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Background: Sleep's impact on the human immune system and inflammatory responses makes it a potential risk factor for lung function impairment. However, the relationship between sleep duration and lung function impairment in middle-aged and young adults has been rarely investigated., Methods: A total of 9,284 aged 20-64 years were categorized into four groups according to sleep duration (≤ 6 h, 7 h, 8 h, and ≥ 9 h), with 7 h as the reference, by using the U.S. NHANES data, 2007-2012. Forced expiratory volume in the 1 s (FEV 1 ), forced vital capacity (FVC), FEV 1 to FVC (FEV 1 /FVC) ratio, peak expiratory flow (PEF), and forced expiratory flow at 25-75% (FEF 25 - 75% ) were measured by spirometry. Restrictive impairment was defined as baseline FVC < 80% predicted and obstructive impairment as FEV 1 /FVC < 0.70. Generalized linear regression and logistic regression were performed to estimate the associations between sleep duration and lung function., Results: Compared with 7 h of sleep duration, shorter and longer sleep duration were associated with decreases in FEV 1 (≤ 6 h: β=-0.010, 95% CI=-0.014 to -0.006; 8 h: β=-0.005, 95% CI=-0.009 to -0.001), FVC (≤ 6 h: β=-0.018, 95% CI=-0.014 to -0.007; 8 h: β=-0.005, 95% CI=-0.009 to -0.002), and PEF (≤ 6 h: β=-0.006, 95% CI=-0.010 to -0.002; 8 h: β=-0.007, 95% CI=-0.011 to -0.002; ≥ 9 h: β=-0.012, 95% CI=-0.020 to -0.004). Similarly, shorter (≤ 6 h: OR = 1.346, 95% CI = 1.065 to 1.700) and longer (≥ 9 h: OR = 1.827, 95% CI = 1.236 to 2.700) sleep duration were associated with increased risks of restrictive impairment. Moreover, the aforementioned associations were more pronounced among male participants., Conclusions: Compared with 7 h of sleep duration, shorter and longer sleep duration were associated with impaired lung function among adults aged 20-64 years, and these associations were stronger among males., Competing Interests: Declarations. Ethics approval and consent to participate: Not applicable. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2024. The Author(s).)

Per the Centers for Disease Control and Prevention, asthma prevalence has steadily risen since the 1980s. Using data from the National Health and Nutrition Examination Survey (NHANES), we investigated associations between milk consumption and pulmonary function (PF). Multivariable analyses were performed, adjusted for a priori potential confounders for lung function, within the eligible total adult population ( n = 11,131) and those self-reporting asthma ( n = 1,542), included the following variables: milk-consumption, asthma diagnosis, forced vital capacity (FVC), FVC%-predicted (%), forced expiratory volume in one-second (FEV 1 ), FEV 1 % and FEV 1 /FVC. Within the total population, FEV 1 % and FVC% were significantly associated with regular (5+ days weekly) consumption of exclusively 1% milk in the prior 30-days (β:1.81; 95% CI: [0.297, 3.325]; p = 0.020 and β:1.27; [0.16, 3.22]; p = 0.046). Among participants with asthma, varied-regular milk consumption in a lifetime was significantly associated with FVC (β:127.3; 95% CI: [13.1, 241.4]; p = 0.002) and FVC% (β:2.62; 95% CI: [0.44, 4.80]; p = 0.006). No association between milk consumption and FEV 1 /FVC was found, while milk-type had variable influence and significance. Taken together, we found certain milk consumption tendencies were associated with pulmonary function values among normal and asthmatic populations. These findings propound future investigations into the potential role of dairy consumption in altering lung function and asthma outcomes, with potential impact on the protection and maintenance of pulmonary health.

Objective: Bronchodilator responsiveness (BDR) is prevalent in COPD, but its clinical implications remain unclear. We explored the significance of BDR, defined by post-bronchodilator change in FEV 1 (BDR FEV1 ) as a measure reflecting the change in flow and in FVC (BDR FVC ) reflecting the change in volume., Methods: We analyzed 2974 participants from a multicenter observational study designed to identify varying COPD phenotypes (SPIROMICS). We evaluated the association of BDR with baseline clinical characteristics, rate of prospective exacerbations and mortality using negative binomial regression and Cox proportional hazards models., Results: A majority of COPD participants exhibited BDR (52.7%). BDR FEV1 occurred more often in earlier stages of COPD, while BDR FVC occurred more frequently in more advanced disease. When defined by increases in either FEV 1 or FVC, BDR was associated with a self-reported history of asthma, but not with blood eosinophil counts. BDR FVC was more prevalent in subjects with greater emphysema and small airway disease on CT. In a univariate analysis, BDR FVC was associated with increased exacerbations and mortality, although no significance was found in a model adjusted for post-bronchodilator FEV 1 ., Conclusion: With advanced airflow obstruction in COPD, BDR FVC is more prevalent in comparison to BDR FEV1 and correlates with the extent of emphysema and degree of small airway disease. Since these associations appear to be related to the impairment of FEV 1 , BDR FVC itself does not define a distinct phenotype nor can it be more predictive of outcomes, but it can offer additional insights into the pathophysiologic mechanism in advanced COPD., Clinical Trials Registration: ClinicalTrials.gov: NCT01969344T4., Competing Interests: IB has received research grants from AMGEN and GE Healthcare; and reports personal fees from Astra Zeneca, GSK, Boehringer Ingelheim, GE Healthcare, Theravance, Mylan, GRIFOLS, CSL Behring, Verona Pharma and Fisher & Pykel Healthcare. SPB is supported by NIH Grant K23HL133438 and he has served on an advisory board for Sunovion and reports grants from NIH, personal fees from Sunovion, personal fees from GlaxoSmithKline, outside the submitted work. JLC is supported by Merit Review award I01 CX000911 from the Department of Veterans Affairs, and reports grants the Department of Defense, the National Institutes of Health, and from MedImmune Corporation, Ltd., and reports grants from NIH/NHLBI, during the conduct of the study; grants from NIH/NIAID, grants from Department of Veterans Affairs, grants from Department of Defense, outside the submitted work. MKH has consulted for GSK, Boehringer Ingelheim and AstraZeneca, has received research support from Novartis and Sunovion and reports grants from NIH, during the conduct of the study; and Consulting for GSK, BI, Mylan and AstraZeneca, research support from Sunovion and Novartis. FJM reports grants from NHLBI, National Institutes of Health, personal fees from Continuing Education, personal fees from Forest Laboratories, Janssen, GlaxoSmithKline, Nycomed/Takeda, AstraZeneca, Boehringer Ingelheim, Bellerophon (formerly Ikaria), Genentech, Novartis, Pearl, Roche, Sunovion, Theravance, CME Incite, Annenberg Center for Health Sciences at Eisenhower, Integritas, InThought, National Association for Continuing Education, Paradigm Medical Communications, LLC, PeerVoice, UpToDate, Haymarket Communications, Western Society of Allergy and Immunology, Proterixbio (formerly Bioscale), Unity Biotechnology, ConCert Pharmaceuticals, Lucid, Methodist Hospital, Columbia University, Prime Healthcare Ltd, WebMD, PeerView Network, California Society of Allergy and Immunology, Chiesi, Puerto Rico Thoracic Society, outside the submitted work, and reports personal fees from Afferent/Merck, personal fees from American Thoracic Society, grants, personal fees, non-financial support from AstraZeneca, personal fees from Bayer, non-financial support from Boehringer Ingelehim, personal fees from ProTerrix Bio, personal fees from Bridge Biotherapeutics, personal fees, non-financial support from Chiesi, personal fees from Gala, personal fees, non-financial support, personal fees from Genentech, grants, personal fees, non-financial support from GlaxoSmithKline, grants, personal fees from Nitto, personal fees from ProMedior, personal fees from ProMetic, personal fees from Patara/Respivant, personal fees from Biogen, personal fees, non-financial support from Sunovion, personal fees, non-financial support from Teva, personal fees from Veracyte, during the conduct of the study. NH reports grants and personal fees from AstraZeneca, GSK, Boehringer Ingelheim, grants from NIH, COPD Foundation, outside the submitted work. GB has grants from the NIH, Foundation for the NIH, COPD Foundation and Alpha-1 Foundation, and reports grants, personal fees from AstraZeneca, grants from Boehringer Ingelheim, grants from NIH, grants from COPD Foundation, personal fees from Mylan, outside the submitted work. JMW has received grant support from the NIH, contracts to conduct research from GSK, Bayer, MereoBioPharma,Quintiles, and reports grants from NIH/NHLBI, during the conduct of the study; grants from NIH/NCATS, grants from Bayer, grants, personal fees from GSK, personal fees from Boehringer Ingelheim, grants, personal fees from Mereo BioPharma, personal fees from Quintiles, outside the submitted work. EAH a founder and shareholder of VIDA Diagnostics, a company commercializing lung image analysis software developed, and reports personal fees from VIDA Diagnostics, during the conduct of the study. VK has consulted for Boehringer Ingelheim, Gala Therapeutics and AstraZeneca and received personal fees from ABIM, and reports personal fees from Medscape, personal fees from Gala Therapeutics, personal fees from ABIM Critical Care Testwriting Committee, personal fees from AstraZeneca, personal fees from Boehringer Ingelheim, outside the submitted work. MTD reports receiving grants from the NIH, the Department of Defense, and the American Heart Association; consulting fees from Boehringer Ingelheim, GlaxoSmithKline, Novartis, Astra Zeneca, Yungjin, PneumRx/BTG, Pulmonx, Genentech, Boston Scientific, Quark Pharmaceuticals, Mereo and received grants from American Lung Association and NIH, and reports grants from NIH, during the conduct of the study; personal fees from Boehringer Ingelheim, personal fees from AstraZeneca, personal fees from GlaxoSmithKline, personal fees from Boston Scientific, grants from American Lung Association, grants from Department of Defense, grants from Department of Veterans Affairs, personal fees from Mereo, personal fees from Quark, outside the submitted work. MBD has received research grants from the NIH and reports personal fees from Boehringer-Ingelheim, GlaxoSmithKline, AstraZeneca, and Mylan-Theravance, outside the submitted work, and reports grants from NIH-NHLBI, during the conduct of the study; grants, personal fees from Boehringer-Ingelheim, personal fees from GlaxoSmithKline, personal fees from AstraZeneca, personal fees from Mylan-Theravance, grants from Department of Defense, personal fees from Novavax, personal fees from Parion, personal fees from Midmark, personal fees from Philips, outside the submitted work. SAC reports personal fees from AstraZeneca, GSK, Amgen, Glenmark, Sunovion, UpToDate, and received personal fees and non-financial support from Genentech, grants from MedImmune, outside the submitted work, and reports personal fees from AstraZeneca, personal fees from GlaxoSmithKline, personal fees from Amgen, personal fees from Glenmark, personal fees from Sunovion, personal fees from Genentech, non-financial support from Medimmune, outside the submitted work. JAK has received research grants from NIH and the Patient Centered Outcomes Research Institute. DPT reports personal fees from Boehringer-Ingelheim, AstraZeneca, Sunovion, Theravance/Innoviva, Mylan, outside the submitted work, and reports personal fees from AstraZeneca, personal fees from Sunovion, during the conduct of the study; personal fees from AstraZeneca, personal fees from Sunovion, personal fees from Boehringer-Ingelheim, personal fees from Mylan, outside the submitted work. CBC has consulted with PulmonX, has received research funding from Equinox Fitness Clubs, Amgen and is employed part-time by the GlaxoSmithKline Global Respiratory Franchise, and reports personal fees from GlaxoSmithKline, outside the submitted work. DC has grants from the NIH, reports grants from NHLBI, grants from COPD Foundation, during the conduct of the study and no other conflicts. RB served on the advisory boards (GlaxoSmithKline, Boehringer Ingelheim, and Mylan Pharmaceuticals) and received research grants from GlaxoSmithKline and Boehringer Ingelheim, and reports personal fees from GlaxoSmithKline, personal fees from Boehringer Ingelheim, personal fees from Mylan Pharmaceuticals, grants from GlaxoSmithKline, grants from Boehringer Ingelheim, outside the submitted work. RP reports grants from NHLBI, grants from COPD Foundation, NHLBI and Department of Veterans Affairs, outside the submitted work. RGB received personal fees from GlaxoSmithKline, grants from NIH/National Center for Advancing Translational Sciences, grants from NIH/NHLBI, and reports grants from NIH/NCATS, during the conduct of the study; personal fees from GlaxoSmithKline, grants from NIH/NHLBI, outside the submitted work; and Dr. Buhr is employed part-time by the Veterans Health Administration; the content of this manuscript does not necessarily reflect the views of the US Department of Veterans Affairs. RJK received grants and personal fees from Genentech, Boehringer Ingelheim, Medimmune/Astra Zeneca, and Gilead and reports grants from NIH, during the conduct of the study; grants, personal fees from Boehringer Ingelheim, grants, personal fees from Roche/Genentech, outside the submitted work. GC reports grants from Boehringer- Ingelheim, Novartis, Astra Zeneca, Respironics, MedImmune, Actelion, Forest, Pearl, Ikaria, Aeris, PneumRx, Pulmonx, personal fees from HGE Health Care Solutions, Inc, Amirall, Boehringer- Ingelheim, Holaira. NB reports grants from NIH, outside the submitted work. PW reports personal fees from Glenmark Pharmaceuticals, personal fees from GSK, personal fees from NGM Pharma, personal fees from Amgen, nothing from Regeneron, nothing from 23andMe, nothing from Theravance, nothing from AstraZeneca, outside the submitted work. CMD reports grants from NIH, during the conduct of the study. SP reports grants from MIH, HNLBI, during the conduct of the study. The authors report no other conflicts of interest in this work., (© 2019 Barjaktarevic et al.)

Background: Pulmonary dysfunction predicts incident cardiovascular disease (CVD)., Objectives: The purpose of this study was to evaluate whether longitudinal decline in lung function is associated with incident heart failure (HF), coronary heart disease (CHD), and stroke., Methods: Among 10,351 participants in the ARIC (Atherosclerosis Risk In Communities) study free of CVD, rapid lung function decline was defined as the greatest quartile (n = 2,585) of decline in either forced expiratory volume in 1 s (FEV 1 ) (>1.9% decline/year) or forced vital capacity (FVC) (>2.1% decline/year) over 2.9 ± 0.2 years. The relationship between rapid decline in FEV 1 or FVC and subsequent incident HF, CHD, stroke, or a composite of these was assessed using multivariable Cox regression adjusting for the baseline spirometry value, demographics, height, body mass index, heart rate, diabetes, hypertension, low-density lipoprotein, use of lipid-lowering medication, N-terminal fragment of prohormone for B-type natriuretic peptide, and smoking., Results: The mean age was 54 ± 6 years, 56% were women, and 81% were white. At 17 ± 6 years of follow-up, HF occurred in 14%, CHD 11%, stroke 6%, and the composite in 24%. Rapid decline in FEV 1 and in FVC were both associated with a heightened risk of incident HF (hazard ratio [HR]: 1.17; 95% confidence interval [CI]: 1.04 to 1.33; p = 0.010; and HR: 1.27; 95% CI: 1.12 to 1.44; p < 0.001; respectively), with rapid decline in FEV 1 most prognostic in the first year of follow-up (HR: 4.22; 95% CI: 1.34 to 13.26; p = 0.01). Rapid decline in FEV 1 was also associated with incident stroke (HR: 1.25; 95% CI: 1.04 to 1.50; p = 0.015)., Conclusions: A rapid decline in lung function, assessed by serial spirometry, is associated with a higher incidence of subsequent CVD, particularly incident HF., (Copyright © 2018 American College of Cardiology Foundation. All rights reserved.)

Background: Globally, 500 million people are chronically infected with Hepatitis B virus (HBV) and Hepatitis C virus (HCV). While these viruses are notorious for their detrimental effect on the liver they are also known to affect multiple organs in the body including the lungs., Aim: To investigate if exposure to HBV and HCV is associated with lung function and respiratory diseases., Methods: Data from the Third National Health and Nutrition Examination Survey (NHANES III) was analysed using multiple linear regressions to investigate the association between exposure to HBV and HCV with the various measures of lung function, while multiple logistic regressions were used to evaluate the association with the respiratory diseases asthma and chronic obstructive pulmonary disease (COPD)., Results: Exposure to HCV was significantly associated with an increase in Forced Expiratory Volume in 1 s, FEV1 (Coef: 97.94 ml, 95% CI: 38.87 to 157.01) and Full Vital Capacity, FVC (Coef: 90 ml, 95% CI: 14.50 to 166.24). Individuals who had been exposed to both HBV and HCV also had a significantly higher FEV1 (Coef: 145.82, CI: 60.68 to 230.94) and FVC (Coef: 195.09, CI: 78.91 to 311.26). There was also a significant association between exposure to HBV and asthma (OR: 1.28, 95% CI: 1.05 to 1.58). These associations were no longer significant after additionally adjusting for cocaine and marijuana use as well as poverty income ratio., Conclusion: Our research implies that hepatotropic viruses may affect the respiratory system, but more work at a population level is needed to further explore these associations., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Background: Lung function is a long-term predictor of mortality and morbidity., Objective: We sought to identify single nucleotide polymorphisms (SNPs) associated with lung function., Methods: We performed a genome-wide association study (GWAS) of FEV1, forced vital capacity (FVC), and FEV1/FVC in 1144 Hutterites aged 6 to 89 years, who are members of a founder population of European descent. We performed least absolute shrinkage and selection operation regression to select the minimum set of SNPs that best predict FEV1/FVC in the Hutterites and used the GRAIL algorithm to mine the Gene Ontology database for evidence of functional connections between genes near the predictive SNPs., Results: Our GWAS identified significant associations between FEV1/FVC and SNPs at the THSD4-UACA-TLE3 locus on chromosome 15q23 (P = 5.7 × 10(-8) to 3.4 × 10(-9)). Nine SNPs at or near 4 additional loci had P < 10(-5) with FEV1/FVC. Only 2 SNPs were found with P < 10(-5) for FEV1 or FVC. We found nominal levels of significance with SNPs at 9 of the 27 previously reported loci associated with lung function measures. Among a predictive set of 80 SNPs, 6 loci were identified that had a significant degree of functional connectivity (GRAIL P < .05), including 3 clusters of β-defensin genes, 2 chemokine genes (CCL18 and CXCL12), and TNFRSF13B., Conclusion: This study identifies genome-wide significant associations and replicates results of previous GWASs. Multimarker modeling implicated for the first time common variation in genes involved in antimicrobial immunity in airway mucosa that influences lung function., (Copyright © 2013 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.)

Background: Vocal cord dysfunction (VCD) is the intermittent paradoxical adduction of the vocal cords during respiration, resulting in variable upper airway obstruction. Exposure to damp indoor environments is associated with adverse respiratory health outcomes, including asthma, but its role in the development of VCD is not well described., Objective: We describe the spectrum of respiratory illness in occupants of 2 water-damaged office buildings., Methods: The National Institute for Occupational Safety and Health conducted a health hazard evaluation that included interviews with managers, a maintenance officer, a remediation specialist who had evaluated the 2 buildings, employees, and consulting physicians. In addition, medical records and reports of building evaluations were reviewed. Diagnostic evaluations for VCD had been conducted at the Asthma and Allergy Center of the Medical College of Wisconsin., Results: Two cases of VCD were temporally related to occupancy of water-damaged buildings. The patients experienced cough, chest tightness, dyspnea, wheezing, and hoarseness when in the buildings. Spirometry was normal. Methacholine challenge did not show bronchial hyperreactivity but did elicit symptoms of VCD and inspiratory flow-volume loop truncation. Direct laryngoscopy revealed vocal cord adduction during inspiration. Coworkers developed upper and lower respiratory symptoms; their diagnoses included sinusitis and asthma, consistent with recognized effects of exposure to indoor dampness. Building evaluations provided evidence of water damage and mold growth., Conclusion: VCD can occur with exposure to water-damaged buildings and should be considered in exposed patients with asthma-like symptoms., (Published by Elsevier Inc.)