Odds Ratio For Chronic Obstructive Pulmonary Disease Research Articles

Prediction of chronic heart failure and chronic obstructive pulmonary disease in a general population: the Tromsø study.

AimsHeart failure (HF) and chronic obstructive pulmonary disease (COPD) are main causes of dyspnoea, and echocardiography and spirometry are essential investigations for these diagnoses. Our aim was to determine the prevalence of HF and COPD in a general population, also how the diseases may be identified, and to what extent their clinical characteristics differ.Methods and resultsIn the seventh survey of Tromsø study (2015–16), subjects aged 40 years or more were examined with echocardiography, spirometry, lung sound recordings, questionnaires, including the modified Medical Research Council (mMRC) questionnaire on dyspnoea, and N‐terminal pro‐brain natriuretic peptide analysis. A diagnosis of HF (HF with reduced ejection fraction, HF with mid‐range ejection fraction, or HF with preserved ejection fraction) or COPD was established according to current guidelines. Predictors of HF and COPD were evaluated by logistic regression and receiver operating characteristic curve analysis. A total of 7110 participants could be evaluated for COPD, 1624 for HF, and 1538 for both diseases. Age‐standardized prevalence of HF was 6.8% for women and 6.1% for men; the respective figures for COPD were 5.2% and 5.1%. Among the 1538 evaluated for both diseases, 139 subjects fulfilled the HF criteria, but only 17.1% reported to have the disease. Of those fulfilling the COPD criteria, 31.6% reported to have the disease. Shortness of breath at exertion was a frequent finding in HF; 59% of those with mMRC ≥2 had HF, while such shortness of breath was found in 24% among those with COPD. Reporting mMRC ≥2 had an odds ratio for HF of 19.5 (95% confidence interval 11.3–33.7), whereas the odds ratio for COPD was 6.3 (95% confidence interval 3.5–11.6). Current smoking was the strongest predictor of COPD but did not predict HF. Basal inspiratory crackles were significant predictors of HF in multivariable analysis. Among the subtypes of HF, an age <70 years was most frequently found in HF with reduced ejection fraction, in 51.7%. Clinical scores based on the predictive value in multivariable analysis of history, symptoms, and signs predicted HF and COPD with areas under the curve of 0.833 and 0.829, respectively.ConclusionsStudy participants with HF and COPD were in most cases not aware of their condition. In general practice, when an elderly patient present with shortness of breath, both diseases should be considered. Previous cardiovascular disease points at HF, while a history of smoking points at COPD. The threshold should be low for ordering echocardiography or spirometry for verifying the suspected cause of dyspnoea.

CHRNA3 and CYP3A5*3 genotype, lung function and chronic obstructive pulmonary disease in the general population

Genetic variations are most likely an additional risk factor besides tobacco smoking per se for the risk of chronic obstructive pulmonary disease (COPD). In this study, we compared genetic variants influencing the effect of smoking on COPD, that is, the effect of the well-known splicing defect polymorphism, CYP3A5*3 (rs776746), identified before genome-wide association studies, with the genome-wide association studies identified CHRNA3 (rs1051730) polymorphism on the risk of decreased lung function and COPD. In all, 10 605 participants from the general population were genotyped. Information on spirometry, hospital admissions and smoking behaviour was recorded. Endpoints were lung function and COPD. For CHRNA3, the percentage of forced expiratory volume in 1 s (FEV1%) predicted was 89.3, 90.6 and 92.4% in homozygous, heterozygous and noncarrier ever-smokers (P-trend<0.001). The corresponding values for forced vital capacity percentage (FVC%) predicted were 94.5, 95.2 and 96.7% (P-trend<0.001), and for FEV1/FVC ratio, the values were 0.753, 0.760 and 0.764 (P-trend=0.008). The odds ratio for COPD in homozygous versus noncarrier ever-smokers was 1.5 [95% confidence interval (CI) 1.3-1.9] for COPD hospitalization, 1.3 (95% CI 1.1-1.6) for COPD defined as FEV1/FVC less than lower limit of normal, 1.3 (95% CI 1.0-1.5) for the Global Initiative for Chronic Obstructive Lung Disease category 1-4 (GOLD 1-4), 1.2 (95% CI 1.0-1.5) for GOLD 2-4 and 1.5 (95% CI 1.1-2.2) for GOLD 3-4. This association could not be found in never-smokers. No association was found for CYP3A5*3. The CHRNA3 genotype is associated with decreased lung function and risk of COPD among ever-smokers, whereas this was not the case for CYP3A5*3.

CHRNA3genotype, nicotine dependence, lung function and disease in the general population

The CHRNA3 rs1051730 polymorphism has been associated to chronic obstructive pulmonary disease (COPD), lung cancer and nicotine dependence in case-control studies with high smoking exposure; however, its influence on lung function and COPD severity in the general population is largely unknown. We genotyped 57,657 adult individuals from the Copenhagen General Population Study, of whom 34,592 were ever-smokers. Information on spirometry, hospital admissions, smoking behaviour and use of nicotinic replacement therapy was recorded. In homozygous (11%), heterozygous (44%) and noncarrier (45%) ever-smokers, forced expiratory volume in 1 s (FEV(1)) was 94.1% predicted, 95.3% pred and 96.5% pred, forced vital capacity (FVC) was 97.1% pred, 97.5% pred and 98.3% pred, and FEV(1)/FVC was 0.770, 0.773 and 0.777, respectively (all p<0.001 for trend). Smoking interacted with genotype on FEV(1) % pred and FEV(1)/FVC (both p<0.001). When adjusted for cumulative tobacco consumption, these associations remained significant. In ever-smokers, odds ratios for COPD in homozygotes versus noncarriers were 1.3 (95% CI 1.2-1.4) for Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages I-IV, 1.4 (95% CI 1.2-1.6) for GOLD II-IV and 1.7 (95% CI 1.3-2.1) for GOLD III-IV. The corresponding value for lung cancer was 1.8 (95% CI 1.2-2.6). Genotype was also associated with daily and cumulative tobacco consumption and with use of nicotinic replacement therapy in former smokers. In ever-smokers, the CHRNA3 rs1051730 genotype associated with reduced lung function and increased COPD severity.

2-adrenergic receptor polymorphisms, asthma and COPD: two large population-based studies

The β(2)-adrenergic receptor (ADRB2) is an important regulator of airway smooth muscle tone. We tested the hypothesis that three functional polymorphisms in the ADRB2 gene (Thr164Ile, Gly16Arg and Gln27Glu) are associated with reduced lung function, asthma or chronic obstructive pulmonary disease (COPD). We first genotyped 8,971 individuals from the Copenhagen City Heart Study for all three polymorphisms. To validate our findings, we genotyped an additional 53,777 individuals from the Copenhagen General Population Study for the Thr164Ile polymorphism. We identified 60,910 Thr164Ile noncarriers, 1,822 heterozygotes and 16 homozygotes. In the Copenhagen City Heart Study, the Thr164Ile genotype was associated with reduced forced expiratory volume in 1 s (FEV(1)) % predicted (trend p = 0.01) and FEV(1)/forced vital capacity (FVC) (p = 0.001): Thr164Ile heterozygotes had 3% and 2% reduced FEV(1) % pred and FEV(1)/FVC, respectively, compared with noncarriers. The odds ratio for COPD in Thr164Ile heterozygotes was 1.46 (95% CI 1.05-2.02). In the Copenhagen General Population Study, the Thr164 genotype associated with reduced FEV(1) % pred (p = 0.04) and FEV(1)/FVC (p < 0.001): Thr164Ile homozygotes and heterozygotes had 7% and 1% reduced FEV(1) % pred and 6% and 1% reduced FEV(1)/FVC, respectively, compared with noncarriers. The odds ratios for COPD in Thr164Ile homozygotes and heterozygotes were 4.53 (95% CI 1.54-13.3) and 1.07 (95% CI 0.92-1.25), respectively. Our results suggest that ADRB2 Thr164Ile is associated with reduced lung function and increased risk of COPD in the general population.

278 Cardiovascular disease is associated with an increased risk of chronic obstructive pulmonary disease in a population screened by spirometry

Chronic Obstructive Pulmonary Disease (COPD) is expected to be the third cause of mortality in the world in 2020. Paradoxically, this disease is widely underdiagnosed and its prevalence remains relatively unknown, in particular in people at cardiovascular risk for whom the association with COPD may worsen the prognosis. The aim of this study was to assess COPD prevalence in a population at cardiovascular risk and to analyse determinants of COPD. Our study was based on patients referred for cardiovascular check-up to a Preventive Cardiology Clinic in a University Hospital in 2009. Participants answered to questionnaires on socio-economic level, medical history and life style. They completed an extensive physical examination and a spirometry test. COPD prevalence was based on the spirometric classification proposed by the Global Initiative for chronic Obstructive Lung Disease. Determinants of COPD were assessed with logistic regression. The sample comprised 502 participants (mean age: 57.4 ± 11.1 years), including 60% of men, 17% of current smokers, 42% of former smokers and 10% of patients with a history of cardiovascular disease (ischemic heart disease, cerebrovascular or peripheral arterial disease). Ten-year risk of coronary heart disease according to the Framingham equation was intermediate (10–20%) for 33% of patients and high (> 20%) for 5%. After exclusion of asthmatic patients, 5.8% [95% CI: 3.9% – 8.2%] were spirometrically screened as COPD patients (Forced Expiratory Volume in one second/Forced Vital Capacity < 0.70). After adjustment for age, gender and smoking, the odds ratio for COPD was 4.44 [1.83–10.78] (p-value = 0.001) in patients with a history of cardiovascular disease compared to those without. Besides, 86% of the patients screened with COPD had never been previously diagnosed. Patients with cardiovascular disease are at increased risk of COPD and thus should beneficiate from COPD screening.

Respiratory symptoms and chronic obstructive pulmonary disease among cement factory workers: Scand J Work Environ Health 2005;31:316–23.

Objectives This study assessed chronic respiratory symptoms and chronic obstructive pulmonary disease (COPD) among workers exposed to cement dust at a Tanzanian cement factory. Methods A total of 120 exposed workers and 107 controls participated in this cross-sectional investigation. Information on demographics, occupational history, chronic respiratory symptoms, smoking habits, and use of respiratory protection equipment was collected by questionnaire. Ventilatory function testing and measurement of personal total dust exposure were also carried out. COPD was diagnosed for workers with chronic bronchitis who also had spirometric airflow obstruction. Chronic respiratory symptoms and COPD were correlated with cumulative total dust exposure and adjusted for age, pack-years, and education. Results The exposed workers had more chronic cough [odds ratio (OR) 4.5, 95% confidence interval (95% CI) 1.9–10.4], chronic sputum production (OR 10.8, 95% CI 4.4–26.4.), dyspnea (OR 5.3, 95% CI 1.9–15.2), work-related shortness of breath (OR 4.8, 95% CI 1.6–14.2), and chronic bronchitis (OR 5.5, 95% CI 2.0–15.3) than the controls. Chronic cough, chronic sputum production, dyspnea, work-related shortness of breath, and chronic bronchitis were significantly related to cumulative dust exposure of 20.0–99.9 and ⩾100.0 versus 3 -years. The prevalence of COPD was higher for the exposed group (18.8%) than for the controls (4.8%). The odds ratio for COPD was significantly increased for cumulative dust exposure, >or=100.0 versus 3 -years (OR 11.2, 95% CI 2.2–56.0). Conclusions Cement workers seem to be at high risk of developing chronic respiratory symptoms and COPD, probably caused by cumulative total dust exposure independent of smoking habits. Reproduced with permission from the Scandinavian Journal of Work, Environment & Health ( www.sjweh.fi ).

Respiratory symptoms and chronic obstructive pulmonary disease among cement factory workers

This study assessed chronic respiratory symptoms and chronic obstructive pulmonary disease (COPD) among workers exposed to cement dust at a Tanzanian cement factory. A total of 120 exposed workers and 107 controls participated in this cross-sectional investigation. Information on demographics, occupational history, chronic respiratory symptoms, smoking habits, and use of respiratory protection equipment was collected by questionnaire. Ventilatory function testing and measurement of personal total dust exposure were also carried out. COPD was diagnosed for workers with chronic bronchitis who also had spirometric airflow obstruction. Chronic respiratory symptoms and COPD were correlated with cumulative total dust exposure and adjusted for age, pack-years, and education. The exposed workers had more chronic cough [odds ratio (OR) 4.5, 95% confidence interval (95% CI) 1.9-10.4], chronic sputum production (OR 10.8, 95% CI 4.4-26.4.), dyspnea (OR 5.3, 95% CI 1.9-15.2), work-related shortness of breath (OR 4.8, 95% CI 1.6-14.2), and chronic bronchitis (OR 5.5, 95% CI 2.0-15.3) than the controls. Chronic cough, chronic sputum production, dyspnea, work-related shortness of breath, and chronic bronchitis were significantly related to cumulative dust exposure of 20.0-99.9 and > or = 100.0 versus <20.0 mg/m3-years. The prevalence of COPD was higher for the exposed group (18.8%) than for the controls (4.8%). The odds ratio for COPD was significantly increased for cumulative dust exposure, > or = 100.0 versus <20.0 mg/m3-years (OR 11.2, 95% CI 2.2-56.0). Cement workers seem to be at high risk of developing chronic respiratory symptoms and COPD, probably caused by cumulative total dust exposure independent of smoking habits.