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1. Multi-View Transformers for Airway-To-Lung Ratio Inference on Cardiac CT Scans: The C4R Study

Author: Naik, Sneha N., Angelini, Elsa D., Hoffman, Eric A., Oelsner, Elizabeth C., Barr, R. Graham, Smith, Benjamin M., and Laine, Andrew F.
Subjects: Electrical Engineering and Systems Science - Image and Video Processing, Computer Science - Computer Vision and Pattern Recognition, Computer Science - Machine Learning
Abstract: The ratio of airway tree lumen to lung size (ALR), assessed at full inspiration on high resolution full-lung computed tomography (CT), is a major risk factor for chronic obstructive pulmonary disease (COPD). There is growing interest to infer ALR from cardiac CT images, which are widely available in epidemiological cohorts, to investigate the relationship of ALR to severe COVID-19 and post-acute sequelae of SARS-CoV-2 infection (PASC). Previously, cardiac scans included approximately 2/3 of the total lung volume with 5-6x greater slice thickness than high-resolution (HR) full-lung (FL) CT. In this study, we present a novel attention-based Multi-view Swin Transformer to infer FL ALR values from segmented cardiac CT scans. For the supervised training we exploit paired full-lung and cardiac CTs acquired in the Multi-Ethnic Study of Atherosclerosis (MESA). Our network significantly outperforms a proxy direct ALR inference on segmented cardiac CT scans and achieves accuracy and reproducibility comparable with a scan-rescan reproducibility of the FL ALR ground-truth., Comment: Accepted to appear in Proceedings of International Symposium on Biomedical Imaging (ISBI), 2025
Published: 2025

2. Demographic and Clinical Factors Associated With SARS-CoV-2 Spike 1 Antibody Response Among Vaccinated US Adults: the C4R Study

Author: Kim, John S., Sun, Yifei, Balte, Pallavi, Cushman, Mary, Boyle, Rebekah, Tracy, Russell P., Styer, Linda M., Bell, Taison D., Anderson, Michaela R., Allen, Norrina B., Schreiner, Pamela J., Bowler, Russell P., Schwartz, David A., Lee, Joyce S., Xanthakis, Vanessa, Doyle, Margaret F., Regan, Elizabeth A., Make, Barry J., Kanaya, Alka M., Wenzel, Sally E., Coresh, Josef, Isasi, Carmen R., Raffield, Laura M., Elkind, Mitchell S. V., Howard, Virginia J., Ortega, Victor E., Woodruff, Prescott, Cole, Shelley A., Henderson, Joel M., Mantis, Nicholas J., Parker, Monica M., Demmer, Ryan T., and Oelsner, Elizabeth C.
Published: 2024
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3. MUC5B, telomere length and longitudinal quantitative interstitial lung changes: the MESA Lung Study

Author: Kim, John S, Manichaikul, Ani W, Hoffman, Eric A, Balte, Pallavi, Anderson, Michaela R, Bernstein, Elana J, Madahar, Purnema, Oelsner, Elizabeth C, Kawut, Steven M, Wysoczanski, Artur, Laine, Andrew F, Adegunsoye, Ayodeji, Z, Jennie, Taub, Margaret A, Mathias, Rasika A, Rich, Stephen S, Rotter, Jerome I, Noth, Imre, Garcia, Christine Kim, Barr, R Graham, and Podolanczuk, Anna J
Subjects: Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Clinical Research, Lung, Atherosclerosis, Genetics, Good Health and Well Being, Adult, Humans, Lung Diseases, Interstitial, Genotype, Telomere, Mucin-5B, Imaging/CT MRI etc, Interstitial Fibrosis, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract: BackgroundThe MUC5B promoter variant (rs35705950) and telomere length are linked to pulmonary fibrosis and CT-based qualitative assessments of interstitial abnormalities, but their associations with longitudinal quantitative changes of the lung interstitium among community-dwelling adults are unknown.MethodsWe used data from participants in the Multi-Ethnic Study of Atherosclerosis with high-attenuation areas (HAAs, Examinations 1-6 (2000-2018)) and MUC5B genotype (n=4552) and telomere length (n=4488) assessments. HAA was defined as the per cent of imaged lung with attenuation of -600 to -250 Hounsfield units. We used linear mixed-effects models to examine associations of MUC5B risk allele (T) and telomere length with longitudinal changes in HAAs. Joint models were used to examine associations of longitudinal changes in HAAs with death and interstitial lung disease (ILD).ResultsThe MUC5B risk allele (T) was associated with an absolute change in HAAs of 2.60% (95% CI 0.36% to 4.86%) per 10 years overall. This association was stronger among those with a telomere length below an age-adjusted percentile of 5% (p value for interaction=0.008). A 1% increase in HAAs per year was associated with 7% increase in mortality risk (rate ratio (RR)=1.07, 95% CI 1.02 to 1.12) for overall death and 34% increase in ILD (RR=1.34, 95% CI 1.20 to 1.50). Longer baseline telomere length was cross-sectionally associated with less HAAs from baseline scans, but not with longitudinal changes in HAAs.ConclusionsLongitudinal increases in HAAs were associated with the MUC5B risk allele and a higher risk of death and ILD.
Published: 2023

4. Bronchodilator Responsiveness in Tobacco-Exposed People With or Without COPD

Author: Fortis, Spyridon, Quibrera, Pedro M, Comellas, Alejandro P, Bhatt, Surya P, Tashkin, Donald P, Hoffman, Eric A, Criner, Gerard J, Han, MeiLan K, Barr, R Graham, Arjomandi, Mehrdad, Dransfield, Mark B, Peters, Stephen P, Dolezal, Brett A, Kim, Victor, Putcha, Nirupama, Rennard, Stephen I, Paine, Robert, Kanner, Richard E, Curtis, Jeffrey L, Bowler, Russell P, Martinez, Fernando J, Hansel, Nadia N, Krishnan, Jerry A, Woodruff, Prescott G, Barjaktarevic, Igor Z, Couper, David, Anderson, Wayne H, Cooper, Christopher B, Investigators, Subpopulations and Intermediate Outcome Measures in COPD Study, Alexis, Neil E, Barjaktarevic, Igor, Basta, Patricia, Bateman, Lori A, Bleecker, Eugene R, Boucher, Richard C, Christenson, Stephanie A, Couper, David J, Crystal, Ronald G, Doerschuk, Claire M, Dransfield, Mark T, Drummond, Brad, Freeman, Christine M, Galban, Craig, Hastie, Annette T, Huang, Yvonne, Kaner, Robert J, Kleerup, Eric C, LaVange, Lisa M, Lazarus, Stephen C, Meyers, Deborah A, Moore, Wendy C, Newell, John D, Paulin, Laura, Pirozzi, Cheryl, Oelsner, Elizabeth C, O’Neal, Wanda K, Ortega, Victor E, Raman, Sanjeev, Wells, J Michael, and Wise, Robert A
Subjects: Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Asthma, Lung, Clinical Research, Chronic Obstructive Pulmonary Disease, Respiratory, Good Health and Well Being, Humans, Bronchodilator Agents, Retrospective Studies, Forced Expiratory Volume, Pulmonary Disease, Chronic Obstructive, Vital Capacity, Tobacco Products, bronchodilator, bronchodilator response, bronchodilator responsiveness, bronchodilator reversibility, COPD, Subpopulations and Intermediate Outcome Measures in COPD Study Investigators, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract: BackgroundBronchodilator responsiveness (BDR) in obstructive lung disease varies over time and may be associated with distinct clinical features.Research questionIs consistent BDR over time (always present) differentially associated with obstructive lung disease features relative to inconsistent (sometimes present) or never (never present) BDR in tobacco-exposed people with or without COPD?Study design and methodsWe retrospectively analyzed data from 2,269 tobacco-exposed participants in the Subpopulations and Intermediate Outcome Measures in COPD Study with or without COPD. We used various BDR definitions: change of ≥ 200 mL and ≥ 12% in FEV1 (FEV1-BDR), change in FVC (FVC-BDR), and change in in FEV1, FVC or both (ATS-BDR). Using generalized linear models adjusted for demographics, smoking history, FEV1 % predicted after bronchodilator administration, and number of visits that the participant completed, we assessed the association of BDR group: (1) consistent BDR, (2) inconsistent BDR, and (3) never BDR with asthma, CT scan features, blood eosinophil levels, and FEV1 decline in participants without COPD (Global Initiative for Chronic Obstructive Lung Disease [GOLD] stage 0) and the entire cohort (participants with or without COPD).ResultsBoth consistent and inconsistent ATS-BDR were associated with asthma history and greater small airways disease (%parametric response mapping functional small airways disease) relative to never ATS-BDR in participants with GOLD stage 0 disease and the entire cohort. We observed similar findings using FEV1-BDR and FVC-BDR definitions. Eosinophils did not vary consistently among BDR groups. Consistent BDR was associated with FEV1 decline over time relative to never BDR in the entire cohort. In participants with GOLD stage 0 disease, both the inconsistent ATS-BDR group (OR, 3.20; 95% CI, 2.21-4.66; P < .001) and consistent ATS-BDR group (OR, 9.48; 95% CI, 3.77-29.12; P < .001) were associated with progression to COPD relative to the never ATS-BDR group.InterpretationDemonstration of BDR, even once, describes an obstructive lung disease phenotype with a history of asthma and greater small airways disease. Consistent demonstration of BDR indicated a high risk of lung function decline over time in the entire cohort and was associated with higher risk of progression to COPD in patients with GOLD stage 0 disease.
Published: 2023

5. Multi-ancestry transcriptome-wide association analyses yield insights into tobacco use biology and drug repurposing

Author: Chen, Fang, Wang, Xingyan, Jang, Seon-Kyeong, Quach, Bryan C, Weissenkampen, J Dylan, Khunsriraksakul, Chachrit, Yang, Lina, Sauteraud, Renan, Albert, Christine M, Allred, Nicholette DD, Arnett, Donna K, Ashley-Koch, Allison E, Barnes, Kathleen C, Barr, R Graham, Becker, Diane M, Bielak, Lawrence F, Bis, Joshua C, Blangero, John, Boorgula, Meher Preethi, Chasman, Daniel I, Chavan, Sameer, Chen, Yii-Der I, Chuang, Lee-Ming, Correa, Adolfo, Curran, Joanne E, David, Sean P, Fuentes, Lisa de las, Deka, Ranjan, Duggirala, Ravindranath, Faul, Jessica D, Garrett, Melanie E, Gharib, Sina A, Guo, Xiuqing, Hall, Michael E, Hawley, Nicola L, He, Jiang, Hobbs, Brian D, Hokanson, John E, Hsiung, Chao A, Hwang, Shih-Jen, Hyde, Thomas M, Irvin, Marguerite R, Jaffe, Andrew E, Johnson, Eric O, Kaplan, Robert, Kardia, Sharon LR, Kaufman, Joel D, Kelly, Tanika N, Kleinman, Joel E, Kooperberg, Charles, Lee, I-Te, Levy, Daniel, Lutz, Sharon M, Manichaikul, Ani W, Martin, Lisa W, Marx, Olivia, McGarvey, Stephen T, Minster, Ryan L, Moll, Matthew, Moussa, Karine A, Naseri, Take, North, Kari E, Oelsner, Elizabeth C, Peralta, Juan M, Peyser, Patricia A, Psaty, Bruce M, Rafaels, Nicholas, Raffield, Laura M, Reupena, Muagututi’a Sefuiva, Rich, Stephen S, Rotter, Jerome I, Schwartz, David A, Shadyab, Aladdin H, Sheu, Wayne H-H, Sims, Mario, Smith, Jennifer A, Sun, Xiao, Taylor, Kent D, Telen, Marilyn J, Watson, Harold, Weeks, Daniel E, Weir, David R, Yanek, Lisa R, Young, Kendra A, Young, Kristin L, Zhao, Wei, Hancock, Dana B, Jiang, Bibo, Vrieze, Scott, and Liu, Dajiang J
Subjects: Genetics, Tobacco, Drug Abuse (NIDA only), Tobacco Smoke and Health, Substance Misuse, Brain Disorders, Human Genome, Good Health and Well Being, Humans, Transcriptome, Drug Repositioning, Genome-Wide Association Study, Tobacco Use, Biology, Polymorphism, Single Nucleotide, Genetic Predisposition to Disease, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract: Most transcriptome-wide association studies (TWASs) so far focus on European ancestry and lack diversity. To overcome this limitation, we aggregated genome-wide association study (GWAS) summary statistics, whole-genome sequences and expression quantitative trait locus (eQTL) data from diverse ancestries. We developed a new approach, TESLA (multi-ancestry integrative study using an optimal linear combination of association statistics), to integrate an eQTL dataset with a multi-ancestry GWAS. By exploiting shared phenotypic effects between ancestries and accommodating potential effect heterogeneities, TESLA improves power over other TWAS methods. When applied to tobacco use phenotypes, TESLA identified 273 new genes, up to 55% more compared with alternative TWAS methods. These hits and subsequent fine mapping using TESLA point to target genes with biological relevance. In silico drug-repurposing analyses highlight several drugs with known efficacy, including dextromethorphan and galantamine, and new drugs such as muscle relaxants that may be repurposed for treating nicotine addiction.
Published: 2023

6. Assessing the contribution of rare genetic variants to phenotypes of chronic obstructive pulmonary disease using whole-genome sequence data

Author: Kim, Wonji, Hecker, Julian, Barr, R Graham, Boerwinkle, Eric, Cade, Brian, Correa, Adolfo, Dupuis, Josée, Gharib, Sina A, Lange, Leslie, London, Stephanie J, Morrison, Alanna C, O'Connor, George T, Oelsner, Elizabeth C, Psaty, Bruce M, Vasan, Ramachandran S, Redline, Susan, Rich, Stephen S, Rotter, Jerome I, Yu, Bing, Lange, Christoph, Manichaikul, Ani, Zhou, Jin J, Sofer, Tamar, Silverman, Edwin K, Qiao, Dandi, Cho, Michael H, and Group, NHLBI Trans-Omics in Precision Medicine Consortium and TOPMed Lung Working
Subjects: Biological Sciences, Genetics, Chronic Obstructive Pulmonary Disease, Lung, Human Genome, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Generic health relevance, Respiratory, Humans, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Pulmonary Disease, Chronic Obstructive, Genome-Wide Association Study, Phenotype, NHLBI Trans-Omics in Precision Medicine (TOPMed) Consortium and TOPMed Lung Working Group, Medical and Health Sciences, Genetics & Heredity
Abstract: RationaleGenetic variation has a substantial contribution to chronic obstructive pulmonary disease (COPD) and lung function measurements. Heritability estimates using genome-wide genotyping data can be biased if analyses do not appropriately account for the nonuniform distribution of genetic effects across the allele frequency and linkage disequilibrium (LD) spectrum. In addition, the contribution of rare variants has been unclear.ObjectivesWe sought to assess the heritability of COPD and lung function using whole-genome sequence data from the Trans-Omics for Precision Medicine program.MethodsUsing the genome-based restricted maximum likelihood method, we partitioned the genome into bins based on minor allele frequency and LD scores and estimated heritability of COPD, FEV1% predicted and FEV1/FVC ratio in 11 051 European ancestry and 5853 African-American participants.Measurements and main resultsIn European ancestry participants, the estimated heritability of COPD, FEV1% predicted and FEV1/FVC ratio were 35.5%, 55.6% and 32.5%, of which 18.8%, 19.7%, 17.8% were from common variants, and 16.6%, 35.8%, and 14.6% were from rare variants. These estimates had wide confidence intervals, with common variants and some sets of rare variants showing a statistically significant contribution (P-value
Published: 2022

7. Rare genetic variants explain missing heritability in smoking.

Author: Jang, Seon-Kyeong, Evans, Luke, Fialkowski, Allison, Arnett, Donna K, Ashley-Koch, Allison E, Barnes, Kathleen C, Becker, Diane M, Bis, Joshua C, Blangero, John, Bleecker, Eugene R, Boorgula, Meher Preethi, Bowden, Donald W, Brody, Jennifer A, Cade, Brian E, Jenkins, Brenda W Campbell, Carson, April P, Chavan, Sameer, Cupples, L Adrienne, Custer, Brian, Damrauer, Scott M, David, Sean P, de Andrade, Mariza, Dinardo, Carla L, Fingerlin, Tasha E, Fornage, Myriam, Freedman, Barry I, Garrett, Melanie E, Gharib, Sina A, Glahn, David C, Haessler, Jeffrey, Heckbert, Susan R, Hokanson, John E, Hou, Lifang, Hwang, Shih-Jen, Hyman, Matthew C, Judy, Renae, Justice, Anne E, Kaplan, Robert C, Kardia, Sharon LR, Kelly, Shannon, Kim, Wonji, Kooperberg, Charles, Levy, Daniel, Lloyd-Jones, Donald M, Loos, Ruth JF, Manichaikul, Ani W, Gladwin, Mark T, Martin, Lisa Warsinger, Nouraie, Mehdi, Melander, Olle, Meyers, Deborah A, Montgomery, Courtney G, North, Kari E, Oelsner, Elizabeth C, Palmer, Nicholette D, Payton, Marinelle, Peljto, Anna L, Peyser, Patricia A, Preuss, Michael, Psaty, Bruce M, Qiao, Dandi, Rader, Daniel J, Rafaels, Nicholas, Redline, Susan, Reed, Robert M, Reiner, Alexander P, Rich, Stephen S, Rotter, Jerome I, Schwartz, David A, Shadyab, Aladdin H, Silverman, Edwin K, Smith, Nicholas L, Smith, J Gustav, Smith, Albert V, Smith, Jennifer A, Tang, Weihong, Taylor, Kent D, Telen, Marilyn J, Vasan, Ramachandran S, Gordeuk, Victor R, Wang, Zhe, Wiggins, Kerri L, Yanek, Lisa R, Yang, Ivana V, Young, Kendra A, Young, Kristin L, Zhang, Yingze, Liu, Dajiang J, Keller, Matthew C, and Vrieze, Scott
Subjects: Smoking, Gene Frequency, Phenotype, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Tobacco, Genetics, Tobacco Smoke and Health, Human Genome, Cancer
Abstract: Common genetic variants explain less variation in complex phenotypes than inferred from family-based studies, and there is a debate on the source of this 'missing heritability'. We investigated the contribution of rare genetic variants to tobacco use with whole-genome sequences from up to 26,257 unrelated individuals of European ancestries and 11,743 individuals of African ancestries. Across four smoking traits, single-nucleotide-polymorphism-based heritability ([Formula: see text]) was estimated from 0.13 to 0.28 (s.e., 0.10-0.13) in European ancestries, with 35-74% of it attributable to rare variants with minor allele frequencies between 0.01% and 1%. These heritability estimates are 1.5-4 times higher than past estimates based on common variants alone and accounted for 60% to 100% of our pedigree-based estimates of narrow-sense heritability ([Formula: see text], 0.18-0.34). In the African ancestry samples, [Formula: see text] was estimated from 0.03 to 0.33 (s.e., 0.09-0.14) across the four smoking traits. These results suggest that rare variants are important contributors to the heritability of smoking.
Published: 2022

8. Collaborative Cohort of Cohorts for COVID-19 Research (C4R) Study: Study Design

Author: Oelsner, Elizabeth C, Krishnaswamy, Akshaya, Balte, Pallavi P, Allen, Norrina Bai, Ali, Tauqeer, Anugu, Pramod, Andrews, Howard F, Arora, Komal, Asaro, Alyssa, Barr, R Graham, Bertoni, Alain G, Bon, Jessica, Boyle, Rebekah, Chang, Arunee A, Chen, Grace, Coady, Sean, Cole, Shelley A, Coresh, Josef, Cornell, Elaine, Correa, Adolfo, Couper, David, Cushman, Mary, Demmer, Ryan T, Elkind, Mitchell SV, Folsom, Aaron R, Fretts, Amanda M, Gabriel, Kelley P, Gallo, Linda C, Gutierrez, Jose, Han, Mei Lan K, Henderson, Joel M, Howard, Virginia J, Isasi, Carmen R, Jacobs, David R, Judd, Suzanne E, Mukaz, Debora Kamin, Kanaya, Alka M, Kandula, Namratha R, Kaplan, Robert C, Kinney, Gregory L, Kucharska-Newton, Anna, Lee, Joyce S, Lewis, Cora E, Levine, Deborah A, Levitan, Emily B, Levy, Bruce D, Make, Barry J, Malloy, Kimberly, Manly, Jennifer J, Mendoza-Puccini, Carolina, Meyer, Katie A, Min, Yuan-I Nancy, Moll, Matthew R, Moore, Wendy C, Mauger, David, Ortega, Victor E, Palta, Priya, Parker, Monica M, Phipatanakul, Wanda, Post, Wendy S, Postow, Lisa, Psaty, Bruce M, Regan, Elizabeth A, Ring, Kimberly, Roger, Véronique L, Rotter, Jerome I, Rundek, Tatjana, Sacco, Ralph L, Schembri, Michael, Schwartz, David A, Seshadri, Sudha, Shikany, James M, Sims, Mario, Stukovsky, Karen D Hinckley, Talavera, Gregory A, Tracy, Russell P, Umans, Jason G, Vasan, Ramachandran S, Watson, Karol E, Wenzel, Sally E, Winters, Karen, Woodruff, Prescott G, Xanthakis, Vanessa, Zhang, Ying, Zhang, Yiyi, and Investigators, for the C4R
Subjects: Public Health, Health Sciences, Social Determinants of Health, Basic Behavioral and Social Science, Infectious Diseases, Behavioral and Social Science, Clinical Research, Prevention, Coronaviruses, Emerging Infectious Diseases, Coronaviruses Disparities and At-Risk Populations, 2.4 Surveillance and distribution, 2.6 Resources and infrastructure (aetiology), Good Health and Well Being, Adolescent, Adult, Aged, Aged, 80 and over, COVID-19, Cohort Studies, Humans, Middle Aged, Pandemics, Prospective Studies, SARS-CoV-2, United States, Young Adult, cohort studies, coronavirus disease 2019, severe acute respiratory syndrome coronavirus 2, %22">>, C4R Investigators, severe acute respiratory syndrome coronavirus 2, Mathematical Sciences, Medical and Health Sciences, Epidemiology
Abstract: The Collaborative Cohort of Cohorts for COVID-19 Research (C4R) is a national prospective study of adults comprising 14 established US prospective cohort studies. Starting as early as 1971, investigators in the C4R cohort studies have collected data on clinical and subclinical diseases and their risk factors, including behavior, cognition, biomarkers, and social determinants of health. C4R links this pre-coronavirus disease 2019 (COVID-19) phenotyping to information on severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and acute and postacute COVID-related illness. C4R is largely population-based, has an age range of 18-108 years, and reflects the racial, ethnic, socioeconomic, and geographic diversity of the United States. C4R ascertains SARS-CoV-2 infection and COVID-19 illness using standardized questionnaires, ascertainment of COVID-related hospitalizations and deaths, and a SARS-CoV-2 serosurvey conducted via dried blood spots. Master protocols leverage existing robust retention rates for telephone and in-person examinations and high-quality event surveillance. Extensive prepandemic data minimize referral, survival, and recall bias. Data are harmonized with research-quality phenotyping unmatched by clinical and survey-based studies; these data will be pooled and shared widely to expedite collaboration and scientific findings. This resource will allow evaluation of risk and resilience factors for COVID-19 severity and outcomes, including postacute sequelae, and assessment of the social and behavioral impact of the pandemic on long-term health trajectories.
Published: 2022

9. Polygenic transcriptome risk scores for COPD and lung function improve cross-ethnic portability of prediction in the NHLBI TOPMed program

Author: Hu, Xiaowei, Qiao, Dandi, Kim, Wonji, Moll, Matthew, Balte, Pallavi P, Lange, Leslie A, Bartz, Traci M, Kumar, Rajesh, Li, Xingnan, Yu, Bing, Cade, Brian E, Laurie, Cecelia A, Sofer, Tamar, Ruczinski, Ingo, Nickerson, Deborah A, Muzny, Donna M, Metcalf, Ginger A, Doddapaneni, Harshavardhan, Gabriel, Stacy, Gupta, Namrata, Dugan-Perez, Shannon, Cupples, L Adrienne, Loehr, Laura R, Jain, Deepti, Rotter, Jerome I, Wilson, James G, Psaty, Bruce M, Fornage, Myriam, Morrison, Alanna C, Vasan, Ramachandran S, Washko, George, Rich, Stephen S, O’Connor, George T, Bleecker, Eugene, Kaplan, Robert C, Kalhan, Ravi, Redline, Susan, Gharib, Sina A, Meyers, Deborah, Ortega, Victor, Dupuis, Josée, London, Stephanie J, Lappalainen, Tuuli, Oelsner, Elizabeth C, Silverman, Edwin K, Barr, R Graham, Thornton, Timothy A, Wheeler, Heather E, Group, TOPMed Lung Working, Cho, Michael H, Im, Hae Kyung, and Manichaikul, Ani
Subjects: Epidemiology, Biological Sciences, Health Sciences, Genetics, Clinical Research, Lung, Prevention, Tobacco, Chronic Obstructive Pulmonary Disease, Tobacco Smoke and Health, Respiratory, Good Health and Well Being, Humans, National Heart, Lung, and Blood Institute (U.S.), Pulmonary Disease, Chronic Obstructive, Risk Factors, Transcriptome, United States, TOPMed Lung Working Group, cross-ethnic portability, gene expression, integrative analysis, polygenic transcriptome risk score, pulmonary disease, risk prediction, Medical and Health Sciences, Genetics & Heredity, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract: While polygenic risk scores (PRSs) enable early identification of genetic risk for chronic obstructive pulmonary disease (COPD), predictive performance is limited when the discovery and target populations are not well matched. Hypothesizing that the biological mechanisms of disease are shared across ancestry groups, we introduce a PrediXcan-derived polygenic transcriptome risk score (PTRS) to improve cross-ethnic portability of risk prediction. We constructed the PTRS using summary statistics from application of PrediXcan on large-scale GWASs of lung function (forced expiratory volume in 1 s [FEV1] and its ratio to forced vital capacity [FEV1/FVC]) in the UK Biobank. We examined prediction performance and cross-ethnic portability of PTRS through smoking-stratified analyses both on 29,381 multi-ethnic participants from TOPMed population/family-based cohorts and on 11,771 multi-ethnic participants from TOPMed COPD-enriched studies. Analyses were carried out for two dichotomous COPD traits (moderate-to-severe and severe COPD) and two quantitative lung function traits (FEV1 and FEV1/FVC). While the proposed PTRS showed weaker associations with disease than PRS for European ancestry, the PTRS showed stronger association with COPD than PRS for African Americans (e.g., odds ratio [OR] = 1.24 [95% confidence interval [CI]: 1.08-1.43] for PTRS versus 1.10 [0.96-1.26] for PRS among heavy smokers with ≥ 40 pack-years of smoking) for moderate-to-severe COPD. Cross-ethnic portability of the PTRS was significantly higher than the PRS (paired t test p
Published: 2022

10. Identification of Sputum Biomarkers Predictive of Pulmonary Exacerbations in COPD

Author: Esther, Charles R, O’Neal, Wanda K, Anderson, Wayne H, Kesimer, Mehmet, Ceppe, Agathe, Doerschuk, Claire M, Alexis, Neil E, Hastie, Annette T, Barr, R Graham, Bowler, Russell P, Wells, J Michael, Oelsner, Elizabeth C, Comellas, Alejandro P, Tesfaigzi, Yohannes, Kim, Victor, Paulin, Laura M, Cooper, Christopher B, Han, MeiLan K, Huang, Yvonne J, Labaki, Wassim W, Curtis, Jeffrey L, Boucher, Richard C, Study, Subpopulations and Intermediate Outcome Measures in COPD, Arjomandi, Mehrdad, Barjaktarevic, Igor, Bateman, Lori A, Bhatt, Surya P, Bleecker, Eugene R, Christenson, Stephanie A, Couper, David J, Criner, Gerard J, Crystal, Ronald G, Dransfield, Mark T, Drummond, Brad, Freeman, Christine M, Galban, Craig, Hansel, Nadia N, Hoffman, Eric A, Huang, Yvonne, Kaner, Robert J, Kanner, Richard E, Kleerup, Eric C, Krishnan, Jerry A, LaVange, Lisa M, Lazarus, Stephen C, Martinez, Fernando J, Meyers, Deborah A, Moore, Wendy C, Newell, John D, Paine, Robert, Paulin, Laura, Peters, Stephen P, Pirozzi, Cheryl, Putcha, Nirupama, Ortega, Victor E, Raman, Sanjeev, Rennard, Stephen I, Tashkin, Donald P, Wise, Robert A, and Woodruff, Prescott G
Subjects: Lung, Chronic Obstructive Pulmonary Disease, Clinical Research, Respiratory, Good Health and Well Being, Biomarkers, Humans, Hypoxanthines, N-Acetylneuraminic Acid, Pulmonary Disease, Chronic Obstructive, Sputum, adenosine, glutathione, inflammation, metabolomics, methionine salvage, mucus, Subpopulations and Intermediate Outcome Measures in COPD Study, Clinical Sciences, Respiratory System
Abstract: BackgroundImproved understanding of the pathways associated with airway pathophysiologic features in COPD will identify new predictive biomarkers and novel therapeutic targets.Research questionWhich physiologic pathways are altered in the airways of patients with COPD and will predict exacerbations?Study design and methodsWe applied a mass spectrometric panel of metabolomic biomarkers related to mucus hydration and inflammation to sputa from the multicenter Subpopulations and Intermediate Outcome Measures in COPD Study. Biomarkers elevated in sputa from patients with COPD were evaluated for relationships to measures of COPD disease severity and their ability to predict future exacerbations.ResultsSputum supernatants from 980 patients were analyzed: 77 healthy nonsmokers, 341 smokers with preserved spirometry, and 562 patients with COPD (178 with Global Initiative on Chronic Obstructive Lung Disease [GOLD] stage 1 disease, 303 with GOLD stage 2 disease, and 81 with GOLD stage 3 disease) were analyzed. Biomarkers from multiple pathways were elevated in COPD and correlated with sputum neutrophil counts. Among the most significant analytes (false discovery rate, 0.1) were sialic acid, hypoxanthine, xanthine, methylthioadenosine, adenine, and glutathione. Sialic acid and hypoxanthine were associated strongly with measures of disease severity, and elevation of these biomarkers was associated with shorter time to exacerbation and improved prediction models of future exacerbations.InterpretationBiomarker evaluation implicated pathways involved in mucus hydration, adenosine metabolism, methionine salvage, and oxidative stress in COPD airway pathophysiologic characteristics. Therapies that target these pathways may be of benefit in COPD, and a simple model adding sputum-soluble phase biomarkers improves prediction of pulmonary exacerbations.Trial registryClinicalTrials.gov; No.: NCT01969344; URL: www.Clinicaltrialsgov.
Published: 2022

11. Comparative Impact of Depressive Symptoms and FEV1% on Chronic Obstructive Pulmonary Disease.

Author: O’Toole, Jacqueline, Woo, Han, Putcha, Nirupama, Cooper, Christopher B, Woodruff, Prescott, Kanner, Richard E, Paine, Robert, Bowler, Russell P, Comellas, Alejandro, Hoth, Karin F, Krishnan, Jerry A, Han, Meilan, Dransfield, Mark, Iyer, Anand S, Couper, David, Peters, Stephen P, Criner, Gerard, Kim, Victor, Barr, R Graham, Martinez, Fernando J, Hansel, Nadia N, Eakin, Michelle N, Alexis, Neil E, Anderson, Wayne H, Arjomandi, Mehrdad, Barjaktarevic, Igor, Bateman, Lori A, Bhatt, Surya P, Bleecker, Eugene R, Boucher, Richard C, Christenson, Stephanie A, Comellas, Alejandro P, Couper, David J, Criner, Gerard J, Crystal, Ronald G, Curtis, Jeffrey L, Doerschuk, Claire M, Dransfield, Mark T, Drummond, Brad, Freeman, Christine M, Galban, Craig, Han, MeiLan K, Hastie, Annette T, Hoffman, Eric A, Huang, Yvonne, Kaner, Robert J, Kleerup, Eric C, LaVange, Lisa M, Lazarus, Stephen C, Meyers, Deborah A, Moore, Wendy C, Newell, John D, Paulin, Laura, Pirozzi, Cheryl, Oelsner, Elizabeth C, O’Neal, Wanda K, Ortega, Victor E, Raman, Sanjeev, Rennard, Stephen I, Tashkin, Donald P, Wells, J Michael, Wise, Robert A, and Woodruff, Prescott G
Subjects: Clinical Research, Behavioral and Social Science, Depression, Chronic Obstructive Pulmonary Disease, Mental Health, Lung, Respiratory, Good Health and Well Being, Female, Forced Expiratory Volume, Humans, Pulmonary Disease, Chronic Obstructive, Quality of Life, Respiratory Function Tests, Smoking, Surveys and Questionnaires, depression, COPD, patient reported outcome measures, SPIROMICS Investigators
Abstract: Rationale: Individuals with chronic obstructive pulmonary disease (COPD) have a high prevalence of depression, which is associated with increased COPD hospitalizations and readmissions. Objectives: Examine the impact of depressive symptoms compared with FEV1% on COPD morbidity. Methods: Using longitudinal data from individuals with COPD in the Subpopulations and Intermediate Outcome Measures in COPD Study, longitudinal growth analysis was performed to assess COPD morbidity by assessing differences in baseline 6-minute walk distance and patient reported outcomes (PROs) and their rate of change over time explained by depressive symptoms or lung function, as measured by Hospital Anxiety and Depression Scale or FEV1% respectively. PROs consisted of in-person completion of St. George's Respiratory Questionnaire, COPD Assessment Test, Functional Assessment of Chronic Illness Therapy Fatigue, and Modified Medical Research Council Dyspnea Scale measures. Results: Of the individuals analyzed (n = 1,830), 43% were female, 81% Caucasian with mean ± SD age of 65.1 ± 8.1, and 52.7 ± 27.5 pack-years smoking. Mean ± SD FEV1% was 60.9 ± 23.0% and 20% had clinically significant depressive symptoms. Adjusted models showed higher Hospital Anxiety and Depression Scale scores and lower FEV1% each were associated with worse PROs at baseline (P ⩽ 0.001). Depression accounted for more baseline variance in St. George's Respiratory Questionnaire, COPD Assessment Test, and Functional Assessment of Chronic Illness Therapy Fatigue than FEV1%, explaining 30-67% of heterogeneity. FEV1% accounted for more baseline variance in Modified Medical Research Council Dyspnea Scale and 6-minute walk distance than depression, explaining 16-32% of heterogeneity. Depressive symptoms accounted for 3-17% variance in change over time in PROs. In contrast, FEV1% accounted for 1-4% variance over time in PROs. Conclusions: Depression is more strongly associated with many PROs at baseline and their change over time compared with FEV1%. Recognizing and incorporating the impact of depressive symptoms into individualized care may improve COPD outcomes.
Published: 2022

12. Author Correction: Genetic regulation of serum IgA levels and susceptibility to common immune, infectious, kidney, and cardio-metabolic traits

Author: Liu, Lili, Khan, Atlas, Sanchez-Rodriguez, Elena, Zanoni, Francesca, Li, Yifu, Steers, Nicholas, Balderes, Olivia, Zhang, Junying, Krithivasan, Priya, LeDesma, Robert A., Fischman, Clara, Hebbring, Scott J., Harley, John B., Moncrieffe, Halima, Kottyan, Leah C., Namjou-Khales, Bahram, Walunas, Theresa L., Knevel, Rachel, Raychaudhuri, Soumya, Karlson, Elizabeth W., Denny, Joshua C., Stanaway, Ian B., Crosslin, David, Rauen, Thomas, Floege, Jürgen, Eitner, Frank, Moldoveanu, Zina, Reily, Colin, Knoppova, Barbora, Hall, Stacy, Sheff, Justin T., Julian, Bruce A., Wyatt, Robert J., Suzuki, Hitoshi, Xie, Jingyuan, Chen, Nan, Zhou, Xujie, Zhang, Hong, Hammarström, Lennart, Viktorin, Alexander, Magnusson, Patrik K. E., Shang, Ning, Hripcsak, George, Weng, Chunhua, Rundek, Tatjana, Elkind, Mitchell S. V., Oelsner, Elizabeth C., Barr, R. Graham, Ionita-Laza, Iuliana, Novak, Jan, Gharavi, Ali G., and Kiryluk, Krzysztof
Published: 2023
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13. A System for Phenotype Harmonization in the National Heart, Lung, and Blood Institute Trans-Omics for Precision Medicine (TOPMed) Program

Author: Stilp, Adrienne M, Emery, Leslie S, Broome, Jai G, Buth, Erin J, Khan, Alyna T, Laurie, Cecelia A, Wang, Fei Fei, Wong, Quenna, Chen, Dongquan, D'Augustine, Catherine M, Heard-Costa, Nancy L, Hohensee, Chancellor R, Johnson, William Craig, Juarez, Lucia D, Liu, Jingmin, Mutalik, Karen M, Raffield, Laura M, Wiggins, Kerri L, de Vries, Paul S, Kelly, Tanika N, Kooperberg, Charles, Natarajan, Pradeep, Peloso, Gina M, Peyser, Patricia A, Reiner, Alex P, Arnett, Donna K, Aslibekyan, Stella, Barnes, Kathleen C, Bielak, Lawrence F, Bis, Joshua C, Cade, Brian E, Chen, Ming-Huei, Correa, Adolfo, Cupples, L Adrienne, de Andrade, Mariza, Ellinor, Patrick T, Fornage, Myriam, Franceschini, Nora, Gan, Weiniu, Ganesh, Santhi K, Graffelman, Jan, Grove, Megan L, Guo, Xiuqing, Hawley, Nicola L, Hsu, Wan-Ling, Jackson, Rebecca D, Jaquish, Cashell E, Johnson, Andrew D, Kardia, Sharon LR, Kelly, Shannon, Lee, Jiwon, Mathias, Rasika A, McGarvey, Stephen T, Mitchell, Braxton D, Montasser, May E, Morrison, Alanna C, North, Kari E, Nouraie, Seyed Mehdi, Oelsner, Elizabeth C, Pankratz, Nathan, Rich, Stephen S, Rotter, Jerome I, Smith, Jennifer A, Taylor, Kent D, Vasan, Ramachandran S, Weeks, Daniel E, Weiss, Scott T, Wilson, Carla G, Yanek, Lisa R, Psaty, Bruce M, Heckbert, Susan R, and Laurie, Cathy C
Subjects: Epidemiology, Health Sciences, Precision Medicine, Human Genome, Networking and Information Technology R&D (NITRD), Genetics, Good Health and Well Being, Data Aggregation, Genetic Association Studies, Humans, Information Dissemination, National Heart, Lung, and Blood Institute (U.S.), Phenomics, Phenotype, Program Evaluation, United States, cardiovascular disease, common data elements, hematologic disease, information dissemination, lung diseases, phenotypes, sleep-wake disorders, Mathematical Sciences, Medical and Health Sciences
Abstract: Genotype-phenotype association studies often combine phenotype data from multiple studies to increase statistical power. Harmonization of the data usually requires substantial effort due to heterogeneity in phenotype definitions, study design, data collection procedures, and data-set organization. Here we describe a centralized system for phenotype harmonization that includes input from phenotype domain and study experts, quality control, documentation, reproducible results, and data-sharing mechanisms. This system was developed for the National Heart, Lung, and Blood Institute's Trans-Omics for Precision Medicine (TOPMed) program, which is generating genomic and other -omics data for more than 80 studies with extensive phenotype data. To date, 63 phenotypes have been harmonized across thousands of participants (recruited in 1948-2012) from up to 17 studies per phenotype. Here we discuss challenges in this undertaking and how they were addressed. The harmonized phenotype data and associated documentation have been submitted to National Institutes of Health data repositories for controlled access by the scientific community. We also provide materials to facilitate future harmonization efforts by the community, which include 1) the software code used to generate the 63 harmonized phenotypes, enabling others to reproduce, modify, or extend these harmonizations to additional studies, and 2) the results of labeling thousands of phenotype variables with controlled vocabulary terms.
Published: 2021

14. Association of Midlife Cardiovascular Risk Factors With the Risk of Heart Failure Subtypes Later in Life

Author: Cohen, Laura P, Vittinghoff, Eric, Pletcher, Mark J, Allen, Norrina B, Shah, Sanjiv J, Wilkins, John T, Chang, Patricia P, Ndumele, Chiadi E, Newman, Anne B, Ives, Diane, Maurer, Mathew S, Oelsner, Elizabeth C, Moran, Andrew E, and Zhang, Yiyi
Subjects: Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Heart Disease, Aging, Prevention, Women's Health, Atherosclerosis, Cardiovascular, 2.1 Biological and endogenous factors, Good Health and Well Being, Adult, Cardiovascular Diseases, Female, Heart Disease Risk Factors, Heart Failure, Humans, Male, Prognosis, Risk Factors, Stroke Volume, Heart failure subtype, heart failure with reduced ejection fraction, heart failure with preserved ejection fraction, risk factors, midlife, Cardiorespiratory Medicine and Haematology, Nursing, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract: BackgroundIndependent associations between cardiovascular risk factor exposures during midlife and later life development of heart failure (HF) with preserved ejection fraction (HFpEF) versus reduced EF (HFrEF) have not been previously studied.MethodsWe pooled data from 4 US cohort studies (Atherosclerosis Risk in Communities, Cardiovascular Health, Health , Aging and Body Composition, and Multi-Ethnic Study of Atherosclerosis) and imputed annual risk factor trajectories for body mass index, systolic and diastolic blood pressure, low-density lipoprotein and high-density lipoprotein cholesterol, and glucose starting from age 40 years. Time-weighted average exposures to each risk factor during midlife and later life were calculated and analyzed for associations with the development of HFpEF or HFrEF.ResultsA total of 23,861 participants were included (mean age at first in-person visit, 61.8 ±1 0.2 years; 56.6% female). During a median follow-up of 12 years, there were 3666 incident HF events, of which 51% had EF measured, including 934 with HFpEF and 739 with HFrEF. A high midlife systolic blood pressure and low midlife high-density lipoprotein cholesterol were associated with HFrEF, and a high midlife body mass index, systolic blood pressure, pulse pressure, and glucose were associated with HFpEF. After adjusting for later life exposures, only midlife pulse pressure remained independently associated with HFpEF.ConclusionsMidlife exposure to cardiovascular risk factors are differentially associated with HFrEF and HFpEF later in life. Having a higher pulse pressure during midlife is associated with a greater risk for HFpEF but not HFrEF, independent of later life exposures.
Published: 2021

15. Multi-ancestry genome-wide association analyses improve resolution of genes and pathways influencing lung function and chronic obstructive pulmonary disease risk

Author: Shrine, Nick, Izquierdo, Abril G., Chen, Jing, Packer, Richard, Hall, Robert J., Guyatt, Anna L., Batini, Chiara, Thompson, Rebecca J., Pavuluri, Chandan, Malik, Vidhi, Hobbs, Brian D., Moll, Matthew, Kim, Wonji, Tal-Singer, Ruth, Bakke, Per, Fawcett, Katherine A., John, Catherine, Coley, Kayesha, Piga, Noemi Nicole, Pozarickij, Alfred, Lin, Kuang, Millwood, Iona Y., Chen, Zhengming, Li, Liming, Wijnant, Sara R. A., Lahousse, Lies, Brusselle, Guy, Uitterlinden, Andre G., Manichaikul, Ani, Oelsner, Elizabeth C., Rich, Stephen S., Barr, R. Graham, Kerr, Shona M., Vitart, Veronique, Brown, Michael R., Wielscher, Matthias, Imboden, Medea, Jeong, Ayoung, Bartz, Traci M., Gharib, Sina A., Flexeder, Claudia, Karrasch, Stefan, Gieger, Christian, Peters, Annette, Stubbe, Beate, Hu, Xiaowei, Ortega, Victor E., Meyers, Deborah A., Bleecker, Eugene R., Gabriel, Stacey B., Gupta, Namrata, Smith, Albert Vernon, Luan, Jian’an, Zhao, Jing-Hua, Hansen, Ailin F., Langhammer, Arnulf, Willer, Cristen, Bhatta, Laxmi, Porteous, David, Smith, Blair H., Campbell, Archie, Sofer, Tamar, Lee, Jiwon, Daviglus, Martha L., Yu, Bing, Lim, Elise, Xu, Hanfei, O’Connor, George T., Thareja, Gaurav, Albagha, Omar M. E., Suhre, Karsten, Granell, Raquel, Faquih, Tariq O., Hiemstra, Pieter S., Slats, Annelies M., Mullin, Benjamin H., Hui, Jennie, James, Alan, Beilby, John, Patasova, Karina, Hysi, Pirro, Koskela, Jukka T., Wyss, Annah B., Jin, Jianping, Sikdar, Sinjini, Lee, Mikyeong, May-Wilson, Sebastian, Pirastu, Nicola, Kentistou, Katherine A., Joshi, Peter K., Timmers, Paul R. H. J., Williams, Alexander T., Free, Robert C., Wang, Xueyang, Morrison, John L., Gilliland, Frank D., Chen, Zhanghua, Wang, Carol A., Foong, Rachel E., Harris, Sarah E., Taylor, Adele, Redmond, Paul, Cook, James P., Mahajan, Anubha, Lind, Lars, Palviainen, Teemu, Lehtimäki, Terho, Raitakari, Olli T., Kaprio, Jaakko, Rantanen, Taina, Pietiläinen, Kirsi H., Cox, Simon R., Pennell, Craig E., Hall, Graham L., Gauderman, W. James, Brightling, Chris, Wilson, James F., Vasankari, Tuula, Laitinen, Tarja, Salomaa, Veikko, Mook-Kanamori, Dennis O., Timpson, Nicholas J., Zeggini, Eleftheria, Dupuis, Josée, Hayward, Caroline, Brumpton, Ben, Langenberg, Claudia, Weiss, Stefan, Homuth, Georg, Schmidt, Carsten Oliver, Probst-Hensch, Nicole, Jarvelin, Marjo-Riitta, Morrison, Alanna C., Polasek, Ozren, Rudan, Igor, Lee, Joo-Hyeon, Sayers, Ian, Rawlins, Emma L., Dudbridge, Frank, Silverman, Edwin K., Strachan, David P., Walters, Robin G., Morris, Andrew P., London, Stephanie J., Cho, Michael H., Wain, Louise V., Hall, Ian P., and Tobin, Martin D.
Published: 2023
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16. Whole genome sequence analysis of pulmonary function and COPD in 19,996 multi-ethnic participants.

Author: Zhao, Xutong, Qiao, Dandi, Yang, Chaojie, Kasela, Silva, Kim, Wonji, Ma, Yanlin, Shrine, Nick, Batini, Chiara, Sofer, Tamar, Taliun, Sarah A Gagliano, Sakornsakolpat, Phuwanat, Balte, Pallavi P, Prokopenko, Dmitry, Yu, Bing, Lange, Leslie A, Dupuis, Josée, Cade, Brian E, Lee, Jiwon, Gharib, Sina A, Daya, Michelle, Laurie, Cecelia A, Ruczinski, Ingo, Cupples, L Adrienne, Loehr, Laura R, Bartz, Traci M, Morrison, Alanna C, Psaty, Bruce M, Vasan, Ramachandran S, Wilson, James G, Taylor, Kent D, Durda, Peter, Johnson, W Craig, Cornell, Elaine, Guo, Xiuqing, Liu, Yongmei, Tracy, Russell P, Ardlie, Kristin G, Aguet, François, VanDenBerg, David J, Papanicolaou, George J, Rotter, Jerome I, Barnes, Kathleen C, Jain, Deepti, Nickerson, Deborah A, Muzny, Donna M, Metcalf, Ginger A, Doddapaneni, Harshavardhan, Dugan-Perez, Shannon, Gupta, Namrata, Gabriel, Stacey, Rich, Stephen S, O'Connor, George T, Redline, Susan, Reed, Robert M, Laurie, Cathy C, Daviglus, Martha L, Preudhomme, Liana K, Burkart, Kristin M, Kaplan, Robert C, Wain, Louise V, Tobin, Martin D, London, Stephanie J, Lappalainen, Tuuli, Oelsner, Elizabeth C, Abecasis, Goncalo R, Silverman, Edwin K, Barr, R Graham, NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium, TOPMed Lung Working Group, Cho, Michael H, and Manichaikul, Ani
Subjects: NHLBI Trans-Omics for Precision Medicine (TOPMed) Consortium, TOPMed Lung Working Group, Lung, Humans, Pulmonary Disease, Chronic Obstructive, Genetic Predisposition to Disease, Intracellular Signaling Peptides and Proteins, Calcium-Binding Proteins, Small Ubiquitin-Related Modifier Proteins, Follow-Up Studies, Feasibility Studies, Polymorphism, Single Nucleotide, Adult, Aged, Aged, 80 and over, Middle Aged, African Americans, Female, Male, Protein Inhibitors of Activated STAT, Respiratory Physiological Phenomena, Genome-Wide Association Study, Genetic Loci, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Whole Genome Sequencing, and over, Polymorphism, Single Nucleotide, Pulmonary Disease, Chronic Obstructive
Abstract: Chronic obstructive pulmonary disease (COPD), diagnosed by reduced lung function, is a leading cause of morbidity and mortality. We performed whole genome sequence (WGS) analysis of lung function and COPD in a multi-ethnic sample of 11,497 participants from population- and family-based studies, and 8499 individuals from COPD-enriched studies in the NHLBI Trans-Omics for Precision Medicine (TOPMed) Program. We identify at genome-wide significance 10 known GWAS loci and 22 distinct, previously unreported loci, including two common variant signals from stratified analysis of African Americans. Four novel common variants within the regions of PIAS1, RGN (two variants) and FTO show evidence of replication in the UK Biobank (European ancestry n ~ 320,000), while colocalization analyses leveraging multi-omic data from GTEx and TOPMed identify potential molecular mechanisms underlying four of the 22 novel loci. Our study demonstrates the value of performing WGS analyses and multi-omic follow-up in cohorts of diverse ancestry.
Published: 2020

17. The Effects of Rare SERPINA1 Variants on Lung Function and Emphysema in SPIROMICS

Author: Ortega, Victor E, Li, Xingnan, O’Neal, Wanda K, Lackey, Lela, Ampleford, Elizabeth, Hawkins, Gregory A, Grayeski, Philip J, Laederach, Alain, Barjaktarevic, Igor, Barr, R Graham, Cooper, Christopher, Couper, David, Han, MeiLan K, Kanner, Richard E, Kleerup, Eric C, Martinez, Fernando J, Paine, Robert, Peters, Stephen P, Pirozzi, Cheryl, Rennard, Stephen I, Woodruff, Prescott G, Hoffman, Eric A, Meyers, Deborah A, Bleecker, Eugene R, Alexis, Neil E, Anderson, Wayne H, Arjomandi, Mehrdad, Bateman, Lori A, Bhatt, Surya P, Boucher, Richard C, Bowler, Russell P, Christenson, Stephanie A, Comellas, Alejandro P, Criner, Gerard J, Crystal, Ronald G, Curtis, Jeffrey L, Doerschuk, Claire M, Dransfield, Mark T, Freeman, Christine M, Galban, Craig, Hansel, Nadia N, Hastie, Annette T, Huang, Yvonne, Kaner, Robert J, Krishnan, Jerry A, LaVange, Lisa M, Lazarus, Stephen C, Moore, Wendy C, Paulin, Laura, Putcha, Nirupama, Oelsner, Elizabeth C, Raman, Sanjeev, Tashkin, Donald P, Wells, J Michael, and Wise, Robert A
Subjects: Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Tobacco, Emphysema, Clinical Research, Genetics, Tobacco Smoke and Health, Lung, Chronic Obstructive Pulmonary Disease, 2.1 Biological and endogenous factors, Aetiology, Respiratory, Adult, Black or African American, Aged, Aged, 80 and over, Female, Forced Expiratory Volume, Genotype, Heterozygote, Hispanic or Latino, Humans, Isoelectric Focusing, Male, Maximal Midexpiratory Flow Rate, Middle Aged, Phenotype, Polymorphism, Genetic, Pulmonary Disease, Chronic Obstructive, Pulmonary Emphysema, Smoking, Tomography, X-Ray Computed, Vital Capacity, White People, alpha 1-Antitrypsin, chronic obstructive pulmonary disease, alpha-1 antitrypsin, SERPINA1, rare variant, emphysema, NHLBI Subpopulations and Intermediate Outcomes Measures in COPD Study, Medical and Health Sciences, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract: Rationale: The role of PI (protease inhibitor) type Z heterozygotes and additional rare variant genotypes in the gene encoding alpha-1 antitrypsin, SERPINA1 (serpin peptidase inhibitor, clade A, member 1), in determining chronic obstructive pulmonary disease risk and severity is controversial.Objectives: To comprehensively evaluate the effects of rare SERPINA1 variants on lung function and emphysema phenotypes in subjects with significant tobacco smoke exposure using deep gene resequencing and alpha-1 antitrypsin concentrations.Methods: DNA samples from 1,693 non-Hispanic white individuals, 385 African Americans, and 90 Hispanics with ≥20 pack-years smoking were resequenced for the identification of rare variants (allele frequency
Published: 2020

18. Genetic diversity fuels gene discovery for tobacco and alcohol use

Author: Saunders, Gretchen R. B., Wang, Xingyan, Chen, Fang, Jang, Seon-Kyeong, Liu, Mengzhen, Wang, Chen, Gao, Shuang, Jiang, Yu, Khunsriraksakul, Chachrit, Otto, Jacqueline M., Addison, Clifton, Akiyama, Masato, Albert, Christine M., Aliev, Fazil, Alonso, Alvaro, Arnett, Donna K., Ashley-Koch, Allison E., Ashrani, Aneel A., Barnes, Kathleen C., Barr, R. Graham, Bartz, Traci M., Becker, Diane M., Bielak, Lawrence F., Benjamin, Emelia J., Bis, Joshua C., Bjornsdottir, Gyda, Blangero, John, Bleecker, Eugene R., Boardman, Jason D., Boerwinkle, Eric, Boomsma, Dorret I., Boorgula, Meher Preethi, Bowden, Donald W., Brody, Jennifer A., Cade, Brian E., Chasman, Daniel I., Chavan, Sameer, Chen, Yii-Der Ida, Chen, Zhengming, Cheng, Iona, Cho, Michael H., Choquet, Hélène, Cole, John W., Cornelis, Marilyn C., Cucca, Francesco, Curran, Joanne E., de Andrade, Mariza, Dick, Danielle M., Docherty, Anna R., Duggirala, Ravindranath, Eaton, Charles B., Ehringer, Marissa A., Esko, Tõnu, Faul, Jessica D., Silva, Lilian Fernandes, Fiorillo, Edoardo, Fornage, Myriam, Freedman, Barry I., Gabrielsen, Maiken E., Garrett, Melanie E., Gharib, Sina A., Gieger, Christian, Gillespie, Nathan, Glahn, David C., Gordon, Scott D., Gu, Charles C., Gu, Dongfeng, Gudbjartsson, Daniel F., Guo, Xiuqing, Haessler, Jeffrey, Hall, Michael E., Haller, Toomas, Harris, Kathleen Mullan, He, Jiang, Herd, Pamela, Hewitt, John K., Hickie, Ian, Hidalgo, Bertha, Hokanson, John E., Hopfer, Christian, Hottenga, JoukeJan, Hou, Lifang, Huang, Hongyan, Hung, Yi-Jen, Hunter, David J., Hveem, Kristian, Hwang, Shih-Jen, Hwu, Chii-Min, Iacono, William, Irvin, Marguerite R., Jee, Yon Ho, Johnson, Eric O., Joo, Yoonjung Y., Jorgenson, Eric, Justice, Anne E., Kamatani, Yoichiro, Kaplan, Robert C., Kaprio, Jaakko, Kardia, Sharon L. R., Keller, Matthew C., Kelly, Tanika N., Kooperberg, Charles, Korhonen, Tellervo, Kraft, Peter, Krauter, Kenneth, Kuusisto, Johanna, Laakso, Markku, Lasky-Su, Jessica, Lee, Wen-Jane, Lee, James J., Levy, Daniel, Li, Liming, Li, Kevin, Li, Yuqing, Lin, Kuang, Lind, Penelope A., Liu, Chunyu, Lloyd-Jones, Donald M., Lutz, Sharon M., Ma, Jiantao, Mägi, Reedik, Manichaikul, Ani, Martin, Nicholas G., Mathur, Ravi, Matoba, Nana, McArdle, Patrick F., McGue, Matt, McQueen, Matthew B., Medland, Sarah E., Metspalu, Andres, Meyers, Deborah A., Millwood, Iona Y., Mitchell, Braxton D., Mohlke, Karen L., Moll, Matthew, Montasser, May E., Morrison, Alanna C., Mulas, Antonella, Nielsen, Jonas B., North, Kari E., Oelsner, Elizabeth C., Okada, Yukinori, Orrù, Valeria, Palmer, Nicholette D., Palviainen, Teemu, Pandit, Anita, Park, S. Lani, Peters, Ulrike, Peters, Annette, Peyser, Patricia A., Polderman, Tinca J. C., Rafaels, Nicholas, Redline, Susan, Reed, Robert M., Reiner, Alex P., Rice, John P., Rich, Stephen S., Richmond, Nicole E., Roan, Carol, Rotter, Jerome I., Rueschman, Michael N., Runarsdottir, Valgerdur, Saccone, Nancy L., Schwartz, David A., Shadyab, Aladdin H., Shi, Jingchunzi, Shringarpure, Suyash S., Sicinski, Kamil, Skogholt, Anne Heidi, Smith, Jennifer A., Smith, Nicholas L., Sotoodehnia, Nona, Stallings, Michael C., Stefansson, Hreinn, Stefansson, Kari, Stitzel, Jerry A., Sun, Xiao, Syed, Moin, Tal-Singer, Ruth, Taylor, Amy E., Taylor, Kent D., Telen, Marilyn J., Thai, Khanh K., Tiwari, Hemant, Turman, Constance, Tyrfingsson, Thorarinn, Wall, Tamara L., Walters, Robin G., Weir, David R., Weiss, Scott T., White, Wendy B., Whitfield, John B., Wiggins, Kerri L., Willemsen, Gonneke, Willer, Cristen J., Winsvold, Bendik S., Xu, Huichun, Yanek, Lisa R., Yin, Jie, Young, Kristin L., Young, Kendra A., Yu, Bing, Zhao, Wei, Zhou, Wei, Zöllner, Sebastian, Zuccolo, Luisa, Batini, Chiara, Bergen, Andrew W., Bierut, Laura J., David, Sean P., Gagliano Taliun, Sarah A., Hancock, Dana B., Jiang, Bibo, Munafò, Marcus R., Thorgeirsson, Thorgeir E., Liu, Dajiang J., and Vrieze, Scott
Published: 2022
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19. Bronchodilator Responsiveness in Tobacco-Exposed People With or Without COPD

Author: Alexis, Neil E., Anderson, Wayne H., Arjomandi, Mehrdad, Barjaktarevic, Igor, Barr, R. Graham, Basta, Patricia, Bateman, Lori A., Bhatt, Surya P., Bleecker, Eugene R., Boucher, Richard C., Bowler, Russell P., Christenson, Stephanie A., Comellas, Alejandro P., Cooper, Christopher B., Couper, David J., Criner, Gerard J., Crystal, Ronald G., Curtis, Jeffrey L., Doerschuk, Claire M., Dransfield, Mark T., Drummond, Brad, Freeman, Christine M., Galban, Craig, Han, MeiLan K., Hansel, Nadia N., Hastie, Annette T., Hoffman, Eric A., Huang, Yvonne, Kaner, Robert J., Kanner, Richard E., Kleerup, Eric C., Krishnan, Jerry A., LaVange, Lisa M., Lazarus, Stephen C., Martinez, Fernando J., Meyers, Deborah A., Moore, Wendy C., Newell, John D., Jr., Paine, Robert, III, Paulin, Laura, Peters, Stephen P., Pirozzi, Cheryl, Putcha, Nirupama, Oelsner, Elizabeth C., O’Neal, Wanda K., Ortega, Victor E., Raman, Sanjeev, Rennard, Stephen I., Tashkin, Donald P., Wells, J. Michael, Wise, Robert A., Woodruff, Prescott G., Fortis, Spyridon, Quibrera, Pedro M., Dransfield, Mark B., Dolezal, Brett A., Kim, Victor, Barjaktarevic, Igor Z., and Couper, David
Published: 2023
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20. Author Correction: Multi-ancestry genome-wide association analyses improve resolution of genes and pathways influencing lung function and chronic obstructive pulmonary disease risk

Author: Shrine, Nick, Izquierdo, Abril G., Chen, Jing, Packer, Richard, Hall, Robert J., Guyatt, Anna L., Batini, Chiara, Thompson, Rebecca J., Pavuluri, Chandan, Malik, Vidhi, Hobbs, Brian D., Moll, Matthew, Kim, Wonji, Tal-Singer, Ruth, Bakke, Per, Fawcett, Katherine A., John, Catherine, Coley, Kayesha, Piga, Noemi Nicole, Pozarickij, Alfred, Lin, Kuang, Millwood, Iona Y., Chen, Zhengming, Li, Liming, Wijnant, Sara R. A., Lahousse, Lies, Brusselle, Guy, Uitterlinden, Andre G., Manichaikul, Ani, Oelsner, Elizabeth C., Rich, Stephen S., Barr, R. Graham, Kerr, Shona M., Vitart, Veronique, Brown, Michael R., Wielscher, Matthias, Imboden, Medea, Jeong, Ayoung, Bartz, Traci M., Gharib, Sina A., Flexeder, Claudia, Karrasch, Stefan, Gieger, Christian, Peters, Annette, Stubbe, Beate, Hu, Xiaowei, Ortega, Victor E., Meyers, Deborah A., Bleecker, Eugene R., Gabriel, Stacey B., Gupta, Namrata, Smith, Albert Vernon, Luan, Jian’an, Zhao, Jing-Hua, Hansen, Ailin F., Langhammer, Arnulf, Willer, Cristen, Bhatta, Laxmi, Porteous, David, Smith, Blair H., Campbell, Archie, Sofer, Tamar, Lee, Jiwon, Daviglus, Martha L., Yu, Bing, Lim, Elise, Xu, Hanfei, O’Connor, George T., Thareja, Gaurav, Albagha, Omar M. E., Suhre, Karsten, Granell, Raquel, Faquih, Tariq O., Hiemstra, Pieter S., Slats, Annelies M., Mullin, Benjamin H., Hui, Jennie, James, Alan, Beilby, John, Patasova, Karina, Hysi, Pirro, Koskela, Jukka T., Wyss, Annah B., Jin, Jianping, Sikdar, Sinjini, Lee, Mikyeong, May-Wilson, Sebastian, Pirastu, Nicola, Kentistou, Katherine A., Joshi, Peter K., Timmers, Paul R. H. J., Williams, Alexander T., Free, Robert C., Wang, Xueyang, Morrison, John L., Gilliland, Frank D., Chen, Zhanghua, Wang, Carol A., Foong, Rachel E., Harris, Sarah E., Taylor, Adele, Redmond, Paul, Cook, James P., Mahajan, Anubha, Lind, Lars, Palviainen, Teemu, Lehtimäki, Terho, Raitakari, Olli T., Kaprio, Jaakko, Rantanen, Taina, Pietiläinen, Kirsi H., Cox, Simon R., Pennell, Craig E., Hall, Graham L., Gauderman, W. James, Brightling, Chris, Wilson, James F., Vasankari, Tuula, Laitinen, Tarja, Salomaa, Veikko, Mook-Kanamori, Dennis O., Timpson, Nicholas J., Zeggini, Eleftheria, Dupuis, Josée, Hayward, Caroline, Brumpton, Ben, Langenberg, Claudia, Weiss, Stefan, Homuth, Georg, Schmidt, Carsten Oliver, Probst-Hensch, Nicole, Jarvelin, Marjo-Riitta, Morrison, Alanna C., Polasek, Ozren, Rudan, Igor, Lee, Joo-Hyeon, Sayers, Ian, Rawlins, Emma L., Dudbridge, Frank, Silverman, Edwin K., Strachan, David P., Walters, Robin G., Morris, Andrew P., London, Stephanie J., Cho, Michael H., Wain, Louise V., Hall, Ian P., and Tobin, Martin D.
Published: 2023
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21. A Genetic Risk Score Associated with Chronic Obstructive Pulmonary Disease Susceptibility and Lung Structure on Computed Tomography

Author: Oelsner, Elizabeth C, Ortega, Victor E, Smith, Benjamin M, Nguyen, Jennifer N, Manichaikul, Ani W, Hoffman, Eric A, Guo, Xiuqing, Taylor, Kent D, Woodruff, Prescott G, Couper, David J, Hansel, Nadia N, Martinez, Fernando J, Paine, Robert, Han, Meilan K, Cooper, Christopher, Dransfield, Mark T, Criner, Gerard, Krishnan, Jerry A, Bowler, Russell, Bleecker, Eugene R, Peters, Stephen, Rich, Stephen S, Meyers, Deborah A, Rotter, Jerome I, and Barr, R Graham
Subjects: Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Prevention, Genetics, Chronic Obstructive Pulmonary Disease, Biomedical Imaging, Lung, Respiratory, Good Health and Well Being, Aged, Female, Genetic Predisposition to Disease, Humans, Male, Middle Aged, Pulmonary Disease, Chronic Obstructive, Risk Assessment, Tomography, X-Ray Computed, United States, spirometry, emphysema, airway remodeling, Medical and Health Sciences, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract: Rationale: Chronic obstructive pulmonary disease (COPD) has been associated with numerous genetic variants, yet the extent to which its genetic risk is mediated by variation in lung structure remains unknown.Objectives: To characterize associations between a genetic risk score (GRS) associated with COPD susceptibility and lung structure on computed tomography (CT).Methods: We analyzed data from MESA Lung (Multi-Ethnic Study of Atherosclerosis Lung Study), a U.S. general population-based cohort, and SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study). A weighted GRS was calculated from 83 SNPs that were previously associated with lung function. Lung density, spatially matched airway dimensions, and airway counts were assessed on full-lung CT. Generalized linear models were adjusted for age, age squared, sex, height, principal components of genetic ancestry, smoking status, pack-years, CT model, milliamperes, and total lung volume.Measurements and Main Results: MESA Lung and SPIROMICS contributed 2,517 and 2,339 participants, respectively. Higher GRS was associated with lower lung function and increased COPD risk, as well as lower lung density, smaller airway lumens, and fewer small airways, without effect modification by smoking. Adjustment for CT lung structure, particularly small airway measures, attenuated associations between the GRS and FEV1/FVC by 100% and 60% in MESA and SPIROMICS, respectively. Lung structure (P 0.10), improved discrimination of moderate-to-severe COPD cases relative to clinical factors alone.Conclusions: A GRS associated with COPD susceptibility was associated with CT lung structure. Lung structure may be an important mediator of heritability and determinant of personalized COPD risk.
Published: 2019

22. Associations of Blood Pressure and Cholesterol Levels During Young Adulthood With Later Cardiovascular Events

Author: Zhang, Yiyi, Vittinghoff, Eric, Pletcher, Mark J, Allen, Norrina B, Hazzouri, Adina Zeki Al, Yaffe, Kristine, Balte, Pallavi P, Alonso, Alvaro, Newman, Anne B, Ives, Diane G, Rana, Jamal S, Lloyd-Jones, Donald, Vasan, Ramachandran S, Bibbins-Domingo, Kirsten, Gooding, Holly C, de Ferranti, Sarah D, Oelsner, Elizabeth C, and Moran, Andrew E
Subjects: Aging, Prevention, Clinical Research, Cardiovascular, Heart Disease, Good Health and Well Being, Adolescent, Adult, Age Factors, Aged, Aged, 80 and over, Blood Pressure, Cardiovascular Diseases, Child, Child, Preschool, Cholesterol, HDL, Cholesterol, LDL, Female, Humans, Male, Middle Aged, Prospective Studies, Risk Factors, Young Adult, blood pressure, cholesterol, coronary heart disease, heart failure, stroke, young adulthood, Cardiorespiratory Medicine and Haematology, Public Health and Health Services, Cardiovascular System & Hematology
Abstract: BackgroundBlood pressure (BP) and cholesterol are major modifiable risk factors for cardiovascular disease (CVD), but effects of exposures during young adulthood on later life CVD risk have not been well quantified.ObjectiveThe authors sought to evaluate the independent associations between young adult exposures to risk factors and later life CVD risk, accounting for later life exposures.MethodsThe authors pooled data from 6 U.S. cohorts with observations spanning the life course from young adulthood to later life, and imputed risk factor trajectories for low-density lipoprotein (LDL) and high-density lipoprotein cholesterols, systolic and diastolic BP starting from age 18 years for every participant. Time-weighted average exposures to each risk factor during young (age 18 to 39 years) and later adulthood (age ≥40 years) were calculated and linked to subsequent risks of coronary heart disease (CHD), heart failure (HF), or stroke.ResultsA total of 36,030 participants were included. During a median follow-up of 17 years, there were 4,570 CHD, 5,119 HF, and 2,862 stroke events. When young and later adult risk factors were considered jointly in the model, young adult LDL ≥100 mg/dl (compared with
Published: 2019

23. Coronary Artery Calcium Scores and Atherosclerotic Cardiovascular Disease Risk Stratification in Smokers

Author: Leigh, Adam, McEvoy, John W, Garg, Parveen, Carr, J Jeffrey, Sandfort, Veit, Oelsner, Elizabeth C, Budoff, Matthew, Herrington, David, and Yeboah, Joseph
Subjects: Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Tobacco, Clinical Research, Heart Disease - Coronary Heart Disease, Cancer, Lung Cancer, Lung, Prevention, Women's Health, Biomedical Imaging, Atherosclerosis, Minority Health, Health Disparities, Aging, Tobacco Smoke and Health, Heart Disease, Cardiovascular, Good Health and Well Being, Aged, Aged, 80 and over, Computed Tomography Angiography, Coronary Angiography, Coronary Artery Disease, Early Detection of Cancer, Female, Humans, Incidence, Incidental Findings, Lung Neoplasms, Male, Middle Aged, Plaque, Atherosclerotic, Predictive Value of Tests, Prevalence, Prognosis, Radiography, Thoracic, Risk Assessment, Risk Factors, Smokers, Smoking, Time Factors, United States, Vascular Calcification, atherosclerotic cardiovascular disease, cigarette smokers, coronary artery calcium, pooled cohort equation, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract: ObjectivesThis study assessed the utility of the pooled cohort equation (PCE) and/or coronary artery calcium (CAC) for atherosclerotic cardiovascular disease (ASCVD) risk assessment in smokers, especially those who were lung cancer screening eligible (LCSE).BackgroundThe U.S. Preventive Services Task Force recommended and the Centers for Medicare & Medicaid Services currently pays for annual screening for lung cancer with low-dose computed tomography scans in a specified group of cigarette smokers. CAC can be obtained from these low-dose scans. The incremental utility of CAC for ASCVD risk stratification remains unclear in this high-risk group.MethodsOf 6,814 MESA (Multi-Ethnic Study of Atherosclerosis) participants, 3,356 (49.2% of total cohort) were smokers (2,476 former and 880 current), and 14.3% were LCSE. Kaplan-Meier, Cox proportional hazards, area under the curve, and net reclassification improvement (NRI) analyses were used to assess the association between PCE and/or CAC and incident ASCVD. Incident ASCVD was defined as coronary death, nonfatal myocardial infarction, or fatal or nonfatal stroke.ResultsSmokers had a mean age of 62.1 years, 43.5% were female, and all had a mean of 23.0 pack-years of smoking. The LCSE sample had a mean age of 65.3 years, 39.1% were female, and all had a mean of 56.7 pack-years of smoking. After a mean of 11.1 years of follow-up 13.4% of all smokers and 20.8% of LCSE smokers had ASCVD events; 6.7% of all smokers and 14.2% of LCSE smokers with CAC = 0 had an ASCVD event during the follow-up. One SD increase in the PCE 10-year risk was associated with a 68% increase risk for ASCVD events in all smokers (hazard ratio: 1.68; 95% confidence interval: 1.57 to 1.80) and a 22% increase in risk for ASCVD events in the LCSE smokers (hazard ratio: 1.22; 95% confidence interval: 1.00 to 1.47). CAC was associated with increased ASCVD risk in all smokers and in LCSE smokers in all the Cox models. The C-statistic of the PCE for ASCVD was higher in all smokers compared with LCSE smokers (0.693 vs. 0.545). CAC significantly improved the C-statistics of the PCE in all smokers but not in LCSE smokers. The event and nonevent net reclassification improvements for all smokers and LCSE smokers were 0.018 and -0.126 versus 0.16 and -0.196, respectively.ConclusionsIn this well-characterized, multiethnic U.S. cohort, CAC was predictive of ASCVD in all smokers and in LCSE smokers but modestly improved discrimination over and beyond the PCE. However, 6.7% of all smokers and 14.2% of LCSE smokers with CAC = 0 had an ASCVD event during follow-up.
Published: 2019

24. Albuminuria, Lung Function Decline, and Risk of Incident Chronic Obstructive Pulmonary Disease. The NHLBI Pooled Cohorts Study

Author: Oelsner, Elizabeth C, Balte, Pallavi P, Grams, Morgan E, Cassano, Patricia A, Jacobs, David R, Barr, R Graham, Burkart, Kristin M, Kalhan, Ravi, Kronmal, Richard, Loehr, Laura R, O'Connor, George T, Schwartz, Joseph E, Shlipak, Michael, Tracy, Russell P, Tsai, Michael Y, White, Wendy, and Yende, Sachin
Subjects: Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Clinical Research, Lung, Women's Health, Health Disparities, Chronic Obstructive Pulmonary Disease, Minority Health, 4.1 Discovery and preclinical testing of markers and technologies, Cardiovascular, Respiratory, Good Health and Well Being, Aged, Albuminuria, Cohort Studies, Comorbidity, Female, Humans, Incidence, Male, Middle Aged, National Heart, Lung, and Blood Institute (U.S.), Pulmonary Disease, Chronic Obstructive, Respiratory Function Tests, Risk Factors, United States, epidemiology, spirometry, asthma, Medical and Health Sciences, Respiratory System, Cardiovascular medicine and haematology, Clinical sciences
Abstract: RationaleChronic lower respiratory diseases (CLRDs), including chronic obstructive pulmonary disease (COPD) and asthma, are the fourth leading cause of death. Prior studies suggest that albuminuria, a biomarker of endothelial injury, is increased in patients with COPD.ObjectivesTo test whether albuminuria was associated with lung function decline and incident CLRDs.MethodsSix U.S. population-based cohorts were harmonized and pooled. Participants with prevalent clinical lung disease were excluded. Albuminuria (urine albumin-to-creatinine ratio) was measured in spot samples. Lung function was assessed by spirometry. Incident CLRD-related hospitalizations and deaths were classified via adjudication and/or administrative criteria. Mixed and proportional hazards models were used to test individual-level associations adjusted for age, height, weight, sex, race/ethnicity, education, birth year, cohort, smoking status, pack-years of smoking, renal function, hypertension, diabetes, and medications.Measurements and main resultsAmong 10,961 participants with preserved lung function, mean age at albuminuria measurement was 60 years, 51% were never-smokers, median albuminuria was 5.6 mg/g, and mean FEV1 decline was 31.5 ml/yr. For each SD increase in log-transformed albuminuria, there was 2.81% greater FEV1 decline (95% confidence interval [CI], 0.86-4.76%; P = 0.0047), 11.02% greater FEV1/FVC decline (95% CI, 4.43-17.62%; P = 0.0011), and 15% increased hazard of incident spirometry-defined moderate-to-severe COPD (95% CI, 2-31%, P = 0.0021). Each SD log-transformed albuminuria increased hazards of incident COPD-related hospitalization/mortality by 26% (95% CI, 18-34%, P
Published: 2019

25. Environmental-level exposure to metals and metal-mixtures associated with spirometry-defined lung disease in American Indian adults: Evidence from the Strong Heart Study

Author: Sobel, Marisa, Navas-Acien, Ana, Powers, Martha, Grau-Perez, Maria, Goessler, Walter, Best, Lyle G., Umans, Jason, Oelsner, Elizabeth C., Podolanczuk, Anna, and Sanchez, Tiffany R.
Published: 2022
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26. Identification of Sputum Biomarkers Predictive of Pulmonary Exacerbations in COPD

Author: Alexis, Neil E., Anderson, Wayne H., Arjomandi, Mehrdad, Barjaktarevic, Igor, Barr, R. Graham, Bateman, Lori A., Bhatt, Surya P., Bleecker, Eugene R., Boucher, Richard C., Bowler, Russell P., Christenson, Stephanie A., Comellas, Alejandro P., Cooper, Christopher B., Couper, David J., Criner, Gerard J., Crystal, Ronald G., Curtis, Jeffrey L., Doerschuk, Claire M., Dransfield, Mark T., Drummond, Brad, Freeman, Christine M., Galban, Craig, Han, MeiLan K., Hansel, Nadia N., Hastie, Annette T., Hoffman, Eric A., Huang, Yvonne, Kaner, Robert J., Kanner, Richard E., Kleerup, Eric C., Krishnan, Jerry A., LaVange, Lisa M., Lazarus, Stephen C., Martinez, Fernando J., Meyers, Deborah A., Moore, Wendy C., Newell, John D., Jr., Paine, Robert, III, Paulin, Laura, Peters, Stephen P., Pirozzi, Cheryl, Putcha, Nirupama, Oelsner, Elizabeth C., O’Neal, Wanda K., Ortega, Victor E., Raman, Sanjeev, Rennard, Stephen I., Tashkin, Donald P., Wells, J. Michael, Wise, Robert A., Woodruff, Prescott G., Esther, Charles R., Jr., Kesimer, Mehmet, Ceppe, Agathe, Tesfaigzi, Yohannes, Kim, Victor, Paulin, Laura M., Huang, Yvonne J., and Labaki, Wassim W.
Published: 2022
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27. Dysanapsis Genetic Risk Predicts Lung Function Across the Lifespan.

Author: Debban, Catherine L., Ambalavanan, Amirthagowri, Ghosh, Auyon, Li, Zhonglin, Buschur, Kristina L., Ma, Yanlin, George, Elizabeth, Pistenmaa, Carrie, Bertoni, Alain G., Oelsner, Elizabeth C., Michos, Erin D., Moraes, Theo J., Jacobs Jr., David R., Christenson, Stephanie, Bhatt, Surya P., Kaner, Robert J., Simons, Elinor, Turvey, Stuart E., Vameghestahbanati, Motahareh, and Engert, James C.
Subjects: GENETIC risk score, CHRONIC obstructive pulmonary disease, GENOME-wide association studies, OBSTRUCTIVE lung diseases, GENETIC variation
Abstract: Rationale: Dysanapsis refers to a mismatch between airway tree caliber and lung size arising early in life. Dysanapsis assessed by computed tomography (CT) is evident by early adulthood and associated with chronic obstructive pulmonary disease (COPD) risk later in life. Objectives: By examining the genetic factors associated with CT-assessed dysanapsis, we aimed to elucidate its molecular underpinnings and physiological significance across the lifespan. Methods: We performed a genome-wide association study of CT-assessed dysanapsis in 11,951 adults, including individuals from two population-based and two COPD-enriched studies. We applied colocalization analysis to integrate genome-wide association study and gene expression data from whole blood and lung. Genetic variants associated with dysanapsis were combined into a genetic risk score that was applied to examine association with lung function in children from a population-based birth cohort (n = 1,278) and adults from the UKBiobank (n = 369,157). Measurements and Main Results: CT-assessed dysanapsis was associated with genetic variants from 21 independent signals in 19 gene regions, implicating HHIP (hedgehog interacting protein), DSP, and NPNT as potential molecular targets based on colocalization of their expression. A higher dysanapsis genetic risk score was associated with obstructive spirometry among 5-year-old children and among adults in the fifth, sixth, and seventh decades of life. Conclusions: CT-assessed dysanapsis is associated with variation in genes previously implicated in lung development, and dysanapsis genetic risk is associated with obstructive lung function from early life through older adulthood. Dysanapsis may represent an endophenotype link between the genetic variations associated with lung function and COPD. [ABSTRACT FROM AUTHOR]
Published: 2024
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28. Low-Density Lipoprotein Cholesterol Level Distributions Across Different Ages: Implications for Screening Children for Severe and Familial Hypercholesterolemia.

Author: Liu, Junxiu, Bellows, Brandon K., Jacobs Jr, David R., Woo, Jessica G., Urbina, Elaine M., Balte, Pallavi P., Oelsner, Elizabeth C., Kazi, Dhruv S., Siscovick, David, Allen, Norrina B., Rana, Jamal S., Wilkins, John T., Hall, Michael E., Bazzano, Lydia A., Burns, Trudy L., Daniels, Stephen R., Dwyer, Terence, Juonala, Markus, Raitakari, Olli T., and Sinaiko, Alan R.
Published: 2024
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29. Non-cigarette tobacco products, aryl-hydrocarbon receptor repressor gene methylation and smoking-related health outcomes.

Author: Eckhardt, Christina M., Balte, Pallavi, Morris, Jack E., Bhatt, Surya P., Couper, David, Fetterman, Jessica, Freedman, Neal, Jacobs, David R., Lifang Hou, Kalhan, Ravi, Yongmei Liu, Loehr, Laura, Lutsey, Pamela L., Schwartz, Joseph E., White, Wendy, Yende, Sachin, London, Stephanie J., Sanchez, Tiffany R., and Oelsner, Elizabeth C.
Subjects: CONSUMER behavior, TOBACCO products, SMOKING, CIGAR smoking, FORCED expiratory volume, COUGH
Published: 2024
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30. Association of Severe Hypercholesterolemia and Familial Hypercholesterolemia Genotype With Risk of Coronary Heart Disease

Author: Zhang, Yiyi, Dron, Jacqueline S., Bellows, Brandon K., Khera, Amit V., Liu, Junxiu, Balte, Pallavi P., Oelsner, Elizabeth C., Amr, Sami Samir, Lebo, Matthew S., Nagy, Anna, Peloso, Gina M., Natarajan, Pradeep, Rotter, Jerome I., Willer, Cristen, Boerwinkle, Eric, Ballantyne, Christie M., Lutsey, Pamela L., Fornage, Myriam, Lloyd-Jones, Donald M., Hou, Lifang, Psaty, Bruce M., Bis, Joshua C., Floyd, James S., Vasan, Ramachandran S., Heard-Costa, Nancy L., Carson, April P., Hall, Michael E., Rich, Stephen S., Guo, Xiuqing, Kazi, Dhruv S., de Ferranti, Sarah D., and Moran, Andrew E.
Published: 2023
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31. Centrilobular emphysema and coronary artery calcification: mediation analysis in the SPIROMICS cohort.

Author: Bhatt, Surya P, Nath, Hrudaya P, Kim, Young-Il, Ramachandran, Rekha, Watts, Jubal R, Terry, Nina LJ, Sonavane, Sushil, Deshmane, Swati P, Woodruff, Prescott G, Oelsner, Elizabeth C, Bodduluri, Sandeep, Han, MeiLan K, Labaki, Wassim W, Michael Wells, J, Martinez, Fernando J, Barr, R Graham, Dransfield, Mark T, and SPIROMICS investigators
Subjects: SPIROMICS investigators, Humans, Pulmonary Disease, Chronic Obstructive, Pulmonary Emphysema, Inflammation Mediators, Vital Capacity, Cohort Studies, Smoking, Aged, Middle Aged, Female, Male, Coronary Artery Disease, Vascular Calcification, Biomarkers, Outcome Assessment, Health Care, COPD, Cardiovascular disease, Coronary artery calcification, Emphysema, Mediators, Pulmonary Disease, Chronic Obstructive, Outcome Assessment, Health Care, Respiratory System, Cardiorespiratory Medicine and Haematology, Clinical Sciences
Abstract: BACKGROUND:Chronic obstructive pulmonary disease (COPD) is associated with a two-to-five fold increase in the risk of coronary artery disease independent of shared risk factors. This association is hypothesized to be mediated by systemic inflammation but this link has not been established. METHODS:We included 300 participants enrolled in the SPIROMICS cohort, 75 each of lifetime non-smokers, smokers without airflow obstruction, mild-moderate COPD, and severe-very severe COPD. We quantified emphysema and airway disease on computed tomography, characterized visual emphysema subtypes (centrilobular and paraseptal) and airway disease, and used the Weston visual score to quantify coronary artery calcification (CAC). We used the Sobel test to determine whether markers of systemic inflammation mediated a link between spirometric and radiographic features of COPD and CAC. RESULTS:FEV1/FVC but not quantitative emphysema or airway wall thickening was associated with CAC (p = 0.036), after adjustment for demographics, diabetes mellitus, hypertension, statin use, and CT scanner type. To explain this discordance, we examined visual subtypes of emphysema and airway disease, and found that centrilobular emphysema but not paraseptal emphysema or bronchial thickening was independently associated with CAC (p = 0.019). MMP3, VCAM1, CXCL5 and CXCL9 mediated 8, 8, 7 and 16% of the association between FEV1/FVC and CAC, respectively. Similar biomarkers partially mediated the association between centrilobular emphysema and CAC. CONCLUSIONS:The association between airflow obstruction and coronary calcification is driven primarily by the centrilobular subtype of emphysema, and is linked through bioactive molecules implicated in the pathogenesis of atherosclerosis. TRIAL REGISTRATION:ClinicalTrials.gov: Identifier: NCT01969344 .
Published: 2018

32. Meta-analysis across Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium provides evidence for an association of serum vitamin D with pulmonary function

Author: Xu, Jiayi, Bartz, Traci M, Chittoor, Geetha, Eiriksdottir, Gudny, Manichaikul, Ani W, Sun, Fangui, Terzikhan, Natalie, Zhou, Xia, Booth, Sarah L, Brusselle, Guy G, de Boer, Ian H, Fornage, Myriam, Frazier-Wood, Alexis C, Graff, Mariaelisa, Gudnason, Vilmundur, Harris, Tamara B, Hofman, Albert, Hou, Ruixue, Houston, Denise K, Jacobs, David R, Kritchevsky, Stephen B, Latourelle, Jeanne, Lemaitre, Rozenn N, Lutsey, Pamela L, O’Connor, George, Oelsner, Elizabeth C, Pankow, James S, Psaty, Bruce M, Rohde, Rebecca R, Rich, Stephen S, Rotter, Jerome I, Smith, Lewis J, Stricker, Bruno H, Voruganti, V Saroja, Wang, Thomas J, Zillikens, M Carola, Barr, R Graham, Dupuis, Josée, Gharib, Sina A, Lahousse, Lies, London, Stephanie J, North, Kari E, Smith, Albert V, Steffen, Lyn M, Hancock, Dana B, and Cassano, Patricia A
Subjects: Biomedical and Clinical Sciences, Nutrition and Dietetics, Aging, Health Disparities, Nutrition, Minority Health, Respiratory, Adult, Aged, Black People, Cross-Sectional Studies, Female, Forced Expiratory Volume, Genome, Human, Heart, Heart Diseases, Humans, Lung, Lung Diseases, Male, Middle Aged, Molecular Epidemiology, Prospective Studies, Regression Analysis, Respiratory Function Tests, Smoking, Vital Capacity, Vitamin D, White People, Black or African American, 1, 25(OH)D 25-hydroxyvitamin D, AA African ancestry, AGES Age, ARIC Atherosclerosis Risk in Communities Study, CARDIA Coronary Artery Risk Development in Young Adults Study, CHARGE Cohorts for Heart and Aging Research in Genomic Epidemiology, CHS Cardiovascular Health Study, COPD chronic obstructive pulmonary disease, EA European ancestry, Environment, FEV1 forced expiratory volume in the 1st second, FHS (Gen3) Framingham Heart Study – Generation 3 Cohort, FHS (Offspring) Framingham Heart Study –Offspring Cohort, FVC forced vital capacity, Gene, HABC Health, Iceland, MESA Multi-Ethnic Study of Atherosclerosis, PFT pulmonary function test, RIA radioimmunoassay, Susceptibility Study − Reykjavik, and Body Composition Study, 25-(OH)2D 1, 25-dihydroxyvitamin D, African Americans, Forced expiratory volume, Respiratory function tests, Vital capacity, Whites, Animal Production, Food Sciences, Nutrition & Dietetics, Animal production, Food sciences, Nutrition and dietetics
Abstract: The role that vitamin D plays in pulmonary function remains uncertain. Epidemiological studies reported mixed findings for serum 25-hydroxyvitamin D (25(OH)D)-pulmonary function association. We conducted the largest cross-sectional meta-analysis of the 25(OH)D-pulmonary function association to date, based on nine European ancestry (EA) cohorts (n 22 838) and five African ancestry (AA) cohorts (n 4290) in the Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium. Data were analysed using linear models by cohort and ancestry. Effect modification by smoking status (current/former/never) was tested. Results were combined using fixed-effects meta-analysis. Mean serum 25(OH)D was 68 (sd 29) nmol/l for EA and 49 (sd 21) nmol/l for AA. For each 1 nmol/l higher 25(OH)D, forced expiratory volume in the 1st second (FEV1) was higher by 1·1 ml in EA (95 % CI 0·9, 1·3; P
Published: 2018

33. Rural Residence and Chronic Obstructive Pulmonary Disease Exacerbations. Analysis of the SPIROMICS Cohort

Author: Burkes, Robert M, Gassett, Amanda J, Ceppe, Agathe S, Anderson, Wayne, O’Neal, Wanda K, Woodruff, Prescott G, Krishnan, Jerry A, Barr, R Graham, Han, MeiLan K, Martinez, Fernando J, Comellas, Alejandro P, Lambert, Allison A, Kaufman, Joel D, Dransfield, Mark T, Wells, J Michael, Kanner, Richard E, Paine, Robert, Bleecker, Eugene R, Paulin, Laura M, Hansel, Nadia N, Drummond, M Bradley, Alexis, Neil E, Anderson, Wayne H, Boucher, Richard C, Bowler, Russell P, Carretta, Elizabeth E, Christenson, Stephanie A, Cooper, Christopher B, Couper, David J, Criner, Gerard J, Crystal, Ronald G, Curtis, Jeffrey L, Doerschuk, Claire M, Freeman, Christine M, Hastie, Annette T, Hoffman, Eric A, Kaner, Robert J, Kleerup, Eric C, LaVange, Lisa M, Lazarus, Stephen C, Meyers, Deborah A, Moore, Wendy C, Newell, John D, Paulin, Laura, Peters, Stephen, Oelsner, Elizabeth C, Ortega, Victor E, Putcha, Nirupama, Rennard, Stephen I, Tashkin, Donald P, Scholand, Mary Beth, Wise, Robert A, Postow, Lisa, and Croxton, Thomas
Subjects: Biomedical and Clinical Sciences, Clinical Sciences, Lung, Rural Health, Chronic Obstructive Pulmonary Disease, Clinical Research, Respiratory, chronic obstructive pulmonary disease, exacerbation, rural health, Current and former investigators of the SPIROMICS sites and reading centers, Cardiovascular medicine and haematology, Clinical sciences
Abstract: Rationale: Rural residence is associated with poor outcomes in several chronic diseases. The association between rural residence and chronic obstructive pulmonary disease (COPD) exacerbations remains unclear.Objectives: In this work, we sought to determine the independent association between rural residence and COPD-related outcomes, including COPD exacerbations, airflow obstruction, and symptom burden.Methods: A total of 1,684 SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study) participants with forced expiratory volume in 1 second/forced vital capacity < 0.70 had geocoding-defined rural-urban residence status determined (N = 204 rural and N = 1,480 urban). Univariate and multivariate logistic and negative binomial regressions were performed to assess the independent association between rurality and COPD outcomes, including exacerbations, lung function, and symptom burden. The primary exposure of interest was rural residence, determined by geocoding of the home address to the block level at the time of study enrollment. Additional covariates of interest included demographic and clinical characteristics, occupation, and occupational exposures. The primary outcome measures were exacerbations determined over a 1-year course after enrollment by quarterly telephone calls and at an annual research clinic visit. The odds ratio (OR) and incidence rate ratio (IRR) of exacerbations that required treatment with medications, including steroids or antibiotics (total exacerbations), and exacerbations leading to hospitalization (severe exacerbations) were determined after adjusting for relevant covariates.Results: Rural residence was independently associated with a 70% increase in the odds of total exacerbations (OR, 1.70 [95% confidence interval (CI), 1.13-2.56]; P = 0.012) and a 46% higher incidence rate of total exacerbations (IRR 1.46 [95% CI, 1.02-2.10]; P = 0.039). There was no association between rural residence and severe exacerbations. Agricultural occupation was independently associated with increased odds and incidence of total and severe exacerbations. Inclusion of agricultural occupation in the analysis attenuated the association between rural residence and the odds and incidence rate of total exacerbations (OR, 1.52 [95% CI, 1.00-2.32]; P = 0.05 and IRR 1.39 [95% CI, 0.97-1.99]; P = 0.07). There was no difference in symptoms or airflow obstruction between rural and urban participants.Conclusions: Rural residence is independently associated with increased odds and incidence of total, but not severe, COPD exacerbations. These associations are not fully explained by agriculture-related exposures, highlighting the need for future research into potential mechanisms of the increased risk of COPD exacerbations in the rural population.
Published: 2018

34. Association of clonal hematopoiesis with chronic obstructive pulmonary disease

Author: Miller, Peter G., Qiao, Dandi, Rojas-Quintero, Joselyn, Honigberg, Michael C., Sperling, Adam S., Gibson, Christopher J., Bick, Alexander G., Niroula, Abhishek, McConkey, Marie E., Sandoval, Brittany, Miller, Brian C., Shi, Weiwei, Viswanathan, Kaushik, Leventhal, Matthew, Werner, Lillian, Moll, Matthew, Cade, Brian E., Barr, R. Graham, Correa, Adolfo, Cupples, L. Adrienne, Gharib, Sina A., Jain, Deepti, Gogarten, Stephanie M., Lange, Leslie A., London, Stephanie J., Manichaikul, Ani, O'Connor, George T., Oelsner, Elizabeth C., Redline, Susan, Rich, Stephen S., Rotter, Jerome I., Ramachandran, Vasan, Yu, Bing, Sholl, Lynette, Neuberg, Donna, Jaiswal, Siddhartha, Levy, Bruce D., Owen, Caroline A., Natarajan, Pradeep, Silverman, Edwin K., van Galen, Peter, Tesfaigzi, Yohannes, Cho, Michael H., and Ebert, Benjamin L.
Published: 2022
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35. Genetic regulation of serum IgA levels and susceptibility to common immune, infectious, kidney, and cardio-metabolic traits

Author: Liu, Lili, Khan, Atlas, Sanchez-Rodriguez, Elena, Zanoni, Francesca, Li, Yifu, Steers, Nicholas, Balderes, Olivia, Zhang, Junying, Krithivasan, Priya, LeDesma, Robert A., Fischman, Clara, Hebbring, Scott J., Harley, John B., Moncrieffe, Halima, Kottyan, Leah C., Namjou-Khales, Bahram, Walunas, Theresa L., Knevel, Rachel, Raychaudhuri, Soumya, Karlson, Elizabeth W., Denny, Joshua C., Stanaway, Ian B., Crosslin, David, Rauen, Thomas, Floege, Jürgen, Eitner, Frank, Moldoveanu, Zina, Reily, Colin, Knoppova, Barbora, Hall, Stacy, Sheff, Justin T., Julian, Bruce A., Wyatt, Robert J., Suzuki, Hitoshi, Xie, Jingyuan, Chen, Nan, Zhou, Xujie, Zhang, Hong, Hammarström, Lennart, Viktorin, Alexander, Magnusson, Patrik K. E., Shang, Ning, Hripcsak, George, Weng, Chunhua, Rundek, Tatjana, Elkind, Mitchell S. V., Oelsner, Elizabeth C., Barr, R. Graham, Ionita-Laza, Iuliana, Novak, Jan, Gharavi, Ali G., and Kiryluk, Krzysztof
Published: 2022
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36. Electronic Cigarette Use in US Adults at Risk for or with COPD: Analysis from Two Observational Cohorts.

Author: Bowler, Russell P, Hansel, Nadia N, Jacobson, Sean, Graham Barr, R, Make, Barry J, Han, MeiLan K, O'Neal, Wanda K, Oelsner, Elizabeth C, Casaburi, Richard, Barjaktarevic, Igor, Cooper, Chris, Foreman, Marilyn, Wise, Robert A, DeMeo, Dawn L, Silverman, Edwin K, Bailey, William, Harrington, Kathleen F, Woodruff, Prescott G, Drummond, M Bradley, and for COPDGene and SPIROMICS Investigators
Subjects: for COPDGene and SPIROMICS Investigators, Humans, Bronchitis, Pulmonary Disease, Chronic Obstructive, Tobacco Use Disorder, Disease Progression, Severity of Illness Index, Prevalence, Cohort Studies, Longitudinal Studies, Harm Reduction, Smoking Cessation, Adult, Aged, Aged, 80 and over, Middle Aged, United States, Female, Male, Vaping, Cigarette Smoking, Electronic Nicotine Delivery Systems, COPD, electronic cigarette, lung function, tobacco, Lung, Drug Abuse (NIDA only), Substance Misuse, Tobacco, Tobacco Smoke and Health, Prevention, Clinical Research, Chronic Obstructive Pulmonary Disease, 3.1 Primary prevention interventions to modify behaviours or promote wellbeing, Prevention of disease and conditions, and promotion of well-being, Respiratory, Good Health and Well Being, Clinical Sciences, General & Internal Medicine
Abstract: BackgroundElectronic cigarettes (e-cigarettes) are battery-operated nicotine-delivery devices used by some smokers as a cessation tool as well as by never smokers.ObjectiveTo determine the usage of e-cigarettes in older adults at risk for or with chronic obstructive pulmonary disease (COPD).DesignProspective cohorts.ParticipantsCOPDGene (N = 3536) and SPIROMICS (N = 1060) subjects who were current or former smokers aged 45-80.Main measuresParticipants were surveyed to determine whether e-cigarette use was associated with longitudinal changes in COPD progression or smoking habits.Key resultsFrom 2010 to 2016, participants who had ever used e-cigarettes steadily increased to 12-16%, but from 2014 to 2016 current use was stable at ~5%. E-cigarette use in African-Americans (AA) and whites was similar; however, AA were 1.8-2.9 times as likely to use menthol-flavored e-cigarettes. Current e-cigarette and conventional cigarette users had higher nicotine dependence and consumed more nicotine than those who smoked only conventional cigarettes. E-cigarette users had a heavier conventional cigarette smoking history and worse respiratory health, were less likely to reduce or quit conventional cigarette smoking, had higher nicotine dependence, and were more likely to report chronic bronchitis and exacerbations. Ever e-cigarette users had more rapid decline in lung function, but this trend did not persist after adjustment for persistent conventional cigarette smoking.ConclusionsE-cigarette use, which is common in adults with or at risk for COPD, was associated with worse pulmonary-related health outcomes, but not with cessation of smoking conventional cigarettes. Although this was an observational study, we find no evidence supporting the use of e-cigarettes as a harm reduction strategy among current smokers with or at risk for COPD.
Published: 2017

37. Association of sputum and blood eosinophil concentrations with clinical measures of COPD severity: an analysis of the SPIROMICS cohort

Author: Hastie, Annette T, Martinez, Fernando J, Curtis, Jeffrey L, Doerschuk, Claire M, Hansel, Nadia N, Christenson, Stephanie, Putcha, Nirupama, Ortega, Victor E, Li, Xingnan, Barr, R Graham, Carretta, Elizabeth E, Couper, David J, Cooper, Christopher B, Hoffman, Eric A, Kanner, Richard E, Kleerup, Eric, O'Neal, Wanda K, Paine, Richard, Peters, Stephen P, Alexis, Neil E, Woodruff, Prescott G, Han, MeiLan K, Meyers, Deborah A, Bleecker, Eugene R, investigators, SPIROMICS, Anderson, Wayne H, Boucher, Richard C, Bowler, Russell P, Christenson, Stephanie A, Comellas, Alejandro P, Criner, Gerard J, Crystal, Ronald G, Dransfield, Mark T, Freeman, Christine M, Kaner, Robert J, Kleerup, Eric C, Krishnan, Jerry A, LaVange, Lisa M, Lazarus, Stephen C, Newell, John D, Oelsner, Elizabeth C, Paine, Robert, Rennard, Stephen I, Tashkin, Donald P, Scholand, Mary Beth, Wells, J Michael, and Wise, Robert A
Subjects: Clinical Research, Lung, Chronic Obstructive Pulmonary Disease, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, Respiratory, Adrenal Cortex Hormones, Aged, Biomarkers, Bronchodilator Agents, Eosinophils, Female, Forced Expiratory Volume, Humans, Leukocyte Count, Male, Middle Aged, Pulmonary Disease, Chronic Obstructive, ROC Curve, Severity of Illness Index, Sputum, SPIROMICS investigators, Clinical Sciences, Public Health and Health Services, Other Medical and Health Sciences
Abstract: BackgroundIncreased concentrations of eosinophils in blood and sputum in chronic obstructive pulmonary disease (COPD) have been associated with increased frequency of exacerbations, reduced lung function, and corticosteroid responsiveness. We aimed to assess whether high eosinophil concentrations in either sputum or blood are associated with a severe COPD phenotype, including greater exacerbation frequency, and whether blood eosinophils are predictive of sputum eosinophils.MethodsWe did a multicentre observational study analysing comprehensive baseline data from SPIROMICS in patients with COPD aged 40-80 years who had a smoking history of at least 20 pack-years, recruited from six clinical sites and additional subsites in the USA between Nov 12, 2010, and April 21, 2015. Inclusion criteria for this analysis were SPIROMICS baseline visit data with complete blood cell counts and, in a subset, acceptable sputum counts. We stratified patients on the basis of blood and sputum eosinophil concentrations and compared their demographic characteristics, as well as results from questionnaires, clinical assessments, and quantitative CT (QCT). We also analysed whether blood eosinophil concentrations reliably predicted sputum eosinophil concentrations. This study is registered with ClinicalTrials.gov (NCT01969344).FindingsOf the 2737 patients recruited to SPIROMICS, 2499 patients were smokers and had available blood counts, and so were stratified by mean blood eosinophil count: 1262 patients with low (
Published: 2017

38. Frequency of exacerbations in patients with chronic obstructive pulmonary disease: an analysis of the SPIROMICS cohort

Author: Han, MeiLan K, Quibrera, Pedro M, Carretta, Elizabeth E, Barr, R Graham, Bleecker, Eugene R, Bowler, Russell P, Cooper, Christopher B, Comellas, Alejandro, Couper, David J, Curtis, Jeffrey L, Criner, Gerard, Dransfield, Mark T, Hansel, Nadia N, Hoffman, Eric A, Kanner, Richard E, Krishnan, Jerry A, Martinez, Carlos H, Pirozzi, Cheryl B, O'Neal, Wanda K, Rennard, Stephen, Tashkin, Donald P, Wedzicha, Jadwiga A, Woodruff, Prescott, Paine, Robert, Martinez, Fernando J, investigators, SPIROMICS, Alexis, Neil E, Anderson, Wayne H, Boucher, Richard C, Christenson, Stephanie A, Comellas, Alejandro P, Criner, Gerard J, Crystal, Ronald G, Doerschuk, Claire M, Freeman, Christine M, Hastie, Annette T, Kaner, Robert J, Kleerup, Eric C, LaVange, Lisa M, Lazarus, Stephen C, Meyers, Deborah A, Newell, John D, Oelsner, Elizabeth C, Putcha, Nirupama, Rennard, Stephen I, Scholand, Mary Beth, Wells, J Michael, Wise, Robert A, and Woodruff, Prescott G
Subjects: Lung, Chronic Obstructive Pulmonary Disease, Clinical Research, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, 2.4 Surveillance and distribution, Aetiology, Respiratory, Adult, Aged, Aged, 80 and over, Biomarkers, Disease Progression, Female, Forced Expiratory Volume, Humans, Interleukin-15, Interleukin-8, Logistic Models, Longitudinal Studies, Male, Middle Aged, Prospective Studies, Pulmonary Disease, Chronic Obstructive, Severity of Illness Index, Spirometry, Time Factors, Tomography, X-Ray Computed, SPIROMICS investigators, Clinical Sciences, Public Health and Health Services, Other Medical and Health Sciences
Abstract: BackgroundPresent treatment strategies to stratify exacerbation risk in patients with chronic obstructive pulmonary disease (COPD) rely on a history of two or more events in the previous year. We aimed to understand year to year variability in exacerbations and factors associated with consistent exacerbations over time.MethodsIn this longitudinal, prospective analysis of exacerbations in the Subpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS) cohort, we analysed patients aged 40-80 years with COPD for whom 3 years of prospective data were available, identified through various means including care at academic and non-academic medical centres, word of mouth, and existing patient registries. Participants were enrolled in the study between Nov 12, 2010, and July 31, 2015. We classified patients according to yearly exacerbation frequency: no exacerbations in any year; one exacerbation in every year during 3 years of follow-up; and those with inconsistent exacerbations (individuals who had both years with exacerbations and years without during the 3 years of follow-up). Participants were characterised by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) spirometric category (1-4) on the basis of post-bronchodilator FEV1. Stepwise logistic regression was used to compare factors associated with one or more acute exacerbations of COPD every year for 3 years versus no exacerbations in the same timeframe. Additionally, a stepwise zero-inflated negative binomial model was used to assess predictors of exacerbation count during follow-up in all patients with available data. Baseline symptom burden was assessed with the COPD assessment test. This trial is registered with ClinicalTrials.gov, number NCT01969344.Findings2981 patients were enrolled during the study. 1843 patients had COPD, of which 1105 patients had 3 years of complete, prospective follow-up data. 538 (49%) of 1105 patients had at least one acute exacerbation during the 3 years of follow-up, whereas 567 (51%) had none. 82 (7%) of 1105 patients had at least one acute exacerbation each year, whereas only 23 (2%) had two or more acute exacerbations in each year. An inconsistent pattern (both years with and without acute exacerbations) was common (456 [41%] of the group), particularly among GOLD stages 3 and 4 patients (256 [56%] of 456). In logistic regression, consistent acute exacerbations (≥1 event per year for 3 years) were associated with higher baseline symptom burden, previous exacerbations, greater evidence of small airway abnormality on CT, lower interleukin-15 concentrations, and higher interleukin-8 concentrations, than were no acute exacerbations.InterpretationAlthough acute exacerbations are common, the exacerbation status of most individuals varies markedly from year to year. Among patients who had any acute exacerbation over 3 years, very few repeatedly had two or more events per year. In addition to symptoms and history of exacerbations in the year before study enrolment, we identified several novel biomarkers associated with consistent exacerbations, including CT-defined small airway abnormality, and interleukin-15 and interleukin-8 concentrations.FundingNational Institutes of Health, and National Heart, Lung, and Blood Institute.
Published: 2017

39. Associations Among 25-Hydroxyvitamin D Levels, Lung Function, and Exacerbation Outcomes in COPD: An Analysis of the SPIROMICS Cohort

Author: Alexis, Neil E., Anderson, Wayne H., Arjomandi, Mehrdad, Barjaktarevic, Igor, Barr, R. Graham, Bateman, Lori A., Bhatt, Surya P., Bleecker, Eugene R., Boucher, Richard C., Bowler, Russell P., Christenson, Stephanie A., Comellas, Alejandro P., Cooper, Christopher B., Couper, David J., Criner, Gerard J., Crystal, Ronald G., Curtis, Jeffrey L., Doerschuk, Claire M., Dransfield, Mark T., Drummond, Brad, Freeman, Christine M., Galban, Craig, Han, MeiLan K., Hansel, Nadia N., Hastie, Annette T., Hoffman, Eric A., Huang, Yvonne, Kaner, Robert J., Kanner, Richard E., Kleerup, Eric C., Krishnan, Jerry A., LaVange, Lisa M., Lazarus, Stephen C., Martinez, Fernando J., Meyers, Deborah A., Moore, Wendy C., Newell, John D., Jr., Paine, Robert, III, Paulin, Laura, Peters, Stephen P., Pirozzi, Cheryl, Putcha, Nirupama, Oelsner, Elizabeth C., O’Neal, Wanda K., Ortega, Victor E., Raman, Sanjeev, Rennard, Stephen I., Tashkin, Donald P., Wells, J. Michael, Wise, Robert A., Woodruff, Prescott G., Postow, Lisa, Viviano, Lisa, Burkes, Robert M., Ceppe, Agathe S., Couper, David, Cooper, Christopher, Labaki, Wassim W., Pirozzi, Cheryl S., Brown, Todd T., and Drummond, M. Bradley
Published: 2020
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40. Unadjusted Lower Limit of Normal for Airflow Obstruction

Author: Bhatt, Surya P, primary, Bodduluri, Sandeep, additional, Nakhmani, Arie, additional, and Oelsner, Elizabeth C., additional
Published: 2024
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41. Lung function decline in former smokers and low-intensity current smokers: a secondary data analysis of the NHLBI Pooled Cohorts Study

Author: Oelsner, Elizabeth C, Balte, Pallavi P, Bhatt, Surya P, Cassano, Patricia A, Couper, David, Folsom, Aaron R, Freedman, Neal D, Jacobs, David R, Jr, Kalhan, Ravi, Mathew, Amanda R, Kronmal, Richard A, Loehr, Laura R, London, Stephanie J, Newman, Anne B, O'Connor, George T, Schwartz, Joseph E, Smith, Lewis J, White, Wendy B, and Yende, Sachin
Published: 2020
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42. Rare and low-frequency exonic variants and gene-by-smoking interactions in pulmonary function

Author: Yang, Tianzhong, Jackson, Victoria E., Smith, Albert V., Chen, Han, Bartz, Traci M., Sitlani, Colleen M., Psaty, Bruce M., Gharib, Sina A., O’Connor, George T., Dupuis, Josée, Xu, Jiayi, Lohman, Kurt, Liu, Yongmei, Kritchevsky, Stephen B., Cassano, Patricia A., Flexeder, Claudia, Gieger, Christian, Karrasch, Stefan, Peters, Annette, Schulz, Holger, Harris, Sarah E., Starr, John M., Deary, Ian J., Manichaikul, Ani, Oelsner, Elizabeth C., Barr, R. G., Taylor, Kent D., Rich, Stephen S., Bonten, Tobias N., Mook-Kanamori, Dennis O., Noordam, Raymond, Li-Gao, Ruifang, Jarvelin, Marjo-Riitta, Wielscher, Matthias, Terzikhan, Natalie, Lahousse, Lies, Brusselle, Guy, Weiss, Stefan, Ewert, Ralf, Gläser, Sven, Homuth, Georg, Shrine, Nick, Hall, Ian P., Tobin, Martin, London, Stephanie J., Wei, Peng, and Morrison, Alanna C.
Published: 2021
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43. Aspirin Use and Respiratory Morbidity in COPD: A Propensity Score-Matched Analysis in Subpopulations and Intermediate Outcome Measures in COPD Study

Author: Alexis, Neil E., Anderson, Wayne H., Barjaktarevic, Igor, Barr, R. Graham, Bleecker, Eugene R., Boucher, Richard C., Bowler, Russell P., Carretta, Elizabeth E., Christenson, Stephanie A., Comellas, Alejandro P., Cooper, Christopher B., Couper, David J., Criner, Gerard J., Crystal, Ronald G., Curtis, Jeffrey L., Doerschuk, Claire M., Dransfield, Mark T., Freeman, Christine M., Han, MeiLan K., Hansel, Nadia N., Hastie, Annette T., Hoffman, Eric A., Kaner, Robert J., Kanner, Richard E., Kleerup, Eric C., Krishnan, Jerry A., LaVange, Lisa M., Lazarus, Stephen C., Martinez, Fernando J., Meyers, Deborah A., Moore, Wendy C., Newell, John D., Jr., Paulin, Laura, Peters, Stephen, Pirozzi, Cheryl, Oelsner, Elizabeth C., O’Neal, Wanda K., Ortega, Victor E., Paine, Robert, III, Putcha, Nirupama, Raman, Sanjeev, Rennard, Stephen I., Tashkin, Donald P., Wells, J. Michael, Wise, Robert A., Woodruff, Prescott G., Fawzy, Ashraf, Aaron, Carrie P., Labaki, Wassim W., Paulin, Laura M., Peters, Stephen P., and Wise, Robert
Published: 2019
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44. Familial Hypercholesterolemia Variant and Cardiovascular Risk in Individuals With Elevated Cholesterol

Author: Zhang, Yiyi, primary, Dron, Jacqueline S., additional, Bellows, Brandon K., additional, Khera, Amit V., additional, Liu, Junxiu, additional, Balte, Pallavi P., additional, Oelsner, Elizabeth C., additional, Amr, Sami Samir, additional, Lebo, Matthew S., additional, Nagy, Anna, additional, Peloso, Gina M., additional, Natarajan, Pradeep, additional, Rotter, Jerome I., additional, Willer, Cristen, additional, Boerwinkle, Eric, additional, Ballantyne, Christie M., additional, Lutsey, Pamela L., additional, Fornage, Myriam, additional, Lloyd-Jones, Donald M., additional, Hou, Lifang, additional, Psaty, Bruce M., additional, Bis, Joshua C., additional, Floyd, James S., additional, Vasan, Ramachandran S., additional, Heard-Costa, Nancy L., additional, Carson, April P., additional, Hall, Michael E., additional, Rich, Stephen S., additional, Guo, Xiuqing, additional, Kazi, Dhruv S., additional, de Ferranti, Sarah D., additional, and Moran, Andrew E., additional
Published: 2024
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45. Repeatability of Pulmonary Quantitative Computed Tomography Measurements in Chronic Obstructive Pulmonary Disease

Author: Motahari, Amin, primary, Barr, R. Graham, additional, Han, MeiLan K., additional, Anderson, Wayne H., additional, Barjaktarevic, Igor, additional, Bleecker, Eugene R., additional, Comellas, Alejandro P., additional, Cooper, Christopher B., additional, Couper, David J., additional, Hansel, Nadia N., additional, Kanner, Richard E., additional, Kazerooni, Ella A., additional, Lynch, David A., additional, Martinez, Fernando J., additional, Newell, John D., additional, Schroeder, Joyce D., additional, Smith, Benjamin M., additional, Woodruff, Prescott G., additional, Hoffman, Eric A., additional, Alexis, Neil E., additional, Arjomandi, Mehrdad, additional, Basta, Patricia, additional, Bateman, Lori A., additional, Bellinger, Christina, additional, Bhatt, Surya P., additional, Boucher, Richard C., additional, Bowler, Russell P., additional, Buhr, Russell G., additional, Christenson, Stephanie A., additional, Criner, Gerard J., additional, Crystal, Ronald G., additional, Curtis, Jeffrey L., additional, Doerschuk, Claire M., additional, Dransfield, Mark T., additional, Drummond, M. Bradley, additional, Freeman, Christine M., additional, Galban, Craig, additional, Gershner, Katherine, additional, Hastie, Annette T., additional, Huang, Yvonne J., additional, Kaner, Robert J., additional, Kesimer, Mehmet, additional, Kleerup, Eric C., additional, Krishnan, Jerry A., additional, Labaki, Wassim W., additional, LaVange, Lisa M., additional, Lazarus, Stephen C., additional, McDonald, Merry-Lynn, additional, Meyers, Deborah A., additional, Moore, Wendy C., additional, Oelsner, Elizabeth C., additional, Ohar, Jill, additional, O’Neal, Wanda K., additional, Ortega, Victor E., additional, Paine, Robert, additional, Paulin, Laura, additional, Peters, Stephen P., additional, Pirozzi, Cheryl, additional, Putcha, Nirupama, additional, Raman, Sanjeev, additional, Rennard, Stephen I., additional, Tashkin, Donald P., additional, Wells, J. Michael, additional, Wise, Robert A., additional, Postow, Lisa, additional, and Viviano, Lisa, additional
Published: 2023
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46. Blood and Urinary Metal Levels among Exclusive Marijuana Users in NHANES (2005–2018)

Author: McGraw, Katlyn E., primary, Nigra, Anne E., additional, Klett, Joshua, additional, Sobel, Marisa, additional, Oelsner, Elizabeth C., additional, Navas-Acien, Ana, additional, Hu, Xin, additional, and Sanchez, Tiffany R., additional
Published: 2023
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47. Association of sputum and blood eosinophil concentrations with clinical measures of COPD severity: an analysis of the SPIROMICS cohort

Author: Alexis, Neil E, Anderson, Wayne H, Barr, R Graham, Bleecker, Eugene R, Boucher, Richard C, Bowler, Russell P, Carretta, Elizabeth E, Christenson, Stephanie A, Comellas, Alejandro P, Cooper, Christopher B, Couper, David J, Criner, Gerard J, Crystal, Ronald G, Curtis, Jeffrey L, Doerschuk, Claire M, Dransfield, Mark T, Freeman, Christine M, Han, MeiLan K, Hansel, Nadia N, Hastie, Annette T, Hoffman, Eric A, Kaner, Robert J, Kanner, Richard E, Kleerup, Eric C, Krishnan, Jerry A, LaVange, Lisa M, Lazarus, Stephen C, Martinez, Fernando J, Meyers, Deborah A, Newell, John D, Jr, Oelsner, Elizabeth C, O'Neal, Wanda K, Paine, Robert, III, Putcha, Nirupama, Rennard, Stephen I., Tashkin, Donald P, Scholand, Mary Beth, Wells, J Michael, Wise, Robert A, Woodruff, Prescott G, Christenson, Stephanie, Ortega, Victor E, Li, Xingnan, Kleerup, Eric, Paine, Richard, III, and Peters, Stephen P
Published: 2017
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48. Frequency of exacerbations in patients with chronic obstructive pulmonary disease: an analysis of the SPIROMICS cohort

Author: Alexis, Neil E, Anderson, Wayne H, Barr, R Graham, Bleecker, Eugene R, Boucher, Richard C, Bowler, Russell P, Carretta, Elizabeth E, Christenson, Stephanie A, Comellas, Alejandro P, Cooper, Christopher B, Couper, David J, Criner, Gerard J, Crystal, Ronald G, Curtis, Jeffrey L, Doerschuk, Claire M, Dransfield, Mark T, Freeman, Christine M, Han, MeiLan K, Hansel, Nadia N, Hastie, Annette T, Hoffman, Eric A, Kaner, Robert J, Kanner, Richard E, Kleerup, Eric C, Krishnan, Jerry A, LaVange, Lisa M, Lazarus, Stephen C, Martinez, Fernando J, Meyers, Deborah A, Newell, John D, Jr, Oelsner, Elizabeth C, O'Neal, Wanda K, Paine, Robert, Putcha, Nirupama, Rennard, Stephen I., Tashkin, Donald P, Scholand, Mary Beth, Wells, J Michael, Wise, Robert A, Woodruff, Prescott G, Quibrera, Pedro M, Comellas, Alejandro, Criner, Gerard, Martinez, Carlos H, Pirozzi, Cheryl B, Rennard, Stephen, Wedzicha, Jadwiga A, Woodruff, Prescott, and Paine, Robert, III
Published: 2017
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49. Smoking intensity (pack/day) is a better measure than pack-years or smoking status for modeling cardiovascular disease outcomes

Author: Nance, Robin, Delaney, Joseph, McEvoy, John W., Blaha, Michael J., Burke, Gregory L., Navas-Acien, Ana, Kaufman, Joel D., Oelsner, Elizabeth C., and McClelland, Robyn L.
Published: 2017
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50. Pulmonary emphysema subtypes defined by unsupervised machine learning on CT scans

Author: Angelini, Elsa D, primary, Yang, Jie, additional, Balte, Pallavi P, additional, Hoffman, Eric A, additional, Manichaikul, Ani W, additional, Sun, Yifei, additional, Shen, Wei, additional, Austin, John H M, additional, Allen, Norrina B, additional, Bleecker, Eugene R, additional, Bowler, Russell, additional, Cho, Michael H, additional, Cooper, Christopher S, additional, Couper, David, additional, Dransfield, Mark T, additional, Garcia, Christine Kim, additional, Han, MeiLan K, additional, Hansel, Nadia N, additional, Hughes, Emlyn, additional, Jacobs, David R, additional, Kasela, Silva, additional, Kaufman, Joel Daniel, additional, Kim, John Shinn, additional, Lappalainen, Tuuli, additional, Lima, Joao, additional, Malinsky, Daniel, additional, Martinez, Fernando J, additional, Oelsner, Elizabeth C, additional, Ortega, Victor E, additional, Paine, Robert, additional, Post, Wendy, additional, Pottinger, Tess D, additional, Prince, Martin R, additional, Rich, Stephen S, additional, Silverman, Edwin K, additional, Smith, Benjamin M, additional, Swift, Andrew J, additional, Watson, Karol E, additional, Woodruff, Prescott G, additional, Laine, Andrew F, additional, and Barr, R Graham, additional
Published: 2023
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