Self-reported influenza vaccination and protective serum antibody titers in a cohort of COPD patients.

BACKGROUND: COPD patients are advised vaccination against seasonal influenza, yet few studies have evaluated the protective antibody titers obtained in this patient group. AIMS: 1) To describe protective titers in COPD patients who self-reported influenza vaccination compared with vaccinated subjects without COPD and unvaccinated COPD patients, 2) analyze whether clinical parameters predicted influenza-specific antibody titers, and 3) whether antibody titers to influenza A at baseline could predict exacerbation risk or 5 years all-cause mortality. METHODS: Influenza A (H1N1 and H3N2) titers were measured by haemagglutination inhibition assay in serum from 432 COPD patients and 77 controls in the Bergen COPD Cohort Study, at yearly visits between 2006/09. Titers of 40 or above were considered protective. We examined the variables sex, age, body composition, smoking, GOLD stage, yearly exacerbations, inhaled steroids, and Charlson score as predictive of titers, both univariately and in a multivariable model estimated by generalized estimating equations. The exacerbation incidence rate ratios and mortality hazard ratios were assessed by negative binominal and cox regression models respectively. RESULTS: At baseline, 59% of COPD patients reported influenza vaccination during the last season. Levels of predictive titers varied considerably each season, but trended lower in COPD patients compared with controls. Neither sex, age, body composition, smoking, comorbidities, GOLD stage nor use of inhaled steroids consistently predicted titers. Having high titers at baseline did not impact later risk for exacerbations, but seemed to be associated with higher all-cause mortality, even after adjustment for COPD disease characteristics. CONCLUSION: Vaccination coverage for influenza is imperfect for COPD patients in Norway, and there is a concern that immunization is suboptimal.

Predictors for PaO2 and hypoxemic respiratory failure in COPD-A three-year follow-up.

BACKGROUND: Knowledge about predictors for developing hypoxemia in the course of chronic obstructive pulmonary disease (COPD) progression is limited. The objective of the present study was to investigate predictors for overall PaO2, for a potential change in PaO2 over time, and for first occurrence of hypoxemia. METHODS: 419 patients aged 40-76 years with COPD GOLD stages II-IV underwent clinical and pulmonary function measurements, including repeated arterial blood gases over three years. Airway obstruction, lung hyperinflation, markers of systemic inflammation and cardiovascular health, exacerbation frequency, smoking habits, and body composition were tested as possible predictors of PaO2 and first episode of hypoxemia. RESULTS: In multivariate adjusted longitudinal analyses, forced expiratory volume in 1 second, total lung capacity and functional residual capacity (all in% predicted), resting heart rate and fat mass index were all associated with overall PaO2 (all P < 0.005). We found no change in PaO2 over time (ρ = 0.33), nor did we find evidence that any of the tested variables predicted change in PaO2 over time. In multivariate adjusted survival analyses, functional residual capacity and resting heart rate were predictors of episodic hypoxemia (both ρ < 0.005). CONCLUSIONS: This longitudinal study identified pulmonary, cardiac and metabolic risk factors for overall PaO2 and episodic hypoxemia, but detected no change in PaO2 over time.

Body composition and plasma levels of inflammatory biomarkers in COPD.

Previous studies suggest a relationship between systemic inflammation and body composition in chronic obstructive pulmonary disease (COPD). We examined the relationships between body composition (fat free mass index (FFMI) kg·m(-2) and fat mass index (FMI) kg·m(-2)) and three plasma inflammatory markers C-reactive Protein (CRP), soluble tumour necrosis factor receptor 1 (sTNF-R1) and osteoprotegerin (OPG) in 409 stable COPD patients (aged 40-75 yrs, Global Initiative for Obstructive Chronic Lung Disease (GOLD) categories II-IV, 249 male) from the Bergen COPD Cohort Study in Norway. FFMI and FMI were measured by bioelectrical impedance. Plasma CRP (µg·mL(-1)), sTNF-R1 (pg·mL(-1)) and OPG (ng·mL(-1)) were determined by enzyme immunoassays. Correlations and Kruskal-Wallis tests were used for bivariate analyses. Linear regression models were fitted for each of the three markers, CRP, sTNF-R1 and OPG, with FFMI and FMI as explanatory variables including sex, age, smoking habits, GOLD category, hypoxaemia, Charlson Comorbidity Index and inhaled steroid use as potential confounders. CRP and sTNF-R1 levels correlated positively with both FFMI and FMI. The adjusted regression coefficients for an increase in logCRP per unit increase in FFMI was 1.23 (1.14-1.33) kg·m(-2) and 24.9 (11.8-38.1) kg·m(-2) for sTNF-R1. Higher FMI was associated with a lower OPG, with adjusted regression coefficient -0.14 (-0.23- -0.04), whereas FFMI was unrelated to OPG. In conclusion, COPD patients with low FFMI had lower not higher plasma levels of CRP and sTNF-R1, whereas higher fat mass was associated with higher CRP and sTNF-R1 and lower OPG.

Socioeconomic risk factors for lung function decline in a general population.

The aim of our study was to examine sex-specific associations between different aspects of socioeconomic status (SES) (educational level, occupational status, income) and lung function in a general adult population. In the Hordaland County Cohort Study, 1,644 subjects aged 26-82 yrs at baseline answered questionnaires and performed post-bronchodilator spirometry both in 1996-1997 and in 2003-2006. We performed adjusted linear regression analysis on the effect of SES on decline in forced experimental volume in 1 s (FEV(1)), forced vital capacity (FVC) and FEV(1)/FVC. Mean annual decline in FEV(1) from baseline to follow-up was 57 mL (se 1.3) and 48 mL (se 1.0) for males and females, respectively. Males had a larger decline in FVC than females, while females had a larger decline in FEV(1)/FVC. Lower education and low occupational status were associated with larger male lung function decline. SES did not affect female lung function decline. However, marital status was a significant predictor; unmarried females had less decline than both married and widowed females in both FEV(1) (adjusted mean annual difference 8 mL and 16 mL) and FVC (adjusted mean annual difference 8 mL and 18 mL). Low SES was associated with increased lung function decline in males. For females, marital status was more important.

Systemic inflammatory markers in COPD: results from the Bergen COPD Cohort Study.

Chronic obstructive pulmonary disease (COPD) is considered an inflammatory pulmonary disorder with systemic inflammatory manifestations. The aim of this study was to assess the systemic levels of six inflammatory mediators in a large cohort of COPD patients and controls. 409 COPD patients and 231 healthy subjects, aged 40-75 yrs, were included from the first phase of the Bergen COPD Cohort Study. All COPD patients were clinically diagnosed by a physician, and had a forced expiratory volume in 1 s/forced vital capacity ratio less than 0.7 and a smoking history of >10 pack-yrs. The plasma levels of C-reactive protein (CRP), soluble tumour necrosis factor receptor (sTNFR)-1, osteoprotegrin, neutrophil activating peptide-2, CXCL16 and monocyte chemoattractant protein-4 were determined by ELISA. After adjustment for all known confounders, COPD patients had significantly lower levels of osteoprotegrin than subjects without COPD (p<0.05), and higher levels of CRP (p<0.01). Among COPD patients, CRP was elevated in patients with frequent exacerbations (p<0.05). sTNFR-1 and osteoprotegrin were both related to Global Initiative for Chronic Obstructive Lung Disease stage and frequency of exacerbations in the last 12 months (p<0.05). In addition, sTNFR-1 was significantly associated with important comorbidities such as hypertension and depression (p<0.05). The present study confirms that certain circulating inflammatory mediators are an important phenotypic feature of COPD.

Decline in respiratory symptoms in service workers five months after a public smoking ban.

OBJECTIVE: To evaluate the effect of a total ban on smoking indoors in restaurants and other hospitality business premises in Norway, on respiratory symptoms among workers in the industry. METHODS: Phone interviews with 1525 employees in the hospitality business were conducted immediately before the enacting of the law. In a follow-up study five months later, 906 of the workers from the baseline sample participated. Questions were asked on demographic variables, passive smoking exposure, personal smoking, attitudes towards the law, and five respiratory symptoms. Change in symptom prevalence was analysed with McNemar's test and with analysis of variance (ANOVA) for repeated measures. RESULTS: The prevalence of all five symptoms declined after the ban; for morning cough from 20.6% to 16.2% (p < 0.01); for daytime cough from 23.2% to 20.9%; for phlegm cough from 15.3% to 11.8% (p < 0.05); for dyspnoea from 19.2% to 13.0% (p < 0.01); and for wheezing from 9.0% to 7.8%. ANOVA showed that the largest decline in symptom prevalence was seen among workers who themselves gave up smoking, and subjects with a positive attitude towards the law before it took effect. CONCLUSION: A significant decrease in respiratory symptoms among service industry workers was found five months after the enacting of a public smoking ban.

Indoor exposures and respiratory symptoms in a Norwegian community sample.

BACKGROUND: Limited data are available on the effect of a poor indoor climate on the respiratory health of adults. No data are available regarding the contribution of indoor exposures to the burden of respiratory symptoms in the population. METHODS: In 1996-7 a community sample of 3181 adults aged 26-82 years was invited to participate in a survey on indoor climate and respiratory health in Hordaland County, Norway. 2401 subjects agreed to take part. Logistic regression was used to examine the relationship between eight markers of indoor exposure and physician diagnosed asthma and five respiratory symptoms, after adjustment for sex, age, smoking, educational level, smoking habits, pack years, and occupational airborne exposure. RESULTS: Mould exposure was associated with all the respiratory symptoms; the adjusted odds ratios (OR) varied from 1.6 (95% confidence interval (CI) 1.0 to 2.4) for cough with phlegm to 2.3 (95% CI 1.4 to 3.9) for grade 2 dyspnoea. Keeping a cat or dog in childhood was associated with grade 2 dyspnoea and attacks of dyspnoea, with adjusted ORs of 1.3 (95% CI 1.0 to 1.7) and 1.4 (95% CI 1.1 to 1.8), respectively. Having a fitted carpet in the bedroom was negatively associated with three of the five respiratory symptoms. 3-5% of the frequency of the respiratory symptoms in the study population could be attributed to exposure to visible moulds. CONCLUSION: Mould exposure is an independent risk factor for several respiratory symptoms in a general population covering a wide age span, but it makes only a small contribution to the respiratory symptom burden in the population at large.

The incidence of adult asthma: a review.

In recent years, several new studies have estimated the incidence of adult asthma. These studies vary in design and quality. The current paper summarises the findings of major population studies in the adult incidence of asthma. The pooled estimate of the adult incidence of asthma was 4.6 per 1000 person-years in women and 3.6 per 1000 person-years in men. The estimate among only general population cohort studies was higher, respectively 5.9 and 4.4 per 1000 person-years in women and men. The adult incidence of asthma was slightly higher in women than men. In the few studies that allowed the incidence of asthma to be estimated among those aged >50 years, there was a trend towards a higher incidence with age. It is thought likely that this is at least partly explained by misclassification with COPD. However, the current findings from these studies may imply that the incidence of asthma in the elderly has previously been under-estimated. Finally, the review shows that estimates of adult asthma incidence have tended to be higher in later studies, implying a rise in asthma incidence in adults within the timeframe of observation.

Remission of respiratory symptoms by smoking and occupational exposure in a cohort study.

Few studies have estimated the remission rates of respiratory symptoms in general populations. No community cohort studies have examined the impact of smoking cessation and previous dust or fumes exposure on the remission of respiratory symptoms. In the Hordaland County Study, an 11-yr community cohort (1985-1996/1997) from Western Norway, data from 2,819 subjects were used to examine the remission of six respiratory symptoms. The measured cumulative remission varied from 42.3% for morning cough to 58.4% for chronic cough. Smoking cessation was a significant predictor of remission of the cough symptoms and wheezing, with odds ratios (OR) (95% confidence intervals (CI)) varying from 2.2 (1.3-3.7) for wheezing to 6.2 (3.5-11.2) for morning cough, after adjustment for sex, age, pack-years smoked, previous dust or fumes exposure, and educational level. In those not previously exposed to dust or fumes, the adjusted OR (95% CI) for the remission of morning cough, phlegm cough, dyspnoea grade 2, attacks of dyspnoea and wheezing varied from 1.5 (0.9-2.5) for attacks of dyspnoea to 2.1 (1.1-3.9) for dyspnoea grade 2, as compared to those previously exposed to dust or fumes. This study suggests a beneficial effect of smoking cessation and an adverse effect of occupational exposure on the remission of respiratory symptoms.

Incidence of asthma and respiratory symptoms by sex, age and smoking in a community study.

The purpose of this study was to establish incidence rates for a wide range of respiratory symptoms and asthma, and relate them to sex, age, and smoking habits. A cohort established in 1985 as a random sample from the population of Western Norway, aged 15-70 yrs, was followed-up in 1996-1997. Of the initial cohort of 3,786 subjects, a total of 2,819 replied to mailed questionnaires at both baseline and follow-up. The 11-yrs cumulative incidence of asthma was 4.0% in males and 3.5% in females. For respiratory symptoms, the cumulative incidences for both sexes varied between 2.0% (dyspnoea grade 4) and 25.8% (wheezing), being higher in females than males for most symptoms. For calculation of odds ratios (ORs) multivariate logistic regression analyses were used. The sex and smoking-adjusted incidences increased by age for all symptoms except wheezing and attacks of dyspnoea. Those starting to smoke within the follow-up had ORs of 1.9-2.2 for the cough symptoms compared to never-smokers, after adjusting for sex, age, and pack-yrs. To conclude, the 11-yrs incidence of dyspnoea increased with increasing pack-yrs, after adjusting for sex, age, and changes in smoking habits. This indicated that when analysing other risk factors, adjustment has to be made for the risks posed by smoking, sex and age.