Loss Of Forced Expiratory Volume Research Articles

The effect of health-related quality of life and physical activity on time to first exacerbation in chronic obstructive pulmonary disease patients.

It is known that there is a relationship between severe exacerbations of chronic obstructive pulmonary disease(COPD) requiring hospitalization with loss of forced expiratory volume in one second (FEV1), impaired quality of life, and increased mortality. The aim of this study was to investigate factors [health-related quality of life with COPD Assessment Test (CAT), physical activity, FEV1, PaO2] affecting the time to first exacerbation (TTFE) after discharge in patients hospitalized with exacerbation. Seventy-five patients who were hospitalized due to COPD acute exacerbation were included in the study and were prospectively monitored. First exacerbation after discharge was recorded. During the first three days of hospitalization, patients were fitted with a pedometer on any of these days; 24-hour step counts were recorded and CAT was administered through face-to-face interviews. Data on age, sex, PaO2, FEV1, and comorbidities were recorded. The median value of the CAT scores of the participants were taken as the cut-off point. High scores were considered as an indicator of poor quality of life. Cox regression models were created for multivariate analyses and hazard ratios (HR) with 95% confidence interval (95% CI) provided. There was a statistically significant relationship between the TTFE and CAT score (p= 0.001), FEV1 (pred %) (p= 0.02) and PaO2 (p= 0.02). No statistically significant relationship was found between TTFE and the number of steps used as an indicator of physical activity (p= 0.3). In multivariate analysis, age and sex adjusted CAT and PaO2 significantly affected the TTFE (HR= 2.06 CI 95%= 1.17-3.65 and HR= 5.50 CI 95%= 2.09-14.49, respectively) while adjusted FEV1 (pred %) was not significantly affected the TTFE (HR= 1.54 CI 95%= 0.88-2.70). The results of this study suggest that using CAT may be an easy-to-apply and practical tool to help identify patients with an increased risk of exacerbation. No significant correlation was found with the daily number of steps, which is an easily measurable indicator of physical activity.

Ever and cumulative occupational exposure and lung function decline in longitudinal population-based studies: a systematic review and meta-analysis

ObjectivesAdverse occupational exposures can accelerate age-related lung function decline. Some longitudinal population-based studies have investigated this association. This study aims to examine this association using findings reported by longitudinal population-based...

Food Intake REstriction for Health OUtcome Support and Education (FIREHOUSE) Protocol: A Randomized Clinical Trial.

Fire Department of New York (FDNY) rescue and recovery workers exposed to World Trade Center (WTC) particulates suffered loss of forced expiratory volume in 1 s (FEV1). Metabolic Syndrome increased the risk of developing WTC-lung injury (WTC-LI). We aim to attenuate the deleterious effects of WTC exposure through a dietary intervention targeting these clinically relevant disease modifiers. We hypothesize that a calorie-restricted Mediterranean dietary intervention will improve metabolic risk, subclinical indicators of cardiopulmonary disease, quality of life, and lung function in firefighters with WTC-LI. To assess our hypothesis, we developed the Food Intake REstriction for Health OUtcome Support and Education (FIREHOUSE), a randomized controlled clinical trial (RCT). Male firefighters with WTC-LI and a BMI > 27 kg/m2 will be included. We will randomize subjects (1:1) to either: (1) Low Calorie Mediterranean (LoCalMed)—an integrative multifactorial, technology-supported approach focused on behavioral modification, nutritional education that will include a self-monitored diet with feedback, physical activity recommendations, and social cognitive theory-based group counseling sessions; or (2) Usual Care. Outcomes include reduction in body mass index (BMI) (primary), improvement in FEV1, fractional exhaled nitric oxide, pulse wave velocity, lipid profiles, targeted metabolic/clinical biomarkers, and quality of life measures (secondary). By implementing a technology-supported LoCalMed diet our FIREHOUSE RCT may help further the treatment of WTC associated pulmonary disease.

Safety and Efficacy of Steroid Pulse Therapy for Acute Loss of FEV1 in Lung Transplant Recipients After Exclusion of Acute Cellular Rejection

BackgroundThe standard treatment of acute cellular rejection after lung transplantation (LTx) is a high-dose steroid pulse therapy. In our center, this therapy is also the standard of care for LTx recipients with acute loss of forced expiratory volume in 1 second (FEV1), after excluding specific causes such as acute rejection on biopsy. The aim of this retrospective study was to evaluate the safety and efficacy of steroid pulse therapy. MethodsFrom 2015 to 2018, 33 consecutive patients (17 male patients, mean age ± SD, 50.5 ± 12.5 years) were included. All patients underwent routine examinations to exclude acute cellular rejection and other specific causes. FEV1 was routinely measured after 5 days, and 1, 3, and 6 months. Positive response to steroid pulse therapy was defined by increase of FEV1 > 10%. ResultsThe mean decrease ± SD from baseline in FEV1 at the start of steroid pulse therapy was 380 ± 630 mL (P = .02). FEV1 changed after 5 days by 170 ± 180 mL (P = .0007), and after 1 month by 140 ± 230 mL (P = .70), 3 months by −60 ± 240 mL (P = .15), and 6 months by −80 ± 290 mL (P = .73). A positive response was observed in 21% of patients after 3 months and 12% after 6 months. High bronchoalveolar lavage (BAL) eosinophil count correlated with a higher FEV1 after steroid pulse therapy. Serious complications were observed in 4 out of 33 patients (12%) with 1 fatal event (pneumonia). ConclusionsOnly a minority of patients after LTx with loss of FEV1 after exclusion of acute cellular rejection benefit from steroid pulse therapy. Patients with BAL eosinophilia are more likely to respond. However, severe complications were observed.

Smoking exposure, loss of forced expiratory volume in one second and the risk of lung cancer among patients with malignant disease who present with cardiac or pulmonary symptoms: a cross-sectional study

BackgroundSmokers with airway obstruction are at a higher risk of lung cancer than smokers without airway obstruction. Inflammation plays a key role in lung carcinogenesis. This single-center study prospectively assessed (i) the relationship between smoking exposure and the loss of forced expiratory volume in 1 s (FEV1) in determining lung cancer risk and (ii) the effect of lung cancer on systemic inflammation.MethodsThe study group comprised 475 consecutively enrolled patients with cancer who presented with pulmonary or cardiac symptoms. The effects of smoking exposure and FEV1 loss on the predicted lung cancer risk were assessed using multiple logistic regression analysis. C-reactive protein (CRP) was used as a marker of inflammation.ResultsThe prevalence of lung cancer was 0.23. The lung cancer risk increased with the number of pack years and FEV1 loss (p < 0.01). Moving from the 5th (−22% of the predicted value) to the 95th percentile of FEV1 loss (56% of the predicted value) increased lung cancer risk from 0.07 to 0.23 (Δ = 0.16) at 0 pack years and from 0.39 to 0.73 (Δ = 0.34) at 70 pack years (95th percentile). The values for Δ peaked at 61 pack years (0.34) and then decreased with a further increase in smoking exposure, without reaching the zero mark. Patients with lung cancer were more likely to have a CRP level above the median (4.05 mg/L) than patients with other cancers (adjusted odds ratio = 2.67).ConclusionsSystemic inflammation is more pronounced in patients with lung cancer than in patients with other cancers. The effect of FEV1 loss on the patients’ predicted risks of lung cancer increases with increasing smoking exposure. Measurements of FEV1 loss are useful to identify patients facing an increased risk of developing lung cancer.

Excessive longitudinal FEV1 decline and risks to future health: A case–control study

Accelerated loss of forced expiratory volume in 1 s (FEV(1)) in an individual is considered an indicator of developing lung disease. We investigated longitudinal FEV(1) slopes, calculated by simple linear regression, and adverse health outcomes after 10-30 years, among 1,428 chemical plant workers. Cases were defined by FEV(1) slopes below 5th percentile values for the cohort. Cases were matched with controls (107 pairs) for race, gender, smoking status, year of birth, age, height, and calendar year at first test. Matched pair statistics were used for comparisons. Cases had a higher proportion, compared to controls, of diagnosis of COPD or emphysema (17.8% vs. 1.9%, P = 0.0002), medication use for respiratory diseases (24.3% vs. 4.7%, P < 0.0001), dyspnea (15% vs. 3.7%, P = 0.0042), and wheezing or rhonchi on examination (10.3% vs. 1.9%, P = 0.0225). Chemical plant workers who experienced accelerated FEV(1) declines experienced four to nine times as many adverse health conditions over 10-30 years.

The chicken or the egg? Perhaps the egg

Impairment in adult lung function has been associated with increased mortality for a wide range of diseases1 and increased morbidity including risk of chronic pulmonary obstructive disease (COPD∥.2 Decrements in...

Influence of chronic obstructive pulmonary disease on postoperative lung function and complications in patients undergoing operations for primary non–small cell lung cancer

Recent data have suggested that there is a flexibility of borderline values of lung function tests in allowing safe lung resection. The aim of this study was to assess the pattern of postoperative lung function change in patients with chronic obstructive pulmonary disease compared with that of patients with normal lung function, and to compare the operative morbidity and mortality between these groups. The study included 35 patients with chronic obstructive pulmonary disease and a control group of 47 patients with normal lung function who underwent lung resection for non-small cell lung cancer. The percent changes of lung function parameters after lung resection and operative morbidity and mortality were compared between groups. The mean postoperative loss in forced expiratory volume in the 1st second was significantly less in patients with chronic obstructive pulmonary disease who underwent lobectomy compared with that of patients with normal lung function (11.88% vs 24.6%, P < .05); forced expiratory flows at low lung volumes (50% and 25%) improved in patients who underwent lobectomy. The lung function change after pneumonectomy followed the same trend as that after lobectomy. In patients with chronic obstructive pulmonary disease, forced expiratory volume in the 1st second and small airways function significantly improved after preoperative bronchodilator therapy. In the group with chronic obstructive pulmonary disease, operative mortality was 0 and operative morbidity was 51.43%. Because the pattern of lung function change is different in patients with chronic obstructive pulmonary disease compared with that of patients with normal lung function, surgery can be offered to carefully selected patients with lung cancer, even in the presence of severely limited lung function.

Functional Advantage After Radical Segmentectomy Versus Lobectomy for Lung Cancer

Although several reports have recently demonstrated that segmentectomy for small-sized N0 lung cancer leads to recurrence and survival rates equivalent to those associated with lobectomy, controversy regarding the postoperative functional advantage in the former over the latter still persists. The purpose of this study was to evaluate the degree of postoperative functional loss in patients undergoing segmentectomy or lobectomy for lung cancer. We analyzed patients able to tolerate lobectomy, who underwent radical segmentectomy (n = 38) or lobectomy (n = 45) for non-small-cell lung cancer. Functional testing included forced vital capacity, forced expiratory volume in 1 second, and anaerobic threshold measured preoperatively and at 2 and 6 months after surgery. Preoperative function tests showed no differences between segmentectomy and lobectomy patients. A positive and significant correlation was found between the number of resected segments versus loss of forced vital capacity (r = 0.518, p < 0.0001 at 2 months; r = 0.604, p < 0.0001 at 6 months) and loss of forced expiratory volume in 1 second (r = 0.492, p < 0.0001 at 2 months; r = 0.512, p < 0.0001 at 6 months). The postoperative reduction of forced vital capacity (p = 0.0006) and forced expiratory volume in 1 second (p = 0.0007) was significantly less in the segmentectomy group; however, a marginally significant benefit was observed in this group for anaerobic threshold (p = 0.0616). The extent of removed lung parenchyma directly affected that of postoperative functional loss even at 6 months after surgery, and segmentectomy offered significantly better functional preservation compared with lobectomy. These results indicate the importance of segmentectomy for early staged lung cancer.

Factor V Leiden Homozygosity, Dyspnea, and Reduced Pulmonary Function

Factor V Leiden homozygosity predisposes patients to deep venous thrombosis and major pulmonary thromboembolism. Consequently, factor V Leiden homozygosity could, via unrecognized repeated minor pulmonary thromboemboli, cause chronic pulmonary disease. We tested the hypothesis that factor V Leiden homozygosity is associated with pulmonary symptoms and signs. We studied a general population sample of 9253 individuals from the Copenhagen City Heart Study who were examined in 1991-1994. Of these, 6475 participants were also examined in 1976-1978 and/or 1981-1983. End points were dyspnea and lung function. Among 20 factor V Leiden homozygotes, a mean +/- SD of 32% +/- 11% had severe dyspnea compared with 6% +/- 0.3% of 8534 noncarriers (chi(2) test; P<.001). The corresponding adjusted odds ratio for severe dyspnea was 5.4 (95% confidence interval, 1.9-15.7). During follow-up, forced expiratory volume in 1 second and forced vital capacity were 5% to 10% lower in homozygotes vs noncarriers (analysis of variance; P = .003 and P = .03). The annual mean +/- SD loss of forced expiratory volume in 1 second and forced vital capacity was 39 +/- 8 mL/y and 35 +/- 8 mL/y in homozygotes vs 21 +/- 10 mL/y and 15 +/- 10 mL/y in noncarriers (t test; P = .03 and P = .04), respectively. Factor V Leiden heterozygosity (n = 699) did not influence pulmonary symptoms and signs. We demonstrate a previously unrecognized clinical presentation of factor V Leiden homozygosity with severe dyspnea and decreased pulmonary function.

Airway remodeling and long-term decline in lung function in asthma.

Asthma is a heterogeneous disease that frequently shows progression of airway obstruction. There are indications that ongoing airway inflammation is responsible for the more severe hyperresponsiveness, lower lung function, and accelerated loss of forced expiratory volume in 1 second. At this moment, we are not well informed about the contributing factors to and the exact relation between airway inflammation and airway remodeling. Exciting new findings during the past years are the potential role of interleukin-13, the further exploration of the epithelial-mesenchymal trophic unit, and the presence of degranulated mast cells in smooth muscle bundles from the bronchi.

New therapeutic drugs in the management of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease remains a major health problem for which new and improved treatments are desperately needed. Recent trials strongly suggest that treatments are improving. Longer-acting bronchodilators will be more convenient and may have additional advantages. Combinations of bronchodilators may offer additive effects and, possibly, synergies. Inhaled glucocorticoids, although unable to alter the loss of forced expiratory volume in 1 second when used alone, may reduce exacerbation frequency and health status deterioration and improve mortality. These clinically meaningful goals represent end points not previously targeted in chronic obstructive pulmonary disease drug development. Moreover, inhaled glucocorticoids may offer benefits in combination with long-acting beta-agonists. Finally, new classes of agents such as the phosphodiesterase inhibitors are on the horizon. The prospect for better treatment of chronic obstructive pulmonary disease looks brighter than ever. Caution is required, however. Much of the excitement has been generated by small studies, presented only in abstract form, and as yet unpublished work. Therapeutic recommendations will require publication of appropriately designed and adequately powered clinical trials.

The role of genotype in determining the effects of cigarette smoking on pulmonary function

The effect of cigarette smoking on pulmonary function is highly variable. Some heavy smokers retain normal pulmonary function and others experience profound pulmonary function loss. The role of genotype in this process is unknown. We tested for gene by environment interaction (GxE) in smoking-associated loss of forced expiratory volume in one second (FEV1) using repeated pulmonary function and smoke-exposure measures from 352 twin pairs enrolled in the NHLBI Male Veteran Twin Study. Inferences using global [Jinks and Fulker, 1970] and dichotomous [Ramakrishnan et al., 1992] procedures were supplemented with a new model for repeatedly observed twinships. The model facilitates testing of standard heritability hypotheses and families of hypotheses regarding the dependence of quantitative twin-twin phenotypic similarity on continuously varying twin-twin exposure concordance. The global and dichotomous procedures were suggestive of GxE in smoke-associated loss of FEV1 (p < 0.01, p = 0.08, respectively). With the new model, overall twin-twin correlation of FEV1 for concordant-smoking MZ and DZ twin pairs was estimated at 0.71 and 0.34, respectively. For twins with little or no difference in cigarette use, the intra-pair correlations of FEV(1) did not differ according to cigarette exposure over a wide range of exposures (0 - > or = 200 pack years). Even great twin-twin discordance in cigarette smoking (> or =10 pack years) had little effect of correlations. We conclude that a constant factor, such as genotype, appears to be interposed between the environmental toxin (cigarette smoke) and phenotype (FEV1).

Loss of lung function among sheet metal workers: ten-year study.

One hundred and twenty-two sheet metal workers in New England were examined over a 10-year interval for loss of pulmonary function and the development of asbestosis or asbestos-related pleural fibrosis. Regression models using the generalized estimating equation (GEE) approach were created to investigate the relationship between exposure and pulmonary function after adjusting for smoking status, age, height, and asbestos-related x-ray changes. A history of shipyard work was a significant contributor to the loss of forced vital capacity (FVC). Among smokers, loss in forced expiratory volume at 1 sec (FEV1) also had a significant relationship to prior shipyard work. There was a borderline significant relationship between percentage predicted FEV1 and cumulative years of asbestos exposure in smokers, as well as years-since-initial-exposure in never-smokers. This study supports previous findings of obstructive airway changes in asbestos-exposed workers and identifies shipboard work as an important predictor of loss in pulmonary function even years after shipyard exposure to asbestos has ceased.

Gender difference in smoking effects on lung function and risk of hospitalization for COPD: results from a Danish longitudinal population study

Recent findings suggest that females may be more susceptible than males to the deleterious influence of tobacco smoking in developing chronic obstructive pulmonary disease (COPD). This paper studies the interaction of gender and smoking on development of COPD as assessed by lung function and hospital admission. A total of 13,897 subjects, born after 1920, from two population studies, 9,083 from the Copenhagen City Heart Study (CCHS) and 4,814 from the Glostrup Population Studies (GPS), were followed for 7-16 yrs. Data were linked with information on hospital admissions caused by COPD. Based on cross-sectional data, in the CCHS the estimated excess loss of forced expiratory volume in one second (FEV1) per pack-year of smoking was 7.4 mL in female smokers who inhaled and 6.3 mL in male smokers who inhaled. In the GPS, the corresponding excess loss of FEV1 was 10.5 and 8.4 mL in females and males, respectively. Two hundred and eighteen subjects in the CCHS and 23 in the GPS were hospitalized during follow-up. Risk associated with pack-years was higher in females than in males (relative risks (RRs) for 1-20, 20-40 and >40 pack-years were 7.0 (3.5-14.1), 9.8 (4.9-19.6) and 23.3 (10.7-50.9) in females, and 3.2 (1.1-9.1), 5.7 (2.2-14.3) and 8.4 (3.3-21.6) in males) but the interaction term gender x pack-years did not reach significance (p=0.08). Results were similar in the GPS. After adjusting for smoking in more detail, females in both cohorts had an increased risk of hospitalization for COPD compared to males with a RR of 1.5 (1.2-2.1) in the CCHS and 3.6 (1.4-9.0) in the GPS. This was not likely to be caused by a generally increased rate of hospital admission for females. Results were similar when including deaths from COPD as endpoint. In two independent population samples, smoking had greater impact on the lung function of females than males, and after adjusting for smoking females subsequently suffered a higher risk of being admitted to hospital for COPD. Results suggest that adverse effects of smoking on lung function may be greater in females than in males.

Occupation and chronic obstructive pulmonary disease (COPD)

Chronic bronchitis, defined as increased cough and sputum production, is well established as an occupational disease independent of cigarette smoking, which is a major confounding factor. The relevance of industrial exposure to the development of airflow obstruction (chronic obstructive pulmonary disease (COPD)) is more controversial. Good data exist linking the inhalation of cadmium fume to the development of emphysema. The pathology of airflow obstruction due to other occupational exposures is less clear. The principal measure of occupational bronchitis with airflow obstruction is accelerated loss of forced expiratory volume in one second (FEV1); and epidemiology is the principal tool for investigation. Using these methods, many workers have established links between occupational exposure and disease, which will be reviewed. From an occupational standpoint tobacco smoking is unique, in that the pollutant is put into the mouth and deliberately inhaled in concentrations far exceeding occupational exposures. Despite this, less than 20% of smokers develop significant airflow obstruction. The factors which determine whether an individual smoker develops airflow obstruction are usually unknown. There are two ways in which an occupational agent may act: 1) by promoting the deleterious effects of smoking; or 2) by acting in a manner similar to tobacco smoking, requiring other promoting factors before an effect is seen. Examples will be given of both of these mechanisms. From a pragmatic point of view, it is highly unlikely that the mixed agents in tobacco smoke are the only cause of significant COPD. The widespread habit of tobacco smoking in industrial populations has delayed the recognition of other factors contributing to disease, as it is only possible to examine the independent risks of smoking and occupational exposures when a reasonable proportion of those occupationally exposed are lifelong nonsmokers. The studies of specific workforces are often difficult to interpret, as workers commencing exposure in jobs with a high risk of lung disease have even better lung function than the normal worker, and losses from a cohort are higher in those with disease, leading to lower estimates of risk as an increasingly smaller proportion of survivors are followed-up. These problems have been overcome by sampling the general population away from the workplace. Such studies suffer from less selection bias (but exclude those who have died prematurely), and have less satisfactory estimates of occupational exposure, usually including a greater proportion of those with low exposure and, thus, reducing the relative risks of exposure. Such studies have included a general older working population in Beijing (China) [1], an urban and rural population in Norway [2], a rural population in Northern Italy [3], and two studies of city dwellers designed to investigate air pollution in France [4] and the USA [5]. Different outcome measures have been used, but all show significant excess risks with occupation. In general, dust exposure is associated with higher risks of reduced lung function than gas or fume exposure [1, 5], with relative risks of around 1.5. General population samples have been studied longitudinally in Paris [6], Cracow (Poland) [7], Zutphen (Holland) [8] and Bergen (Norway) [9]. The Zutphen study again started with a community sample, using a job matrix to link symptoms and diagnoses with the occupation. The study has been analyzed longitudinally, initially using the time, intensity and duration of exposure. The longitudinal analysis found a cumulative 25 yr incidence of chronic nonspecific lung disease of 27.9%. Incidence density ratios were calculated, and ratios for smoking increased from 1.5 for light smokers to 4.5 for those smoking more than 20 cigarettes daily. Increased risks of chronic nonspecific lung disease (which includes asthma), were found in a number of occupations which are shown in table 1. A further analysis of this study, by the same group, appears in this issue of the Journal [10], using a different job exposure matrix generated from the sample itself. It is disappointing that the results of the reanalysis are less clear than the original analysis, perhaps because of the lack of differentiation between the proportion of the workforce exposed to a particular agent, and its intensity. The mortality analysis was limited by the small number of deaths (33 out of 799) due to chronic nonspecific lung disease. Nevertheless, for occupational groups where at

Risk factors associated with longitudinal change in pulmonary function.

In a longitudinal study of pulmonary function, we investigated the relationship between loss of forced expiration over time and a series of potential risk factors, as well as 4 other measures of pulmonary function at initial visit. Data on 1,912 adults tested twice, with an average of 4.7 yr between visits, were used. Of the potential risk factors examined, only age and smoking were consistently associated with increased loss of forced expiratory function in both men and women. Statistically significant differences among ABO blood types and among Pi types were also seen in women, although the direction of these differences was unexpected in that non-Z Pi variant phenotypes showed less decline in pulmonary function than did the most common Pi M phenotypes. Similar patterns of differences were seen in men, although these were not statistically significant. Of 4 initial-visit pulmonary function measures examined, only closing capacity at initial visit was consistently associated with subsequent loss of forced expiratory volume in one second (delta FEV1) in both men and women. The final predictive model for delta FEV1 accounted for a modest proportion of the total variation seen in this sample, however, limiting its potential use for predicting decline in pulmonary function over a 5-yr span in individual subjects.

Precipitous fall of the forced expiratory volume

Two patients are described who showed a precipitous loss of forced expiratory volume from normal to low levels within a few years. They did not have bronchial asthma and we suggest that this pattern of deterioration may occur occasionally in patients before they attend hospital with the symptoms of chronic bronchitis.