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BACKGROUND: Improved understanding of the pathways associated with airway pathophysiologic features in COPD will identify new predictive biomarkers and novel therapeutic targets. RESEARCH QUESTION: Which physiologic pathways are altered in the airways of patients with COPD and will predict exacerbations? STUDY DESIGN AND METHODS: We 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. RESULTS: Sputum 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. INTERPRETATION: Biomarker 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 REGISTRY: ClinicalTrials.gov; No.: NCT01969344; URL: www.clinicaltrials.gov

Rationale: Ambient air pollution exposure is associated with respiratory morbidity among individuals with chronic obstructive pulmonary disease (COPD), particularly among those with concomitant obesity. Although people with COPD report high incidence of poor sleep quality, no studies have evaluated the association between air pollution exposure, obesity, and sleep disturbances in COPD. Methods: We analyzed data collected from current and former smokers with COPD enrolled in the Subpopulations and Intermediate Outcome Measures in COPD -Air Pollution ancillary study (SPIROMICS AIR). Socio-demographics and anthropometric measurements were collected, and 1-year mean historical ambient particulate matter (PM(2.5)) and ozone concentrations at participants’ residences were estimated by cohort-specific spatiotemporal modeling. Sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI), and regression models were constructed to determine the association of 1-year PM(2.5 )(1Yr-PM(2.5)) and 1-year ozone (1Yr-ozone) with the PSQI score, and whether obesity modified the association. Results: In 1308 participants (age: 65.8±7.8 years, 42% women), results of regression analyses suggest that each 10µg/m(3) increase in 1Yr-PM(2.5 )was associated with a 2.1-point increase in PSQI (P=0.03). Obesity modified the association between 1Yr-PM(2.5) and PSQI (P=0.03). In obese and overweight participants, a 10µg/m(3) increase in 1Yr-PM(2.5) was associated with a higher PSQI (4.0 points, P

Rationale: Racial residential segregation has been associated with worse health outcomes, but the link with chronic obstructive pulmonary disease (COPD) morbidity has not been established.Objective...

Purpose: Individuals in rural areas of the United States have a greater risk of chronic obstructive pulmonary disease (COPD) and have worse COPD outcomes. New Hampshire (NH) is split between non-rural and rural counties. Methods: We examined differences in COPD exacerbation rates ([encounters per county/county population of 35 years of age and older] × 100), length of stay (LOS), and total charges by rurality, determined by the 2013 National Center for Health Statistics rural-urban classification. Linear regression analysis determined the association of rural status on COPD outcomes, adjusting for age, gender, insurance status, and county-level smoking prevalence. Findings: A total of 15,916 encounters were analyzed, of which 5805 were inpatient and 10,111 were from the emergency department, 7058 (44%) were male, and the mean age was 65.6. A total of 31% were from large, fringe metro counties, 25.9% were from medium metro counties, 37.6% were from micropolitan counties, and 5.5% were from non-core counties. In multivariable regression, rural counties had higher COPD exacerbation rates compared to urban counties (non-core beta=0.18, [confidence interval (CI) 0.16, 0.20]; micropolitan beta=0.02, CI [0.01, 0.03]); medium metro counties (beta=-0.07, Cl [-0.09, -0.06]) had lower rates of COPD exacerbations (P < 0.001 for all). Compared to urban counties, encounters from rural counties had lower total charges (medium metro beta=-1695 [-2410, -980]; micropolitan beta=-2701 [-3315, -2088]; non-core beta=-4453 [-5646, -3260], all p

Background Little is known about the concordance of atopy with asthma COPD overlap. Among individuals with COPD, a better understanding of the phenotypes characterized by asthma overlap and atopy is needed to better target therapies. Research Question What is the overlap between atopy and asthma status among individuals with COPD, and how are categories defined by the presence of atopy and asthma status associated with clinical and radiologic phenotypes and outcomes in the Genetic Epidemiology of COPD Study (COPDGene) and Subpopulation and Intermediate Outcome Measures in COPD Study (SPIROMICS)? Study Design and Methods Four hundred three individuals with COPD from SPIROMICS and 696 individuals from COPDGene with data about specific IgEs to 10 common allergens and mixes (simultaneous assessment of combination of allergens in similar category) were included. Comparison groups were defined by atopic and asthma status (neither, atopy alone, atopic asthma, nonatopic asthma, with atopy defined as any positive specific IgE (≥0.35 KU/L) to any of the 10 allergens or mixes and asthma defined as self-report of doctor-diagnosed current asthma). Multivariable regression analyses (linear, logistic, and zero inflated negative binomial where appropriate) adjusted for age, sex, race, lung function, smoking status, pack-years smoked, and use of inhaled corticosteroids were used to determine characteristics of groups and relationship with outcomes (exacerbations, clinical outcomes, CT metrics) separately in COPDGene and SPIROMICS, and then adjusted results were combined using meta-analysis. Results The prevalence of atopy was 35% and 36% in COPD subjects from SPIROMICS and COPDGene, respectively, and less than 50% overlap was seen between atopic status with asthma in both cohorts. In meta-analysis, individuals with nonatopic asthma had the most impaired symptom scores (effect size for St. George's Respiratory Questionnaire total score, 4.2; 95% CI, 0.4-7.9; effect size for COPD Assessment Test score, 2.8; 95% CI, 0.089-5.4), highest risk for exacerbations (incidence rate ratio, 1.41; 95% CI, 1.05-1.88) compared with the group without atopy or asthma. Those with atopy and atopic asthma were not at increased risk for adverse outcomes. Interpretation Asthma and atopy had incomplete overlap among former and current smokers with COPD in COPDGene and SPIROMICS. Nonatopic asthma was associated with adverse outcomes and exacerbation risk in COPD, whereas groups having atopy alone and atopic asthma had less risk.

BackgroundResearch on cigarettes and adult asthma offers mixed findings, perhaps due to overlap with chronic obstructive pulmonary disease (COPD) and inadequate adjustment for other smoke exposures. Associations between other tobacco products, including e-cigarettes, and asthma are also understudied.Research questionUsing Population Assessment of Tobacco and Health Study waves 2–4 (2014/2015–2016/2017) data, we assessed the relation between tobacco product use and asthma in persons unlikely to have COPD.Study design and methodsProspective study of 10 267 adults aged 18–39 years without COPD diagnoses. Past-month tobacco use at wave 2 was modelled first as combustible versus non-combustible use and second as specific product categories (former, cigarettes, e-cigarettes, cigars, hookah, smokeless tobacco). Outcomes included lifetime asthma prevalence at wave 2, incidence (waves 3 and 4) and Asthma Control Test score (lower=worse). Multivariable regressions adjusted for predictors of asthma, including other smoke exposures: cigarette pack-years, secondhand smoke and marijuana use. Sensitivity analyses examined findings when persons >39 years and those with both COPD and asthma were added, and when smoke exposure adjustments were removed.ResultsNo product, including cigarettes and e-cigarettes, was associated with prevalence or incidence of asthma. Among people with asthma at wave 2, combustible tobacco (beta=−0.86, 95% CI (−1.32 to –0.39)) and cigarettes (beta=−1.14, 95% CI (−1.66 to –0.62)) were associated with worse asthma control. No tobacco product was associated with asthma control over time. In sensitivity analyses, tobacco use became associated with incident asthma as adults >39 years and those with asthma+COPD were added, and as adjustments for other smoke exposures were omitted.InterpretationAlthough cigarette use was associated with worse asthma control, there were no longitudinal associations between combustible tobacco or e-cigarette use and new onset or worsening asthma in these preliminary analyses. Research on tobacco and asthma should exclude COPD and adjust for smoking history and other smoke exposures.

Background: Little is known of the repeatability and reliability of mucociliary clearance (MCC) in former tobacco smokers who have both chronic obstructive pulmonary disease (COPD) and chronic bronchitis (CB). Less is known of the effect of roflumilast, a selective inhibitor of PDE4, on MCC in these patients. Methods: Former tobacco smokers with COPD and CB were treated for 4 weeks with either roflumilast, or placebo, in a randomized, crossover trial. The following were measured on two baseline and two posttreatment visits: MCC values through 90 minutes, following inhalation of (99m)technetium sulfur colloid and gamma camera imaging; outer:inner (O:I) deposition ratio; forced expiratory volume in 1 second (FEV(1)); and symptom scores. Comparisons included: MCC measures through 30 minutes (MCC30), 60 minutes (MCC60), and 90 minutes (MCC90) on the two baseline visits (n = 9) and mean change [(roflumilast − baseline)-(placebo − baseline)] for MCC30, MCC60, MCC90, and FEV(1) (n = 8). Associations between MCC measurements, FEV(1) and O:I ratio with symptom scores were also examined. Results: Pearson correlation tests indicated good repeatability for baseline measures of MCC30, MCC60, and MCC90 and intraclass correlation coefficients indicated good reliability. Only FEV(1) (percent predicted) improved significantly following roflumilast treatment. There were no statistically significant correlations between MCC measures and symptom scores. Lower FEV(1) values were significantly associated with increased shortness of breath (dyspnea), and lower O:I ratios (more inner region deposition) were significantly associated with increased cough and sputum. Conclusions: Measurements of MCC30, MCC60, and MCC90 are repeatable and reliable in former tobacco smokers with both COPD and CB. One month of treatment with roflumilast did not improve MCC in this limited study. Airway narrowing in the larger, central airways of these subjects could lead to decreased FEV(1), increased inner region deposition of the radiolabeled particles, and the associated increase in symptoms of dyspnea, cough, and sputum.

Background Aspirin use in COPD has been associated with reduced all-cause mortality in meta-regression analysis with few equivocal studies. However, the effect of aspirin on COPD morbidity is unknown. Methods Self-reported daily aspirin use was obtained at baseline from SPIROMICS participants with COPD (FEV1/FVC Results Among 1,698 participants, 45% reported daily aspirin use at baseline. Propensity score matching resulted in 503 participant pairs. Aspirin users had a lower incidence rate of total AECOPD (adjusted incidence rate ratio [IRR], 0.78; 95% CI, 0.65-0.94), with similar effect for moderate but not severe AECOPD (IRR, 0.86; 95% CI, 0.63-1.18). Aspirin use was associated with lower total St. George's Respiratory Questionnaire score (β, –2.2; 95% CI, –4.1 to –0.4), reduced odds of moderate-severe dyspnea (modified Medical Research Council questionnaire score ≥ 2; adjusted odds ratio, 0.69; 95% CI, 0.51-0.93), and COPD Assessment Test score (β, –1.1; 95% CI, –1.9 to –0.2) but not 6-min walk distance (β, 0.7 m; 95% CI, –14.3 to 15.6). Conclusions Daily aspirin use is associated with reduced rate of COPD exacerbations, less dyspnea, and better quality of life. Randomized clinical trials of aspirin use in COPD are warranted to account for unmeasured and residual confounding. Trial Registry ClinicalTrials.gov; No.: NCT01969344; URL: www.clinicaltrials.gov

Background Millions of Americans are living in food deserts in the United States, however the role of the local food environment on COPD has not been studied. The aim of this study is to determine the association between food deserts and COPD-related outcomes. Method In this cross-sectional analysis we linked data collected from SPIROMICS (SubPopulations and InteRmediate Outcome Measures in COPD Study) between 2010 and 2015 and food desert data, defined as an underserved area that lacks access to affordable healthy foods, from the Food Access Research Atlas. COPD outcomes include percentage of predicted forced expiratory volume in one second (FEV1%), St. George’s Respiratory Questionnaire (SGRQ), COPD Assessment Test (CAT), 6-min walk distance test (6MWD), exacerbations, and air trapping. We used generalized linear mixed models to evaluate the association between living in food deserts and respiratory outcomes, adjusting for age, gender, race, education, income, marital status, BMI, smoking status, pack years, and urban status Results Among 2713 participants, 22% lived in food deserts. Participants living in food deserts were less likely to be white and more likely to have a lower income than those who did not live in food deserts. In the adjusted model controlling for demographics and individual income, living in food deserts was associated lower FEV1% (β = – 2.51, P = 0.046), higher air trapping (β = 2.47, P = 0.008), worse SGRQ (β = 3.48, P = 0.001) and CAT (β = 1.20, P = 0.003) scores, and 56% greater odds of severe exacerbations (P = 0.004). Results were consistent when looking at food access alone, regardless of whether participants lived in low income areas. Conclusions Findings suggest an independent association between food desert and food access alone with COPD outcomes. Health program planning may benefit from addressing disparities in access to food.

Rationale: Black adults have worse health outcomes compared with white adults in certain chronic diseases, including chronic obstructive pulmonary disease (COPD).Objectives: To determine to what degree disadvantage by individual and neighborhood socioeconomic status (SES) may contribute to racial disparities in COPD outcomes.Methods: Individual and neighborhood-scale sociodemographic characteristics were determined in 2,649 current or former adult smokers with and without COPD at recruitment into SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study). We assessed whether racial differences in symptom, functional, and imaging outcomes (St. George's Respiratory Questionnaire, COPD Assessment Test score, modified Medical Research Council dyspnea scale, 6-minute-walk test distance, and computed tomography [CT] scan metrics) and severe exacerbation risk were explained by individual or neighborhood SES. Using generalized linear mixed model regression, we compared respiratory outcomes by race, adjusting for confounders and individual-level and neighborhood-level descriptors of SES both separately and sequentially.Measurements and Main Results: After adjusting for COPD risk factors, Black participants had significantly worse respiratory symptoms and quality of life (modified Medical Research Council scale, COPD Assessment Test, and St. George's Respiratory Questionnaire), higher risk of severe exacerbations and higher percentage of emphysema, thicker airways (internal perimeter of 10 mm), and more air trapping on CT metrics compared with white participants. In addition, the association between Black race and respiratory outcomes was attenuated but remained statistically significant after adjusting for individual-level SES, which explained up to 12-35% of racial disparities. Further adjustment showed that neighborhood-level SES explained another 26-54% of the racial disparities in respiratory outcomes. Even after accounting for both individual and neighborhood SES factors, Black individuals continued to have increased severe exacerbation risk and persistently worse CT outcomes (emphysema, air trapping, and airway wall thickness).Conclusions: Disadvantages by individual- and neighborhood-level SES each partly explain disparities in respiratory outcomes between Black individuals and white individuals. Strategies to narrow the gap in SES disadvantages may help to reduce race-related health disparities in COPD; however, further work is needed to identify additional risk factors contributing to persistent disparities.

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.

This study aims to determine the impact of physical activity on asthma symptom reporting among children living in an inner city. Among 147 children aged 5–12 years with physician-diagnosed asthma, we assessed asthma symptoms using twice-daily diaries and physical activity using the physical activity questionnaire for children during three 8-day periods (baseline, 3 and 6 months). Linear, logistic, and quasi-poisson regression models were used to determine the association between physical activity and asthma symptoms; adjusting for age, sex, race, BMI, caregiver’s education, asthma severity, medication use, and season. A 1-unit increase in PAQ score was significantly associated with reporting more nocturnal symptoms [risk ratio (RR): 1.03; 95% CI 1.00–1.06], daytime symptoms (RR: 1.04; 95% CI 1.00–1.09), being bothered by asthma (RR: 1.05; 95% CI 1.00–1.09), and trouble breathing (RR: 1.05; 95% CI 1.00–1.10). Level of physical activity should be taken into account in clinical management of asthma and epidemiological studies of asthma symptom burden.

Rationale: Benzodiazepines are associated with mortality and poor outcomes among patients with chronic obstructive pulmonary disease (COPD), but use of benzodiazepines for dyspnea among patients with end-stage disease may confound this relationship. Objectives: Assess the mortality risks of long-term benzodiazepine exposure among patients with COPD and comorbid post-traumatic stress disorder (PTSD), patients with chronic nonrespiratory indications for benzodiazepines. Methods: We identified all patients with COPD and PTSD within the Veteran’s Health Administration between 2010 and 2012. We calculated propensity scores for benzodiazepine use and compared overall and cause-specific mortality of patients with long-term (≥90 d) benzodiazepine use relative to matched patients without use. Secondary analyses assessed propensity-adjusted survival by characteristics of benzodiazepine exposure. Results: Among 44,555 eligible patients with COPD and PTSD, 23.6% received benzodiazepines long term. In the matched sample of 19,552 patients, we observed no mortality difference (hazard ratio [HR] for long-term use, 1.06; 95% confidence interval [CI], 0.95–1.18) but greater risk of death by suicide among those with long-term use (HR, 2.33; 95% CI, 1.14–4.79). Among matched and unmatched patients, short-term benzodiazepine use, but not long-term use, was associated with increased mortality (short-term: HR, 1.16; 95% CI, 1.05–1.28; long-term: HR, 1.03; 95% CI, 0.94–1.13). Conclusions: Risks for respiratory compromise related to long-term benzodiazepine use in COPD may be less than previously estimated, but short-term use of benzodiazepines could still pose a mortality risk. Suicide associated with benzodiazepine use in this population warrants further investigation.

Rationale: In developing countries, poor and rural areas have a high burden of chronic obstructive pulmonary disease (COPD), and environmental pollutants and indoor burning of biomass have been implicated as potential causal exposures. Less is known about the prevalence of COPD in the United States with respect to urban–rural distribution, poverty, and factors that uniquely contribute to COPD among never-smokers. Objectives: To understand the impact of urban–rural status, poverty, and other community factors on COPD prevalence nationwide and among never-smokers. Methods: We studied a nationally representative sample of adults in the National Health Interview Survey 2012–2015, with data linkage between neighborhood data from the U.S. Census’s American Community Survey and the National Center for Health Statistics Urban–Rural Classification Scheme. The main outcome was COPD prevalence. Measurements and Main Results: The prevalence of COPD in poor, rural areas was almost twice that in the overall population (15.4% vs. 8.4%). In adjusted models, rural residence (odds ratio [OR], 1.23; P

Quantitative computed tomographic (CT) imaging can aid in chronic obstructive pulmonary disease (COPD) phenotyping. Few studies have identified whether occupational exposures are associated with distinct CT imaging characteristics.To examine the association between occupational exposures and CT-measured patterns of disease in the SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study).Participants underwent whole-lung multidetector helical CT at full inspiration and expiration. The association between occupational exposures (self-report of exposure to vapors, gas, dust, or fumes [VGDF] at the longest job) and CT metrics of emphysema (percentage of total voxels -950 Hounsfield units at total lung capacity), large airways (wall area percent [WAP] and square-root wall area of a single hypothetical airway with an internal perimeter of 10 mm [Pi10]), and small airways (percent air trapping [percent total voxels -856 Hounsfield units at residual volume] and parametric response mapping of functional small-airway abnormality [PRM fSAD]) were explored by multivariate linear regression, and for central airway measures by generalized estimating equations to account for multiple measurements per individual. Models were adjusted for age, sex, race, current smoking status, pack-years of smoking, body mass index, and site. Airway measurements were additionally adjusted for total lung volume.A total of 2,736 participants with available occupational exposure data (n = 927 without airflow obstruction and 1,809 with COPD) were included. The mean age was 64 years, 78% were white, and 54% were male. Forty percent reported current smoking, and mean (SD) pack-years was 49.3 (26.9). Mean (SD) post-bronchodilator forced expiratory volume in 1 second (FEVIn an analysis of SPIROMICS participants, we found that VGDF exposure in the longest job was associated with an increase in emphysema, and in large- and small-airway disease, as measured by quantitative CT imaging.

Rationale: Links between occupational exposures and morbidity in individuals with established chronic obstructive pulmonary disease (COPD) remain unclear.Objectives: To determine the impact of occupational exposures on COPD morbidity.Methods: A job exposure matrix (JEM) determined occupational exposure likelihood based on longest job in current/former smokers (n = 1,075) recruited as part of the Subpopulations and Intermediate Outcomes in COPD Study, of whom 721 had established COPD. Bivariate and multivariate linear regression models estimated the association of occupational exposure with COPD, and among those with established disease, the occupational exposure associations with 6-minute-walk distance (6MWD), the Modified Medical Research Council Dyspnea Scale (mMRC), the COPD Assessment Test (CAT), St. George’s Respiratory Questionnaire (SGRQ), 12-item Short-Form Physical Component (SF-12), and COPD exacerbations requiring health care utilization, adjusting for demographics, current smoking status, and ...

Introduction Population-based epidemiological evidence suggests that exposure to ambient air pollutants increases hospitalisations and mortality from chronic obstructive pulmonary disease (COPD), but less is known about the impact of exposure to air pollutants on patient-reported outcomes, morbidity and progression of COPD. Methods and analysis The Subpopulations and Intermediate Outcome Measures in COPD (SPIROMICS) Air Pollution Study (SPIROMICS AIR) was initiated in 2013 to investigate the relation between individual-level estimates of short-term and long-term air pollution exposures, day-to-day symptom variability and disease progression in individuals with COPD. SPIROMICS AIR builds on a multicentre study of smokers with COPD, supplementing it with state-of-the-art air pollution exposure assessments of fine particulate matter, oxides of nitrogen, ozone, sulfur dioxide and black carbon. In the parent study, approximately 3000 smokers with and without airflow obstruction are being followed for up to 3 years for the identification of intermediate biomarkers which predict disease progression. Subcohorts undergo daily symptom monitoring using comprehensive daily diaries. The air monitoring and modelling methods employed in SPIROMICS AIR will provide estimates of individual exposure that incorporate residence-specific infiltration characteristics and participant-specific time-activity patterns. The overarching study aim is to understand the health effects of short-term and long-term exposures to air pollution on COPD morbidity, including exacerbation risk, patient-reported outcomes and disease progression. Ethics and dissemination The institutional review boards of all the participating institutions approved the study protocols. The results of the trial will be presented at national and international meetings and published in peer-reviewed journals.

Physical activity enhances uptake of air pollutants in the lung, possibly augmenting their harmful effects on chronic lung disease during exercise.To examine whether benefits of physical activity with respect to the risk of asthma and chronic obstructive pulmonary disease (COPD) are moderated by exposure to high air pollution levels in an urban setting.A total of 53,113 subjects (50-65 yr) from the Danish Diet, Cancer, and Health cohort reported physical activity at recruitment (1993-1997) and were followed until 2013 in the National Patient Register for incident hospitalizations for asthma and COPD. Levels of nitrogen dioxide (NOA total of 1,151 subjects were hospitalized for asthma and 3,225 for COPD during 16 years. We found inverse associations of participation in sports (hazard ratio [95% confidence interval]: 0.85 [0.75-0.96]) and cycling (0.85 [0.75-0.96]) with incident asthma, and of participation in sports (0.82 [0.77-0.89]), cycling (0.81 [0.76-0.87]), gardening (0.88 [0.81-0.94]), and walking (0.85 [0.75-0.95]) with incident COPD admissions. We found positive associations between NOIncreased exposure to air pollution during exercise does not outweigh beneficial effects of physical activity on the risk of asthma and COPD.

Cold temperatures lead to worse outcomes in those with COPD, even after accounting for other environmental factors http://ow.ly/ltCG30bRWnT

Background Ultrasound guidance commonly is used for the placement of central venous catheters (CVCs). The Agency for Healthcare Research and Quality recommends the use of ultrasound for CVC placement as one of its 11 practices to improve patient care. Despite increased access to portable ultrasound machines and comfort with ultrasound-guided CVC access, fewer clinicians are familiar with ultrasound-guided techniques of arterial catheterization. The goal of this systematic review and meta-analysis was to determine the utility of real-time two-dimensional ultrasound guidance for radial artery catheterization. Methods A comprehensive literature search of Medline, Excerpta Medica Database, and the Cochrane Central Register of Controlled Trials by two independent reviewers identified prospective, randomized controlled trials comparing ultrasound guidance with traditional palpation techniques of radial artery catheterization. Data were extracted on study design, study size, operator and patient characteristics, and the rate of first-attempt success. A meta-analysis was constructed to analyze the data. Results Four trials with a total of 311 subjects were included in the review, with 152 subjects included in the palpation group and 159 in the ultrasound-guided group. Compared with the palpation method, ultrasound guidance for arterial catheterization was associated with a 71% improvement in the likelihood of first-attempt success (relative risk, 1.71; 95% CI, 1.25-2.32). Conclusions The use of real-time two-dimensional ultrasound guidance for radial artery catheterization improved first-pass success rate.