Maintenance Pulmonary Rehabilitation: An Update and Future Directions.

The Global Initiative for Chronic Obstructive Lung Disease guidelines recommend pulmonary rehabilitation (PR) for individuals with COPD to improve exercise capacity and health-related quality of life (HRQOL) and reduce symptoms of dyspnea. For cost-effectiveness in COPD care, PR is second only to smoking cessation. However, PR programs typically last 9-12 weeks. The benefits of PR in terms of exercise capacity and HRQOL often decrease toward pre-PR levels as early as 3-6 months after completing PR if patients do not continue to engage in exercise. This review will (1) briefly summarize the efficacy data that informed the 2023 American Thoracic Society (ATS) clinical practice guidelines for maintenance PR, (2) discuss exercise components of maintenance PR studied since 2020 when the last papers were included in the ATS guidelines, (3) explore future directions for delivery of maintenance PR using technology-mediated models, and (4) examine the need for behavior change techniques informed by theoretical models that underpin long-term behavior change. This review will focus on persons with COPD who have completed an out-patient core initial PR program as most of the data on maintenance PR have been published in this patient population. Core PR typically implies a facility-based initial intensive structured program. All patients who complete a core initial PR program should be counseled by PR staff at the discharge visit to engage in ongoing exercise. This usual care is equally as important as referral to a formal PR maintenance program. It is critical to emphasize that usual care after core initial PR means all patients should be supported to participate in regular ongoing exercise, regardless of whether supervised maintenance PR is available. Currently, the optimal frequency, exercise and/or physical activity content, and delivery mode for maintenance PR in persons with COPD and other chronic respiratory diseases remain unknown. Patient safety and degree of in-person supervision required due to the severity of the underlying lung disease need to be considered. Future research of maintenance PR should be underpinned by behavior change techniques. Finally, in the setting of finite resources, balancing the competing priorities of core initial programs with those of maintenance PR programs needs to be achieved.

Indoor and ambient black carbon and fine particulate matter associations with blood biomarkers in COPD patients.

BACKGROUND: Systemic inflammation contributes to cardiovascular risk and chronic obstructive pulmonary disease (COPD) pathophysiology. Associations between systemic inflammation and exposure to ambient fine particulate matter (PM ≤ 2.5 µm diameter; PM2.5), and black carbon (BC), a PM2.5 component attributable to traffic and other sources of combustion, infiltrating indoors are not well described. METHODS: Between 2012 and 2017, COPD patients completed in-home air sampling over one-week intervals, up to four times (seasonally), followed by measurement of plasma biomarkers of systemic inflammation, C-reactive protein (CRP) and interleukin-6 (IL-6), and endothelial activation, soluble vascular adhesion molecule-1 (sVCAM-1). Ambient PM2.5, BC and sulfur were measured at a central site. The ratio of indoor/ambient sulfur in PM2.5, a surrogate for fine particle infiltration, was used to estimate indoor BC and PM2.5 of ambient origin. Linear mixed effects regression with a random intercept for each participant was used to assess associations between indoor and indoor of ambient origin PM2.5 and BC with each biomarker. RESULTS: 144 participants resulting in 482 observations were included in the analysis. There were significant positive associations between indoor BC and indoor BC of ambient origin with CRP [%-increase per interquartile range (IQR);95 % CI (13.2 %;5.2-21.8 and 11.4 %;1.7-22.1, respectively)]. Associations with indoor PM2.5 and indoor PM2.5 of ambient origin were weaker. There were no associations with IL-6 or sVCAM-1. CONCLUSIONS: In homes of patients with COPD without major sources of combustion, indoor BC is mainly attributable to the infiltration of ambient sources of combustion indoors. Indoor BC of ambient origin is associated with increases in systemic inflammation in patients with COPD, even when staying indoors.

Indoor (residential) and ambient particulate matter associations with urinary oxidative stress biomarkers in a COPD cohort.

OBJECTIVES: Oxidative stress contributes to chronic obstructive pulmonary disease (COPD) pathophysiology. Associations between indoor (residential) exposure to particulate matter ≤2.5 µm in diameter (PM2.5) and one of its components, black carbon (BC), and oxidative stress are ill-defined. METHODS: Between 2012 and 2017, 140 patients with COPD completed in-home air sampling over one week intervals, followed by collection of urine samples to measure oxidative stress biomarkers, malondialdehyde (MDA), a marker of lipid peroxidation, and 8-hydroxy-2' -deoxyguanosine (8-OHdG), a marker of oxidative DNA damage. Ambient (central site) BC and PM2.5 were measured, and the ratio of indoor/ambient sulfur in PM2.5, a surrogate for residential ventilation and particle infiltration, was used to estimate indoor BC and PM2.5 of outdoor origin. Mixed effects linear regression models with a participant-specific random intercept were used to assess associations with oxidative biomarkers, adjusting for personal characteristics. RESULTS: There were positive associations (% increase per IQR; 95 % CI) of directly measured indoor BC with total MDA (6.96; 1.54, 12.69) and 8-OHdG (4.18; -0.67, 9.27), and similar associations with both indoor BC of outdoor origin and ambient BC. There were no associations with directly measured indoor PM2.5, but there were positive associations between indoor PM2.5 of outdoor origin and total MDA (5.40; -0.91, 12.11) and 8-OHdG (8.02; 2.14, 14.25). CONCLUSIONS: In homes with few indoor combustion sources, directly measured indoor BC, estimates of indoor BC and PM2.5 of outdoor origin, and ambient BC, were positively associated with urinary biomarkers of oxidative stress. This suggests that the infiltration of particulate matter from outdoor sources, attributable to traffic and other sources of combustion, promotes oxidative stress in COPD patients.

Modification of associations between indoor particulate matter and systemic inflammation in individuals with COPD.

RATIONALE: Little is known about personal characteristics and systemic responses to particulate pollution in patients with COPD. OBJECTIVES: Assess whether diabetes, obesity, statins and non-steroidal anti-inflammatory medications (NSAIDs) modify associations between indoor black carbon (BC) and fine particulate matter ≤2.5 µm in diameter (PM2.5) on systemic inflammation and endothelial activation. METHODS: 144 individuals with COPD without current smoking and without major in-home combustion sources were recruited at Veterans Affairs Boston Healthcare System. PM2.5 and BC were measured in each participant's home seasonally for a week (up to 4 times; 482 observations) and plasma biomarkers of systemic inflammation [C-reactive protein (CRP); interleukin-6 (IL-6)] and endothelial activation [soluble vascular adhesion molecule-1 (sVCAM-1)] measured. Linear mixed effects regression with a random intercept was used, and effect modification assessed with multiplicative interaction terms and stratum specific estimates. RESULTS: Median (25%ile, 75%ile) indoor BC and PM2.5 were 0.6 (0.5,0.7) µg/m3 and 6.8 (4.8,10.4) µg/m3, respectively. Although p-values for effect modification were not statistically significant, there were positive associations (%-increase/interquartile range; 95% CI) between CRP and BC greater among non-statin (18.8%; 3.6-36.3) than statin users (11.1%; 2.1-20.9). There were also positive associations greater among non-statin users between PM2.5 and CRP. For IL-6, associations with BC and PM2.5 were also greater among non-statin users. Associations between CRP and BC were greater (20.3%; 4.5-38.5) in persons with diabetes than without diabetes (10.3%; 0.92-20.6) with similar effects of PM2.5. There were no consistent associations that differed based on obesity. Effect modification was not observed for NSAID use, or with any factor considered with sVCAM-1. CONCLUSIONS: Associations between indoor BC and PM2.5 and CRP were greater in patients with diabetes and those not taking statins, and with IL-6 if not taking statins. These results suggest that these characteristics may modify the systemic response to indoor BC and PM2.5 in persons with COPD.

Predictors of Outpatient Pulmonary Rehabilitation Uptake, Adherence, Completion, and Treatment Response Among Male U.S. Veterans With Chronic Obstructive Pulmonary Disease.

OBJECTIVE: To examine predictors of uptake (never start), adherence (drop out), and completion of pulmonary rehabilitation (PR), as well as PR treatment response based on minimal clinically important difference (MCID) on the 6-minute walk test (6MWT) distance and Chronic Respiratory Questionnaire-Self-Report (CRQ-SR). DESIGN: Retrospective, cohort study. SETTING: Veterans Health Administration. PARTICIPANTS: U.S. veterans with chronic obstructive pulmonary disease (COPD) (N=253) referred to PR between 2010 and 2018. INTERVENTIONS: Outpatient PR program. MAIN OUTCOME MEASURES: Participants completed baseline (time 1) measures of depression (Beck Depression Inventory-II), health-related quality of life (CRQ-SR), self-efficacy (Exercise Self-Regulatory Efficacy Scale [Ex-SRES]), and COPD knowledge. Exercise capacity was assessed with the 6MWT. Participants who completed all 18 sessions of PR repeated assessments (time 2). Logistic regression models examined predictors of uptake, adherence, and completion of PR as well as treatment response based on MCID. RESULTS: Participants were referred to PR with 24.90% never starting, 28.90% dropping out, and 46.20% completing. No differences emerged between never starters and dropouts. Having a history of any cancer increased the likelihood of completing PR (vs never starting; odds ratio [OR], 3.18; P=.003). Greater CRQ-SR dyspnea score, indicating less dyspnea, was associated with increased likelihood of completing PR (OR, 1.12; P=.006). Past smoking compared with current smoking was associated with increased likelihood of completion (OR, 3.89; P≤.002). Those without a history of alcohol use disorder had increased likelihood of completing PR (OR, 2.23; P=.048). Greater baseline 6MWT distance was associated with lower likelihood of achieving MCID in 6MWT (OR, 0.99; P<.001). Greater Ex-SRES was associated with decreased likelihood of achieving 6MWT MCID (OR, 0.98; P=.023). CONCLUSIONS: Findings suggest that early psychoeducation on dyspnea management and smoking and alcohol cessation may increase completion of PR.

The Effect of a web-based physical activity intervention on COPD knowledge: A secondary cohort study.

BACKGROUND: Novel strategies to complement current methods of education delivery by healthcare providers in clinic encounters or in pulmonary rehabilitation are needed to promote COPD self-management. METHODS: We developed a COPD web-based platform that delivers education as part of a physical activity intervention. We examined COPD knowledge in persons with COPD who used a web-mediated, pedometer-based physical activity intervention. Knowledge was assessed with the Bristol COPD Knowledge Questionnaire (BCKQ) at baseline, 3, 6, 9, and 12 months. Scores range from 0 to 100, with higher scores indicating greater knowledge. Repeated measures ANOVA (PROC MIXED, SAS 9.4) examined trends across the 12 months and identified changes from baseline at 3, 6, 9, and 12 months. RESULTS: We enrolled 72 participants with COPD, 93% males with mean ± sd age of 69 ± 7 years and FEV1% predicted of 60 ± 23%. There was a significant increase from baseline to 9 months (p = 0.012), although this increase did not persist at 12 months. Among the 13 topics, participants scored the highest at baseline on smoking knowledge (65.3 ± 17.4) and the lowest on inhaled steroids (9.7 ± 15.4). Across the 12 months, there were significant increases in knowledge about inhaled bronchodilators (p = 0.011) and inhaled steroids (p = 0.035). At 12 months, there were significant improvements in knowledge about exercise (p = 0.004), vaccination (p = 0.027), inhaled bronchodilators (p = 0.002), and inhaled steroids (p = 0.002). CONCLUSION: An internet-mediated intervention may provide another option for COPD education delivery and support for disease self-management.

Molecular markers of aging, exercise capacity, & physical activity in COPD.

BACKGROUND: Exercise capacity (EC) and physical activity (PA) are independent, potentially modifiable predictors of clinical outcomes in COPD. Molecular measures of biological age may help characterize variability in EC and PA observed among COPD patients. METHODS: Veterans with COPD (FEV1/FVC<0.7 or emphysema on chest computed tomography) enrolled in 2 cohorts at VA Boston completed questionnaires, a 6-min walk distance (6MWD) for EC, and blood collection at enrollment. PA data (average daily step count) was collected using an HJ-720 ITC pedometer over ≥5 days. A subset of subjects returned for repeat assessment after 12 weeks. DNA methylation data was generated using the HumanMethylationEPIC platform; epigenetic estimates of biological age and age acceleration were generated using established algorithms. Multivariable models examined the associations between biological age, 6MWD, PA and future acute exacerbations (AEs), adjusting for chronological age, sex, race, smoking status, pack-years, body mass index, cohort, and estimated cell counts. RESULTS: Subjects (n = 269) were predominantly male (98.5%), white (92.9%), and elderly (70.6 ± 8.5 years) with average FEV1% of 57.7 ± 21.1, 6MWD of 374.3 ± 93.5 m, and daily steps of 3043.4 ± 2374 at baseline. In adjusted models, multiple measures of baseline epigenetic age and age acceleration were inversely associated with 6MWD; only GrimAge was inversely associated with PA. Longitudinal change in Hannum-Age was inversely associated with change in EC at 12 weeks (n = 94). No measures of biological age were significantly associated with prospective AEs over 1.3 ± 0.3 years. CONCLUSIONS: Epigenetic measures of biological age are independent predictors of EC and PA, but not AEs, among individuals with COPD.

Physical Activity in Overlap Syndrome of COPD and Obstructive Sleep Apnea: Relationship With Markers of Systemic Inflammation.

STUDY OBJECTIVES: Low physical activity (PA) is associated with poor health outcomes in chronic obstructive pulmonary disease (COPD). Overlap syndrome (OVS), the co-occurrence of COPD and obstructive sleep apnea (OSA), is highly prevalent. Little is known about PA in OVS, and its relationship with markers of systemic inflammation. METHODS: We studied 256 persons with stable COPD, 61 (24%) of whom had OVS, who were well characterized in two previous PA studies. PA was directly assessed with the Omron HJ-720ITC pedometer. C-reactive protein (CRP) and interleukin-6 (IL-6) were assayed from peripheral blood. Linear regression models, adjusting for age and forced expiratory volume in 1 second (FEV1) % predicted, assessed daily step counts and CRP and IL-6 levels in OVS, compared to COPD alone. Linear regression models, adjusting for age, FEV1 % predicted, and coronary artery disease, assessed the relationships between PA and CRP and IL-6 in those with OVS versus those with COPD alone. RESULTS: Compared to COPD alone, persons with OVS walked 672 fewer steps per day (95% CI -1,317 to -28, P = .041). Those with OVS had significantly higher levels of CRP and IL-6 compared to COPD alone. In OVS, each 1,000 fewer steps walked was associated with a 0.875 ng/mL (95% CI 0.767 to 0.997) increase in IL-6, independent of lung function. CONCLUSIONS: Persons with OVS have significantly lower levels of PA and higher levels of inflammatory biomarkers, compared to COPD alone. Lower PA is significantly associated with higher IL-6 levels in OVS.

Effects of Indoor and Ambient Black Carbon and [Formula: see text] on Pulmonary Function among Individuals with COPD.

BACKGROUND: Particulate matter (PM) air pollution has been associated with decreased pulmonary function, but the exposure­response relationship in chronic obstructive pulmonary disease (COPD) patients is uncertain, and most studies have only focused on exposures to ambient pollution. OBJECTIVES: We aimed to assess associations between pulmonary function and indoor and ambient PM [Formula: see text] ([Formula: see text]) and black carbon (BC). METHODS: Between November 2012 and December 2014, 125 patients with COPD (mean age, 73.4 y) who were not currently smoking and without known indoor BC sources were recruited. Indoor BC and [Formula: see text] were measured in each home for a week in each season, up to four times a year, followed by in-person spirometry pre- and post-bronchodilator. Ambient exposures were available from a central site monitor. Multivariable adjusted mixed effects regression models were used to assess associations scaled per interquartile range (IQR) of exposure. RESULTS: There were 367 study visits; the median (IQR) indoor BC and [Formula: see text] were 0.19 (0.22) [Formula: see text] and 6.67 (5.80) [Formula: see text], respectively. Increasing indoor exposures to BC were associated with decreases in pre-bronchodilator forced expiratory volume in 1 s [Formula: see text] and forced vital capacity (FVC), and [Formula: see text]. For example, in multivariable adjusted models, each IQR increase in indoor BC from the weekly integrated filter was associated with a [Formula: see text] [95% confidence interval (CI): [Formula: see text], [Formula: see text]] decrease in pre-bronchodilator [Formula: see text]. Increases in indoor [Formula: see text] were associated with decreases in [Formula: see text] and FVC of smaller magnitude than those for indoor BC; however, the results were less precise. Ambient BC was not associated with pre-bronchodilator pulmonary function, ambient [Formula: see text] was only associated with decreases in FVC and increases in [Formula: see text], and neither indoor nor ambient BC or [Formula: see text] were associated with post-bronchodilator pulmonary function. CONCLUSIONS: Low-level exposures to indoor BC and [Formula: see text], but not ambient exposures, were consistently associated with decreases in pre-bronchodilator pulmonary function. There was no association between exposures and post-bronchodilator pulmonary function. https://doi.org/10.1289/EHP3668.

Indoor black carbon and biomarkers of systemic inflammation and endothelial activation in COPD patients.

RATIONALE: Evidence linking traffic-related particle exposure to systemic effects in chronic obstructive lung disease (COPD) patients is limited. OBJECTIVES: Assess relationships between indoor black carbon (BC), a tracer of traffic-related particles, and plasma biomarkers of systemic inflammation and endothelial activation. METHODS: BC was measured by reflectance in fine particle samples over a mean of 7.6 days in homes of 85 COPD patients up to 4 times seasonally over a year. After the completion of sampling, plasma C-reactive protein (CRP), interleukin-6 (IL-6), and soluble vascular adhesion molecule-1 (sVCAM-1) were measured. Current smokers and homes with major sources of BC were excluded; therefore, indoor BC was primarily a measure of infiltrated outdoor BC. Mixed effects regression models with a random intercept for each participant were used to assess BC effects at different times (1-9 days before phlebotomy) and in the multi-day sample. RESULTS: Measured median BC was 0.19 µg/m3 (interquartile range, IQR=0.22 µg/m3). Adjusting for season, race, age, BMI, heart disease, diabetes, ambient temperature, relative humidity, a recent cold or similar illness, and blood draw time, there was a positive relationship between BC and CRP. The largest effect size was for BC averaged over the previous seven days (11.8% increase in CRP per IQR; 95%CI = 1.8-22.9). Effects were greatest among non-statin users and persons with diabetes. There were positive effects of BC on IL-6 only in non-statin users. There were no associations with sVCAM-1. CONCLUSIONS: These results demonstrate exposure-response relationships between indoor BC with biomarkers of systemic inflammation in COPD patients, with stronger relationships in persons not using statins and with diabetes.

Indoor black carbon of outdoor origin and oxidative stress biomarkers in patients with chronic obstructive pulmonary disease.

OBJECTIVES: We assessed relationships between indoor black carbon (BC) exposure and urinary oxidative stress biomarkers, 8-hydroxy-2'-deoxyguanosine (8-OHdG) and malondialdehyde (MDA), in participants with chronic obstructive pulmonary disease (COPD). METHODS: Eighty-two participants completed in-home air sampling for one week prior to providing urine samples up to four times in a year. Weekly indoor and daily outdoor concentrations were used to estimate indoor daily lags and moving averages. There were no reported in-home BC sources, thus indoor levels closely represented outdoor BC infiltration. Mixed effects regression models with a random intercept for each participant were used to assess relationships between indoor BC and 8-OHdG and MDA, adjusting for age, race, BMI, diabetes, heart disease, season, time of urine collection, urine creatinine, and outdoor humidity and temperature. RESULTS: There were positive effects of BC on 8-OHdG and MDA, with the greatest effect the day before urine collection (6.9% increase; 95% CI 0.9-13.3%, per interquartile range: 0.22 µg/m3) for 8-OHdG and 1 to 4 days before collection (8.3% increase; 95% CI 0.03-17.3% per IQR) for MDA. Results were similar in models adjusting for PM2.5 not associated with BC and NO2 (10.4% increase, 95% CI: 3.5-17.9 for 8-OHdG; 8.1% increase, 95% CI: -1.1-18.1 for MDA). Effects on 8-OHdG were greater in obese participants. CONCLUSIONS: We found positive associations between BC exposure and 8-OHdG and MDA, in which associations with 8-OHdG were stronger in obese participants. These results suggest that exposure to low levels of traffic-related pollution results in lipid peroxidation and oxidative DNA damage in individuals with COPD.

An index of daily step count and systemic inflammation predicts clinical outcomes in chronic obstructive pulmonary disease.

BACKGROUND: Identification of persons with chronic obstructive pulmonary disease (COPD) at risk for acute exacerbations (AEs) targets them for close monitoring. OBJECTIVES: We examined the ability of a novel index combining physical activity and systemic inflammation to identify persons at risk for AEs. METHODS: In an observational cohort study of 167 persons with COPD, we assessed daily step count, a direct measure of physical activity, with the StepWatch Activity Monitor and measured plasma C-reactive protein (CRP) and IL-6 levels. AEs and COPD-related hospitalizations were assessed prospectively over a median of 16 months. Predictors of AEs and COPD-related hospitalizations were assessed using negative binomial models. MEASUREMENTS AND MAIN RESULTS: Median daily step count was 5,203 steps (interquartile range, 3,627-7,024). Subjects with daily step count ≤ 5,203 and CRP > 3 mg/l had an increased rate of AEs (rate ratio [RR], 2.06; 95% confidence interval [CI], 1.30-3.27) and COPD-related hospitalizations (RR, 3.51; 95% CI, 1.73-7.11) compared with subjects with daily step count > 5,203 and CRP ≤ 3 mg/l, adjusting for FEV1% predicted and prednisone use for AE in the previous year. Similarly, subjects with daily step count ≤ 5,203 and IL-6 > 2 pg/ml had an increased rate of AEs (RR, 2.04; 95% CI, 1.14-3.63) and COPD-related hospitalizations (RR, 4.27; 95% CI, 1.56-11.7) compared with subjects with daily step count > 5,203 and IL-6 ≤ 2 pg/ml. CONCLUSIONS: An index combining daily step count and systemic inflammation can predict AEs and COPD-related hospitalizations. A validation study in a separate cohort is needed to confirm the utility of the proposed index as a clinical tool to risk stratify persons with COPD.

Daily step count is associated with plasma C-reactive protein and IL-6 in a US cohort with COPD.

BACKGROUND: Physical activity is an important clinical marker of disease status in COPD. COPD is also characterized by low-grade systemic inflammation. However, the relationship between physical activity and systemic inflammation in COPD is unclear. METHODS: We monitored daily step count, a directly measured physical activity, using the StepWatch Activity Monitor, an ankle-worn accelerometer, in 171 people with stable COPD. Exercise capacity was assessed with the 6-min walk test (6MWT). We measured plasma C-reactive protein (CRP) and IL-6 levels. Linear regression models examined the cross-sectional associations of daily step count and 6MWT distance with CRP and IL-6 levels. RESULTS: Subjects had a mean age 72±8 years and mean FEV1 1.5±0.57 L (54±20% predicted). Median daily step count was 5,203 (interquartile range [IQR], 3,627-7,024], CRP level was 2.4 mg/L (IQR, 1.2-5.0), and IL-6 level was 2.9 pg/mL (IQR, 2.0-5.1). Each 1,000-step increase in daily step count was associated with a 0.94 mg/L and 0.96 pg/mL decrease in CRP (P=.020) and IL-6 (P=.044) levels, respectively, adjusting for age, FEV1 % predicted, pack-years smoked, cardiac disease, current statin use, history of acute exacerbations, and season. There was a significant linear trend of increasing daily step count by quartiles and decreasing CRP (P=.0007) and IL-6 (P=.023) levels. Higher 6MWT distance was also significantly associated with lower CRP and IL-6 values. CONCLUSION: People with COPD who walked the most had the lowest plasma CRP and IL-6 levels. These results provide the conceptual basis to study whether an intervention to promote walking will reduce systemic inflammation in people with COPD.

Dynamic lung mechanics in late-stage emphysema before and after lung volume reduction surgery.

This study evaluated the effects of lung volume reduction surgery (LVRS) on the heterogeneity of lung function in awake, late-stage emphysema patients with measurements taken before and after full recovery from LVRS. We assessed standard clinical measures of lung function and functional heterogeneity in six awake, late-stage emphysema patients before and 6 months after LVRS. Functional heterogeneity was quantified by measuring dynamic inspiratory resistance (R(L)(insp)) and elastance (E(L)(insp)) over a frequency range that included normal breathing ( approximately 0.33-8 Hz). Since LVRS involves targeted resection of emphysematous regions of the lung, we hypothesized that emphysema patients would be functionally more homogeneous post-LVRS. We also compared our measures of functional heterogeneity with indices of anatomic heterogeneity and severity using high-resolution computed tomography (HRCT). After LVRS, 6 min walk distance increased by 22% (940+/-91 versus 1158+/-299, p=0.031) and recoil pressure at TLC increased (9.0+/-2.0 versus 14+/-5, p=0.031), but changes in R(L)(insp) and E(L)(insp) varied greatly between subjects. A measure of anatomic severity quantified using HRCT positively correlated with airway resistance (r(s)=0.89, p=0.048). These results suggest that subjects with more severe disease as assessed by HRCT criteria had reduced overall effective airway caliber consequent to active airway constriction, reduced parenchymal tethering, and/or loss of parallel lung units. Furthermore, LVRS may not necessarily improve lung function via a substantial reduction in mechanical heterogeneity.

Respiratory symptoms and intensity of occupational dust exposure.

OBJECTIVES: Occupational exposure to dusts may result in chronic respiratory symptoms. METHODS: To investigate the utility of obtaining a history of occupational exposure to dust in US veterans, a respiratory health survey was conducted between 1988 and 1992 in a community-based cohort of US veterans in southeastern Massachusetts that were eligible for Veterans' Affairs (VA) healthcare benefits but were not regular users. A mail questionnaire was used to obtain a history of cough, phlegm, and wheeze, work in a dusty job, and duration, type, and intensity of dust exposure. Information on cigarette use and other possible confounders was obtained. RESULTS: In 2,617 white men, after the data had been adjusted for cigarette smoking, age, distance to the nearest major roadway, and chronic respiratory disease, the relative odds of chronic cough, chronic phlegm, and persistent wheeze attributable to occupational dust exposure was increased twofold. Risk also increased, based on exposure intensity. For heavy dust exposure the OR was 1.98 (95% CI 1.39-2.81) for chronic cough, 2.82 (95% CI 2.03-3.93) for chronic phlegm, and 2.70 (95% CI 1.95-3.75) for persistent wheeze. CONCLUSIONS: After active cigarette smoking and other possible confounders had been considered, it was found that dust exposure was related to respiratory symptoms in US veterans and that the greatest risk was attributable to heavy intensity exposure.

Physiological characterization of variability in response to lung volume reduction surgery.

This paper examines potential physiological mechanisms responsible for improvement after lung volume reduction surgery (LVRS). In 25 patients (63 +/- 9 yr; 11 men, 14 women), spirometry [forced expiratory volume in 1 s (FEV(1)) and forced vital capacity (FVC)], lung volumes [residual volume (RV) and total lung capacity (TLC)], small airway resistance, recoil pressures, and respiratory muscle contractility (RMC) were measured before and 4-6 mo after LVRS. Data were interpreted to assess how changes in each component of lung mechanics affect overall function. Among responders (DeltaFEV(1) > or = 12%; 150 ml), improvement was primarily due to an increase in FVC, not to FEV(1)-to-FVC ratio. Among nonresponders, FEV(1), FVC, and RV/TLC did not change after surgery, although recoil pressure increased in both groups. Both groups experienced a reduction in RMC after LVRS. In conclusion, LVRS improves function in emphysema by resizing the lung relative to the chest wall by reducing RV. LVRS does not change airway resistance but decreases RMC, which attenuates the potential benefits of LVRS that are generated by reducing RV/TLC. Among nonresponders, recoil pressure increased out of proportion to reduced volume, such that no increase in vital capacity or improvement in FEV(1) occurred.