studies were included: 11 for VOCs (7 for incidenceand 4 for impact), 25 for cleaning agents (7 for incidenceand 8 for impact), 48 for damp/mould (26 for incidence and 22 for impact) and 10 for pesticides (8 for incidence and 2 for impact). Exposure to damp/mould increases the risk of new-onset wheeze (moderate certainty evidence). Exposure to cleaning agents may be associated with a higher risk of new-onset asthma and with asthma severity (low level of certainty). Exposure to pesticides and VOCs may increase the risk of new-onset asthma (very low certainty evidence). The impact on asthma-related outcomes of all major indoor pollutants is uncertain. As the level of certainty is low or very low for most of the available evidence on the impact of indoor pollutants on asthma-related outcomes more rigorous research in the field is warranted.

Journal article

Cookson W, Cuthbertson L, Moffatt M, 2024, GENOMIC ATTRIBUTES OF AIRWAY COMMENSAL BACTERIA AND MUCOSA, Communications Biology, ISSN: 2399-3642

Journal article

Xu T, Chen Y, Zhan W, Chung KF, Qiu Z, Huang K, Chen R, Xie J, Wang G, Zhang M, Wang X, Yao H, Liao X, Zhang Y, Zhang G, Zhang W, Sun D, Zhu J, Jiang S, Feng J, Zhao J, Sun G, Huang H, Zhang J, Wang L, Wu F, Li S, Xu P, Chi C, Chen P, Jiang M, He W, Huang L, Luo W, Li S, Zhong N, Lai K, China Cough Coalitionet al., 2024, Profiles of Cough and Associated Risk Factors in Nonhospitalized Individuals With SARS-CoV-2 Omicron Variant Infection: Cross-Sectional Online Survey in China., JMIR Public Health Surveill, Vol: 10

BACKGROUND: Cough is a common symptom during and after COVID-19 infection; however, few studies have described the cough profiles of COVID-19. OBJECTIVE: The aim of this study was to investigate the prevalence, severity, and associated risk factors of severe and persistent cough in individuals with COVID-19 during the latest wave of the Omicron variant in China. METHODS: In this nationwide cross-sectional study, we collected information of the characteristics of cough from individuals with infection of the SARS-CoV-2 Omicron variant using an online questionnaire sent between December 31, 2022, and January 11, 2023. RESULTS: There were 11,718 (n=7978, 68.1% female) nonhospitalized responders, with a median age of 37 (IQR 30-47) years who responded at a median of 16 (IQR 12-20) days from infection onset to the time of the survey. Cough was the most common symptom, occurring in 91.7% of participants, followed by fever, fatigue, and nasal congestion (68.8%-87.4%). The median cough visual analog scale (VAS) score was 70 (IQR 50-80) mm. Being female (odds ratio [OR] 1.31, 95% CI 1.20-1.43), having a COVID-19 vaccination history (OR 1.71, 95% CI 1.37-2.12), current smoking (OR 0.48, 95% CI 0.41-0.58), chronic cough (OR 2.04, 95% CI 1.69-2.45), coronary heart disease (OR 1.71, 95% CI 1.17-2.52), asthma (OR 1.22, 95% CI 1.02-1.46), and gastroesophageal reflux disease (GERD) (OR 1.21, 95% CI 1.01-1.45) were independent factors for severe cough (VAS>70, 37.4%). Among all respondents, 35.0% indicated having a productive cough, which was associated with risk factors of being female (OR 1.44, 95% CI 1.31-1.57), having asthma (OR 1.84, 95% CI 1.52-2.22), chronic cough (OR 1.44, 95% CI 1.19-1.74), and GERD (OR 1.22, 95% CI 1.01-1.47). Persistent cough (>3 weeks) occurred in 13.0% of individuals, which was associated with the risk factors of having diabetes (OR 2.24, 95% CI 1.30-3.85), asthma (OR 1.70, 95% CI 1.11-2.62), and chronic cough (OR 1.97, 95% CI 1.32-2.94). CONCLUSIO

Journal article

Agache I, Canelo-Aybar C, Annesi-Maesano I, Cecchi L, Rigau D, Rodríguez-Tanta LY, Nieto-Gutierrez W, Song Y, Cantero-Fortiz Y, Roqué M, Vasquez JC, Sola I, Biagioni B, Chung F, D'Amato G, Damialis A, Del Giacco S, Vecillas LDL, Dominguez-Ortega J, Galàn C, Gilles S, Giovannini M, Holgate S, Jeebhay M, Nadeau K, Papadopoulos N, Quirce S, Sastre J, Traidl-Hoffmann C, Walusiak-Skorupa J, Sousa-Pinto B, Alonso-Coello P, Salazar J, Jutel M, Akdis Cet al., 2024, The impact of outdoor pollution and extreme temperatures on asthma-related outcomes: A systematic review for the EAACI guidelines on environmental science for allergic diseases and asthma., Allergy

Air pollution is one of the biggest environmental threats for asthma. Its impact is augmented by climate change. To inform the recommendations of the EAACI Guidelines on the environmental science for allergic diseases and asthma, a systematic review (SR) evaluated the impact on asthma-related outcomes of short-term exposure to outdoor air pollutants (PM2.5, PM10, NO2 , SO2 , O3 , and CO), heavy traffic, outdoor pesticides, and extreme temperatures. Additionally, the SR evaluated the impact of the efficacy of interventions reducing outdoor pollutants. The risk of bias was assessed using ROBINS-E tools and the certainty of the evidence by using GRADE. Short-term exposure to PM2.5, PM10, and NO2 probably increases the risk of asthma-related hospital admissions (HA) and emergency department (ED) visits (moderate certainty evidence). Exposure to heavy traffic may increase HA and deteriorate asthma control (low certainty evidence). Interventions reducing outdoor pollutants may reduce asthma exacerbations (low to very low certainty evidence). Exposure to fumigants may increase the risk of new-onset asthma in agricultural workers, while exposure to 1,3-dichloropropene may increase the risk of asthma-related ED visits (low certainty evidence). Heatwaves and cold spells may increase the risk of asthma-related ED visits and HA and asthma mortality (low certainty evidence).

Journal article

Chung KF, 2024, Defining cough phenotypes: chronic productive cough with obstructive lung function trajectory., Lancet Respir Med, Vol: 12, Pages: 91-93

Journal article

Moe AAK, Singh N, Dimmock M, Cox K, McGarvey L, Chung KF, McGovern AE, McMahon M, Richards AL, Farrell MJ, Mazzone SBet al., 2024, Brainstem processing of cough sensory inputs in chronic cough hypersensitivity., EBioMedicine, Vol: 100

BACKGROUND: Chronic cough is a prevalent and difficult to treat condition often accompanied by cough hypersensitivity, characterised by cough triggered from exposure to low level sensory stimuli. The mechanisms underlying cough hypersensitivity may involve alterations in airway sensory nerve responsivity to tussive stimuli which would be accompanied by alterations in stimulus-induced brainstem activation, measurable with functional magnetic resonance imaging (fMRI). METHODS: We investigated brainstem responses during inhalation of capsaicin and adenosine triphosphate (ATP) in 29 participants with chronic cough and 29 age- and sex-matched controls. Psychophysical testing was performed to evaluate individual sensitivities to inhaled stimuli and fMRI was used to compare neural activation in participants with cough and control participants while inhaling stimulus concentrations that evoked equivalent levels of urge-to-cough sensation. FINDINGS: Participants with chronic cough were significantly more sensitive to inhaled capsaicin and ATP and showed a change in relationship between urge-to-cough perception and cough induction. When urge-to-cough levels were matched, participants with chronic cough displayed significantly less neural activation in medullary regions known to integrate airway sensory inputs. By contrast, neural activations did not differ significantly between the two groups in cortical brain regions known to encode cough sensations whereas activation in a midbrain region of participants with chronic cough was significantly increased compared to controls. INTERPRETATION: Cough hypersensitivity in some patients may occur in brain circuits above the level of the medulla, perhaps involving midbrain regions that amplify ascending sensory signals or change the efficacy of central inhibitory control systems that ordinarily serve to filter sensory inputs. FUNDING: Supported in part by a research grant from Investigator-Initiated Studies Program of Merck Sharp &

Journal article

Bunyavanich S, Becker PM, Altman MC, Lasky-Su J, Ober C, Zengler K, Berdyshev E, Bonneau R, Chatila T, Chatterjee N, Chung KF, Cutcliffe C, Davidson W, Dong G, Fang G, Fulkerson P, Himes BE, Liang L, Mathias RA, Ogino S, Petrosino J, Price ND, Schadt E, Schofield J, Seibold MA, Steen H, Wheatley L, Zhang H, Togias A, Hasegawa Ket al., 2024, Analytical Challenges in Omics Research on Asthma and Allergy: A National Institute of Allergy and Infectious Diseases Workshop., J Allergy Clin Immunol

Studies of asthma and allergy are generating increasing volumes of omics data for analysis and interpretation. The National Institute of Allergy and Infectious Diseases (NIAID) assembled a workshop comprised of investigators studying asthma and allergic diseases using omics approaches, omics investigators from outside the field, and NIAID medical and scientific officers to discuss the following areas in asthma and allergy research: genomics, epigenomics, transcriptomics, microbiomics, metabolomics, proteomics, lipidomics, integrative omics, systems biology, and causal inference. Current states-of-the art, present challenges, novel and emerging strategies, and priorities for progress were presented and discussed for each area. This workshop report summarizes the major points and conclusions from this NIAID workshop. As a group, the investigators underscored the imperatives for rigorous analytic frameworks, integration of different omics data types, cross-disciplinary interaction, strategies for overcoming current limitations, and the overarching goal to improve scientific understanding and care of asthma and allergic diseases.

Journal article

Pham DD, Lee J-H, Kwon H-S, Song W-J, Cho YS, Kim H, Kwon J-W, Park S-Y, Kim S, Hur GY, Kim BK, Nam Y-H, Yang M-S, Kim M-Y, Kim S-H, Lee B-J, Lee T, Park S-Y, Kim M-H, Cho Y-J, Park C, Jung J-W, Park HK, Kim J-H, Moon J-Y, Bhavsar P, Adcock I, Chung KF, Kim T-Bet al., 2024, Predictors of Early and Late Lung Function Improvement in Severe Eosinophilic Asthma on Type2-Biologics in the PRISM Study., Lung

BACKGROUND: The determinants linked to the short- and long-term improvement in lung function in patients with severe eosinophilic asthma (SEA) on biological treatment (BioT) remain elusive. OBJECTIVE: We sought to identify the predictors of early and late lung function improvement in patients with SEA after BioT. METHODS: 140 adult patients with SEA who received mepolizumab, dupilumab, or reslizumab were followed up for 6 months to evaluate improvement in forced expiratory volume in one second (FEV1). Logistic regression was used to determine the association between potential prognostic factors and improved lung function at 1 and 6 months of treatment. RESULTS: More than a third of patients with SEA using BioT showed early and sustained improvements in FEV1 after 1 month. A significant association was found between low baseline FEV1 and high blood eosinophil count and sustained FEV1 improvement after 1 month (0.54 [0.37-0.79] and 1.88 [1.28-2.97] odds ratios and 95% confidence interval, respectively). Meanwhile, among patients who did not experience FEV1 improvement after 1 month, 39% exhibited improvement at 6 months follow-up. A high ACT score measured at this visit was the most reliable predictor of late response after 6 months of treatment (OR and 95% CI 1.75 [1.09-2.98]). CONCLUSION: Factors predicting the efficacy of biological agents that improve lung function in SEA vary according to the stage of response.

Journal article

Kalaiarasan G, Kumar P, Tomson M, Zavala-Reyes JC, Porter AE, Young G, Sephton MA, Abubakar-Waziri H, Pain CC, Adcock IM, Mumby S, Dilliway C, Fang F, Arcucci R, Chung KFet al., 2024, Particle number size distribution in three different microenvironments of London, Atmosphere, Vol: 15, ISSN: 2073-4433

We estimated the particle number distributions (PNDs), particle number concentrations (PNCs), physicochemical characteristics, meteorological effects, and respiratory deposition doses (RDD) in the human respiratory tract for three different particle modes: nucleation (N6–30), accumulation (N30–300), and coarse (N300–10,000) modes. This study was conducted in three different microenvironments (MEs) in London (indoor, IN; traffic intersection, TI; park, PK) measuring particles in the range of 6 nm–10,000 nm using an electrical low-pressure impactor (ELPI+). Mean PNCs were 1.68 ± 1.03 × 104 #cm−3, 7.00 ± 18.96 × 104 #cm−3, and 0.76 ± 0.95 × 104 #cm−3 at IN, TI, and PK, respectively. The PNDs were high for nucleation-mode particles at the TI site, especially during peak traffic hours. Wind speeds ranging from 0 to 6 ms−1 exhibit higher PNCs for nucleation- and accumulation-mode particles at TI and PK sites. Physicochemical characterisation shows trace metals, including Fe, O, and inorganic elements, that were embedded in a matrix of organic material in some samples. Alveolar RDD was higher for the nucleation and accumulation modes than the coarse-mode particles. The chemical signatures from the physicochemical characterisation indicate the varied sources at different MEs. These findings enhance our understanding of the different particle profiles at each ME and should help devise ways of reducing personal exposure at each ME.

Journal article

Asamoah K, Chung K, Bodinier B, Dahlen S-E, Djukanovic R, Bhavsar P, Adcock I, Vuckovic D, Chadeau Met al., 2024, Proteomic signatures of eosinophilic and neutrophilic asthma from serum and sputum, EBioMedicine, Vol: 99, ISSN: 2352-3964

BackgroundEosinophilic and neutrophilic asthma defined by high levels of blood and sputum eosinophils and neutrophils exemplifies the inflammatory heterogeneity of asthma, particularly severe asthma. We analysed the serum and sputum proteome to identify biomarkers jointly associated with these different phenotypes.MethodsProteomic profiles (N = 1129 proteins) were assayed in sputum (n = 182) and serum (n = 574) from two cohorts (U-BIOPRED and ADEPT) of mild-moderate and severe asthma by SOMAscan. Using least absolute shrinkage and selection operator (LASSO)-penalised logistic regression in a stability selection framework, we sought sparse sets of proteins associated with either eosinophilic or neutrophilic asthma with and without adjustment for established clinical factors including oral corticosteroid use and forced expiratory volume.FindingsWe identified 13 serum proteins associated with eosinophilic asthma, including 7 (PAPP-A, TARC/CCL17, ALT/GPT, IgE, CCL28, CO8A1, and IL5-Rα) that were stably selected while adjusting for clinical factors yielding an AUC of 0.84 (95% CI: 0.83–0.84) compared to 0.62 (95% CI: 0.61–0.63) for clinical factors only. Sputum protein analysis selected only PAPP-A (AUC = 0.81 [95% CI: 0.80–0.81]). 12 serum proteins were associated with neutrophilic asthma, of which 5 (MMP-9, EDAR, GIIE/PLA2G2E, IL-1-R4/IL1RL1, and Elafin) complemented clinical factors increasing the AUC from 0.63 (95% CI: 0.58–0.67) for the model with clinical factors only to 0.89 (95% CI: 0.89–0.90). Our model did not select any sputum proteins associated with neutrophilic status.InterpretationTargeted serum proteomic profiles are a non-invasive and scalable approach for subtyping of neutrophilic and eosinophilic asthma and for future functional understanding of these phenotypes.FundingU-BIOPRED has received funding from the Innovative Medicines Initiative (IMI) Joint Undertaking under grant agreement no. 115010, resources of which a

Journal article

Makrufardi F, Triasih R, Nurnaningsih N, Chung KF, Lin S-C, Chuang H-Cet al., 2024, Extreme temperatures increase the risk of pediatric pneumonia: a systematic review and meta-analysis., Front Pediatr, Vol: 12, ISSN: 2296-2360

INTRODUCTION: The impact of climate change on ambient temperatures threatens to worsen pediatric pneumonia-related outcomes considerably. This study examined the associations of temperature variation and extreme temperature with pediatric pneumonia-related events using a meta-analysis. METHODS: We systematically searched PubMed, Medline, Embase, and Web of Science databases for relevant literature, and the quality of evidence was assessed. Fixed and random-effects meta-analyses were performed to calculate the pooled relative risks (RRs) of the associations with pneumonia-related events. RESULTS: We observed that a 1°C temperature variation increased the RR of pneumonia events by 1.06-fold (95% confidence interval (CI): 1.03-1.10). A 1°C temperature variation increased the RR by 1.10-fold of the pediatric pneumonia hospital admissions (95% CI: 1.00-1.21) and 1.06-fold of the pediatric pneumonia emergency department visits (95% CI: 1.01-1.10). Extreme cold increased the RR by 1.25-fold of the pediatric pneumonia events (95% CI: 1.07-1.45). A 1°C temperature variation increased the RR of pneumonia events in children by 1.19-fold (95% CI: 1.08-1.32), girls by 1.03-fold (95% CI: 1.02-1.05), and in temperate climate zones by 1.07-fold (95% CI: 1.03-1.11). Moreover, an increase in extreme cold increased the RR of pneumonia events in children by 2.43-fold (95% CI: 1.72-3.43), girls by 1.96-fold (95% CI: 1.29-2.98) and in temperate climate zones by 2.76-fold (95% CI: 1.71-4.47). CONCLUSION: Our study demonstrated that pediatric pneumonia events are more prevalent among children, particularly girls, and individuals residing in temperate climate zones. Climate change represents an emergent public health threat, affecting pediatric pneumonia treatment and prevention.. SYSTEMATIC REVIEW REGISTRATION: PROSPERO (CRD42022378610).

Journal article

Edwards DA, Chung KF, 2023, Mucus Transpiration as the Basis for Chronic Cough and Cough Hypersensitivity., Lung

Chronic cough is characterized by a state of cough hypersensitivity. We analyze the process of transpiration, by which water appears to evaporate from laryngeal and tracheal mucus as from the surface of a leaf, as a potential cause of cough hypersensitivity. In this process, osmotic pressure differences form across mucus, pulling water toward the air, and preventing mucus dehydration. Recent research suggests that these osmotic differences grow on encounter with dry and dirty air, amplifying pressure on upper airway epithelia and initiating a cascade of biophysical events that potentially elevate levels of ATP, promote inflammation and acidity, threaten water condensation, and diminish mucus water permeability. Among consequences of this inflammatory cascade is tendency to cough. Studies of isotonic, hypotonic, and hypertonic aerosols targeted to the upper airways give insights to the nature of mucus transpiration and its relationship to a water layer that forms by condensation in the upper airways on exhalation. They also suggest that, while hypertonic NaCl and mannitol may provoke cough and bronchoconstriction, hypertonic salts with permeating anions and non-permeating cations may relieve these same upper respiratory dysfunctions. Understanding of mucus transpiration and its role in cough hypersensitivity can lead to new treatment modalities for chronic cough and other airway dysfunctions promoted by the breathing of dry and dirty air.

Journal article

Li C, Liu Q, Chang Q, Xie M, Weng J, Wang X, Li M, Chen J, Huang Y, Yang X, Wang K, Zhang N, Chung KF, Adcock IM, Zhang H, Li Fet al., 2023, Role of mitochondrial fusion proteins MFN2 and OPA1 on lung cellular senescence in chronic obstructive pulmonary disease, Respiratory Research, Vol: 24, ISSN: 1465-9921

BACKGROUND: Mitochondrial dysfunction and lung cellular senescence are significant features involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) stands as the primary contributing factor to COPD. This study examined mitochondrial dynamics, mitophagy and lung cellular senescence in COPD patients and investigated the effects of modulation of mitochondrial fusion [mitofusin2 (MFN2) and Optic atrophy 1 (OPA1)] on CS extract (CSE)-induced lung cellular senescence. METHODS: Senescence-associated secretory phenotype (SASP) component mRNAs (IL-1β, IL-6, CXCL1 and CXCL8), mitochondrial morphology, mitophagy and mitochondria-related proteins (including phosphorylated-DRP1(p-DRP1), DRP1, MFF, MNF2, OPA1, PINK1, PARK2, SQSTM1/p62 and LC3b) and senescence-related proteins (including P16, H2A.X and Klotho) were measured in lung tissues or primary alveolar type II (ATII) cells of non-smokers, smokers and COPD patients. Alveolar epithelial (A549) cells were exposed to CSE with either pharmacologic inducer (leflunomide and BGP15) or genetic induction of MFN2 and OPA1 respectively. RESULTS: There were increases in mitochondrial number, and decreases in mitochondrial size and activity in lung tissues from COPD patients. SASP-related mRNAs, DRP1 phosphorylation, DRP1, MFF, PARK2, SQSTM1/p62, LC3B II/LC3B I, P16 and H2A.X protein levels were increased, while MFN2, OPA1, PINK1 and Klotho protein levels were decreased in lung tissues from COPD patients. Some similar results were identified in primary ATII cells of COPD patients. CSE induced increases in oxidative stress, SASP-related mRNAs, mitochondrial damage and dysfunction, mitophagy and cellular senescence in A549 cells, which were ameliorated by both pharmacological inducers and genetic overexpression of MFN2 and OPA1. CONCLUSIONS: Impaired mitochondrial fusion, enhanced mitophagy and lung cellular senescence are observed in the lung of COPD patients. Up-regulation of MFN2 and OPA1

Journal article

Roth-Walter F, Adcock IM, Benito-Villalvilla C, Bianchini R, Bjermer L, Caramori G, Cari L, Chung KF, Diamant Z, Eguiluz-Gracia I, Knol EF, Jesenak M, Levi-Schaffer F, Nocentini G, O'Mahony L, Palomares O, Redegeld F, Sokolowska M, Van Esch BCAM, Stellato Cet al., 2023, Metabolic pathways in immune senescence and inflammaging: Novel therapeutic strategy for chronic inflammatory lung diseases. An EAACI position paper from the Task Force for Immunopharmacology., Allergy

The accumulation of senescent cells drives inflammaging and increases morbidity of chronic inflammatory lung diseases. Immune responses are built upon dynamic changes in cell metabolism that supply energy and substrates for cell proliferation, differentiation, and activation. Metabolic changes imposed by environmental stress and inflammation on immune cells and tissue microenvironment are thus chiefly involved in the pathophysiology of allergic and other immune-driven diseases. Altered cell metabolism is also a hallmark of cell senescence, a condition characterized by loss of proliferative activity in cells that remain metabolically active. Accelerated senescence can be triggered by acute or chronic stress and inflammatory responses. In contrast, replicative senescence occurs as part of the physiological aging process and has protective roles in cancer surveillance and wound healing. Importantly, cell senescence can also change or hamper response to diverse therapeutic treatments. Understanding the metabolic pathways of senescence in immune and structural cells is therefore critical to detect, prevent, or revert detrimental aspects of senescence-related immunopathology, by developing specific diagnostics and targeted therapies. In this paper, we review the main changes and metabolic alterations occurring in senescent immune cells (macrophages, B cells, T cells). Subsequently, we present the metabolic footprints described in translational studies in patients with chronic asthma and chronic obstructive pulmonary disease (COPD), and review the ongoing preclinical studies and clinical trials of therapeutic approaches aiming at targeting metabolic pathways to antagonize pathological senescence. Because this is a recently emerging field in allergy and clinical immunology, a better understanding of the metabolic profile of the complex landscape of cell senescence is needed. The progress achieved so far is already providing opportunities for new therapies, as well as for st

Journal article

Shim J-S, Kim H, Kwon J-W, Park S-Y, Kim S, Kim B-K, Nam Y-H, Yang M-S, Kim M-Y, Kim S-H, Lee B-J, Lee T, Kim S-H, Park SY, Cho Y-J, Park CS, Jung J-W, Park H-K, Kim J-H, Choi J-H, Moon J-Y, Adcock I, Chung KF, Kim M-H, Kim T-B, Precision Intervention in Severe Asthma PRISM study investigatorsaet al., 2023, A comparison of treatment response to biologics in asthma-COPD overlap and pure asthma: Findings from the PRISM study, The World Allergy Organization Journal, Vol: 16, ISSN: 1939-4551

BACKGROUND: Despite the increasing use of biologics in severe asthma, there is limited research on their use in asthma-chronic obstructive pulmonary disease overlap (ACO). We compared real-world treatment responses to biologics in ACO and asthma. METHODS: We conducted a multicenter, retrospective, cohort study using data from the Precision Medicine Intervention in Severe Asthma (PRISM). ACO was defined as post-bronchodilator forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) <0.7 and a smoking history of >10 pack-years. Physicians selected biologics (omalizumab, mepolizumab, reslizumab, benralizumab, and dupilumab) based on each United States Food & Drug Administration (FDA) approval criteria. RESULTS: After six-month treatment with biologics, both patients with ACO (N = 13) and asthma (N = 81) showed positive responses in FEV1 (10.69 ± 17.17 vs. 11.25 ± 12.87 %, P = 0.652), Asthma Control Test score (3.33 ± 5.47 vs. 5.39 ± 5.42, P = 0.290), oral corticosteroid use (-117.50 ± 94.38 vs. -115.06 ± 456.85 mg, P = 0.688), fractional exhaled nitric oxide levels (-18.62 ± 24.68 vs. -14.66 ± 45.35 ppb, P = 0.415), sputum eosinophils (-3.40 ± 10.60 vs. -14.48 ± 24.01 %, P = 0.065), blood eosinophils (-36.47 ± 517.02 vs. -363.22 ± 1294.59, P = 0.013), and exacerbation frequency (-3.07 ± 4.42 vs. -3.19 ± 5.11, P = 0.943). The odds ratio for exacerbation and time-to-first exacerbation showed no significant difference after full adjustments, and subgroup analysis according to biologic type was also showed similar results. CONCLUSIONS: Biologics treatment response patterns in p

Journal article

Chang J-H, Lee Y-L, Chang L-T, Chang T-Y, Hsiao T-C, Chung KF, Ho KF, Kuo H-P, Lee K-Y, Chuang K-J, Chuang H-Cet al., 2023, Climate change, air quality, and respiratory health: a focus on particle deposition in the lungs, ANNALS OF MEDICINE, Vol: 55, ISSN: 0785-3890

Journal article

Tran HM, Lin Y-C, Tsai F-J, Lee K-Y, Chang J-H, Chung C-L, Chung KF, Chuang K-J, Chuang H-Cet al., 2023, Short-term mediating effects of PM2.5 on climate-associated COPD severity, SCIENCE OF THE TOTAL ENVIRONMENT, Vol: 903, ISSN: 0048-9697

Journal article

Chen X-Y, Kao C, Peng S-W, Chang J-H, Lee Y-L, Laiman V, Chung KF, Bhavsar PK, Heriyanto DS, Chuang K-J, Chuang H-Cet al., 2023, Role of DCLK1/Hippo pathway in type II alveolar epithelial cells differentiation in acute respiratory distress syndrome., Mol Med, Vol: 29

BACKGROUND: Delay in type II alveolar epithelial cell (AECII) regeneration has been linked to higher mortality in patients with acute respiratory distress syndrome (ARDS). However, the interaction between Doublecortin-like kinase 1 (DCLK1) and the Hippo signaling pathway in ARDS-associated AECII differentiation remains unclear. Therefore, the objective of this study was to understand the role of the DCLK1/Hippo pathway in mediating AECII differentiation in ARDS. MATERIALS AND METHODS: AECII MLE-12 cells were exposed to 0, 0.1, or 1 μg/mL of lipopolysaccharide (LPS) for 6 and 12 h. In the mouse model, C57BL/6JNarl mice were intratracheally (i.t.) injected with 0 (control) or 5 mg/kg LPS and were euthanized for lung collection on days 3 and 7. RESULTS: We found that LPS induced AECII markers of differentiation by reducing surfactant protein C (SPC) and p53 while increasing T1α (podoplanin) and E-cadherin at 12 h. Concurrently, nuclear YAP dynamic regulation and increased TAZ levels were observed in LPS-exposed AECII within 12 h. Inhibition of YAP consistently decreased cell levels of SPC, claudin 4 (CLDN-4), galectin 3 (LGALS-3), and p53 while increasing transepithelial electrical resistance (TEER) at 6 h. Furthermore, DCLK1 expression was reduced in isolated human AECII of ARDS, consistent with the results in LPS-exposed AECII at 6 h and mouse SPC-positive (SPC+) cells after 3-day LPS exposure. We observed that downregulated DCLK1 increased p-YAP/YAP, while DCLK1 overexpression slightly reduced p-YAP/YAP, indicating an association between DCLK1 and Hippo-YAP pathway. CONCLUSIONS: We conclude that DCLK1-mediated Hippo signaling components of YAP/TAZ regulated markers of AECII-to-AECI differentiation in an LPS-induced ARDS model.

Journal article

Pham DD, Lee J-H, Kwon H-S, Song W-J, Cho YS, Kim H, Kwon J-W, Park S-Y, Kim S, Hur GY, Kim BK, Nam Y-H, Yang M-S, Kim M-Y, Kim S-H, Lee B-J, Lee T, Park SY, Kim M-H, Cho Y-J, Park C, Jung J-W, Park HK, Kim J-H, Moon J-Y, Adcock I, Bhavsar P, Chung KF, Kim T-Bet al., 2023, Prospective direct comparison of biologic treatments for severe eosinophilic asthma: Findings from the PRISM study., Ann Allergy Asthma Immunol

BACKGROUND: Although various monoclonal antibodies have been used as add-on therapy for severe eosinophilic asthma (SEA), to the best of our knowledge, no direct head-to-head comparative study has evaluated their efficacy. OBJECTIVE: To compare the efficacy of reslizumab, mepolizumab, and dupilumab in patients with SEA. METHODS: This was a multicenter, prospective observational study in patients with SEA who had received 1 of these biologic agents for at least 6 months. Cox proportional hazard models were used to compare the risk of the first exacerbation event, adjusting for sputum or blood eosinophils and common asthma-related covariates. The annual exacerbation rate was analyzed using a negative binomial model, and a mixed-effect model was used to analyze changes in forced expiratory volume in 1 second and asthma control test score over time. RESULTS: A total of 141 patients with SEA were included in the analysis; 71 (50%) received dupilumab; 40 (28%) received reslizumab, and 30 (21%) received mepolizumab. During the 12-month follow-up, 27.5%, 43.3%, and 38.0% of patients in the reslizumab, mepolizumab, and dupilumab groups, respectively, experienced at least 1 exacerbation. However, after adjusting for confounding factors, the dupilumab and mepolizumab groups showed similar outcomes in time-to-first exacerbation, exacerbation rate, forced expiratory volume in 1 second, and asthma control test score to those of the reslizumab group. CONCLUSION: In patients with SEA, treatment with reslizumab, mepolizumab, and dupilumab resulted in comparable clinical outcomes within a 12-month period. The cohort protocol was sanctioned by the Institutional Review Board of each study center (clinicaltrial.gov identifier NCT05164939).

Journal article

Faiz A, Mahbub RM, Boedijono FS, Tomassen MI, Kooistra W, Timens W, Nawijn M, Hansbro PM, Johansen MD, Pouwels SD, Heijink IH, Massip F, de Biase MS, Schwarz RF, Adcock IM, Chung KF, van der Does A, Hiemstra PS, Goulaouic H, Xing H, Abdulai R, de Rinaldis E, Cunoosamy D, Harel S, Lederer D, Nivens MC, Wark PA, Kerstjens HAM, Hylkema MN, Brandsma C-A, van den Berge Met al., 2023, IL-33 Expression Is Lower in Current Smokers at both Transcriptomic and Protein Levels., Am J Respir Crit Care Med, Vol: 208, Pages: 1075-1087

Rationale: IL-33 is a proinflammatory cytokine thought to play a role in the pathogenesis of asthma and chronic obstructive pulmonary disease (COPD). A recent clinical trial using an anti-IL-33 antibody showed a reduction in exacerbation and improved lung function in ex-smokers but not current smokers with COPD. Objectives: This study aimed to understand the effects of smoking status on IL-33. Methods: We investigated the association of smoking status with the level of gene expression of IL-33 in the airways in eight independent transcriptomic studies of lung airways. Additionally, we performed Western blot analysis and immunohistochemistry for IL-33 in lung tissue to assess protein levels. Measurements and Main Results: Across the bulk RNA-sequencing datasets, IL-33 gene expression and its signaling pathway were significantly lower in current versus former or never-smokers and increased upon smoking cessation (P < 0.05). Single-cell sequencing showed that IL-33 is predominantly expressed in resting basal epithelial cells and decreases during the differentiation process triggered by smoke exposure. We also found a higher transitioning of this cellular subpopulation into a more differentiated cell type during chronic smoking, potentially driving the reduction of IL-33. Protein analysis demonstrated lower IL-33 levels in lung tissue from current versus former smokers with COPD and a lower proportion of IL-33-positive basal cells in current versus ex-smoking controls. Conclusions: We provide strong evidence that cigarette smoke leads to an overall reduction in IL-33 expression in transcriptomic and protein level, and this may be due to the decrease in resting basal cells. Together, these findings may explain the clinical observation that a recent antibody-based anti-IL-33 treatment is more effective in former than current smokers with COPD.

Journal article

Tran HM, Tsai F-J, Lee Y-L, Chang J-H, Chang L-T, Chang T-Y, Chung KF, Kuo H-P, Lee K-Y, Chuang K-J, Chuang H-Cet al., 2023, The impact of air pollution on respiratory diseases in an era of climate change: A review of the current evidence, SCIENCE OF THE TOTAL ENVIRONMENT, Vol: 898, ISSN: 0048-9697

Journal article

Versi A, Ivan FX, Abdel-Aziz MI, Bates S, Riley J, Baribaud F, Kermani NZ, Montuschi P, Dahlen S-E, Djukanovic R, Sterk P, Maitland-Van Der Zee AH, Chotirmall SH, Howarth P, Adcock IM, Chung KF, U-BIOPRED consortiumet al., 2023, Haemophilus influenzae and Moraxella catarrhalis in sputum of severe asthma with inflammasome and neutrophil activation, Allergy, Vol: 78, Pages: 2906-2920, ISSN: 0105-4538

BACKGROUND: Because of altered airway microbiome in asthma, we analysed the bacterial species in sputum of patients with severe asthma. METHODS: Whole genome sequencing was performed on induced sputum from non-smoking (SAn) and current or ex-smoker (SAs/ex) severe asthma patients, mild/moderate asthma (MMA) and healthy controls (HC). Data were analysed by asthma severity, inflammatory status and transcriptome-associated clusters (TACs). RESULTS: α-diversity at the species level was lower in SAn and SAs/ex, with an increase in Haemophilus influenzae and Moraxella catarrhalis, and Haemophilus influenzae and Tropheryma whipplei, respectively, compared to HC. In neutrophilic asthma, there was greater abundance of Haemophilus influenzae and Moraxella catarrhalis and in eosinophilic asthma, Tropheryma whipplei was increased. There was a reduction in α-diversity in TAC1 and TAC2 that expressed high levels of Haemophilus influenzae and Tropheryma whipplei, and Haemophilus influenzae and Moraxella catarrhalis, respectively, compared to HC. Sputum neutrophils correlated positively with Moraxella catarrhalis and negatively with Prevotella, Neisseria and Veillonella species and Haemophilus parainfluenzae. Sputum eosinophils correlated positively with Tropheryma whipplei which correlated with pack-years of smoking. α- and β-diversities were stable at one year. CONCLUSIONS: Haemophilus influenzae and Moraxella catarrhalis were more abundant in severe neutrophilic asthma and TAC2 linked to inflammasome and neutrophil activation, while Haemophilus influenzae and Tropheryma whipplei were highest in SAs/ex and in TAC1 associated with highest expression of IL-13 type 2 and ILC2 signatures with the abundance of Tropheryma whipplei correlating positively with sputum eosinophils. Whether these bacterial species drive the inflammatory response in asthma needs evaluation.

Journal article

Song W-J, Dupont L, Birring SS, Chung KF, Dąbrowska M, Dicpinigaitis P, Ribas CD, Fontana G, Gibson PG, Guilleminault L, Hull JH, Idzko M, Kardos P, Kim HJ, Lai K, Lavorini F, Millqvist E, Morice AH, Niimi A, Parker SM, Satia I, Smith JA, van den Berg JW, McGarvey LPet al., 2023, Consensus goals and standards for specialist cough clinics: the NEUROCOUGH international Delphi study., ERJ Open Res, Vol: 9, ISSN: 2312-0541

BACKGROUND: Current guidelines on the management of chronic cough do not provide recommendations for the operation of specialist cough clinics. The objective of the present study was to develop expert consensus on goals and standard procedures for specialist cough clinics. METHODS: We undertook a modified Delphi process, whereby initial statements proposed by experts were categorised and presented back to panellists over two ranking rounds using an 11-point Likert scale to identify consensus. RESULTS: An international panel of 57 experts from 19 countries participated, with consensus reached on 15 out of 16 statements, covering the aims, roles and standard procedures of specialist cough clinics. Panellists agreed that specialist cough clinics offer optimal care for patients with chronic cough. They also agreed that history taking should enquire as to cough triggers, cough severity rating scales should be routinely used, and a minimum of chest radiography, spirometry and measurements of type 2 inflammatory markers should be undertaken in newly referred patients. The importance of specialist cough clinics in promoting clinical research and cough specialty training was acknowledged. Variability in healthcare resources and clinical needs between geographical regions was noted. CONCLUSIONS: The Delphi exercise provides a platform and guidance for both established cough clinics and those in planning stages.

Journal article

Jin FD, Wang J, Deng SJ, Song W-J, Zhang X, Wang CY, Gao SY, Chung KF, Yang Y, Vertigan AE, Luo FM, Birring SS, Li WM, Liu D, Wang Get al., 2023, Interaction effect of chronic cough and ageing on increased risk of exacerbation in patients with asthma: a prospective cohort study in a real-world setting., ERJ Open Res, Vol: 9, ISSN: 2312-0541

BACKGROUND: Older adults with asthma have the greatest burden and worst outcomes, and there is increasing evidence that chronic cough (CC) is associated with asthma severity and poor prognosis. However, the clinical characteristics of older adult patients with both asthma and CC remain largely unknown. METHODS: Participants with stable asthma underwent two cough assessments within 3 months to define the presence of CC. Patients were divided into four groups based on CC and age (cut-off ≥60 years). Multidimensional assessment was performed at baseline, followed by a 12-month follow-up to investigate asthma exacerbations. Logistic regression models were used to explore the interaction effect of CC and age on asthma control and exacerbations. RESULTS: In total, 310 adult patients were prospectively recruited and divided into four groups: older CC group (n=46), older non-CC group (n=20), younger CC group (n=112) and younger non-CC group (n=132). Compared with the younger non-CC group, the older CC group had worse asthma control and quality of life and increased airflow obstruction. The older CC group showed an increase in moderate-to-severe exacerbations during the 12-month follow-up. There was a significant interaction effect of CC and ageing on the increased moderate-to-severe exacerbations (adjusted risk ratio 2.36, 95% CI 1.47-3.30). CONCLUSION: Older asthma patients with CC have worse clinical outcomes, including worse asthma control and quality of life, increased airway obstruction and more frequent moderate-to-severe exacerbations, which can be partly explained by the interaction between CC and ageing.

Journal article

Lee S-E, Rudd M, Kim T-H, Oh J-Y, Lee J-H, Jover L, Small PM, Chung KF, Song W-Jet al., 2023, Feasibility and Utility of a Smartphone Application-Based Longitudinal Cough Monitoring in Chronic Cough Patients in a Real-World Setting, LUNG, ISSN: 0341-2040

Journal article

Liu Z, Qin R, Hu XJ, Liu LJ, Xu SQ, Shi GC, Zhou H, Bai J, Zhang CM, Qi Y, Zhou W, Lan SH, Tong J, Su TS, Wang Q, Yang XY, Sun DJ, Zhu LM, Chen XY, Chen H, Xie YP, Xiao ZH, Chen YB, Zhao B, Wu QG, Chen WL, Li DY, Liu H, Cheng AQ, Cui ZY, Zhao L, Li JX, Wei XW, Zhou XM, Su Z, Chung KF, Chen ZM, Xiao D, Wang Cet al., 2023, Real-world tobacco cessation practice in China: findings from the prospective, nationwide multicenter China National Tobacco Cessation Cohort Study (CNTCCS), The Lancet Regional Health - Western Pacific, Vol: 39

Background: Tobacco cessation is proven to be the most effective and cost-effective strategy for smokers to reduce their risk of smoking-related disease and premature death. Providing effective, efficient, safe, and patient-centred tobacco cessation treatment to reach those who need them is a significant challenge. To date, only a few nationwide studies in China have assessed the overall clinical care practice and treatment outcome of tobacco cessation. Methods: This a prospective, nationwide, multicenter, cohort study covering all Eastern China, Northwest China, Central China, North China, Southwest China, Northeast China, and South China. Participants who were current smokers aged 18–85 years attending clinic for smoking cessation were included. All the participants were treated with 3-month cessation treatment and followed up for 3 months. Data were collected prospectively using online system. The primary outcome was 7-day point abstinence rate at 24 weeks, validated biochemically by an expired carbon monoxide level of less than 10 ppm. The participants lost to follow-up or not providing validation were included as non-abstainers. Findings: A representative sample of 3557 participants were recruited and 2943 participants were included into this analysis. These participants had mean age of 53.05 years, and 94.8% were males, with 75.8% showing symptoms of tobacco dependence. A total of 965 (32.8%) participants were treated with Bupropion + behavioural counselling, followed by 935 (31.8%) with behavioural counselling, 778 (26.4%) with Varenicline + behavioural counselling, 135 (4.6%) with alternative treatments + behavioural counselling, and 130 (4.4%) with nicotine replacement therapy (NRT) + behavioural counselling. After 3-month treatment and 3-month follow-up, 21.74% of the participants quit smoking at 24 weeks. In the multivariable-adjusted analyses, quitting smoking was significantly associated with female, higher socioeconomic status, poor health condit

Journal article

Liu Z, Qin R, Hu X-J, Liu L-J, Xu S-Q, Shi G-C, Zhou H, Bai J, Zhang C-M, Qi Y, Zhou W, Lan S-H, Tong J, Su T-S, Wang Q, Yang X-Y, Sun D-J, Zhu L-M, Chen X-Y, Chen H, Xie Y-P, Xiao Z-H, Chen Y-B, Zhao B, Wu Q-G, Chen W-L, Li D-Y, Liu H, Cheng A-Q, Cui Z-Y, Zhao L, Li J-X, Wei X-W, Zhou X-M, Su Z, Chung KF, Chen Z-M, Xiao D, Wang Cet al., 2023, Real-world tobacco cessation practice in China: findings from the prospective, nationwide multicenter China National Tobacco Cessation Cohort Study (CNTCCS)., Lancet Reg Health West Pac, Vol: 39

BACKGROUND: Tobacco cessation is proven to be the most effective and cost-effective strategy for smokers to reduce their risk of smoking-related disease and premature death. Providing effective, efficient, safe, and patient-centred tobacco cessation treatment to reach those who need them is a significant challenge. To date, only a few nationwide studies in China have assessed the overall clinical care practice and treatment outcome of tobacco cessation. METHODS: This a prospective, nationwide, multicenter, cohort study covering all Eastern China, Northwest China, Central China, North China, Southwest China, Northeast China, and South China. Participants who were current smokers aged 18-85 years attending clinic for smoking cessation were included. All the participants were treated with 3-month cessation treatment and followed up for 3 months. Data were collected prospectively using online system. The primary outcome was 7-day point abstinence rate at 24 weeks, validated biochemically by an expired carbon monoxide level of less than 10 ppm. The participants lost to follow-up or not providing validation were included as non-abstainers. FINDINGS: A representative sample of 3557 participants were recruited and 2943 participants were included into this analysis. These participants had mean age of 53.05 years, and 94.8% were males, with 75.8% showing symptoms of tobacco dependence. A total of 965 (32.8%) participants were treated with Bupropion + behavioural counselling, followed by 935 (31.8%) with behavioural counselling, 778 (26.4%) with Varenicline + behavioural counselling, 135 (4.6%) with alternative treatments + behavioural counselling, and 130 (4.4%) with nicotine replacement therapy (NRT) + behavioural counselling. After 3-month treatment and 3-month follow-up, 21.74% of the participants quit smoking at 24 weeks. In the multivariable-adjusted analyses, quitting smoking was significantly associated with female, higher socioe

Journal article

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