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1. Age and Attitudes Towards an Internet-Mediated, Pedometer-Based Physical Activity Intervention for Chronic Obstructive Pulmonary Disease: Secondary Analysis

Author

Robinson, Stephanie A, Wan, Emily S, Shimada, Stephanie L, Richardson, Caroline R, and Moy, Marilyn L

Subjects
Geriatrics, RC952-954.6
Abstract

BackgroundChronic obstructive pulmonary disease (COPD) is prevalent among older adults. Promoting physical activity and increasing exercise capacity are recommended for all individuals with COPD. Pulmonary rehabilitation is the standard of care to improve exercise capacity, although there are barriers that hinder accessibility. Technology has the potential to overcome some of these barriers, but it is unclear how aging adults with a chronic disease like COPD perceive technology-based platforms to support their disease self-management. ObjectiveGuided by the unified theory of acceptance and use of technology, the current retrospective secondary analysis explores if age moderates multiple factors that influence an individual with COPD’s openness toward an internet-mediated, pedometer-based physical activity intervention. MethodsAs part of an efficacy study, participants with COPD (N=59) were randomly assigned to use an internet-mediated, pedometer-based physical activity intervention for 12 weeks. At completion, they were asked about their experience with the intervention using a survey, including their performance expectancy and effort expectancy, facilitating conditions (ie, internet use frequency and ability), and use of the intervention technology. Logistic regression and general linear modeling examined the associations between age and these factors. ResultsParticipants ranged in age from 49 to 89 years (mean 68.66, SD 8.93). Disease severity was measured by forced expiratory volume in the first second percent predicted (mean 60.01, SD 20.86). Nearly all participants (54/59) believed the intervention was useful. Regarding effort expectancy, increasing age was associated with reporting that it was easy to find the time to engage in the intervention. Regarding facilitating conditions, approximately half of the participants believed the automated step count goals were too high (23/59) and many did not feel comfortable reaching their goals (22/59). The probability of these perceptions increased with age, even after accounting for disease severity. Age was not associated with other facilitating conditions or use of the technology. ConclusionsAge does not influence performance expectancy or use of technology with an internet-mediated, pedometer-based physical activity intervention. Age is associated with certain expectations of effort and facilitating conditions. Consideration of age of the user is needed when personalizing step count goals and time needed to log in to the website. Trial RegistrationClinicalTrials.gov NCT01772082; https://clinicaltrials.gov/ct2/show/NCT01772082

Published
2020
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2. Chronic respiratory symptoms following deployment-related occupational and environmental exposures among US veterans.

Author

Garshick, Eric, Redlich, Carrie, Korpak, Anna, Timmons, Andrew, Smith, Nicholas, Nakayama, Karen, Baird, Coleen, Ciminera, Paul, Kheradmand, Farrah, Fan, Vincent, Hart, Jaime, Koutrakis, Petros, Kuschner, Ware, Ioachimescu, Octavian, Jerrett, Michael, Montgrain, Phillipe, Proctor, Susan, Wan, Emily, Wendt, Christine, Wongtrakool, Cherry, and Blanc, Paul

Subjects
air pollution, occupational health, respiratory system, Humans, Adult, Veterans, Bronchitis, Chronic, Occupational Exposure, Cross-Sectional Studies, Environmental Exposure, Smoke, Dyspnea, Gases, Dust
Abstract

OBJECTIVES: Characterise inhalational exposures during deployment to Afghanistan and Southwest Asia and associations with postdeployment respiratory symptoms. METHODS: Participants (n=1960) in this cross-sectional study of US Veterans (Veterans Affairs Cooperative Study Service and Health Among Deployed Veterans) completed an interviewer-administered questionnaire regarding 32 deployment exposures, grouped a priori into six categories: burn pit smoke; other combustion sources; engine exhaust; mechanical and desert dusts; toxicants; and military job-related vapours gas, dusts or fumes (VGDF). Responses were scored ordinally (0, 1, 2) according to exposure frequency. Factor analysis supported item reduction and category consolidation yielding 28 exposure items in 5 categories. Generalised linear models with a logit link tested associations with symptoms (by respiratory health questionnaire) adjusting for other covariates. OR were scaled per 20-point score increment (normalised maximum=100). RESULTS: The cohort mean age was 40.7 years with a median deployment duration of 11.7 months. Heavy exposures to multiple inhalational exposures were commonly reported, including burn pit smoke (72.7%) and VGDF (72.0%). The prevalence of dyspnoea, chronic bronchitis and wheeze in the past 12 months was 7.3%, 8.2% and 15.6%, respectively. Burn pit smoke exposure was associated with dyspnoea (OR 1.22; 95% CI 1.06 to 1.47) and chronic bronchitis (OR 1.22; 95% CI 1.13 to 1.44). Exposure to VGDF was associated with dyspnoea (OR 1.29; 95% CI 1.14 to 1.58) and wheeze (OR 1.18; 95% CI 1.02 to 1.35). CONCLUSION: Exposures to burn pit smoke and military occupational VGDF during deployment were associated with an increased odds of chronic respiratory symptoms among US Veterans.

Published
2024

4. Sinusitis and rhinitis among US veterans deployed to Southwest Asia and Afghanistan after September 11, 2001

Author

Maccarone, Jennifer, Redlich, Carrie A., Timmons, Andrew, Korpak, Anna M., Smith, Nicholas L., Nakayama, Karen S., Baird, Coleen P., Ciminera, Paul, Kheradmand, Farrah, Fan, Vincent S., Hart, Jaime E., Koutrakis, Petros, Kuschner, Ware G., Ioachimescu, Octavian C., Jerrett, Michael, Montgrain, Philippe R., Proctor, Susan P., Wendt, Christine H., Wongtrakool, Cherry, Wan, Emily S., Blanc, Paul D., and Garshick, Eric

Published
2025
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7. Prevalence of abnormal spirometry in individuals with a smoking history and no known obstructive lung disease.

Author

Tran, Thuonghien, Kinney, Gregory, Comellas, Alejandro, Hoth, Karin, Baldomero, Arianne, Mamary, A, Curtis, Jeffrey, Hanania, Nicola, Casaburi, Richard, Young, Kendra, Kim, Victor, Make, Barry, Wan, Emily, Diaz, Alejandro, Hokanson, John, Crapo, James, Silverman, Edwin, Bhatt, Surya, Regan, Elizabeth, and Fortis, Spyridon

Subjects
Chronic obstructive pulmonary disease, Diagnosis, Humans, Female, Prevalence, Pulmonary Disease, Chronic Obstructive, Lung, Smoking, Risk Factors, Spirometry
Abstract

INTRODUCTION: Recent evidence suggests a high prevalence of undiagnosed chronic obstructive pulmonary disease (COPD). These individuals are at risk of exacerbations and delayed treatment. We analyzed an at-risk population for the prevalence of abnormal spirometry to provide clarity into who should undergo early spirometry. METHODS: We analyzed data from the COPDGene study. Participants with ≥10 pack-years of smoking were included. Individuals with self-reported or physician-diagnosed COPD, asthma, chronic bronchitis, emphysema and/or were on inhalers were excluded. Parsimonious multivariable logistic regression models identified factors associated with abnormal spirometry, defined as either airflow obstruction (AFO) or preserved ratio impaired spirometry. Variables were selected for the final model using a stepwise backward variable elimination process which minimized Akaike information criterion (AIC). Similarly, during the 5-year follow-up period, we assessed factors associated with incident diagnosis of COPD. RESULTS: Of 5055 individuals, 1064 (21%) had undiagnosed AFO. Age, pack-years, current smoking and a history of acute bronchitis were associated with AFO while body mass index, female sex, and Black race were inversely associated. Among 2800 participants with 5-year follow-up, 532 (19%) had an incident diagnosis of COPD. Associated risk factors included mMRC ≥2, chronic productive cough, respiratory exacerbations during the follow-up period, and abnormal spirometry. Age was inversely associated. CONCLUSIONS: The prevalence of undiagnosed COPD is high in at-risk populations. We found multiple factors associated with undiagnosed COPD and incident diagnosis of COPD at follow up. These results can be used to identify those at risk for undiagnosed COPD to facilitate earlier diagnosis and treatment.

Published
2023

8. A MUC5B Gene Polymorphism, rs35705950-T, Confers Protective Effects Against COVID-19 Hospitalization but Not Severe Disease or Mortality

Author

Verma, Anurag, Minnier, Jessica, Wan, Emily S, Huffman, Jennifer E, Gao, Lina, Joseph, Jacob, Ho, Yuk-Lam, Wu, Wen-Chih, Cho, Kelly, Gorman, Bryan R, Rajeevan, Nallakkandi, Pyarajan, Saiju, Garcon, Helene, Meigs, James B, Sun, Yan V, Reaven, Peter D, McGeary, John E, Suzuki, Ayako, Gelernter, Joel, Lynch, Julie A, Petersen, Jeffrey M, Zekavat, Seyedeh Maryam, Natarajan, Pradeep, Dalal, Sharvari, Jhala, Darshana N, Arjomandi, Mehrdad, Gatsby, Elise, Lynch, Kristine E, Bonomo, Robert A, Freiberg, Matthew, Pathak, Gita A, Zhou, Jin J, Donskey, Curtis J, Madduri, Ravi K, Wells, Quinn S, Huang, Rose DL, Polimanti, Renato, Chang, Kyong-Mi, Liao, Katherine P, Tsao, Philip S, Wilson, Peter WF, Hung, Adriana M, O’Donnell, Christopher J, Gaziano, John M, Hauger, Richard L, Iyengar, Sudha K, Luoh, Shiuh-Wen, and Initiative, the Million Veteran Program COVID-19 Science

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Women's Health, Emerging Infectious Diseases, Autoimmune Disease, Genetics, Rare Diseases, Coronaviruses, Lung, Infectious Diseases, 2.1 Biological and endogenous factors, Respiratory, Good Health and Well Being, Humans, COVID-19, Mucin-5B, Polymorphism, Genetic, Idiopathic Pulmonary Fibrosis, Genotype, Hospitalization, Genetic Predisposition to Disease, coronavirus disease 2019, severe acute respiratory syndrome coronavirus 2, idiopathic pulmonary fibrosis, electronic health records, genetic association, Million Veteran Program COVID-19 Science Initiative, Medical and Health Sciences, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract

Rationale: A common MUC5B gene polymorphism, rs35705950-T, is associated with idiopathic pulmonary fibrosis (IPF), but its role in severe acute respiratory syndrome coronavirus 2 infection and disease severity is unclear. Objectives: To assess whether rs35705950-T confers differential risk for clinical outcomes associated with coronavirus disease (COVID-19) infection among participants in the Million Veteran Program (MVP). Methods: The MUC5B rs35705950-T allele was directly genotyped among MVP participants; clinical events and comorbidities were extracted from the electronic health records. Associations between the incidence or severity of COVID-19 and rs35705950-T were analyzed within each ancestry group in the MVP followed by transancestry meta-analysis. Replication and joint meta-analysis were conducted using summary statistics from the COVID-19 Host Genetics Initiative (HGI). Sensitivity analyses with adjustment for additional covariates (body mass index, Charlson comorbidity index, smoking, asbestosis, rheumatoid arthritis with interstitial lung disease, and IPF) and associations with post-COVID-19 pneumonia were performed in MVP subjects. Measurements and Main Results: The rs35705950-T allele was associated with fewer COVID-19 hospitalizations in transancestry meta-analyses within the MVP (Ncases = 4,325; Ncontrols = 507,640; OR = 0.89 [0.82-0.97]; P = 6.86 × 10-3) and joint meta-analyses with the HGI (Ncases = 13,320; Ncontrols = 1,508,841; OR, 0.90 [0.86-0.95]; P = 8.99 × 10-5). The rs35705950-T allele was not associated with reduced COVID-19 positivity in transancestry meta-analysis within the MVP (Ncases = 19,168/Ncontrols = 492,854; OR, 0.98 [0.95-1.01]; P = 0.06) but was nominally significant (P

Published
2022

9. Alpha-1 Antitrypsin MZ Heterozygosity Is an Endotype of Chronic Obstructive Pulmonary Disease.

Author

Ghosh, Auyon J, Hobbs, Brian D, Moll, Matthew, Saferali, Aabida, Boueiz, Adel, Yun, Jeong H, Sciurba, Frank, Barwick, Lucas, Limper, Andrew H, Flaherty, Kevin, Criner, Gerard, Brown, Kevin K, Wise, Robert, Martinez, Fernando J, Lomas, David, Castaldi, Peter J, Carey, Vincent J, DeMeo, Dawn L, Cho, Michael H, Silverman, Edwin K, Hersh, Craig P, Crapo, James D, Make, Barry J, Regan, Elizabeth A, Beaty, Terri H, El-Boueiz, Adel, Foreman, Marilyn G, Hayden, Lystra P, Hetmanski, Jacqueline, Hokanson, John E, Kim, Wonji, Laird, Nan, Lange, Christoph, Lutz, Sharon M, McDonald, Merry-Lynn, Prokopenko, Dmitry, Morrow, Jarrett, Qiao, Dandi, Sakornsakolpat, Phuwanat, Wan, Emily S, Centeno, Juan Pablo, Charbonnier, Jean-Paul, Coxson, Harvey O, Galban, Craig J, Han, MeiLan K, Hoffman, Eric A, Humphries, Stephen, Jacobson, Francine L, Judy, Philip F, Kazerooni, Ella A, Kluiber, Alex, Lynch, David A, Nardelli, Pietro, Newell, John D, Notary, Aleena, Oh, Andrea, Ross, James C, Estepar, Raul San Jose, Schroeder, Joyce, Sieren, Jered, Stoel, Berend C, Tschirren, Juerg, Van Beek, Edwin, van Ginneken, Bram, van Rikxoort, Eva, Sanchez-Ferrero, Gonzalo Vegas, Veitel, Lucas, Washko, George R, Wilson, Carla G, Jensen, Robert, Everett, Douglas, Crooks, Jim, Pratte, Katherine, Strand, Matt, Austin, Erin, Kinney, Gregory, Young, Kendra A, Bhatt, Surya P, Bon, Jessica, Diaz, Alejandro A, Make, Barry, Murray, Susan, Regan, Elizabeth, Soler, Xavier, Bowler, Russell P, Kechris, Katerina, Banaei-Kashani, Farnoush, Curtis, Jeffrey L, Pernicano, Perry G, and Hanania, Nicola

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Chronic Obstructive Pulmonary Disease, Lung, Emphysema, Clinical Research, Aetiology, 2.1 Biological and endogenous factors, Respiratory, Adult, Aged, Aged, 80 and over, Case-Control Studies, Female, Genetic Markers, Genotype, Heterozygote, Humans, Longitudinal Studies, Male, Middle Aged, Phenotype, Pulmonary Disease, Chronic Obstructive, Respiratory Function Tests, Survival Analysis, Whole Genome Sequencing, alpha 1-Antitrypsin, COPDGene Investigators, RNA sequencing, alpha-1 antitrypsin, chronic obstructive pulmonary disease, meta-analysis, Medical and Health Sciences, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract

Rationale: Multiple studies have demonstrated an increased risk of chronic obstructive pulmonary disease (COPD) in heterozygous carriers of the AAT (alpha-1 antitrypsin) Z allele. However, it is not known if MZ subjects with COPD are phenotypically different from noncarriers (MM genotype) with COPD. Objectives: To assess if MZ subjects with COPD have different clinical features compared with MM subjects with COPD. Methods: Genotypes of SERPINA1 were ascertained by using whole-genome sequencing data in three independent studies. We compared outcomes between MM subjects with COPD and MZ subjects with COPD in each study and combined the results in a meta-analysis. We performed longitudinal and survival analyses to compare outcomes in MM and MZ subjects with COPD over time. Measurements and Main Results: We included 290 MZ subjects with COPD and 6,184 MM subjects with COPD across the three studies. MZ subjects had a lower FEV1% predicted and greater quantitative emphysema on chest computed tomography scans compared with MM subjects. In a meta-analysis, the FEV1 was 3.9% lower (95% confidence interval [CI], -6.55% to -1.26%) and emphysema (the percentage of lung attenuation areas

Published
2022

10. Genetic variation in genes regulating skeletal muscle regeneration and tissue remodelling associated with weight loss in chronic obstructive pulmonary disease

Author

Kumar, Preeti Lakshman, Wilson, Ava C, Rocco, Alison, Cho, Michael H, Wan, Emily, Hobbs, Brian D, Washko, George R, Ortega, Victor E, Christenson, Stephanie A, Li, Xingnan, Wells, J Michael, Bhatt, Surya P, DeMeo, Dawn L, Lutz, Sharon M, Rossiter, Harry, Casaburi, Richard, Rennard, Stephen I, Lomas, David A, Labaki, Wassim W, Tal‐Singer, Ruth, Bowler, Russel P, Hersh, Craig P, Tiwari, Hemant K, Dransfield, Mark, Thalacker‐Mercer, Anna, Meyers, Deborah A, Silverman, Edwin K, McDonald, Merry‐Lynn N, and COPDGene, ECLIPSE and SPIROMICS investigators

Subjects
Epidemiology, Health Sciences, Nutrition, Lung, Genetics, Prevention, Chronic Obstructive Pulmonary Disease, Human Genome, Clinical Research, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Respiratory, Adult, Bayes Theorem, Genetic Variation, Genome-Wide Association Study, Humans, Muscle, Skeletal, Nerve Tissue Proteins, Pulmonary Disease, Chronic Obstructive, Regeneration, Weight Loss, GWAS, Cachexia, Weight loss, COPD, Biomarkers, Skeletal muscle regeneration, Tissue remodelling, COPDGene, ECLIPSE and SPIROMICS investigators, Physiology, Clinical Sciences, Human Movement and Sports Sciences, Clinical sciences, Allied health and rehabilitation science, Sports science and exercise
Abstract

BackgroundChronic obstructive pulmonary disease (COPD) is the third leading cause of death globally. COPD patients with cachexia or weight loss have increased risk of death independent of body mass index (BMI) and lung function. We tested the hypothesis genetic variation is associated with weight loss in COPD using a genome-wide association study approach.MethodsParticipants with COPD (N = 4308) from three studies (COPDGene, ECLIPSE, and SPIROMICS) were analysed. Discovery analyses were performed in COPDGene with replication in SPIROMICS and ECLIPSE. In COPDGene, weight loss was defined as self-reported unintentional weight loss > 5% in the past year or low BMI (BMI

Published
2021

11. Emphysema Progression and Lung Function Decline Among Angiotensin Converting Enzyme Inhibitors and Angiotensin-Receptor Blockade Users in the COPDGene Cohort

Author

Tejwani, Vickram, Fawzy, Ashraf, Putcha, Nirupama, Castaldi, Peter J, Cho, Michael H, Pratte, Katherine A, Bhatt, Surya P, Lynch, David A, Humphries, Stephen M, Kinney, Gregory L, D’Alessio, Franco R, Hansel, Nadia N, Crapo, James D, Silverman, Edwin K, Make, Barry J, Regan, Elizabeth A, Beaty, Terri, Begum, Ferdouse, Cho, Michael, DeMeo, Dawn L, Boueiz, Adel R, Foreman, Marilyn G, Halper-Stromberg, Eitan, Hayden, Lystra P, Hersh, Craig P, Hetmanski, Jacqueline, Hobbs, Brian D, Hokanson, John E, Laird, Nan, Lange, Christoph, Lutz, Sharon M, McDonald, Merry-Lynn, Parker, Margaret M, Prokopenko, Dmitry, Qiao, Dandi, Regan, Elizabeth, Sakornsakolpat, Phuwanat, Wan, Emily S, Won, Sungho, Centeno, Juan Pablo, Charbonnier, Jean-Paul, Coxson, Harvey O, Galban, Craig J, Han, MeiLan K, Hoffman, Eric A, Humphries, Stephen, Jacobson, Francine L, Judy, Philip F, Kazerooni, Ella A, Kluiber, Alex, Nardelli, Pietro, Newell, John D, Notary, Aleena, Oh, Andrea, Ross, James C, San Jose Estepar, Raul, Schroeder, Joyce, Sieren, Jered, Stoel, Berend C, Tschirren, Juerg, Van Beek, Edwin, Ginneken, Bramvan, van Rikxoort, Eva, Sanchez-Ferrero, Gonzalo Vegas, Veitel, Lucas, Washko, George R, Wilson, Carla G, Jensen, Robert, Everett, Douglas, Crooks, Jim, Pratte, Katherine, Strand, Matt, Kinney, Gregory, Young, Kendra A, Bon, Jessica, Diaz, Alejandro A, Make, Barry, Murray, Susan, Soler, Xavier, Bowler, Russell P, Kechris, Katerina, Banaei-Kashani, Farnoush, Curtis, Jeffrey L, Pernicano, Perry G, Hanania, Nicola, Atik, Mustafa, Boriek, Aladin, Guntupalli, Kalpatha, and Guy, Elizabeth

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Clinical Research, Emphysema, Lung, Tobacco, Chronic Obstructive Pulmonary Disease, Tobacco Smoke and Health, Cancer, Respiratory, Aged, Angiotensin Receptor Antagonists, Angiotensin-Converting Enzyme Inhibitors, Cohort Studies, Disease Progression, Female, Forced Expiratory Volume, Humans, Lung Volume Measurements, Male, Middle Aged, Prospective Studies, Protective Factors, Pulmonary Disease, Chronic Obstructive, Pulmonary Emphysema, Spirometry, Tomography, X-Ray Computed, Vital Capacity, Walk Test, angiotensin II, COPD, emphysema progression, COPDGene Investigators, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract

BackgroundAttenuation of transforming growth factor β by blocking angiotensin II has been shown to reduce emphysema in a murine model. General population studies have demonstrated that the use of angiotensin converting enzyme inhibitors (ACEis) and angiotensin-receptor blockers (ARBs) is associated with reduction of emphysema progression in former smokers and that the use of ACEis is associated with reduction of FEV1 progression in current smokers.Research questionIs use of ACEi and ARB associated with less progression of emphysema and FEV1 decline among individuals with COPD or baseline emphysema?MethodsFormer and current smokers from the Genetic Epidemiology of COPD Study who attended baseline and 5-year follow-up visits, did not change smoking status, and underwent chest CT imaging were included. Adjusted linear mixed models were used to evaluate progression of adjusted lung density (ALD), percent emphysema (%total lung volume

Published
2021

12. The Association Between Lung Hyperinflation and Coronary Artery Disease in Smokers

Author

Chandra, Divay, Gupta, Aman, Kinney, Gregory L, Fuhrman, Carl R, Leader, Joseph K, Diaz, Alejandro A, Bon, Jessica, Barr, R Graham, Washko, George, Budoff, Matthew, Hokanson, John, Sciurba, Frank C, Crapo, James D, Silverman, Edwin K, Make, Barry J, Regan, Elizabeth A, Beaty, Terri, Begum, Ferdouse, Boueiz, Adel R, Castaldi, Peter J, Cho, Michael, DeMeo, Dawn L, Foreman, Marilyn G, Halper-Stromberg, Eitan, Hayden, Lystra P, Hersh, Craig P, Hetmanski, Jacqueline, Hobbs, Brian D, Hokanson, John E, Laird, Nan, Lange, Christoph, Lutz, Sharon M, McDonald, Merry-Lynn, Parker, Margaret M, Prokopenko, Dmitry, Qiao, Dandi, Sakornsakolpat, Phuwanat, Wan, Emily S, Won, Sungho, Al Qaisi, Mustafa, Coxson, Harvey O, Gray, Teresa, Han, MeiLan K, Hoffman, Eric A, Humphries, Stephen, Jacobson, Francine L, Judy, Philip F, Kazerooni, Ella A, Kluiber, Alex, Lynch, David A, Newell, John D, Ross, James C, San Jose Estepar, Raul, Schroeder, Joyce, Sieren, Jered, Stinson, Douglas, Stoel, Berend C, Tschirren, Juerg, Van Beek, Edwin, van Ginneken, Bram, van Rikxoort, Eva, Wilson, Carla G, Jensen, Robert, Crooks, Jim, Everett, Douglas, Moore, Camille, Strand, Hughes, John, Kinney, Gregory, Pratte, Katherine, Young, Kendra A, Bhatt, Surya, Martinez, Carlos, Murray, Susan, Soler, Xavier, Banaei-Kashani, Farnoush, Bowler, Russell P, Kechris, Katerina, Curtis, Jeffrey L, Pernicano, Perry G, Hanania, Nicola, Atik, Mustafa, Boriek, Aladin, Guntupalli, Kalpatha, Guy, Elizabeth, and Parulekar, Amit

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Lung, Heart Disease, Prevention, Atherosclerosis, Heart Disease - Coronary Heart Disease, Chronic Obstructive Pulmonary Disease, Emphysema, Tobacco Smoke and Health, Biomedical Imaging, Tobacco, Cardiovascular, Clinical Research, Respiratory, Good Health and Well Being, Airway Obstruction, Airway Remodeling, Asymptomatic Diseases, Biological Variation, Population, Coronary Artery Disease, Coronary Vessels, Female, Humans, Male, Middle Aged, Organ Size, Plethysmography, Pulmonary Emphysema, Respiratory Function Tests, Risk Factors, Smoking, Tomography, X-Ray Computed, United States, COPD, coronary artery disease, lung hyperinflation, smoking, COPDGene Investigators, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract

BackgroundSmokers manifest varied phenotypes of pulmonary impairment.Research questionWhich pulmonary phenotypes are associated with coronary artery disease (CAD) in smokers?Study design and methodsWe analyzed data from the University of Pittsburgh COPD Specialized Center for Clinically Oriented Research (SCCOR) cohort (n = 481) and the Genetic Epidemiology of COPD (COPDGene) cohort (n = 2,580). Participants were current and former smokers with > 10 pack-years of tobacco exposure. Data from the two cohorts were analyzed separately because of methodologic differences. Lung hyperinflation was assessed by plethysmography in the SCCOR cohort and by inspiratory and expiratory CT scan lung volumes in the COPDGene cohort. Subclinical CAD was assessed as the coronary artery calcium score, whereas clinical CAD was defined as a self-reported history of CAD or myocardial infarction (MI). Analyses were performed in all smokers and then repeated in those with airflow obstruction (FEV1 to FVC ratio, < 0.70).ResultsPulmonary phenotypes, including airflow limitation, emphysema, lung hyperinflation, diffusion capacity, and radiographic measures of airway remodeling, showed weak to moderate correlations (r < 0.7) with each other. In multivariate models adjusted for pulmonary phenotypes and CAD risk factors, lung hyperinflation was the only phenotype associated with calcium score, history of clinical CAD, or history of MI (per 0.2 higher expiratory and inspiratory CT scan lung volume; coronary calcium: OR, 1.2; 95% CI, 1.1-1.5; P = .02; clinical CAD: OR, 1.6; 95% CI, 1.1-2.3; P = .01; and MI in COPDGene: OR, 1.7; 95% CI, 1.0-2.8; P = .05). FEV1 and emphysema were associated with increased risk of CAD (P < .05) in models adjusted for CAD risk factors; however, these associations were attenuated on adjusting for lung hyperinflation. Results were the same in those with airflow obstruction and were present in both cohorts.InterpretationLung hyperinflation is associated strongly with clinical and subclinical CAD in smokers, including those with airflow obstruction. After lung hyperinflation was accounted for, FEV1 and emphysema no longer were associated with CAD. Subsequent studies should consider measuring lung hyperinflation and examining its mechanistic role in CAD in current and former smokers.

Published
2021

13. Pulmonary Arterial Pruning and Longitudinal Change in Percent Emphysema and Lung Function The Genetic Epidemiology of COPD Study

Author

Pistenmaa, Carrie L, Nardelli, P, Ash, SY, Come, CE, Diaz, AA, Rahaghi, FN, Barr, RG, Young, KA, Kinney, GL, Simmons, JP, Wade, RC, Wells, JM, Hokanson, JE, Washko, GR, San José Estépar, R, Crapo, James D, Silverman, Edwin K, Make, Barry J, Regan, Elizabeth A, Beaty, Terri H, Castaldi, Peter J, Cho, Michael H, DeMeo, Dawn L, Boueiz, Adel El, Foreman, Marilyn G, Ghosh, Auyon, Hayden, Lystra P, Hersh, Craig P, Hetmanski, Jacqueline, Hobbs, Brian D, Hokanson, John E, Kim, Wonji, Laird, Nan, Lange, Christoph, Lutz, Sharon M, McDonald, Merry-Lynn, Prokopenko, Dmitry, Moll, Matthew, Morrow, Jarrett, Qiao, Dandi, Regan, Elizabeth, Saferali, Aabida, Sakornsakolpat, Phuwanat, Wan, Emily S, Yun, Jeong, Centeno, Juan Pablo, Charbonnier, Jean-Paul, Coxson, Harvey O, Galban, Craig J, Han, MeiLan K, Hoffman, Eric A, Humphries, Stephen, Jacobson, Francine L, Judy, Philip F, Kazerooni, Ella A, Kluiber, Alex, Lynch, David A, Nardelli, Pietro, Newell, John D, Notary, Aleena, Oh, Andrea, Ross, James C, San Jose Estepar, Raul, Schroeder, Joyce, Sieren, Jered, Stoel, Berend C, Tschirren, Juerg, Van Beek, Edwin, Ginneken, Bramvan, van Rikxoort, Eva, Ferrero, Gonzalo Vegas Sanchez-, Veitel, Lucas, Washko, George R, Wilson, Carla G, Jensen, Robert, Everett, Douglas, Crooks, Jim, Pratte, Katherine, Strand, Matt, Austin, Erin, Kinney, Gregory, Young, Kendra A, Bhatt, Surya P, Bon, Jessica, Diaz, Alejandro A, Make, Barry, Murray, Susan, Soler, Xavier, Bowler, Russell P, Kechris, Katerina, Banaei-Kashani, Farnoush, and Curtis, Jeffrey L

Subjects
Emphysema, Tobacco, Tobacco Smoke and Health, Lung, Chronic Obstructive Pulmonary Disease, Clinical Research, Biomedical Imaging, Respiratory, Disease Progression, Endothelium, Vascular, Female, Humans, Longitudinal Studies, Male, Middle Aged, Pulmonary Artery, Pulmonary Disease, Chronic Obstructive, Respiratory Function Tests, Smokers, Tomography, X-Ray Computed, emphysema, imaging, longitudinal, lung function, pulmonary circulation, COPDGene Investigators, Clinical Sciences, Respiratory System
Abstract

BackgroundPulmonary endothelial damage has been shown to precede the development of emphysema in animals, and vascular changes in humans have been observed in COPD and emphysema.Research questionIs intraparenchymal vascular pruning associated with longitudinal progression of emphysema on CT imaging or decline in lung function over 5 years?Study design and methodsThe Genetic Epidemiology of COPD Study enrolled ever smokers with and without COPD from 2008 through 2011. The percentage of emphysema-like lung, or "percent emphysema," was assessed at baseline and after 5 years on noncontrast CT imaging as the percentage of lung voxels < -950 Hounsfield units. An automated CT imaging-based tool assessed and classified intrapulmonary arteries and veins. Spirometry measures are postbronchodilator. Pulmonary arterial pruning was defined as a lower ratio of small artery volume (< 5 mm2 cross-sectional area) to total lung artery volume. Mixed linear models included demographics, anthropomorphics, smoking, and COPD, with emphysema models also adjusting for CT imaging scanner and lung function models adjusting for clinical center and baseline percent emphysema.ResultsAt baseline, the 4,227 participants were 60 ± 9 years of age, 50% were women, 28% were Black, 47% were current smokers, and 41% had COPD. Median percent emphysema was 2.1 (interquartile range, 0.6-6.3) and progressed 0.24 percentage points/y (95% CI, 0.22-0.26 percentage points/y) over 5.6 years. Mean FEV1 to FVC ratio was 68.5 ± 14.2% and declined 0.26%/y (95% CI, -0.30 to -0.23%/y). Greater pulmonary arterial pruning was associated with more rapid progression of percent emphysema (0.11 percentage points/y per 1-SD increase in arterial pruning; 95% CI, 0.09-0.16 percentage points/y), including after adjusting for baseline percent emphysema and FEV1. Arterial pruning also was associated with a faster decline in FEV1 to FVC ratio (-0.04%/y per 1-SD increase in arterial pruning; 95% CI, -0.008 to -0.001%/y).InterpretationPulmonary arterial pruning was associated with faster progression of percent emphysema and more rapid decline in FEV1 to FVC ratio over 5 years in ever smokers, suggesting that pulmonary vascular differences may be relevant in disease progression.Trial registryClinicalTrials.gov; No.: NCT00608764; URL: www.clinicaltrials.gov.

Published
2021

14. Machine Learning Characterization of COPD Subtypes Insights From the COPDGene Study

Author

Castaldi, Peter J, Boueiz, Adel, Yun, Jeong, San Jose Estepar, Raul, Ross, James C, Washko, George, Cho, Michael H, Hersh, Craig P, Kinney, Gregory L, Young, Kendra A, Regan, Elizabeth A, Lynch, David A, Criner, Gerald J, Dy, Jennifer G, Rennard, Stephen I, Casaburi, Richard, Make, Barry J, Crapo, James, Silverman, Edwin K, Hokanson, John E, Crapo, James D, Beaty, Terri, Begum, Ferdouse, Cho, Michael, DeMeo, Dawn L, Boueiz, Adel R, Foreman, Marilyn G, Halper-Stromberg, Eitan, Hayden, Lystra P, Hetmanski, Jacqueline, Hobbs, Brian D, Laird, Nan, Lange, Christoph, Lutz, Sharon M, McDonald, Merry-Lynn, Parker, Margaret M, Prokopenko, Dmitry, Qiao, Dandi, Regan, Elizabeth, Sakornsakolpat, Phuwanat, Wan, Emily S, Won, Sungho, Centeno, Juan Pablo, Charbonnier, Jean-Paul, Coxson, Harvey O, Galban, Craig J, Han, MeiLan K, Hoffman, Eric A, Humphries, Stephen, Jacobson, Francine L, Judy, Philip F, Kazerooni, Ella A, Kluiber, Alex, Nardelli, Pietro, Newell, John D, Notary, Aleena, Oh, Andrea, Schroeder, Joyce, Sieren, Jered, Stoel, Berend C, Tschirren, Juerg, Van Beek, Edwin, van Ginneken, Bram, van Rikxoort, Eva, Sanchez-Ferrero, Gonzalo Vegas, Veitel, Lucas, Washko, George R, Wilson, Carla G, Jensen, Robert, Everett, Douglas, Crooks, Jim, Pratte, Katherine, Strand, Matt, Kinney, Gregory, Bhatt, Surya P, Bon, Jessica, Diaz, Alejandro A, Make, Barry, Murray, Susan, Soler, Xavier, Bowler, Russell P, and Kechris, Katerina

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Genetics, Chronic Obstructive Pulmonary Disease, Lung, 2.1 Biological and endogenous factors, Aetiology, Respiratory, Cluster Analysis, Diagnostic Imaging, Disease Progression, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Machine Learning, Molecular Epidemiology, Phenotype, Pulmonary Disease, Chronic Obstructive, Respiratory Function Tests, COPD, emphysema, machine learning, COPDGene Investigators, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract

COPD is a heterogeneous syndrome. Many COPD subtypes have been proposed, but there is not yet consensus on how many COPD subtypes there are and how they should be defined. The COPD Genetic Epidemiology Study (COPDGene), which has generated 10-year longitudinal chest imaging, spirometry, and molecular data, is a rich resource for relating COPD phenotypes to underlying genetic and molecular mechanisms. In this article, we place COPDGene clustering studies in context with other highly cited COPD clustering studies, and summarize the main COPD subtype findings from COPDGene. First, most manifestations of COPD occur along a continuum, which explains why continuous aspects of COPD or disease axes may be more accurate and reproducible than subtypes identified through clustering methods. Second, continuous COPD-related measures can be used to create subgroups through the use of predictive models to define cut-points, and we review COPDGene research on blood eosinophil count thresholds as a specific example. Third, COPD phenotypes identified or prioritized through machine learning methods have led to novel biological discoveries, including novel emphysema genetic risk variants and systemic inflammatory subtypes of COPD. Fourth, trajectory-based COPD subtyping captures differences in the longitudinal evolution of COPD, addressing a major limitation of clustering analyses that are confounded by disease severity. Ongoing longitudinal characterization of subjects in COPDGene will provide useful insights about the relationship between lung imaging parameters, molecular markers, and COPD progression that will enable the identification of subtypes based on underlying disease processes and distinct patterns of disease progression, with the potential to improve the clinical relevance and reproducibility of COPD subtypes.

Published
2020

15. Prevalence of abnormal spirometry in individuals with a smoking history and no known obstructive lung disease

Author

Crapo, James D., Silverman, Edwin K., Make, Barry J., Regan, Elizabeth A., Beaty, Terri H., Castaldi, Peter J., Cho, Michael H., DeMeo, Dawn L., El Boueiz, Adel, Foreman, Marilyn G., Ghosh, Auyon, Hayden, Lystra P., Hersh, Craig P., Hetmanski, Jacqueline, Hobbs, Brian D., Hokanson, John E., Kim, Wonji, Laird, Nan, Lange, Christoph, Lutz, Sharon M., McDonald, Merry-Lynn, Prokopenko, Dmitry, Moll, Matthew, Morrow, Jarrett, Qiao, Dandi, Saferali, Aabida, Sakornsakolpat, Phuwanat, Wan, Emily S., Yun, Jeong, Centeno, Juan Pablo, Charbonnier, Jean-Paul, Coxson, Harvey O., Galban, Craig J., Han, MeiLan K., Hoffman, Eric A., Humphries, Stephen, Jacobson, Francine L., Judy, Philip F., Kazerooni, Ella A., Kluiber, Alex, Lynch, David A., Nardelli, Pietro, Newell, John D., Jr., Notary, Aleena, Oh, Andrea, Ross, James C., San Jose Estepar, Raul, Schroeder, Joyce, Sieren, Jered, Stoel, Berend C., Tschirren, Juerg, Van Beek, Edwin, van Ginneken, Bram, van Rikxoort, Eva, Sanchez Ferrero, Gonzalo Vegas, Veitel, Lucas, Washko, George R., Wilson, Carla G., Jensen, Robert, Everett, Douglas, Crooks, Jim, Pratte, Katherine, Strand, Matt, Austin, Erin, Kinney, Gregory, Young, Kendra A., Bhatt, Surya P., Bon, Jessica, Diaz, Alejandro A., Make, Barry, Murray, Susan, Regan, Elizabeth, Soler, Xavier, Bowler, Russell P., Kechris, Katerina, BanaeiKashani, Farnoush, Curtis, Jeffrey L., Pernicano, Perry G., Hanania, Nicola, Atik, Mustafa, Boriek, Aladin, Guntupalli, Kalpatha, Guy, Elizabeth, Parulekar, Amit, Hersh, Craig, Washko, George, Barr, R. Graham, Austin, John, D'Souza, Belinda, Thomashow, Byron, MacIntyre, Neil, Jr., McAdams, H. Page, Washington, Lacey, McEvoy, Charlene, Tashjian, Joseph, Wise, Robert, Brown, Robert, Hansel, Nadia N., Horton, Karen, Lambert, Allison, Putcha, Nirupama, Casaburi, Richard, Adami, Alessandra, Budoff, Matthew, Fischer, Hans, Porszasz, Janos, Rossiter, Harry, Stringer, William, Sharafkhaneh, Amir, Lan, Charlie, Wendt, Christine, Bell, Brian, Kunisaki, Ken M., Flenaugh, Eric L., Gebrekristos, Hirut, Ponce, Mario, Terpenning, Silanath, Westney, Gloria, Bowler, Russell, Rosiello, Richard, Pace, David, Criner, Gerard, Ciccolella, David, Cordova, Francis, Dass, Chandra, D'Alonzo, Gilbert, Desai, Parag, Jacobs, Michael, Kelsen, Steven, Kim, Victor, Mamary, A. James, Marchetti, Nathaniel, Satti, Aditi, Shenoy, Kartik, Steiner, Robert M., Swift, Alex, Swift, Irene, Vega-Sanchez, Maria Elena, Dransfield, Mark, Bailey, William, Iyer, Anand, Nath, Hrudaya, Wells, J. Michael, Conrad, Douglas, Yen, Andrew, Comellas, Alejandro P., Hoth, Karin F., Newell, John, Jr., Thompson, Brad, Kazerooni, Ella, Labaki, Wassim, Galban, Craig, Vummidi, Dharshan, Billings, Joanne, Begnaud, Abbie, Allen, Tadashi, Sciurba, Frank, Chandra, Divay, Weissfeld, Joel, Anzueto, Antonio, Adams, Sandra, Maselli-Caceres, Diego, Ruiz, Mario E., Singh, Harjinder, Tran, Thuonghien V., Kinney, Gregory L., Comellas, Alejandro, Baldomero, Arianne K., Hokanson, John, and Fortis, Spyridon

Published
2023
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16. Clinical Markers Associated With Risk of Suicide or Drug Overdose Among Individuals With Smoking Exposure: A Longitudinal Follow-up Study of the COPDGene Cohort

Author

Crapo, James D., Silverman, Edwin K., Make, Barry J., Regan, Elizabeth A., Beaty, Terri H., Castaldi, Peter J., Cho, Michael H., DeMeo, Dawn L., El Boueiz, Adel, Foreman, Marilyn G., Ghosh, Auyon, Hayden, Lystra P., Hersh, Craig P., Hetmanski, Jacqueline, Hobbs, Brian D., Hokanson, John E., Kim, Wonji, Laird, Nan, Lange, Christoph, Lutz, Sharon M., McDonald, Merry-Lynn, Prokopenko, Dmitry, Moll, Matthew, Morrow, Jarrett, Qiao, Dandi, Saferali, Aabida, Sakornsakolpat, Phuwanat, Wan, Emily S., Yun, Jeong, Centeno, Juan Pablo, Charbonnier, Jean-Paul, Coxson, Harvey O., Galban, Craig J., Han, MeiLan K., Hoffman, Eric A., Humphries, Stephen, Jacobson, Francine L., Judy, Philip F., Kazerooni, Ella A., Kluiber, Alex, Lynch, David A., Nardelli, Pietro, Newell, John D., Jr., Notary, Aleena, Oh, Andrea, Ross, James C., San Jose Estepar, Raul, Schroeder, Joyce, Sieren, Jered, Stoel, Berend C., Tschirren, Juerg, Van Beek, Edwin, van Ginneken, Bram, van Rikxoort, Eva, Sanchez-Ferrero, Gonzalo Vegas, Veitel, Lucas, Washko, George R., Wilson, Carla G., Jensen, Robert, Strand, Matthew, Crooks, Jim, Pratte, Katherine, Khatiwada, Aastha, Austin, Erin, Kinney, Gregory, Young, Kendra A., Bhatt, Surya P., Bon, Jessica, Diaz, Alejandro A., Make, Barry, Murray, Susan, Regan, Elizabeth, Soler, Xavier, Bowler, Russell P., Kechris, Katerina, Banaei-Kashani, Farnoush, Curtis, Jeffrey L., Pernicano, Perry G., Hanania, Nicola, Atik, Mustafa, Boriek, Aladin, Guntupalli, Kalpatha, Guy, Elizabeth, Parulekar, Amit, Hersh, Craig, Washko, George, Barr, R. Graham, Austin, John, D’Souza, Belinda, Thomashow, Byron, MacIntyre, Neil, Jr., McAdams, H. Page, Washington, Lacey, McEvoy, Charlene, Tashjian, Joseph, Wise, Robert, Brown, Robert, Hansel, Nadia N., Horton, Karen, Lambert, Allison, Putcha, Nirupama, Casaburi, Richard, Adami, Alessandra, Budoff, Matthew, Fischer, Hans, Porszasz, Janos, Rossiter, Harry, Stringer, William, Sharafkhaneh, Amir, Lan, Charlie, Wendt, Christine, Bell, Brian, Kunisaki, Ken M., Flenaugh, Eric L., Gebrekristos, Hirut, Ponce, Mario, Terpenning, Silanath, Westney, Gloria, Bowler, Russell, Rosiello, Richard, Pace, David, Criner, Gerard, Ciccolella, David, Cordova, Francis, Dass, Chandra, D’Alonzo, Gilbert, Desai, Parag, Jacobs, Michael, Kelsen, Steven, Kim, Victor, Mamary, A. James, Marchetti, Nathaniel, Satti, Aditi, Shenoy, Kartik, Steiner, Robert M., Swift, Alex, Swift, Irene, Vega-Sanchez, Maria Elena, Dransfield, Mark, Bailey, William, Iyer, Anand, Nath, Hrudaya, Wells, J. Michael, Conrad, Douglas, Yen, Andrew, Comellas, Alejandro P., Hoth, Karin F., Newell, John, Jr., Thompson, Brad, Kazerooni, Ella, Labaki, Wassim, Galban, Craig, Vummidi, Dharshan, Billings, Joanne, Begnaud, Abbie, Allen, Tadashi, Sciurba, Frank, Chandra, Divay, Weissfeld, Joel, Anzueto, Antonio, Adams, Sandra, Maselli-Caceres, Diego, Ruiz, Mario E., Singh, Harjinder, Adviento, Brigid A., Iyer, Anand S., Kinney, Gregory L., Hanania, Nicola A., Lowe, Katherine E., Holm, Kristen E., Yohannes, Abebaw M., Shinozaki, Gen, and Fiedorowicz, Jess G.

Published
2023
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17. Low FVC/TLC in Preserved Ratio Impaired Spirometry (PRISm) is associated with features of and progression to obstructive lung disease.

Author

Fortis, Spyridon, Comellas, Alejandro, Kim, Victor, Casaburi, Richard, Hokanson, John E, Crapo, James D, Silverman, Edwin K, and Wan, Emily S

Subjects
Lung, Humans, Pulmonary Disease, Chronic Obstructive, Pulmonary Emphysema, Disease Progression, Tomography, X-Ray Computed, Respiratory Function Tests, Total Lung Capacity, Vital Capacity, Forced Expiratory Volume, Spirometry, Aged, Middle Aged, Female, Male
Abstract

One quarter of individuals with Preserved Ratio Impaired Spirometry (PRISm) will develop airflow obstruction, but there are no established methods to identify these individuals. We examined the utility of FVC/TLC in identifying features of obstructive lung disease. The ratio of post-bronchodilator FVC and TLCCT from chest CT (FVC/TLCCT) among current and former smokers with PRISm (FEV1/FVC ≥ 0.7 and FEV1

Published
2020

18. Disease Progression Modeling in Chronic Obstructive Pulmonary Disease

Author

Young, Alexandra L, Bragman, Felix JS, Rangelov, Bojidar, Han, MeiLan K, Galbán, Craig J, Lynch, David A, Hawkes, David J, Alexander, Daniel C, Hurst, John R, Crapo, James D, Silverman, Edwin K, Make, Barry J, Regan, Elizabeth A, Beaty, Terri, Begum, Ferdouse, Castaldi, Peter J, Cho, Michael, DeMeo, Dawn L, Boueiz, Adel R, Foreman, Marilyn G, Halper-Stromberg, Eitan, Hayden, Lystra P, Hersh, Craig P, Hetmanski, Jacqueline, Hobbs, Brian D, Hokanson, John E, Laird, Nan, Lange, Christoph, Lutz, Sharon M, McDonald, Merry-Lynn, Parker, Margaret M, Qiao, Dandi, Wan, Emily S, Won, Sungho, Sakornsakolpat, Phuwanat, Prokopenko, Dmitry, Al Qaisi, Mustafa, Coxson, Harvey O, Gray, Teresa, Hoffman, Eric A, Humphries, Stephen, Jacobson, Francine L, Judy, Philip F, Kazerooni, Ella A, Kluiber, Alex, Newell, John D, Ross, James C, Estepar, Raul San Jose, Schroeder, Joyce, Sieren, Jered, Stinson, Douglas, Stoel, Berend C, Tschirren, Juerg, Van Beek, Edwin, van Ginneken, Bram, van Rikxoort, Eva, Washko, George, Wilson, Carla G, Jensen, Robert, Everett, Douglas, Crooks, Jim, Moore, Camille, Strand, Matt, Hughes, John, Kinney, Gregory, Pratte, Katherine, Young, Kendra A, Bhatt, Surya, Bon, Jessica, Martinez, Carlos, Murray, Susan, Soler, Xavier, Bowler, Russell P, Kechris, Katerina, Banaei-Kashani, Farnoush, Curtis, Jeffrey L, Martinez, Carlos H, Pernicano, Perry G, Hanania, Nicola, Alapat, Philip, Atik, Mustafa, Bandi, Venkata, Boriek, Aladin, Guntupalli, Kalpatha, Guy, Elizabeth, Nachiappan, Arun, Parulekar, Amit, Barr, R Graham, Austin, John, D’Souza, Belinda, Pearson, Gregory DN, Rozenshtein, Anna, Thomashow, Byron, MacIntyre, Neil, McAdams, H Page, Washington, Lacey, McEvoy, Charlene, and Tashjian, Joseph

Subjects
Biomedical Imaging, Lung, Clinical Research, Chronic Obstructive Pulmonary Disease, Aetiology, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, 4.1 Discovery and preclinical testing of markers and technologies, 2.1 Biological and endogenous factors, Respiratory, Aged, Disease Progression, Female, Humans, Male, Middle Aged, Models, Theoretical, Pulmonary Disease, Chronic Obstructive, Tomography, X-Ray Computed, clustering, CT imaging, emphysema, bronchitis, chronic obstructive pulmonary disease, COPDGene Investigators, Medical and Health Sciences, Respiratory System
Abstract

Rationale: The decades-long progression of chronic obstructive pulmonary disease (COPD) renders identifying different trajectories of disease progression challenging.Objectives: To identify subtypes of patients with COPD with distinct longitudinal progression patterns using a novel machine-learning tool called "Subtype and Stage Inference" (SuStaIn) and to evaluate the utility of SuStaIn for patient stratification in COPD.Methods: We applied SuStaIn to cross-sectional computed tomography imaging markers in 3,698 Global Initiative for Chronic Obstructive Lung Disease (GOLD) 1-4 patients and 3,479 controls from the COPDGene (COPD Genetic Epidemiology) study to identify subtypes of patients with COPD. We confirmed the identified subtypes and progression patterns using ECLIPSE (Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints) data. We assessed the utility of SuStaIn for patient stratification by comparing SuStaIn subtypes and stages at baseline with longitudinal follow-up data.Measurements and Main Results: We identified two trajectories of disease progression in COPD: a "Tissue→Airway" subtype (n = 2,354, 70.4%), in which small airway dysfunction and emphysema precede large airway wall abnormalities, and an "Airway→Tissue" subtype (n = 988, 29.6%), in which large airway wall abnormalities precede emphysema and small airway dysfunction. Subtypes were reproducible in ECLIPSE. Baseline stage in both subtypes correlated with future FEV1/FVC decline (r = -0.16 [P

Published
2020

20. Chest Computed Tomography to Improve Phenotyping in Pulmonary Hypertension Associated with Chronic Obstructive Pulmonary Disease.

Author

Johnson, Shelsey W., Wan, Emily S., San Jose Estépar, Raul, Nardelli, Pietro, Pistenmaa, Carrie, Piccari, Lucilla, Nathan, Steven D., Waxman, Aaron B., Washko, George R., and Rahaghi, Farbod N.

Subjects
BRAIN natriuretic factor, LUNGS, PULMONARY artery diseases, LUNG volume, PULMONARY emphysema, VASCULAR remodeling, PULMONARY arterial hypertension
Abstract

The article from the Annals of the American Thoracic Society discusses the impact of chronic obstructive pulmonary disease (COPD) on pulmonary hypertension, affecting nearly 40% of COPD patients. The text highlights the need for improved phenotyping and diagnosis of COPD-PH, emphasizing the role of chest computed tomography (CT) in identifying pulmonary vascular disease. The article also reviews ongoing clinical trials investigating the efficacy of therapies for COPD-PH, such as phosphodiesterase 5-inhibitors, and the potential benefits of CT imaging in enhancing treatment response assessment. [Extracted from the article]

Published
2025
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22. Longitudinal Association Between Muscle Loss and Mortality in Ever Smokers

Author

Crapo, James D., Silverman, Edwin K., Cummings, Sara, Madden, Kelley, Make, Barry J., Nabbosa, Juliet, Port, Emily, Rashdi, Serine, Regan, Elizabeth A., Stepp, Lori, Watts, Shandi, Weaver, Michael, Beaty, Terri, Bowler, Russell P., Curtis, Jeffrey L., Han, MeiLan K., Hokanson, John E., Lynch, David A., Strand, Matthew J., Anderson, Gary, Bleecker, Eugene R., Coxson, Harvey O., Crystal, Ronald G., Hogg, James C., Province, Michael A., Rennard, Stephen I., Croxton, Thomas, Gan, Weiniu, Postow, Lisa A., Viviano, Lisa M., Costa-Davis, Corinne, Malanga, Elisha, Prieto, Delia, Tal-Singer, Ruth, Farzadegan, Homayoon, Hadji, Akila, Sathe, Leena, Baraghoshi, David, Chen, Grace, Crooks, James, Knowles, Ruthie, Pratte, Katherine, Wilson, Carla, Zelarney, Pearlanne T., Kechris, Katerina J., Leach, Sonia, Austin, Erin E., Czizik, Annika, Kinney, Gregory, Li, Yisha, Lutz, Sharon M., Ragland, Margaret F., Richmond, Nicole, Young, Kendra A., Cho, Michael, Castaldi, Peter J., Glass, Kimberly, Hersh, Craig, Kim, Wonji, Liu, Yang-Yu, Hersh, Craig P., Bidinger, Jacqueline, Cho, Michael H., Conrad, Douglas, DeMeo, Dawn L., El-Boueiz, Adel R., Foreman, Marilyn G., Ghosh, Auyon, Hahn, Georg, Hansel, Nadia N., Hayden, Lystra P., Hobbs, Brian, Kim, Woori, Lange, Christoph, McDonald, Merry- Lynn, McGeachie, Michael, Moll, Matthew, Morris, Melody, Patsopoulos, Nikolaos A., Qiao, Dandi, Ruczinski, Ingo, Wan, Emily S., Dy, Jennifer G., Fain, Sean B., Ginsburg, Shoshana, Hoffman, Eric A., Humphries, Stephen, Judy, Philip F., Stefanie Mason, Alex Kluiber, Oh, Andrea, Poynton, Clare, Reinhardt, Joseph M., Ross, James, San Jose Estepar, Raul, Schroeder, Joyce D., Sitek, Arkadiusz, Steiner, Robert M., van Beek, Edwin, Ginneken, Bram van, van Rikxoort, Eva, Washko, George R., Jensen, Robert, John E. Hokanson, Co-Chair, Bhatt, Surya P., Casaburi, Richard, Kim, Victor, Putcha, Nirupama, Han, MeiLan, Bon, Jessica, Diaz, Alejandro A., Regan, Elizabeth, Anzueto, Antonio, Bailey, William C., Criner, Gerard J., Dransfield, Mark T., Kinney, Greg, Sprenger, Kim, Benos, Takis, Hanania, Nicola A., Hoth, Karin F., Lambert, Allison, Lowe, Katherine, Oates, Gabriela, Parekh, Trisha, Westney, Gloria, Young, Kendra, Balasubramanian, Aparna, Boriek, Aladin, Fawzy, Ashraf, Jacobson, Francine, LaFon, David C., MacIntyre, Neil, Maselli-Caceres, Diego, McCormack, Meredith C., McDonald, Merry-Lynn, Sciurba, Frank, Soler, Xavier, Tejwani, Vickram, van Beek, Edwin JR., Wade, Raymond C., Wells, Mike, Wendt, Chris H., Yun, Jeong H., Zhang, Jingzhou, Gillenwater, Lucas, Lowe, Katherine E., Pratte, Katherine A., Ragland, Margaret, Attaway, Amy, Mason, Stefanie, Rossiter, Harry B., Saha, Punam Kumar, Wilson, Ava, Amaza, Hannatu, Baldomero, Adrienne, Mamary, A. James, O’Brien, James, Wise, Robert A., Eakin, Michelle, Fiedorowicz, Jess G., Henkle, Ben, Holm, Kristen, Iyer, Anand, Kunisaki, Ken M., McEvoy, Charlene, Mkorombindo, Takudzwa, Shinozaki, Gen, Yohannes, Abebaw, Hobbs, Brian D., Miller, Bruce E., Retson, Tara, McCloskey, Lisa, Pernicano, Perry G., Atik, Mustafa, Bertrand, Laura, Monaco, Thomas, Narendra, Dharani, Lenge de Rosen, Veronica V., Badu-Danso, Kwame, Jacobson, Francine L., Kaufman, Laura, Maguire, Cherie, Struble, Sophie, Wilson, Seth, Barr, R. Graham, Almonte, Casandra, Austin, John H.M., Gomez Blum, Maria Lorena, D’Souza, Belinda M., Florez, Emilay, Martinez, Rodney, MacIntyre, Neil, Jr., Curry, Wendy, McAdams, H. Page, Reikofski, Charlotte V., Washington, Lacey, Brown, Robert, Clare, Cheryl, Daniel, Marie, Horton, Karen, Ting “Tony” Lin, Cheng, Mirza, Tahira, Scott, Meagan, Shade, Becky, Budoff, Matt, Calmelat, Robert, Cavanaugh, Deborah, Dailing, Chris, Diaz, Leticia, Fischer, Hans, Indelicato, Renee Love, Porszasz, Janos, Soriano, April, Stringer, William, Urrutia, Miriam, Baldomero, Arianne, Bell, Brian, Deconcini, Miranda, Loes, Linda, Phelan, Jonathan, Robichaux, Camille, Sasse, Cheryl, Tashjian, Joseph H., Flenaugh, Eric L., Abson, Kema, Gebrekristos, Hirut, Johnson, Priscilla, Jordan, Jessica, Ponce, Mario, Terpenning, Silanath, Wilson, Derrick, Broadhurst, Grace, Dyer, Debra, Engel, Elena, Finigan, Jay, Hill, Andrew, Jones, Alex, Jones, Ryan, Owen, Jordan, Rosiello, Richard, Andries, Nicole, Charpentier, Mary, Kirk, Diane, Pace, David, Ciccolella, David, Cordova, Francis, Dass, Chandra, D’Alonzo, Gilbert, Davis, Valena, Desai, Parag, Fehrle, Dee, Grabianowski, Carla, Jacobs, Michael, Jameson, Laurie, Jones, Gayle M., Kelsen, Steven, Marchetti, Nathaniel, McGonagle, Francine, Satti, Aditi, Shenoy, Kartik, Sheridan, Regina, Vega-Sanchez, Maria, Wallace, Samantha, Akinseye-kolapo, Samuel, Baker, Matthew, Goggins, Arnissa, McClain, Anny, Nath, Hrudaya, Singh, Satinder P., Sonavane, Sushil K., Westfall, Elizabeth, Gil, Marissa, El Hajjaoui, Tarek, Hsiao, Albert, Martineau, Amber, Mielke, Jenna, Perez, Karl, Querido, Gabriel, Reston, Tara, Yen, Andrew, Comellas, Alejandro, Fortis, Spyridon, Galizia, Mauricio, Garcia, Eric, Keating, Janet, Laroia, Archana, Lee, Changhyun, Meyer, Amber, Mullan, Brian, Nagpal, Prashant, Ofori, Oloigbe, Suiter, Sierra, Mason, Stefanie E., Moreta-Martinez, Rafael, Labaki, Wassim W., San Jose Estepar, Ruben, Make, Barry, and Stringer, Kathleen

Published
2022
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23. Longitudinal Phenotypes and Mortality in Preserved Ratio Impaired Spirometry in the COPDGene Study.

Author

Wan, Emily S, Fortis, Spyridon, Regan, Elizabeth A, Hokanson, John, Han, MeiLan K, Casaburi, Richard, Make, Barry J, Crapo, James D, DeMeo, Dawn L, Silverman, Edwin K, and COPDGene Investigators

Subjects
COPDGene Investigators, Lung, Humans, Pulmonary Disease, Chronic Obstructive, Respiratory Function Tests, Spirometry, Risk Factors, Longitudinal Studies, Follow-Up Studies, Phenotype, Aged, Aged, 80 and over, Middle Aged, United States, Female, Male, Surveys and Questionnaires, Smokers, lung disease epidemiology, spirometry classification, spirometry mortality, spirometry statistics and numerical data, Clinical Research, Respiratory, Good Health and Well Being, Medical and Health Sciences, Respiratory System
Abstract

RationaleIncreasing awareness of the prevalence and significance of Preserved Ratio Impaired Spirometry (PRISm), alternatively known as restrictive or Global Initiative for Chronic Obstructive Lung Disease (GOLD)-unclassified spirometry, has expanded the body of knowledge on cross-sectional risk factors. However, longitudinal studies of PRISm remain limited.ObjectivesTo examine longitudinal patterns of change in lung function, radiographic characteristics, and mortality of current and former smokers with PRISm.MethodsCurrent and former smokers, aged 45 to 80 years, were enrolled in COPDGene (phase 1, 2008-2011) and returned for a 5-year follow-up (phase 2, 2012-2016). Subjects completed questionnaires, spirometry, chest computed tomography scans, and 6-minute-walk tests at both study visits. Baseline characteristics, longitudinal change in lung function, and mortality were assessed by post-bronchodilator lung function categories: PRISm (FEV1/FVC  0.7 and FEV1 > 80%), and GOLD1-4 (FEV1/FVC

Published
2018

24. Blood eosinophil count thresholds and exacerbations in patients with chronic obstructive pulmonary disease

Author

Yun, Jeong H, Lamb, Andrew, Chase, Robert, Singh, Dave, Parker, Margaret M, Saferali, Aabida, Vestbo, Jørgen, Tal-Singer, Ruth, Castaldi, Peter J, Silverman, Edwin K, Hersh, Craig P, Crapo, James D, Make, Barry J, Regan, Elizabeth A, Beaty, Terri, Begum, Ferdouse, Busch, Robert, Cho, Michael, DeMeo, Dawn L, Boueiz, Adel R, Foreman, Marilyn G, Halper-Stromberg, Eitan, Hansel, Nadia N, Hardin, Megan E, Hayden, Lystra P, Hetmanski, Jacqueline, Hobbs, Brian D, Hokanson, John E, Laird, Nan, Lange, Christoph, Lutz, Sharon M, McDonald, Merry-Lynn, Qiao, Dandi, Santorico, Stephanie, Silverman, E, Wan, Emily S, Won, Sungho, Qaisi, Mustafa Al, Coxson, Harvey O, Gray, Teresa, Han, MeiLan K, Hoffman, Eric A, Humphries, Stephen, Jacobson, Francine L, Judy, Philip F, Kazerooni, Ella A, Kluiber, Alex, Lynch, David A, Newell, John D, Ross, James C, San Jose Estepar, Raul, Schroeder, Joyce, Sieren, Jered, Stinson, Douglas, Stoel, Berend C, Tschirren, Juerg, Van Beek, Edwin, van Ginneken, Bram, van Rikxoort, Eva, Washko, George, Wilson, Carla G, Jensen, Robert, Everett, Douglas, Crooks, Jim, Moore, Camille, Strand, Matt, Hughes, John, Kinney, Gregory, Pratte, Katherine, Young, Kendra A, Curtis, Jeffrey L, Martinez, Carlos H, Pernicano, Perry G, Hanania, Nicola, Alapat, Philip, Atik, Mustafa, Bandi, Venkata, Boriek, Aladin, Guntupalli, Kalpatha, Guy, Elizabeth, Nachiappan, Arun, Parulekar, Amit, Hersh, Craig, Barr, R Graham, Austin, John, D'Souza, Belinda, Pearson, Gregory DN, and Rozenshtein, Anna

Subjects
Lung, Chronic Obstructive Pulmonary Disease, Clinical Research, Respiratory, Aged, Disease Progression, Eosinophils, Female, Humans, Leukocyte Count, Longitudinal Studies, Male, Middle Aged, Observational Studies as Topic, Pulmonary Disease, Chronic Obstructive, Chronic obstructive pulmonary disease, asthma, eosinophil, exacerbation, COPDGene and ECLIPSE Investigators, Immunology, Allergy
Abstract

BACKGROUND:Eosinophilic airway inflammation in patients with chronic obstructive pulmonary disease (COPD) is associated with exacerbations and responsivity to steroids, suggesting potential shared mechanisms with eosinophilic asthma. However, there is no consistent blood eosinophil count that has been used to define the increased exacerbation risk. OBJECTIVE:We sought to investigate blood eosinophil counts associated with exacerbation risk in patients with COPD. METHODS:Blood eosinophil counts and exacerbation risk were analyzed in patients with moderate-to-severe COPD by using 2 independent studies of former and current smokers with longitudinal data. The Genetic Epidemiology of COPD (COPDGene) study was analyzed for discovery (n = 1,553), and the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE) study was analyzed for validation (n = 1,895). A subset of the ECLIPSE study subjects were used to assess the stability of blood eosinophil counts over time. RESULTS:COPD exacerbation risk increased with higher eosinophil counts. An eosinophil count threshold of 300 cells/μL or greater showed adjusted incidence rate ratios for exacerbations of 1.32 in the COPDGene study (95% CI, 1.10-1.63). The cutoff of 300 cells/μL or greater was validated for prospective risk of exacerbation in the ECLIPSE study, with adjusted incidence rate ratios of 1.22 (95% CI, 1.06-1.41) using 3-year follow-up data. Stratified analysis confirmed that the increased exacerbation risk associated with an eosinophil count of 300 cells/μL or greater was driven by subjects with a history of frequent exacerbations in both the COPDGene and ECLIPSE studies. CONCLUSIONS:Patients with moderate-to-severe COPD and blood eosinophil counts of 300 cells/μL or greater had an increased risk exacerbations in the COPDGene study, which was prospectively validated in the ECLIPSE study.

Published
2018

28. Emphysema Progression and Lung Function Decline Among Angiotensin Converting Enzyme Inhibitors and Angiotensin-Receptor Blockade Users in the COPDGene Cohort

Author

Crapo, James D., Silverman, Edwin K., Make, Barry J., Regan, Elizabeth A., Beaty, Terri, Begum, Ferdouse, Castaldi, Peter J., Cho, Michael, DeMeo, Dawn L., Boueiz, Adel R., Foreman, Marilyn G., Halper-Stromberg, Eitan, Hayden, Lystra P., Hersh, Craig P., Hetmanski, Jacqueline, Hobbs, Brian D., Hokanson, John E., Laird, Nan, Lange, Christoph, Lutz, Sharon M., McDonald, Merry-Lynn, Parker, Margaret M., Prokopenko, Dmitry, Qiao, Dandi, Sakornsakolpat, Phuwanat, Wan, Emily S., Won, Sungho, Centeno, Juan Pablo, Charbonnier, Jean-Paul, Coxson, Harvey O., Galban, Craig J., Han, MeiLan K., Hoffman, Eric A., Humphries, Stephen, Jacobson, Francine L., Judy, Philip F., Kazerooni, Ella A., Kluiber, Alex, Lynch, David A., Nardelli, Pietro, Newell, John D., Jr., Notary, Aleena, Oh, Andrea, Ross, James C., San Jose Estepar, Raul, Schroeder, Joyce, Sieren, Jered, Stoel, Berend C., Tschirren, Juerg, Van Beek, Edwin, Ginneken, Bramvan, van Rikxoort, Eva, Sanchez-Ferrero, Gonzalo Vegas, Veitel, Lucas, Washko, George R., Wilson, Carla G., Jensen, Robert, Everett, Douglas, Crooks, Jim, Pratte, Katherine, Strand, Matt, Kinney, Gregory, Young, Kendra A., Bhatt, Surya P., Bon, Jessica, Diaz, Alejandro A., Make, Barry, Murray, Susan, Regan, Elizabeth, Soler, Xavier, Bowler, Russell P., Kechris, Katerina, Banaei-Kashani, Farnoush, Curtis, Jeffrey L., Pernicano, Perry G., Hanania, Nicola, Atik, Mustafa, Boriek, Aladin, Guntupalli, Kalpatha, Guy, Elizabeth, Parulekar, Amit, Hersh, Craig, Washko, George, Barr, R. Graham, Austin, John, D’Souza, Belinda, Thomashow, Byron, MacIntyre, Neil, Jr., McAdams, H. Page, Washington, Lacey, Flenaugh, Eric, Terpenning, Silanth, McEvoy, Charlene, Tashjian, Joseph, Wise, Robert, Brown, Robert, Hansel, Nadia N., Horton, Karen, Lambert, Allison, Putcha, Nirupama, Casaburi, Richard, Adami, Alessandra, Budoff, Matthew, Fischer, Hans, Porszasz, Janos, Rossiter, Harry, Stringer, William, Sharafkhaneh, Amir, Lan, Charlie, Wendt, Christine, Bell, Brian, Kunisaki, KenM., Bowler, Russell, Rosiello, Richard, Pace, David, Criner, Gerard, Ciccolella, David, Cordova, Francis, Dass, Chandra, D’Alonzo, Gilbert, Desai, Parag, Jacobs, Michael, Kelsen, Steven, Kim, Victor, Mamary, A. James, Marchetti, Nathaniel, Satti, Aditi, Shenoy, Kartik, Steiner, Robert M., Swift, Alex, Swift, Irene, Vega-Sanchez, Maria Elena, Dransfield, Mark, Bailey, William, Iyer, Anand, Nath, Hrudaya, Wells, J. Michael, Conrad, Douglas, Yen, Andrew, Comellas, Alejandro P., Hoth, Karin F., Newell, John, Jr., Thompson, Brad, Kazerooni, Ella, Labaki, Wassim, Galban, Craig, Vummidi, Dharshan, Billings, Joanne, Begnaud, Abbie, Allen, Tadashi, Sciurba, Frank, Chandra, Divay, Fuhrman, Carl, Weissfeld, Joel, Tejwani, Vickram, Fawzy, Ashraf, Cho, Michael H., Pratte, Katherine A., Humphries, Stephen M., Kinney, Gregory L., and D’Alessio, Franco R.

Published
2021
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29. Lobar Emphysema Distribution Is Associated With 5-Year Radiological Disease Progression

Author

Boueiz, Adel, Chang, Yale, Cho, Michael H, Washko, George R, San José Estépar, Raul, Bowler, Russell P, Crapo, James D, DeMeo, Dawn L, Dy, Jennifer G, Silverman, Edwin K, Castaldi, Peter J, Crapo, James, Silverman, Edwin, Make, Barry, Regan, Elizabeth, Beaty, Terri, Laird, Nan, Lange, Christoph, Santorico, Stephanie, Hokanson, John, DeMeo, Dawn, Hansel, Nadia, Hersh, Craig, Castaldi, Peter, McDonald, Merry-Lynn, Wan, Emily, Hardin, Megan, Hetmanski, Jacqueline, Parker, Margaret, Foreman, Marilyn, Hobbs, Brian, Busch, Robert, Qiao, Dandi, Halper-Stromberg, Eitan, Begum, Ferdouse, Won, Sungho, Lutz, Sharon, Lynch, David A, Coxson, Harvey O, Han, MeiLan K, Hoffman, Eric A, Humphries, Stephen, Jacobson, Francine L, Judy, Philip F, Kazerooni, Ella A, Newell, John D, Ross, James C, Estépar, Raul José, Stoel, Berend C, Tschirren, Juerg, van Rikxoort, Eva, van Ginneken, Bram, Wilson, Carla G, Qaisi, Mustafa Al, Gray, Teresa, Kluiber, Alex, Mann, Tanya, Sieren, Jered, Stinson, Douglas, Schroeder, Joyce, Van Beek, Edwin, Jensen, Robert, Everett, Douglas, Faino, Anna, Strand, Matt, Wilson, Carla, Hokanson, John E, Kinney, Gregory, Young, Kendra, Pratte, Katherine, Duca, Lindsey, Curtis, Jeffrey L, Martinez, Carlos H, Pernicano, Perry G, Hanania, Nicola, Alapat, Philip, Bandi, Venkata, Atik, Mustafa, Boriek, Aladin, Guntupalli, Kalpatha, Guy, Elizabeth, Parulekar, Amit, Nachiappan, Arun, Jacobson, Francine, Barr, R Graham, Thomashow, Byron, Austin, John, D’Souza, Belinda, and Pearson, Gregory DN

Subjects
Clinical Research, Chronic Obstructive Pulmonary Disease, Lung, Emphysema, Prevention, 2.1 Biological and endogenous factors, Aetiology, Respiratory, Aged, Comorbidity, Disease Progression, Female, Forced Expiratory Volume, Humans, Male, Middle Aged, Pulmonary Emphysema, Severity of Illness Index, Tomography, X-Ray Computed, clustering, COPD, COPD disease progression, emphysema distribution, machine learning, COPDGene Investigators, Clinical Sciences, Respiratory System
Abstract

BackgroundEmphysema has considerable variability in its regional distribution. Craniocaudal emphysema distribution is an important predictor of the response to lung volume reduction. However, there is little consensus regarding how to define upper lobe-predominant and lower lobe-predominant emphysema subtypes. Consequently, the clinical and genetic associations with these subtypes are poorly characterized.MethodsWe sought to identify subgroups characterized by upper-lobe or lower-lobe emphysema predominance and comparable amounts of total emphysema by analyzing data from 9,210 smokers without alpha-1-antitrypsin deficiency in the Genetic Epidemiology of COPD (COPDGene) cohort. CT densitometric emphysema was measured in each lung lobe. Random forest clustering was applied to lobar emphysema variables after regressing out the effects of total emphysema. Clusters were tested for association with clinical and imaging outcomes at baseline and at 5-year follow-up. Their associations with genetic variants were also compared.ResultsThree clusters were identified: minimal emphysema (n = 1,312), upper lobe-predominant emphysema (n = 905), and lower lobe-predominant emphysema (n = 796). Despite a similar amount of total emphysema, the lower-lobe group had more severe airflow obstruction at baseline and higher rates of metabolic syndrome compared with subjects with upper-lobe predominance. The group with upper-lobe predominance had greater 5-year progression of emphysema, gas trapping, and dyspnea. Differential associations with known COPD genetic risk variants were noted.ConclusionsSubgroups of smokers defined by upper-lobe or lower-lobe emphysema predominance exhibit different functional and radiological disease progression rates, and the upper-lobe predominant subtype shows evidence of association with known COPD genetic risk variants. These subgroups may be useful in the development of personalized treatments for COPD.

Published
2018

31. The Association Between Lung Hyperinflation and Coronary Artery Disease in Smokers

Author

Crapo, James D., Silverman, Edwin K., Make, Barry J., Regan, Elizabeth A., Beaty, Terri, Begum, Ferdouse, Boueiz, Adel R., Castaldi, Peter J., Cho, Michael, DeMeo, Dawn L., Foreman, Marilyn G., Halper-Stromberg, Eitan, Hayden, Lystra P., Hersh, Craig P., Hetmanski, Jacqueline, Hobbs, Brian D., Hokanson, John E., Laird, Nan, Lange, Christoph, Lutz, Sharon M., McDonald, Merry-Lynn, Parker, Margaret M., Prokopenko, Dmitry, Qiao, Dandi, Sakornsakolpat, Phuwanat, Wan, Emily S., Won, Sungho, Al Qaisi, Mustafa, Coxson, Harvey O., Gray, Teresa, Han, MeiLan K., Hoffman, Eric A., Humphries, Stephen, Jacobson, Francine L., Judy, Philip F., Kazerooni, Ella A., Kluiber, Alex, Lynch, David A., Newell, John D., Jr., Ross, James C., San Jose Estepar, Raul, Schroeder, Joyce, Sieren, Jered, Stinson, Douglas, Stoel, Berend C., Tschirren, Juerg, Van Beek, Edwin, Ginneken, Bram van, van Rikxoort, Eva, Washko, George, Wilson, Carla G., Jensen, Robert, Crooks, Jim, Everett, Douglas, Moore, Camille, Strand, Hughes, John, Kinney, Gregory, Pratte, Katherine, Young, Kendra A., Bhatt, Surya, Bon, Jessica, Martinez, Carlos, Murray, Susan, Soler, Xavier, Banaei-Kashani, Farnoush, Bowler, Russell P., Kechris, Katerina, Curtis, Jeffrey L., Pernicano, Perry G., Hanania, Nicola, Atik, Mustafa, Boriek, Aladin, Guntupalli, Kalpatha, Guy, Elizabeth, Parulekar, Amit, Diaz, Alejandro A., Hersh, Craig, Barr, R. Graham, Austin, John, D’Souza, Belinda, Thomashow, Byron, MacIntyre, Neil, Jr., McAdams, H. Page, Washington, Lacey, McEvoy, Charlene, Tashjian, Joseph, Wise, Robert, Brown, Robert, Hansel, Nadia N., Horton, Karen, Lambert, Allison, Putcha, Nirupama, Casaburi, Richard, Adami, Alessandra, Budoff, Matthew, Fischer, Hans, Porszasz, Janos, Rossiter, Harry, Stringer, William, DeBakey, Michael E., Sharafkhaneh, Amir, Lan, Charlie, Wendt, Christine, Bell, Brian, Kunisaki, Ken M., Berkowitz, Eugene, Westney, Gloria, Bowler, Russell, Rosiello, Richard, Pace, David, Criner, Gerard, Ciccolella, David, Cordova, Francis, Dass, Chandra, D’Alonzo, Gilbert, Desai, Parag, Jacobs, Michael, Kelsen, Steven, Kim, Victor, Mamary, A. James, Marchetti, Nathaniel, Satti, Aditi, Shenoy, Kartik, Steiner, Robert M., Swift, Alex, Swift, Irene, Vega-Sanchez, Maria Elena, Dransfield, Mark, Bailey, William, Bhatt, Surya P., Iyer, Anand, Nath, Hrudaya, Wells, J. Michael, Ramsdell, Joe, Friedman, Paul, Yen, Andrew, Comellas, Alejandro P., Hoth, Karin F., Newell, John, Jr., Thompson, Brad, Kazerooni, Ella, Martinez, Carlos H., Billings, Joanne, Begnaud, Abbie, Allen, Tadashi, Sciurba, Frank, Chandra, Divay, Fuhrman, Carl, Weissfeld, Joel, Anzueto, Antonio, Adams, Sandra, Maselli-Caceres, Diego, Ruiz, Mario E., Gupta, Aman, Kinney, Gregory L., Fuhrman, Carl R., Leader, Joseph K., Hokanson, John, and Sciurba, Frank C.

Published
2021
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32. Pulmonary Arterial Pruning and Longitudinal Change in Percent Emphysema and Lung Function: The Genetic Epidemiology of COPD Study

Author

Crapo, James D., Silverman, Edwin K., Make, Barry J., Regan, Elizabeth A., Beaty, Terri H., Castaldi, Peter J., Cho, Michael H., DeMeo, Dawn L., El Boueiz, Adel, Foreman, Marilyn G., Ghosh, Auyon, Hayden, Lystra P., Hersh, Craig P., Hetmanski, Jacqueline, Hobbs, Brian D., Hokanson, John E., Kim, Wonji, Laird, Nan, Lange, Christoph, Lutz, Sharon M., McDonald, Merry-Lynn, Prokopenko, Dmitry, Moll, Matthew, Morrow, Jarrett, Qiao, Dandi, Saferali, Aabida, Sakornsakolpat, Phuwanat, Wan, Emily S., Yun, Jeong, Centeno, Juan Pablo, Charbonnier, Jean-Paul, Coxson, Harvey O., Galban, Craig J., Han, MeiLan K., Hoffman, Eric A., Humphries, Stephen, Jacobson, Francine L., Judy, Philip F., Kazerooni, Ella A., Kluiber, Alex, Lynch, David A., Nardelli, Pietro, Newell, John D., Jr., Notary, Aleena, Oh, Andrea, Ross, James C., San Jose Estepar, Raul, Schroeder, Joyce, Sieren, Jered, Stoel, Berend C., Tschirren, Juerg, Van Beek, Edwin, Ginneken, Bramvan, van Rikxoort, Eva, Sanchez- Ferrero, Gonzalo Vegas, Veitel, Lucas, Washko, George R., Wilson, Carla G., Jensen, Robert, Everett, Douglas, Crooks, Jim, Pratte, Katherine, Strand, Matt, Austin, Erin, Kinney, Gregory, Young, Kendra A., Bhatt, Surya P., Bon, Jessica, Diaz, Alejandro A., Make, Barry, Murray, Susan, Regan, Elizabeth, Soler, Xavier, Bowler, Russell P., Kechris, Katerina, Banaei-Kashani, Farnoush, Curtis, Jeffrey L., Pernicano, Perry G., Hanania, Nicola, Atik, Mustafa, Boriek, Aladin, Guntupalli, Kalpatha, Guy, Elizabeth, Parulekar, Amit, Hersh, Craig, Washko, George, Barr, R. Graham, Austin, John, D’Souza, Belinda, Thomashow, Byron, MacIntyre, Neil, Jr., McAdams, H. Page, Washington, Lacey, McEvoy, Charlene, Tashjian, Joseph, Wise, Robert, Brown, Robert, Hansel, Nadia N., Horton, Karen, Lambert, Allison, Putcha, Nirupama, Casaburi, Richard, Adami, Alessandra, Budoff, Matthew, Fischer, Hans, Porszasz, Janos, Rossiter, Harry, Stringer, William, Sharafkhaneh, Amir, Lan, Charlie, Wendt, Christine, Bell, Brian, Kunisaki, Ken M., Flenaugh, Eric L., Gebrekristos, Hirut, Ponce, Mario, Terpenning, Silanath, Westney, Gloria, Bowler, Russell, Rosiello, Richard, Pace, David, Criner, Gerard, Ciccolella, David, Cordova, Francis, Dass, Chandra, D’Alonzo, Gilbert, Desai, Parag, Jacobs, Michael, Kelsen, Steven, Kim, Victor, Mamary, A. James, Marchetti, Nathaniel, Satti, Aditi, Shenoy, Kartik, Steiner, Robert M., Swift, Alex, Swift, Irene, Vega-Sanchez, Maria Elena, Dransfield, Mark, Bailey, William, Iyer, Anand, Nath, Hrudaya, Wells, J. Michael, Conrad, Douglas, Yen, Andrew, Comellas, Alejandro P., Hoth, Karin F., Newell, John, Jr., Thompson, Brad, Kazerooni, Ella, Labaki, Wassim, Galban, Craig, Vummidi, Dharshan, Billings, Joanne, Begnaud, Abbie, Allen, Tadashi, Sciurba, Frank, Chandra, Divay, Weissfeld, Joel, Pistenmaa, Carrie L., Nardelli, P., Ash, S.Y., Come, C.E., Diaz, A.A., Rahaghi, F.N., Barr, R.G., Young, K.A., Kinney, G.L., Simmons, J.P., Wade, R.C., Wells, J.M., Hokanson, J.E., Washko, G.R., and San José Estépar, R.

Published
2021
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33. Machine Learning Characterization of COPD Subtypes: Insights From the COPDGene Study

Author

Crapo, James D., Silverman, Edwin K., Make, Barry J., Regan, Elizabeth A., Beaty, Terri, Begum, Ferdouse, Castaldi, Peter J., Cho, Michael, DeMeo, Dawn L., Boueiz, Adel R., Foreman, Marilyn G., Halper-Stromberg, Eitan, Hayden, Lystra P., Hersh, Craig P., Hetmanski, Jacqueline, Hobbs, Brian D., Hokanson, John E., Laird, Nan, Lange, Christoph, Lutz, Sharon M., McDonald, Merry-Lynn, Parker, Margaret M., Prokopenko, Dmitry, Qiao, Dandi, Sakornsakolpat, Phuwanat, Wan, Emily S., Won, Sungho, Centeno, Juan Pablo, Charbonnier, Jean-Paul, Coxson, Harvey O., Galban, Craig J., Han, MeiLan K., Hoffman, Eric A., Humphries, Stephen, Jacobson, Francine L., Judy, Philip F., Kazerooni, Ella A., Kluiber, Alex, Lynch, David A., Nardelli, Pietro, Newell, John D., Jr., Notary, Aleena, Oh, Andrea, Ross, James C., Estepar, Raul San Jose, Schroeder, Joyce, Sieren, Jered, Stoel, Berend C., Tschirren, Juerg, Van Beek, Edwin, van Ginneken, Bram, van Rikxoort, Eva, Sanchez-Ferrero, Gonzalo Vegas, Veitel, Lucas, Washko, George R., Wilson, Carla G., Jensen, Robert, Everett, Douglas, Crooks, Jim, Pratte, Katherine, Strand, Matt, Kinney, Gregory, Young, Kendra A., Bhatt, Surya P., Bon, Jessica, Diaz, Alejandro A., Make, Barry, Murray, Susan, Regan, Elizabeth, Soler, Xavier, Bowler, Russell P., Kechris, Katerina, Banaei-Kashani, Farnoush, Boueiz, Adel, Yun, Jeong, Washko, George, Cho, Michael H., Kinney, Gregory L., Criner, Gerald J., Dy, Jennifer G., Rennard, Stephen I., Casaburi, Richard, and Crapo, James

Published
2020
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34. Association between Functional Small Airway Disease and FEV1 Decline in Chronic Obstructive Pulmonary Disease.

Author

Bhatt, Surya P, Soler, Xavier, Wang, Xin, Murray, Susan, Anzueto, Antonio R, Beaty, Terri H, Boriek, Aladin M, Casaburi, Richard, Criner, Gerard J, Diaz, Alejandro A, Dransfield, Mark T, Curran-Everett, Douglas, Galbán, Craig J, Hoffman, Eric A, Hogg, James C, Kazerooni, Ella A, Kim, Victor, Kinney, Gregory L, Lagstein, Amir, Lynch, David A, Make, Barry J, Martinez, Fernando J, Ramsdell, Joe W, Reddy, Rishindra, Ross, Brian D, Rossiter, Harry B, Steiner, Robert M, Strand, Matthew J, van Beek, Edwin JR, Wan, Emily S, Washko, George R, Wells, J Michael, Wendt, Chris H, Wise, Robert A, Silverman, Edwin K, Crapo, James D, Bowler, Russell P, Han, MeiLan K, and COPDGene Investigators

Subjects
COPDGene Investigators, Respiratory System, Lung, Humans, Pulmonary Disease, Chronic Obstructive, Tomography, X-Ray Computed, Forced Expiratory Volume, Spirometry, Middle Aged, Female, Male, FEV1, lung function, parametric response mapping, Chronic Obstructive Pulmonary Disease, Clinical Research, Respiratory, Medical and Health Sciences
Abstract

RationaleThe small conducting airways are the major site of airflow obstruction in chronic obstructive pulmonary disease and may precede emphysema development.ObjectivesWe hypothesized a novel computed tomography (CT) biomarker of small airway disease predicts FEV1 decline.MethodsWe analyzed 1,508 current and former smokers from COPDGene with linear regression to assess predictors of change in FEV1 (ml/yr) over 5 years. Separate models for subjects without and with airflow obstruction were generated using baseline clinical and physiologic predictors in addition to two novel CT metrics created by parametric response mapping (PRM), a technique pairing inspiratory and expiratory CT images to define emphysema (PRM(emph)) and functional small airways disease (PRM(fSAD)), a measure of nonemphysematous air trapping.Measurements and main resultsMean (SD) rate of FEV1 decline in ml/yr for GOLD (Global Initiative for Chronic Obstructive Lung Disease) 0-4 was as follows: 41.8 (47.7), 53.8 (57.1), 45.6 (61.1), 31.6 (43.6), and 5.1 (35.8), respectively (trend test for grades 1-4; P

Published
2016

36. Genome-wide association study of preserved ratio impaired spirometry (PRISm)

Author

Higbee, Daniel H., Lirio, Alvin, Hamilton, Fergus, Granell, Raquel, Wyss, Annah B., London, Stephanie J., Bartz, Traci M., Gharib, Sina A., Cho, Michael H., Wan, Emily, Silverman, Edwin, Crapo, James D., Lominchar, Jesus V.T., Hansen, Torben, Grarup, Niels, Dantoft, Thomas, Kårhus, Line, Linneberg, Allan, O'Connor, George T., Dupuis, Josée, Xu, Hanfie, De Vries, Maaike M., Hu, Xiaowei, Rich, Stephen S., Barr, R. Graham, Manichaikul, Ani, Wijnant, Sara R.A., Brusselle, Guy G., Lahousse, Lies, Li, Xuan, Hernández Cordero, Ana I., Obeidat, Ma'en, Sin, Don D., Harris, Sarah E., Redmond, Paul, Taylor, Adele M., Cox, Simon R., Williams, Alexander T., Shrine, Nick, John, Catherine, Guyatt, Anna L., Hall, Ian P., Davey Smith, George, Tobin, Martin D., Dodd, James W., Higbee, Daniel H., Lirio, Alvin, Hamilton, Fergus, Granell, Raquel, Wyss, Annah B., London, Stephanie J., Bartz, Traci M., Gharib, Sina A., Cho, Michael H., Wan, Emily, Silverman, Edwin, Crapo, James D., Lominchar, Jesus V.T., Hansen, Torben, Grarup, Niels, Dantoft, Thomas, Kårhus, Line, Linneberg, Allan, O'Connor, George T., Dupuis, Josée, Xu, Hanfie, De Vries, Maaike M., Hu, Xiaowei, Rich, Stephen S., Barr, R. Graham, Manichaikul, Ani, Wijnant, Sara R.A., Brusselle, Guy G., Lahousse, Lies, Li, Xuan, Hernández Cordero, Ana I., Obeidat, Ma'en, Sin, Don D., Harris, Sarah E., Redmond, Paul, Taylor, Adele M., Cox, Simon R., Williams, Alexander T., Shrine, Nick, John, Catherine, Guyatt, Anna L., Hall, Ian P., Davey Smith, George, Tobin, Martin D., and Dodd, James W.

Abstract

Background Preserved ratio impaired spirometry (PRISm) is defined as a forced expiratory volume in 1 s (FEV 1) <80% predicted and FEV 1/forced vital capacity ≤0.70. PRISm is associated with respiratory symptoms and comorbidities. Our objective was to discover novel genetic signals for PRISm and see if they provide insight into the pathogenesis of PRISm and associated comorbidities. Methods We undertook a genome-wide association study (GWAS) of PRISm in UK Biobank participants (Stage 1), and selected single nucleotide polymorphisms (SNPs) reaching genome-wide significance for replication in 13 cohorts (Stage 2). A combined meta-analysis of Stage 1 and Stage 2 was done to determine top SNPs. We used cross-trait linkage disequilibrium score regression to estimate genome-wide genetic correlation between PRISm and pulmonary and extrapulmonary traits. Phenome-wide association studies of top SNPs were performed. Results 22 signals reached significance in the joint meta-analysis, including four signals novel for lung function. A strong genome-wide genetic correlation (r g) between PRISm and spirometric COPD (r g=0.62, p<0.001) was observed, and genetic correlation with type 2 diabetes (r g=0.12, p=0.007). Phenome-wide association studies showed that 18 of 22 signals were associated with diabetic traits and seven with blood pressure traits. Conclusion This is the first GWAS to successfully identify SNPs associated with PRISm. Four of the signals, rs7652391 (nearest gene MECOM), rs9431040 (HLX), rs62018863 (TMEM114) and rs185937162 (HLA-B), have not been described in association with lung function before, demonstrating the utility of using different lung function phenotypes in GWAS. Genetic factors associated with PRISm are strongly correlated with risk of both other lung diseases and extrapulmonary comorbidity.

Published
2024

37. Genome-wide association study of preserved ratio impaired spirometry (PRISm)

Author

Higbee, Daniel H, Lirio, Alvin, Hamilton, Fergus, Granell, Raquel, Wyss, Annah B, London, Stephanie J, Bartz, Traci M, Gharib, Sina A, Cho, Michael H, Wan, Emily, Silverman, Edwin, Crapo, James D, Lominchar, Jesus V T, Hansen, Torben, Grarup, Niels, Dantoft, Thomas, Kårhus, Line, Linneberg, Allan, O'Connor, George T, Dupuis, Josée, Xu, Hanfie, De Vries, Maaike M, Hu, Xiaowei, Rich, Stephen S, Barr, R Graham, Manichaikul, Ani, Wijnant, Sara R A, Brusselle, Guy G, Lahousse, Lies, Li, Xuan, Hernández Cordero, Ana I, Obeidat, Ma'en, Sin, Don D, Harris, Sarah E, Redmond, Paul, Taylor, Adele M, Cox, Simon R, Williams, Alexander T, Shrine, Nick, John, Catherine, Guyatt, Anna L, Hall, Ian P, Davey Smith, George, Tobin, Martin D, Dodd, James W, Higbee, Daniel H, Lirio, Alvin, Hamilton, Fergus, Granell, Raquel, Wyss, Annah B, London, Stephanie J, Bartz, Traci M, Gharib, Sina A, Cho, Michael H, Wan, Emily, Silverman, Edwin, Crapo, James D, Lominchar, Jesus V T, Hansen, Torben, Grarup, Niels, Dantoft, Thomas, Kårhus, Line, Linneberg, Allan, O'Connor, George T, Dupuis, Josée, Xu, Hanfie, De Vries, Maaike M, Hu, Xiaowei, Rich, Stephen S, Barr, R Graham, Manichaikul, Ani, Wijnant, Sara R A, Brusselle, Guy G, Lahousse, Lies, Li, Xuan, Hernández Cordero, Ana I, Obeidat, Ma'en, Sin, Don D, Harris, Sarah E, Redmond, Paul, Taylor, Adele M, Cox, Simon R, Williams, Alexander T, Shrine, Nick, John, Catherine, Guyatt, Anna L, Hall, Ian P, Davey Smith, George, Tobin, Martin D, and Dodd, James W

Abstract

BACKGROUND: Preserved ratio impaired spirometry (PRISm) is defined as a forced expiratory volume in 1 s (FEV 1) <80% predicted and FEV 1/forced vital capacity ≥0.70. PRISm is associated with respiratory symptoms and comorbidities. Our objective was to discover novel genetic signals for PRISm and see if they provide insight into the pathogenesis of PRISm and associated comorbidities. METHODS: We undertook a genome-wide association study (GWAS) of PRISm in UK Biobank participants (Stage 1), and selected single nucleotide polymorphisms (SNPs) reaching genome-wide significance for replication in 13 cohorts (Stage 2). A combined meta-analysis of Stage 1 and Stage 2 was done to determine top SNPs. We used cross-trait linkage disequilibrium score regression to estimate genome-wide genetic correlation between PRISm and pulmonary and extrapulmonary traits. Phenome-wide association studies of top SNPs were performed.RESULTS: 22 signals reached significance in the joint meta-analysis, including four signals novel for lung function. A strong genome-wide genetic correlation (r g) between PRISm and spirometric COPD (r g=0.62, p<0.001) was observed, and genetic correlation with type 2 diabetes (r g=0.12, p=0.007). Phenome-wide association studies showed that 18 of 22 signals were associated with diabetic traits and seven with blood pressure traits. CONCLUSION: This is the first GWAS to successfully identify SNPs associated with PRISm. Four of the signals, rs7652391 (nearest gene MECOM), rs9431040 ( HLX), rs62018863 ( TMEM114) and rs185937162 ( HLA-B), have not been described in association with lung function before, demonstrating the utility of using different lung function phenotypes in GWAS. Genetic factors associated with PRISm are strongly correlated with risk of both other lung diseases and extrapulmonary comorbidity.

Published
2024

38. Reduced Bone Density and Vertebral Fractures in Smokers. Men and COPD Patients at Increased Risk.

Author

Jaramillo, Joshua D, Wilson, Carla, Stinson, Douglas S, Lynch, David A, Bowler, Russell P, Lutz, Sharon, Bon, Jessica M, Arnold, Ben, McDonald, Merry-Lynn N, Washko, George R, Wan, Emily S, DeMeo, Dawn L, Foreman, Marilyn G, Soler, Xavier, Lindsay, Sarah E, Lane, Nancy E, Genant, Harry K, Silverman, Edwin K, Hokanson, John E, Make, Barry J, Crapo, James D, Regan, Elizabeth A, and COPDGene Investigators

Subjects
COPDGene Investigators, Humans, Osteoporosis, Pulmonary Disease, Chronic Obstructive, Spinal Fractures, Tomography, X-Ray Computed, Incidence, Risk Factors, Smoking, Bone Density, Adult, Middle Aged, United States, Female, Male, COPD, low bone density, quantitative computed tomography, smoking, vertebral fractures, Pulmonary Disease, Chronic Obstructive, Tomography, X-Ray Computed, Respiratory System, Clinical Sciences
Abstract

RationaleFormer smoking history and chronic obstructive pulmonary disease (COPD) are potential risk factors for osteoporosis and fractures. Under existing guidelines for osteoporosis screening, women are included but men are not, and only current smoking is considered.ObjectivesTo demonstrate the impact of COPD and smoking history on the risk of osteoporosis and vertebral fracture in men and women.MethodsCharacteristics of participants with low volumetric bone mineral density (vBMD) were identified and related to COPD and other risk factors. We tested associations of sex and COPD with both vBMD and fractures adjusting for age, race, body mass index (BMI), smoking, and glucocorticoid use.Measurements and main resultsvBMD by calibrated quantitative computed tomography (QCT), visually scored vertebral fractures, and severity of lung disease were determined from chest CT scans of 3,321 current and ex-smokers in the COPDGene study. Low vBMD as a surrogate for osteoporosis was calculated from young adult normal values. Male smokers had a small but significantly greater risk of low vBMD (2.5 SD below young adult mean by calibrated QCT) and more fractures than female smokers. Low vBMD was present in 58% of all subjects, was more frequent in those with worse COPD, and rose to 84% among subjects with very severe COPD. Vertebral fractures were present in 37% of all subjects and were associated with lower vBMD at each Global Initiative for Chronic Obstructive Lung Disease stage of severity. Vertebral fractures were most common in the midthoracic region. COPD and especially emphysema were associated with both low vBMD and vertebral fractures after adjustment for steroid use, age, pack-years of smoking, current smoking, and exacerbations. Airway disease was associated with higher bone density after adjustment for other variables. Calibrated QCT identified more subjects with abnormal values than the standard dual-energy X-ray absorptiometry in a subset of subjects and correlated well with prevalent fractures.ConclusionsMale smokers, with or without COPD, have a significant risk of low vBMD and vertebral fractures. COPD was associated with low vBMD after adjusting for race, sex, BMI, smoking, steroid use, exacerbations, and age. Screening for low vBMD by using QCT in men and women who are smokers will increase opportunities to identify and treat osteoporosis in this at-risk population.

Published
2015

39. Whole Genome Sequencing Identifies CRISPLD2 as a Lung Function Gene in Children With Asthma

Author

Abe, Namiko, Abecasis, Goncalo, Albert, Christine, Palmer Allred, Nicholette (Nichole), Almasy, Laura, Alonso, Alvaro, Ament, Seth, Anderson, Peter, Anugu, Pramod, Applebaum-Bowden, Deborah, Arking, Dan, Arnett, Donna K., Ashley-Koch, Allison, Aslibekyan, Stella, Assimes, Tim, Auer, Paul, Avramopoulos, Dimitrios, Barnard, John, Barnes, Kathleen, Barr, R. Graham, Barron-Casella, Emily, Beaty, Terri, Becker, Diane, Becker, Lewis, Beer, Rebecca, Begum, Ferdouse, Beitelshees, Amber, Benjamin, Emelia, Bezerra, Marcos, Bielak, Larry, Bis, Joshua, Blackwell, Thomas, Blangero, John, Boerwinkle, Eric, Borecki, Ingrid, Bowler, Russell, Brody, Jennifer, Broeckel, Ulrich, Broome, Jai, Bunting, Karen, Burchard, Esteban, Cardwell, Jonathan, Carty, Cara, Casaburi, Richard, Casella, James, Chaffin, Mark, Chang, Christy, Chasman, Daniel, Chavan, Sameer, Chen, Bo-Juen, Chen, Wei-Min, Chen, Yii-Der Ida, Cho, Michael H., Choi, Seung Hoan, Chuang, Lee-Ming, Chung, Mina, Cornell, Elaine, Correa, Adolfo, Crandall, Carolyn, Crapo, James, Cupples, L. Adrienne, Curran, Joanne, Curtis, Jeffrey, Custer, Brian, Damcott, Coleen, Darbar, Dawood, Das, Sayantan, David, Sean, Davis, Colleen, Daya, Michelle, de Andrade, Mariza, DeBaun, Michael, Deka, Ranjan, DeMeo, Dawn, Devine, Scott, Do, Ron, Duan, Qing, Duggirala, Ravi, Durda, Peter, Dutcher, Susan, Eaton, Charles, Ekunwe, Lynette, Ellinor, Patrick, Emery, Leslie, Farber, Charles, Farnam, Leanna, Fingerlin, Tasha, Flickinger, Matthew, Fornage, Myriam, Franceschini, Nora, Fu, Mao, Fullerton, Stephanie M., Fulton, Lucinda, Gabriel, Stacey, Gan, Weiniu, Gao, Yan, Gass, Margery, Gelb, Bruce, Geng, Xiaoqi (Priscilla), Germer, Soren, Gignoux, Chris, Gladwin, Mark, Glahn, David, Gogarten, Stephanie, Gong, Da-Wei, Goring, Harald, Gu, C. Charles, Guan, Yue, Guo, Xiuqing, Haessler, Jeff, Hall, Michael, Harris, Daniel, Hawley, Nicola, He, Jiang, Heavner, Ben, Heckbert, Susan, Hernandez, Ryan, Herrington, David, Hersh, Craig, Hidalgo, Bertha, Hixson, James, Hokanson, John, Holly, Kramer, Hong, Elliott, Hoth, Karin, (Agnes) Hsiung, Chao, Huston, Haley, Hwu, Chii Min, Irvin, Marguerite Ryan, Jackson, Rebecca, Jain, Deepti, Jaquish, Cashell, Jhun, Min A., Johnsen, Jill, Johnson, Andrew, Johnson, Craig, Johnston, Rich, Jones, Kimberly, Kachroo, Priyadarshini, Kang, Hyun Min, Kaplan, Robert, Kardia, Sharon, Kathiresan, Sekar, Kaufman, Laura, Kelly, Shannon, Kenny, Eimear, Kessler, Michael, Khan, Alyna, Kinney, Greg, Konkle, Barbara, Kooperberg, Charles, Krauter, Stephanie, Lange, Christoph, Lange, Ethan, Lange, Leslie, Laurie, Cathy, Laurie, Cecelia, LeBoff, Meryl, Lee, Seunggeun Shawn, Lee, Wen-Jane, LeFaive, Jonathon, Levine, David, Levy, Dan, Lewis, Joshua, Li, Yun, Lin, Honghuang, Lin, Keng Han, Liu, Simin, Liu, Yongmei, Loos, Ruth, Lubitz, Steven, Lunetta, Kathryn, Luo, James, Mahaney, Michael, Make, Barry, Manichaikul, Ani, Manson, JoAnn, Margolin, Lauren, Martin, Lisa, Mathai, Susan, Mathias, Rasika, McArdle, Patrick, McDonald, Merry-Lynn, McFarland, Sean, McGarvey, Stephen, Mei, Hao, Meyers, Deborah A., Mikulla, Julie, Min, Nancy, Minear, Mollie, Minster, Ryan L., Mitchell, Braxton, Montasser, May E., Musani, Solomon, Mwasongwe, Stanford, Mychaleckyj, Josyf C., Nadkarni, Girish, Naik, Rakhi, Natarajan, Pradeep, Nekhai, Sergei, Nickerson, Deborah, North, Kari, O'Connell, Jeff, O'Connor, Tim, Ochs-Balcom, Heather, Pankow, James, Papanicolaou, George, Parker, Margaret, Parsa, Afshin, Penchev, Sara, Peralta, Juan Manuel, Perez, Marco, Perry, James, Peters, Ulrike, Peyser, Patricia, Phillips, Lawrence S., Phillips, Sam, Pollin, Toni, Post, Wendy, Becker, Julia Powers, Boorgula, Meher Preethi, Preuss, Michael, Prokopenko, Dmitry, Psaty, Bruce, Qasba, Pankaj, Qiao, Dandi, Qin, Zhaohui, Rafaels, Nicholas, Raffield, Laura, Ramachandran, Vasan, Rao, D.C., Rasmussen-Torvik, Laura, Ratan, Aakrosh, Redline, Susan, Reed, Robert, Regan, Elizabeth, Reiner, Alex, Rice, Ken, Rich, Stephen, Roden, Dan, Roselli, Carolina, Rotter, Jerome, Ruczinski, Ingo, Russell, Pamela, Ruuska, Sarah, Ryan, Kathleen, Sakornsakolpat, Phuwanat, Salimi, Shabnam, Salzberg, Steven, Sandow, Kevin, Sankaran, Vijay, Scheller, Christopher, Schmidt, Ellen, Schwander, Karen, Schwartz, David, Sciurba, Frank, Seidman, Christine, Seidman, Jonathan, Sheehan, Vivien, Shetty, Amol, Shetty, Aniket, Sheu, Wayne Hui-Heng, Shoemaker, M. Benjamin, Silver, Brian, Silverman, Edwin, Smith, Jennifer, Smith, Josh, Smith, Nicholas, Smith, Tanja, Smoller, Sylvia, Snively, Beverly, Sofer, Tamar, Sotoodehnia, Nona, Stilp, Adrienne, Streeten, Elizabeth, Sung, Yun Ju, Su-Lasky, Jessica, Sylvia, Jody, Szpiro, Adam, Sztalryd, Carole, Taliun, Daniel, Tang, Hua, Taub, Margaret, Taylor, Kent, Taylor, Simeon, Telen, Marilyn, Thornton, Timothy A., Tinker, Lesley, Tirschwell, David, Tiwari, Hemant, Tracy, Russell, Tsai, Michael, Vaidya, Dhananjay, VandeHaar, Peter, Vrieze, Scott, Walker, Tarik, Wallace, Robert, Walts, Avram, Wan, Emily, Wang, Fei Fei, Watson, Karol, Weeks, Daniel E., Weir, Bruce, Weiss, Scott, Weng, Lu-Chen, Willer, Cristen, Williams, Kayleen, Williams, L. Keoki, Wilson, Carla, Wilson, James, Wong, Quenna, Xu, Huichun, Yanek, Lisa, Yang, Ivana, Yang, Rongze, Zaghloul, Norann, Zekavat, Maryam, Zhang, Yingze, Zhao, Snow Xueyan, Zhao, Wei, Zheng, Xiuwen, Zhi, Degui, Zhou, Xiang, Zody, Michael, Zoellner, Sebastian, Hecker, Julian, Chawes, Bo L., Ahluwalia, Tarunveer S., Kelly, Rachel S., Chu, Su H., Virkud, Yamini V., Huang, Mengna, Barnes, Kathleen C., Burchard, Esteban G., Eng, Celeste, Hu, Donglei, Celedón, Juan C., Levin, Albert M., Gui, Hongsheng, Forno, Erick, Mak, Angel C.Y., Avila, Lydiana, Soto-Quiros, Manuel E., Cloutier, Michelle M., Acosta-Pérez, Edna, Canino, Glorisa, Bønnelykke, Klaus, Bisgaard, Hans, Raby, Benjamin A., Weiss, Scott T., and Lasky-Su, Jessica A.

Published
2019
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40. The St. George’s Respiratory Questionnaire Definition of Chronic Bronchitis May Be a Better Predictor of COPD Exacerbations Compared With the Classic Definition

Author

Crapo, James D., Silverman, Edwin K., Make, Barry J., Regan, Elizabeth A., Beaty, Terri, Begum, Ferdouse, Busch, Robert, Castaldi, Peter J., Cho, Michael, DeMeo, Dawn L., Boueiz, Adel R., Foreman, Marilyn G., Halper-Stromberg, Eitan, Hansel, Nadia N., Hardin, Megan E., Hayden, Lystra P., Hersh, Craig P., Hetmanski, Jacqueline, Hobbs, Brian D., Hokanson, John E., Laird, Nan, Lange, Christoph, Lutz, Sharon M., McDonald, Merry-Lynn, Parker, Margaret M., Qiao, Dandi, Santorico, Stephanie, Wan, Emily S., Won, Sungho, Charbonnier, Jean-Paul, Coxson, Harvey O., Han, MeiLan K., Hoffman, Eric A., Humphries, Stephen, Jacobson, Francine L., Judy, Philip F., Kazerooni, Ella A., Kluiber, Alex, Lynch, David A., Newell, John D., Jr., Ross, James C., San Jose Estepar, Raul, Sieren, Jered, Stoel, Berend C., Tschirren, Juerg, Van Beek, Edwin, van Ginneken, Bram, van Rikxoort, Eva, Washko, George, Wilson, Carla G., Jensen, Robert, Everett, Douglas, Crooks, Jim, Moore, Camille, Strand, Matt, Hughes, John, Kinney, Gregory, Pratte, Katherine, Young, Kendra A., Curtis, Jeffrey L., Martinez, Carlos H., Pernicano, Perry G., Hanania, Nicola, Alapat, Philip, Atik, Mustafa, Bandi, Venkata, Boriek, Aladin, Guntupalli, Kalpatha, Guy, Elizabeth, Nachiappan, Arun, Parulekar, Amit, Hersh, Craig, Barr, R. Graham, Austin, John, D’Souza, Belinda, Pearson, Gregory D.N., Rozenshtein, Anna, Thomashow, Byron, MacIntyre, Neil, Jr., McAdams, H. Page, Washington, Lacey, McEvoy, Charlene, Tashjian, Joseph, Wise, Robert, Brown, Robert, Horton, Karen, Lambert, Allison, Putcha, Nirupama, Casaburi, Richard, Adami, Alessandra, Budoff, Matthew, Fischer, Hans, Porszasz, Janos, Rossiter, Harry, Stringer, William, Sharafkhaneh, Amir, Lan, Charlie, Wendt, Christine, Bell, Brian, Berkowitz, Eugene, Flenaugh, Eric L., Westney, Gloria, Bowler, Russell, Rosiello, Richard, Pace, David, Criner, Gerard, Ciccolella, David, Cordova, Francis, Dass, Chandra, D’Alonzo, Gilbert, Desai, Parag, Jacobs, Michael, Kelsen, Steven, Kim, Victor, Mamary, A. James, Marchetti, Nathaniel, Satti, Aditi, Shenoy, Kartik, Steiner, Robert M., Vega-Sanchez, Maria Elena, Dransfield, Mark, Bailey, William, Bhatt, Surya, Iyer, Anand, Nath, Hrudaya, Oates, Gabriela, Sonavane, Sushil, Wells, J. Michael, Ramsdell, Joe, Friedman, Paul, Soler, Xavier, Yen, Andrew, Comellas, Alejandro P., Newell, John, Jr., Thompson, Brad, Kazerooni, Ella, Billings, Joanne, Begnaud, Abbie, Allen, Tadashi, Sciurba, Frank, Bon, Jessica, Chandra, Divay, Fuhrman, Carl, Weissfeld, Joel, Anzueto, Antonio, Adams, Sandra, Maselli-Caceres, Diego, Ruiz, Mario E., Zhao, Huaqing, Regan, Elizabeth, Jones, Paul W., and Criner, Gerard J.

Published
2019
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41. Clinical Epidemiology of COPD: Insights From 10 Years of the COPDGene Study

Author

Maselli, Diego J., Bhatt, Surya P., Anzueto, Antonio, Bowler, Russell P., DeMeo, Dawn L., Diaz, Alejandro A., Dransfield, Mark T., Fawzy, Ashraf, Foreman, Marilyn G., Hanania, Nicola A., Hersh, Craig P., Kim, Victor, Kinney, Gregory L., Putcha, Nirupama, Wan, Emily S., Wells, J. Michael, Westney, Gloria E., Young, Kendra A., Silverman, Edwin K., Han, MeiLan K., and Make, Barry J.

Published
2019
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42. The Need of Safety-Net Programme for a Mass Education System

Author

Wong, Edwin K. P., Ngai, Sze Wan Emily, and Lo, King Shuen

Abstract

Background: The Project Yi Jin (PYJ), an alternative pathway for secondary school leavers and adults to further their education, has been receiving full support from the government, the Federation for Continuing Education in Tertiary Institutions (FCE) in Hong Kong and the public. Graduates of PYJ have the equivalent academic status of their counterparts in the main stream education. It was first implemented in 2000/01 by the FCE and has been offered to more than 35,000 students by 2006/07. With the success of the programme as a safety-net for a mass education system, it should continue to function more vigorously as new reforms are being implemented in the Hong Kong education scene in the future. The Chief Executive in his 2004 Policy Address has set out the direction to develop a new secondary and university system, i.e., (3+3) for secondary + 4 (tertiary) [the old one is (3+2+2)+3], to be launched in 2010/11, that will effectively prepare the next generation to cope with the challenges of the 21st century and the demands of the rapidly developing knowledge-based society. The new system, together with substantial modified curricula including the newly developed applied learning courses (ApL), is supposed to be able to look after all secondary students. Aims and focus of discussion: This paper aims to argue the necessity of launching a new version of Project Yi Jin (nPYJ) concurrently together with the new 3+3+4 academic system. In light of the contemporary global educational systems as compared to that of Hong Kong, it is postulated that the launching of nPYJ as a continuation of the successful PYJ is both legitimate and indispensable with regard to the carefully observed current global fashion of lifelong learning and continuing education in which diversity, equity, and flexibility are highly valued. Method: A comprehensive comparative review was carried out on eleven selected oriental and occidental countries and regions, namely, Australia, Canada, Germany, Japan, South Korea, United Kingdom, United States, China, Taiwan, Singapore and Macao, focusing on the worldwide trend of constant high school drop-out rate as well as the mentioned countries' respective senior secondary schooling articulation policy leading to higher education, in particular shedding light on the establishment of alternative pathways towards tertiary education alongside the conventional educational track. Conclusion: With the literature backdrop and empirical support, it is shown that high school drop-outs are inevitable no matter how well-defined an education system may be. Thus this is where the "safety-net" contingency plan is found essential. A new version of Project Yi Jin (nPYJ), to be offered in parallel with the Hong Kong's new 3+3+4 secondary academic curricula, is indispensable to the new educational structure in the territory which fundamentally helps transform the conventionally somewhat segregated and elite educational system into a mass one. Regarding the curricular design, both PYJ and nPYJ will focus on generic skills and a wide range of electives will be offered as well to arouse students' interest of study. (Contains 1 figure, 1 table and 5 footnotes.)

Published
2006

43. Deployment-related Cigarette Smoking Behaviors and Pulmonary Function Among U.S. Veterans

Author

Maccarone, Jennifer R, primary, Sterns, Olivia R, additional, Timmons, Andrew, additional, Korpak, Anna M, additional, Smith, Nicholas L, additional, Nakayama, Karen S, additional, Baird, Coleen P, additional, Ciminera, Paul, additional, Kheradmand, Farrah, additional, Fan, Vincent S, additional, Hart, Jaime E, additional, Koutrakis, Petros, additional, Jerrett, Michael, additional, Kuschner, Ware G, additional, Ioachimescu, Octavian C, additional, Montgrain, Philippe R, additional, Proctor, Susan P, additional, Redlich, Carrie A, additional, Wendt, Christine H, additional, Blanc, Paul D, additional, Garshick, Eric, additional, and Wan, Emily S, additional

Published
2024
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46. Epidemiology, genetics, and subtyping of preserved ratio impaired spirometry (PRISm) in COPDGene

Author

Wan, Emily S, Castaldi, Peter J, Cho, Michael H, Hokanson, John E, Regan, Elizabeth A, Make, Barry J, Beaty, Terri H, Han, MeiLan K, Curtis, Jeffrey L, Curran-Everett, Douglas, Lynch, David A, DeMeo, Dawn L, Crapo, James D, and Silverman, Edwin K

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Tobacco Smoke and Health, Clinical Research, Chronic Obstructive Pulmonary Disease, Genetics, Human Genome, Tobacco, Lung, 2.1 Biological and endogenous factors, Aetiology, Respiratory, Good Health and Well Being, Aged, Aged, 80 and over, Cluster Analysis, Cohort Studies, Cross-Sectional Studies, Female, Genome-Wide Association Study, Humans, Male, Middle Aged, Pulmonary Disease, Chronic Obstructive, Spirometry, COPDGene Investigators, Lung diseases, Restriction, Smoking, Cardiorespiratory Medicine and Haematology, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract

BackgroundPreserved Ratio Impaired Spirometry (PRISm), defined as a reduced FEV1 in the setting of a preserved FEV1/FVC ratio, is highly prevalent and is associated with increased respiratory symptoms, systemic inflammation, and mortality. Studies investigating quantitative chest tomographic features, genetic associations, and subtypes in PRISm subjects have not been reported.MethodsData from current and former smokers enrolled in COPDGene (n = 10,192), an observational, cross-sectional study which recruited subjects aged 45-80 with ≥10 pack years of smoking, were analyzed. To identify epidemiological and radiographic predictors of PRISm, we performed univariate and multivariate analyses comparing PRISm subjects both to control subjects with normal spirometry and to subjects with COPD. To investigate common genetic predictors of PRISm, we performed a genome-wide association study (GWAS). To explore potential subgroups within PRISm, we performed unsupervised k-means clustering.ResultsThe prevalence of PRISm in COPDGene is 12.3%. Increased dyspnea, reduced 6-minute walk distance, increased percent emphysema and decreased total lung capacity, as well as increased segmental bronchial wall area percentage were significant predictors (p-value

Published
2014

48. Blood eosinophil count thresholds and exacerbations in patients with chronic obstructive pulmonary disease

Author

Crapo, James D., Silverman, Edwin K., Make, Barry J., Regan, Elizabeth A., Beaty, Terri, Begum, Ferdouse, Busch, Robert, Castaldi, Peter J., Cho, Michael, DeMeo, Dawn L., Boueiz, Adel R., Foreman, Marilyn G., Halper-Stromberg, Eitan, Hansel, Nadia N., Hardin, Megan E., Hayden, Lystra P., Hersh, Craig P., Hetmanski, Jacqueline, Hobbs, Brian D., Hokanson, John E., Laird, Nan, Lange, Christoph, Lutz, Sharon M., McDonald, Merry-Lynn, Parker, Margaret M., Qiao, Dandi, Santorico, Stephanie, Wan, Emily S., Won, Sungho, Al Qaisi, Mustafa, Coxson, Harvey O., Gray, Teresa, Han, MeiLan K., Hoffman, Eric A., Humphries, Stephen, Jacobson, Francine L., Judy, Philip F., Kazerooni, Ella A., Kluiber, Alex, Lynch, David A., Newell, John D., Jr., Ross, James C., San Jose Estepar, Raul, Schroeder, Joyce, Sieren, Jered, Stinson, Douglas, Stoel, Berend C., Tschirren, Juerg, Van Beek, Edwin, van Ginneken, Bram, van Rikxoort, Eva, Washko, George, Wilson, Carla G., Jensen, Robert, Everett, Douglas, Crooks, Jim, Moore, Camille, Strand, Matt, Hughes, John, Kinney, Gregory, Pratte, Katherine, Young, Kendra A., Curtis, Jeffrey L., Martinez, Carlos H., Pernicano, Perry G., Hanania, Nicola, Alapat, Philip, Atik, Mustafa, Bandi, Venkata, Boriek, Aladin, Guntupalli, Kalpatha, Guy, Elizabeth, Nachiappan, Arun, Parulekar, Amit, Hersh, Craig, Barr, R. Graham, Austin, John, D'Souza, Belinda, Pearson, Gregory D.N., Rozenshtein, Anna, Thomashow, Byron, MacIntyre, Neil, Jr., McAdams, H. Page, Washington, Lacey, McEvoy, Charlene, Tashjian, Joseph, Wise, Robert, Brown, Robert, Horton, Karen, Lambert, Allison, Putcha, Nirupama, Casaburi, Richard, Adami, Alessandra, Budoff, Matthew, Fischer, Hans, Porszasz, Janos, Rossiter, Harry, Stringer, William, Sharafkhaneh, Amir, Lan, Charlie, Wendt, Christine, Bell, Brian, Berkowitz, Eugene, Westney, Gloria, Bowler, Russell, Rosiello, Richard, Pace, David, Criner, Gerard, Ciccolella, David, Cordova, Francis, Dass, Chandra, D'Alonzo, Gilbert, Desai, Parag, Jacobs, Michael, Kelsen, Steven, Kim, Victor, Mamary, A. James, Marchetti, Nathaniel, Satti, Aditi, Shenoy, Kartik, Steiner, Robert M., Swift, Alex, Swift, Irene, Vega-Sanchez, Maria Elena, Dransfield, Mark, Bailey, William, Bhatt, Surya, Iyer, Anand, Nath, Hrudaya, Wells, J. Michael, Ramsdell, Joe, Friedman, Paul, Soler, Xavier, Yen, Andrew, Comellas, Alejandro P., Newell, John, Jr., Thompson, Brad, Kazerooni, Ella, Billings, Joanne, Begnaud, Abbie, Allen, Tadashi, Sciurba, Frank, Bon, Jessica, Chandra, Divay, Fuhrman, Carl, Weissfeld, Joel, Anzueto, Antonio, Adams, Sandra, Maselli-Caceres, Diego, Ruiz, Mario E., Ivanov, Y., Kostov, K., Bourbeau, J., Fitzgerald, M., Hernandez, P., Killian, K., Levy, R., Maltais, F., O'Donnell, D., Krepelka, J., Vestbo, J., Wouters, E., Quinn, D., Bakke, P., Kosnik, M., Agusti, A., Sauleda, J., de Mallorca, P., Feschenko, Y., Gavrisyuk, V., Kiev, L. Yashina, Monogarova, N., Calverley, P., Lomas, D., MacNee, W., Singh, D., Wedzicha, J., Anzueto, A., Braman, S., Casaburi, R., Celli, B., Giessel, G., Gotfried, M., Greenwald, G., Hanania, N., Mahler, D., Make, B., Rennard, S., Rochester, C., Scanlon, P., Schuller, D., Sciurba, F., Sharafkhaneh, A., Siler, T., Silverman, E., Wanner, A., Wise, R., ZuWallack, R., Coxson, H., Crim, C., Edwards, L., Singer, R. Tal, Yates, J., Miller, B., Tal-Singer, R., Yun, Jeong H., Lamb, Andrew, Chase, Robert, Singh, Dave, Saferali, Aabida, Vestbo, Jørgen, and Tal-Singer, Ruth

Published
2018
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49. Pulmonary Function Reduction in Diabetes With and Without Chronic Obstructive Pulmonary Disease

Author

Kinney, Gregory L, Black-Shinn, Jennifer L, Wan, Emily S, Make, Barry, Regan, Elizabeth, Lutz, Sharon, Soler, Xavier, Silverman, Edwin K, Crapo, James, Hokanson, John E, and Investigators, the COPDGene

Subjects
Epidemiology, Health Sciences, Chronic Obstructive Pulmonary Disease, Clinical Research, Tobacco Smoke and Health, Diabetes, Prevention, Tobacco, Lung, Metabolic and endocrine, Respiratory, Aged, Case-Control Studies, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Female, Forced Expiratory Volume, Humans, Male, Middle Aged, Pulmonary Disease, Chronic Obstructive, Risk Factors, Smoking, Vital Capacity, COPDGene Investigators, Medical and Health Sciences, Endocrinology & Metabolism, Biomedical and clinical sciences, Health sciences
Abstract

ObjectiveDiabetes damages major organ systems through disrupted glycemic control and increased inflammation. The effects of diabetes on the lung have been of interest for decades, but the modest reduction in pulmonary function and its nonprogressive nature have limited its investigation. A recent systematic review found that diabetes was associated with reductions in forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), and diffusing capacity for carbon monoxide of the lung and increased FEV1/FVC. They reported pooled results including few smokers. This study will examine measures of pulmonary function in participants with extensive smoking exposure.Research design and methodsWe examined pulmonary function in participants with a >10-pack-year history of smoking with and without diabetes with and without chronic obstructive pulmonary disease (COPD). We measured pulmonary function, exercise capacity, and pulmonary-related quality of life in 10,129 participants in the Genetic Epidemiology of Chronic Obstructive Pulmonary Disease (COPDGene) Study.ResultsParticipants with diabetes were observed to have reduced pulmonary function after controlling for known risk factors and also significant reductions in exercise capacity and quality of life across functional stages of COPD.ConclusionsPulmonary function in patients with ≥10 pack-years of smoking and diabetes is reduced, and this decrease is associated with significant reductions in activity-related quality of life and exercise capacity.

Published
2014

50. Asthma Is a Risk Factor for Respiratory Exacerbations Without Increased Rate of Lung Function Decline: Five-Year Follow-up in Adult Smokers From the COPDGene Study

Author

Crapo, James D., Make, Barry J., Regan, Elizabeth A., Silverman, Edwin K., Beaty, Terri, Begum, Ferdouse, Boueiz, Adel R., Busch, Robert, Castaldi, Peter J., Cho, Michael, DeMeo, Dawn L., Foreman, Marilyn G., Halper-Stromberg, Eitan, Hansel, Nadia N., Hardin, Megan E., Hayden, Lystra P., Hersh, Craig P., Hetmanski, Jacqueline, Hobbs, Brian D., Hokanson, John E., Laird, Nan, Lange, Christoph, Lutz, Sharon M., McDonald, Merry-Lynn, Parker, Margaret M., Qiao, Dandi, Santorico, Stephanie, Wan, Emily S., Al Qaisi, Mustafa, Coxson, Harvey O., Gray, Teresa, Han, MeiLan K., Hoffman, Eric A., Humphries, Stephen, Jacobson, Francine L., Judy, Philip F., Kazerooni, Ella A., Kluiber, Alex, Lynch, David A., Newell, John D., Jr., Ross, James C., Estepar, Raul San Jose, Schroeder, Joyce, Sieren, Jered, Stinson, Douglas, Stoel, Berend C., Tschirren, Juerg, Van Beek, Edwin, van Ginneken, Bram, van Rikxoort, Eva, Washko, George, Wilson, Carla G., Jensen, Robert, Crooks, Jim, Everett, Douglas, Moore, Camille, Strand, Matt, Hughes, John, Kinney, Gregory, Pratte, Katherine, Young, Kendra A., Qiu, Weiliang, Strand, Matthew J., and van Beek, Edwin J.

Published
2018
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