Risk Of Obstructive Pulmonary Disease Research Articles

Follow-up Study A Children Who Are Disordered Pneumonia

Pneumonia is one of significant problems among infections of low airways in children. Morbidity of common-acquired pneumonia (CAP) continues to go in last year’s. Data available in the literature show, that pneumonia with empyema possibly associated with high risk of chronic obstructive pulmonary diseases, asthma and recurrent case of pneumonia in last life. Fatal pneumonia or developing chronic obstruction lung diseases occur mainly in children after severe and complicated forms of pneumonia, this information is presented in native and foreign literature. Currently pneumonia with the heavy and complicated current is a major cause of infant mortality or promotes development of a chronic obstruction lung diseases. Mortality from pneumonia is 3-19% according to different authors. The risk of respiratory diseases in the 3-6 months after pneumonia increased in children who underwent pneumonia. After complicated CAP the complete resolution of the inflammatory happens on 6-9 month. After not complicated САР forms at 10-30% of children radiological changes within 2-6 weeks were noted. In one research it is reported that the full recovery from slow resolving pneumonia at 96% of children has come on 6-8 month of the dispensary period. Some authors in the scientific works use immunomodulators and vaccinations to reduce the residual variation in the lungs and improve recovery time dramatically of pneumonia. In follow up study the important task is a identifying and elimination of risk factors for improvement of treatment and dispensary period for slow resolving pneumonia, recurrent case of pneumonia, sever pneumonia.

Implementation of a COPD Screening Questionnaire in an Outpatient HIV Clinic

ABSTRACTHuman immunodeficiency virus (HIV) is associated with increased risk for chronic obstructive pulmonary disease (COPD); yet substantial under-recognition of COPD exists. We administered a patient-completed, physician-reviewed COPD screening tool in an outpatient HIV clinic to determine whether screening is feasible or possible. Patients attending nonacute, routine HIV care visits were provided a brief COPD screening tool, which included three questions focused on age, respiratory symptoms, and smoking history. Providers were given completed forms for review and ordered spirometry at their discretion. Forms and medical records were subsequently reviewed to determine completion and results of spirometry testing. Of the 1,510 patients screened during the study period, 968 (64%) forms were completed. After excluding 79 incomplete forms, 889 (92%) unique patient forms were included in this analysis. Among these, 204 (23%) met criteria for spirometry referral, among whom physicians ordered spirometry in 64 (31%). At 6 months following study completion, 19 (30%) of the patients referred for spirometry had the test completed, with 5 (26%) demonstrating airflow obstruction. Nearly one out of four HIV patients met indication for screening spirometry and roughly one out of four undergoing spirometry had COPD. Critical drop-offs in the screening and diagnostic process occurred at questionnaire completion and spirometry ordering. Interventions tailored to these critical steps could improve the yield from COPD screening and help to optimize the identification of COPD in high-risk HIV-infected populations. COPD screening in a clinic focused on longitudinal HIV care can effectively identify COPD among those completing the screening continuum.

Nano zerovalent iron particles induce pulmonary and cardiovascular toxicity in an in vitro human co-culture model

Despite promising environmental applications for nano zerovalent iron (nZVI), concerns remain about the potential accumulation and toxic effects of nZVI particles. Here, we use an alveolar-capillary co-culture model to investigate a possible link between low-level epithelial exposure to nZVI and pulmonary and cardiovascular toxicity. While nZVI was unable to pass through the epithelial barrier into the endothelium, nZVI exposure did cause oxidative and inflammatory responses in both epithelial and endothelial cells. Therefore, toxic effects induced by nZVI are not restricted to epithelial cells but can be transferred into the endothelium. Communication between A549 and EA.hy926 cells is responsible for amplification of nZVI-induced toxic responses. Decreases in transepithelial electrical resistance and zonula occludens proteins after epithelial exposure to nZVI impaired epithelial barrier integrity. Increases in oxidized α1-antitrypsin and oxidized low-density lipoprotein in the co-culture model suggest that nZVI exposure increases the risk of chronic obstructive pulmonary disease and atherosclerosis. Therefore, inhalation of nZVI has the potential to induce cardiovascular disease through oxidative and inflammatory mediators produced from the damaged lung epithelium in chronic lung diseases.

DHA May Have a Profoundly Protective Impact on the Lungs of Smokers

Evidence has accumulated over the last twenty years that smokers who frequently ingest fish are at lower risk for both chronic obstructive pulmonary disease (COPD) and lung cancer. Plasma phospholipid levels of DHA, but not EPA, have been reported to correlate inversely with risk for COPD in smokers, suggesting that DHA may be primarily responsible for the apparent protection afforded to lungs of smokers by fish consumption. Meanwhile, evidence is emerging that certain metabolites of DHA - including 4 - hydroxy hexenal (4-HHE), 17 - oxo - DHA, and resolvin D1 - can activate Nrf2 - mediated transcription of heme oxygenase - 1 and other antioxidant / cytoprotective enzymes. Since the oxidant stress imposed by cigarette smoke exposure could be expected to promote peroxidation of membrane DHA and hence boost production of 4 - HHE, DHA in lung membranes may in effect up-regulate the protective feedback mechanism whereby oxidative stress provokes Nrf2 - mediated induction of cytoprotective enzymes. DHA can also give rise to the autacoid resolvin D1, which, via activation of a receptor, suppresses NF - kappaB activation and the consequent production of pro-inflammatory cytokines. Resolvin D1 can also inhibit macrophage NADPH oxidase and promote an anti-inflammatory M2 phenotype in lung macrophages. Not surprisingly, inhalation of resolvin D1 has a marked anti-inflammatory impact on the lungs of mice exposed to tobacco smoke. These considerations help to rationalize the epidemiology linking fish consumption to lung health, and suggest that smokers who can’t or won’t quit their habit would be well advised to consume fish or DHA supplements regularly. Higher intakes of fruits and vegetables - likely in part because many of these contain Nrf2 - activating phytochemicals - likewise are associated with lower risk for COPD, and can be recommended for smokers.

Lung development in the late preterm

An increasing incidence of moderate-to-late prematurity is observed worldwide (6-7% of all births). Moderate-to-late prematurity is a cause of important mortality and morbidity, even when it is just a few weeks before term gestation [1]. Respiratory issues related to moderate prematurity include delayed neonatal transition to air breathing, respiratory distress resulting from delayed fluid clearance, surfactant deficiency, and pulmonary hypertension. There is increasing evidence to support the hypothesis that preterm delivery, even in the absence of any neonatal respiratory disease, may have adverse effects on subsequent lung growth and development, and that these alterations may persist during the early years of life. Premature birth interrupts normal in utero lung development and results in an early transition from the hypoxic intrauterine environment to a comparatively hyperoxic atmospheric environment [2]. Alveolar walls may be thicker, impairing optimal gas exchange. Colin et al. proposed that preterm birth leads to decreased parenchyma elasticity and subsequent airway tethering, a mechanism by which airway wall compliance keeps surrounding alveoli well opened [3]. The long-term significance of reduced airway function early in life has been emphasized in a longitudinal study involving a large group of non-selected infants who had participated in the Tucson Children’s Respiratory study [4]. In this study Stern et al. showed that infants whose pulmonary function was in the lowest quartile also had pulmonary function in the lowest quartile through the years of follow-up until early adulthood. These findings in a normal unselected population, suggest that the level of pulmonary function in early life tracks and changes little with growth. Several authors suggest that deficits in lung function during early life, especially if associated with lower respiratory illnesses, increase the risk of chronic obstructive pulmonary disease in late adult life [5-7]. Of particular importance in this context may be the role played by RSV, which affects most children during their first year of life. The risk of life-threatening RSV infection appears relevant up to a post-conceptional age of 44 weeks. Stein et al. reported that RSV lower respiratory tract illness during the first 3 years of life in a healthy birth cohort was associated with recurrent wheeze up to age 11 [8]. In conclusion altered lung development is a characteristic feature of the late preterm infants and its impact on neonatal and postnatal morbidity needs to be considered.

Chronic Obstructive Pulmonary Disease (COPD) and Vapors, Gases, Dusts, or Fumes (VGDF): A Meta-analysis

To evaluate the association between the risk of chronic obstructive pulmonary disease (COPD) and exposure to vapors, gases, dusts, or fumes (VGDF), we conducted a meta-analysis of epidemiological studies. We searched for studies investigating the relationship between COPD and occupational exposure to VGDF in the adult population. The bibliographic search was conducted in databases (PubMed and Google Scholar). Eleven studies that met predetermined inclusion criteria were included in the meta-analysis. We calculated the pooled odds ratio (OR) with its 95% confidence interval (CI) of COPD for exposure to VGDF using a random-effects model. The presence of publication bias was explored. There was moderate heterogeneity among the included studies (I2 = 54.3%). In a random-effects model meta-analysis, the pooled OR for exposure to VGDF was 1.43 for COPD (95% CI: 1.19–1.73) compared with no exposure to VGDF. Publication bias was not observed in this study. Our study suggests that exposure to VGDF is associated with a higher risk of COPD. Further prospective cohort studies are needed to confirm this association.

Psychosocial Risk Factors for Hospitalisation and Death from Chronic Obstructive Pulmonary Disease: A Prospective Cohort Study

Only a few smaller studies have addressed the effect of psychosocial factors on risk of chronic obstructive pulmonary disease (COPD) in spite of the potential for psychosocial stress to affect development of the disease through immunological and behavioural pathways. The aim of this study is to determine the relation between various psychosocial risk factors, individually and accumulated, and COPD hospitalisation and deaths. A total of 8728 women and men free of asthma and COPD participating in the Copenhagen City Heart Study, were asked comprehensive questions on major life events, work-related stress, social network, vital exhaustion, economic hardship, and sleep medication in 1991–1993 and followed in nationwide registers until 2009, with <2% loss to follow-up. During follow-up, 461 women and 352 men were hospitalized with or died from COPD. Major life events in adult life and vital exhaustion were both associated with a higher risk of COPD in an exposure-dependent manner, with high vital exhaustion being associated with a hazard ratio [HR] of 2.31 (95% CI 1.69–3.16) for women and 2.48 (1.69–3.64) for men. A higher risk of COPD was also found in participants who experienced economic hardship or had a dysfunctional social network. Furthermore, the accumulation of psychosocial risk factors was associated with a higher risk of COPD in both women (HR = 2.40, 1.78–3.22) and men (HR = 1.93, 1.33–2.80). Psychosocial vulnerability may be important to consider both in clinical practice and when planning future preventive strategies against COPD.

Elevated risk of chronic obstructive pulmonary disease in systemic lupus erythematosus: a population-based study

Elevated risk of chronic obstructive pulmonary disease in systemic lupus erythematosus: a population-based study

Conflicting Effects of Occupational Endotoxin Exposure on Lung Health - A Hypothesis- Generating Review of Cancer and COPD Risk

128 Journal of Environmental Immunology and Toxicology Volume 1 Issue 3 Abstract Occupational exposure to endotoxin has been previously associated with increased risk of chronic obstructive pulmonary disease (COPD) and other chronic lung conditions. However, occupational endotoxin exposure has been shown to be associated with a decreased risk of several cancers, including lung cancer. The purpose of this review is to assess the current literature on endotoxin, COPD and lung cancer and generate directions for future research assessing the mechanisms of these contradictory effects of endotoxin on lung health. A systematic literature search was conducted to locate relevant papers in English, published up to June 2012, using Medline and NIOSH-TIC2. Based on the current literature, the mechanisms of endotoxin-related COPD causation and lung cancer protection appear to operate through differential effects of an inflammatory response to inhaled endotoxin. In particular, COPD risk and cancer prevention appear to both be driven by activation of cytokines, including TNF-α and IL-12, through inhaled endotoxin. In addition, genetic polymorphisms and both duration and level of exposure may be important determinants of disease. We recommend that further research on the role of endotoxin and lung disease focus on understanding the effects of the duration or level of exposure to endotoxin necessary for development of COPD, and on determining the stage of tumor development most affected by endotoxins.

Nursing care of painless gastroscopy in patients with presence of hypoxemia risk

Objective To explore the safety of undergoing painless gastroscopy in patients with presence of hypoxemia risk,and summarize the nursing experience.Methods Two hundreds and seven patients undergoing painless gastroscopy from May 2010 to October 2012 were enrolled in this study,who combined with the risk of obesity,age,smoking and chronic obstructive pulmonary disease,etc..The characteristics of hypoxemia and nursing care were analyzed.Results Eighty-seven patients (87/207,42％) occurred hypoxemia in painless gastroscopy,85 cases of which were corrected after increasing oxygen flow and giving high frequency breathing machine ventilation,and 2 cases of which terminated the inspection and recovered after giving mask oxygen and completed the conventional gastroscopy.Conclusions The incidence of hypoxemia in patients with risk factors and painless gastroscopy is higher.Nursing assessment and pre-oxygenation treatment before examination,enhancement the monitoring of respiratory function,management of respiratory tract and cooperation of doctors and nursesnursing are important guarantees to complete examination and reduce hypoxemia risk. Key words: Gastroscopes; Hypoxemia; Nursing care

Angiotensin-converting Enzyme I/D Polymorphism is Associated with COPD Risk in Asian Population: Evidence from a Meta-analysis

Several molecular epidemiological studies were conducted in recent years to evaluate the risk of chronic obstructive pulmonary disease (COPD) associated with insertion/deletion (I/D) polymorphism of angiotensin-converting enzyme (ACE). However, the results remain conflicting rather than conclusive. To derive a more precise estimation of association between ACE polymorphism and the risk of COPD, we performed a meta-analysis from all available relevant studies. We used odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of the association. There was a markedly positive association between the D allele or DD genotype and COPD risk in Asians (D vs. I: OR = 1.55, 95% CI = 1.407–2.44; DD vs. II: OR = 2.53, 95% CI = 1.65–3.89; DD vs. DI/II: OR = 2.09, 95% CI = 1.09–4.03), but this association was not observed in Europeans (D vs. I: OR = 0.93, 95% CI = 0.75–1.15; DD vs. II: OR = 0.86, 95% CI = 0.56–1.33; DD vs. DI/II: OR = 0.88, 95% CI = 0.63–1.23). Our meta-analysis provides strong evidence that D allele and DD homozygous might be significant genetic molecular markers for COPD susceptibility in Asians, but not for Europeans. Additional well-designed large studies were required for the validation of our results.

ANALYSIS OF RISK FACTORS OF RESPIRATORY PATHOLOGY IN FAR NORTH NICKEL INDUSTRY WORKERS

It is known that development of health problems is caused by a combination of genetic, behavioral, environmental and occupational factors. The aim of the study was to identify and quantify the importance of production and non-production risk factors for chronic bronchopulmonary diseases (CBPD) in 1 530 employees of the nickel industry in the Kola North. The study of the structure and prevalence of CBPD showed that the risk of their development was higher in the employees of the electrolysis shop as compared to the workers of the auxiliary shops (RR = 1.81). In the former group of the employees, the highest risk for chronic bronchitis (CB) and chronic obstructive pulmonary disease (COPD) was found in the electrolysis workers (RR = 1.54). In both groups of the workers, the most significant risk factors in the CB and COPD were exposure to tobacco smoke (RR = 2.42-1 1.73) and harmful production impacts (RR = 2.05-13.22). The risk of the developing CB and COPD was also increased by misuse of alcohol (OR = 1.59-2.32) and low physical activity (RR = 1.61-1.97). Causal risk factors for toxic fibrosis were different — age of an employee over 40 years (RR = 6.75) and overweight (OR = 4.44). No risk factors for asthma have been found within the scope of the studied causes. It has been concluded that in determination of the degree of the CBPD development risks in the nickel industry workers, a combination of production and non-production impacts should be taken into consideration. Only improvement of working conditions is not enough to reduce the CBPD risk. The task also requires influence of modifiable non-work related adverse factors, with tobacco smoking being the most important of them.

Roflumilast: A Novel Treatment for Chronic Obstructive Pulmonary Disease

To evaluate the efficacy and safety of roflumilast, approved by the Food and Drug Administration in February 2011 as a treatment to reduce the risk of chronic obstructive pulmonary disease (COPD) exacerbations in patients with severe COPD associated with chronic bronchitis and a history of exacerbations. Literature was retrieved through MEDLINE (1977-December 2011), using the terms roflumilast and COPD. In addition, US government Web sites, including clinicaltrials.gov and fda.gov, were reviewed for pertinent information. Lastly, reference citations from publications identified were reviewed. All articles published in English identified from the data sources were evaluated. For the evaluation of clinical efficacy and safety, only Phase 3 studies were included. Limited treatment options are available for patients with moderate-to-severe COPD and repeated exacerbations. In 6 published Phase 3 trials to date, roflumilast 500 μg daily exhibited modest improvements in lung function, measured by pre- and postbronchodilator forced expiratory volume in 1 second, and reduced rates of moderate and severe exacerbations. Roflumilast was generally well tolerated, with diarrhea, nausea, and headache the most common adverse events seen in clinical trials, although it has also been associated with an increased risk of neuropsychiatric abnormalities and dose-limiting weight loss. The greatest benefit seen with roflumilast was among patients with moderate-to-severe COPD associated with chronic bronchitis along with a recent history of exacerbations. The benefits were demonstrated with monotherapy and in combination with long-acting β(2)-agonists or anticholinergic agents. Despite its only modest benefits in improving lung function and reducing exacerbation rates, roflumilast serves as a safe and effective option in the treatment of COPD.

Geographic Isolation and the Risk for Chronic Obstructive Pulmonary Disease–Related Mortality: A Cohort Study

Geographic Isolation and the Risk for Chronic Obstructive Pulmonary Disease–Related Mortality: A Cohort Study

Hematopoietic cell kinase gene polymorphisms and the risk of chronic obstructive pulmonary disease in a Chinese population

ABSTRACTHematopoietic cell kinase (Hck), a Src family kinase, has been recently suggested to be implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). The present study aims to analyze the association of polymorphism of Hck gene with COPD in a Chinese population. Polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) and polymerase chain reaction–sequence-specific primer method (PCR-SSP) were used to type Hck polymorphisms in 120 patients with COPD and 100 healthy controls. There were significant differences in the genotype and allele distribution of −627 G/T polymorphism in Hck gene between cases and controls (P < .05). The GT genotype was associated with a significantly increased risk of COPD as compared with the GG genotype (Odds ratio [OR] = 2.60, 95% confidence interval [CI]: 1.39–4.48; P = .002). Moreover, individuals carrying T allele had a significantly higher risk for developing COPD than those carrying G allele (OR = 2.19, 95% CI: 1.26–3.79; P = .005). In haplotype analysis, compared with CG(deletion) haplotype, CT(insertion) haplotype was associated with a significantly increased risk of COPD (OR = 2.66, 95% CI: 1.22–5.78; P = .011). These findings suggest the Hck gene polymorphisms may contribute to COPD susceptibility in Chinese population.

Association of SERPINE2 gene with the risk of chronic obstructive pulmonary disease and spirometric phenotypes in northern Han Chinese population

Chronic obstructive pulmonary disease (COPD) is a complex human disease influenced by multiple genes and environmental factors. The SERPINE2 gene has recently been demonstrated to be associated with COPD onset in a non-East Asian population. In this study, we genotyped 20 single nucleotide polymorphisms (SNPs) in SERPINE2 from 310 cases and 203 controls, all of which belong to the Han from North China. Genotype frequencies were compared between the cases and the controls and analyzed for statistical significance. Two SNPs (rs729631 and rs975278), which are in strong linkage disequilibrium (LD) and locate in block 1 on the LD map of our samples, showed significant association both with the risk of COPD and decline in baseline lung function after Bonferroni correction (P < 0.05). This study provides further evidences for SERPINE2 gene as a COPD susceptible gene, and block 1 of SERPINE2 appears to be the genetic variant region that affects the Han Chinese.

XRCC1 Arg194Trp polymorphism and risk of chronic obstructive pulmonary disease

The DNA damage, caused by cigarette smoking, can cause airway cell apoptosis and death, which may be associated with the development of chronic obstructive pulmonary disease (COPD). However, just 20%-30% smokers develop COPD, which suggests that different degrees of DNA repair cause different outcomes in smokers. X-ray repair cross-complementing group 1 (XRCC1), a base excision repair protein, has multiple roles in repairing ROS-mediated, basal DNA damage and single-strand DNA breaks. The present study investigated the association between polymorphism in XRCC1 (Arg399Gln) and susceptibility of COPD. A total of 201 COPD cases and 309 controls were recruited and frequency-matched on age and sex. XRCC1 genotype was determined by PCR-restriction fragment length polymorphism analysis. Overall, compared with those with the XRCC1 Arg/Arg genotype, the risk for COPD had no significant difference among individuals with Trp/Trp genotype. However, after stratifying by smoking status, in former smokers, compared with those with the XRCC1 Arg/Arg genotype, the risk for COPD was significantly reduced among individuals with Trp/Trp genotype (adjusted OR=0.22, 95% CI 0.06-0.85, P=0.028); after stratifying by smoking exposure, in light smokers, compared with those with the XRCC1 Arg/Arg genotype, the risk for COPD was significantly reduced among individuals with Arg/Trp genotype and Trp/Trp genotype (adjusted OR=0.39, 95% CI 0.16-0.94, P=0.036; 0.24, 95% CI 0.07-0.79, P=0.019, respectively). In conclusion, XRCC1 Arg194Trp genotype is associated with a reduced risk of developing COPD among former and light smokers.

Evaluation of Primary DNA Damage, Cytogenetic Biomarkers and Genetic Polymorphisms for CYP1A1 and GSTM1 in Road Tunnel Construction Workers

In tunnel construction workers, occupational exposure to dust (α-quartz and other particles from blasting), gases (nitrogen dioxide, NO2), diesel exhausts, and oil mist has been associated with lung function decline, induction of inflammatory reactions in the lungs with release of mediators that may influence blood coagulation, and increased risk of chronic obstructive pulmonary disease. The present molecular epidemiology study was designed to evaluate whether occupational exposure to indoor pollutants during road tunnel construction might result in genotoxic effects. A study group of 39 underground workers and a reference group of 34 unexposed subjects were examined. Primary and oxidative DNA damage, sister-chromatid exchanges (SCE), and micronuclei (MN) were measured in peripheral blood cells. The possible influences of polymorphisms in gene encoding for CYP1A1 and GSTM1 xenobiotic-metabolizing enzymes were also investigated. Exposure assessment was performed with detailed interviews and questionnaires. There were no significant differences in the level of primary and oxidative DNA damage and frequency of SCE between the tunnel workers and controls, whereas the frequency of MN showed a significant increase in exposed subjects compared to controls. No effects of CYP1A1 or GSTM1 variants were observed for the analyzed biomarkers. Since MN in peripheral blood lymphocytes are recognized as a predictive biomarker of cancer risk within a population of healthy subjects, the genotoxic risk of occupational exposure to various indoor environmental pollutants during road tunnel construction cannot be excluded by this biomonitoring study.

SLC11A1 Polymorphisms Are Associated with the Risk of Chronic Obstructive Pulmonary Disease in a Korean Population

The solute carrier family 11 member 1 (SLC11A1) protein plays important roles in macrophage activation and displays pleiotropic effects on various macrophage functions, including the regulation of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and oxidative burst. Considering the important roles of macrophage in the pathogenesis of chronic obstructive pulmonary disease (COPD), we hypothesized that the SLC11A1 gene may act as a low-penetrance susceptibility gene for COPD. To test this hypothesis, we first examined the frequencies of 12 candidate polymorphisms in the SLC11A1 gene in 27 healthy Korean individuals, and then genotyped 3 haplotype-tagging polymorphisms [IVS4 + 14G > C (rs3731865), D543 N (rs17235409), and (*)86A > G (rs1059823)] in 83 COPD patients and 203 healthy controls. Individuals with at least one variant allele of the D543 N and (*)86A > G polymorphisms were at a significantly increased risk for COPD compared with carriers with each homozygous wild-type allele [adjusted odds ratio (OR) = 2.23, 95% confidence interval (CI) = 1.24-4.02, P = 0.007; and adjusted OR = 1.92, 95% CI = 1.10-3.35, P = 0.022, respectively]. Consistent with the findings of the genotyping analysis, the 122 haplotype carrying both the 543 N and (*)86G alleles was associated with a significantly increased risk for COPD compared with the 111 haplotype with the 542D and (*)86A alleles (adjusted OR = 2.05, 95% CI = 1.19-3.51, P = 0.009 and Bonferroni corrected P = 0.027). These findings suggest that the SLC11A1 polymorphisms could be used as markers for genetic susceptibility to COPD. However, further studies with large numbers of subjects are needed to confirm our findings.

Regular Physical Activity Modifies Smoking-related Lung Function Decline and Reduces Risk of Chronic Obstructive Pulmonary Disease: A Population-based Cohort Study

Regular Physical Activity Modifies Smoking-related Lung Function Decline and Reduces Risk of Chronic Obstructive Pulmonary Disease: A Population-based Cohort Study