Expiratory flow limitation (EFL) during tidal breathing is a major determinant of dynamic hyperinflation and exercise limitation in chronic obstructive pulmonary disease (COPD). Current methods of detecting this are either invasive or unsuited to following changes breath-by-breath. It was hypothesised that tidal flow limitation would substantially reduce the total respiratory system reactance (X_rs) during expiration, and that this reduction could be used to reliably detect if EFL was present.To test this, 5‐Hz forced oscillations were applied at the mouth in seven healthy subjects and 15 COPD patients (mean±sd forced expiratory volume in one second was 36.8±11.5 % predicted) during quiet breathing. COPD breaths were analysed (n=206) and classified as flow-limited if flow decreased as alveolar pressure increased, indeterminate if flow decreased at constant alveolar pressure, or nonflow-limited.Of these, 85 breaths were flow-limited, 80 were not and 41 were indeterminate. Among other indices, mean inspiratory minus mean expiratory X_rs(ΔX_rs) and minimum expiratory X_rs(X_exp,min) identified flow-limited breaths with 100% specificity and sensitivity using a threshold between 2.53–3.12 cmH₂O·s·L⁻¹(ΔX_rs) and −7.38– −6.76 cmH₂O·s·L⁻¹(X_exp,min) representing 6.0% and 3.9% of the total range of values respectively. No flow-limited breaths were seen in the normal subjects by either method.Within-breath respiratory system reactance provides an accurate, reliable and noninvasive technique to detect expiratory flow limitation in patients with chronic obstructive pulmonary disease.

Indacaterol is a novel, inhaled, once-daily, ultra-long-acting β₂-agonist bronchodilator recently approved in Europe for the treatment of chronic obstructive pulmonary disease (COPD). The aim of the present study was to investigate the efficacy and safety of indacaterol compared with placebo and the twice-daily β₂-agonist, salmeterol, as an active control.Patients with moderate-to-severe COPD were randomised to 6 months double-blind treatment with indacaterol (150 μg once daily), salmeterol (50 μg twice daily) or placebo. The primary efficacy end-point was trough (24 h post-dose) forced expiratory volume in 1 s (FEV₁) after 12 weeks.1,002 patients were randomised and 838 (84%) completed the study. Indacaterol increased trough FEV₁at week 12 by 170 mL over placebo (p<0.001) and by 60 mL over salmeterol (p<0.001). Both active treatments improved health status (St George's Respiratory Questionnaire) and dyspnoea (transition dyspnoea index) compared with placebo, with differences between them favouring indacaterol. Safety profiles were similar across the treatment groups, and both indacaterol and salmeterol were well tolerated.Once-daily treatment with 150 μg indacaterol had a significant and clinically relevant bronchodilator effect over 24 h post-dose and improved health status and dyspnoea to a greater extent than twice-daily 50 μg salmeterol. Indacaterol should prove a useful additional treatment for patients with COPD.

Background: Environmental pollution is a known risk factor for multiple diseases and furthermore increases rate of hospitalisations. We investigated the correlation between emergency room admissions (ERAs) of the general population for respiratory diseases and the environmental pollutant levels in Milan, a metropolis in northern Italy. Methods: We collected data from 45770 ERAs for respiratory diseases. A time-stratified case-crossover design was used to investigate the association between air pollution levels and ERAs for acute respiratory conditions. The effects of air pollutants were investigated at lag 0 to lag 5, lag 0–2 and lag 3–5 in both single and multi-pollutant models, adjusted for daily weather variables. Results: An increase in ozone (O₃) levels at lag 3–5 was associated with a 78% increase in the number of ERAs for asthma, especially during the warm season. Exposure to carbon monoxide (CO) proved to be a risk factor for pneumonia at lag 0–2 and in the warm season increased the risk of ERA by 66%. A significant association was found between ERAs for COPD exacerbation and levels of sulphur dioxide (SO₂), CO, nitrate dioxide (NO₂), and particulate matter (PM₁₀ and PM_2.5). The multipollutant model that includes all pollutants showed a significant association between CO (26%) and ERA for upper respiratory tract diseases at lag 0–2. For chronic obstructive pulmonary disease (COPD) exacerbations, only CO (OR 1.19) showed a significant association. Conclusions: Exposure to environmental pollution, even at typical low levels, can increase the risk of ERA for acute respiratory diseases and exacerbation of obstructive lung diseases in the general population.