Systematic review with meta-analysis of the epidemiological evidence relating smoking to COPD, chronic bronchitis and emphysema

<p>Abstract</p> <p>Background</p> <p>Smoking is a known cause of the outcomes COPD, chronic bronchitis (CB) and emphysema, but no previous systematic review exists. We summarize evidence for various smoking indices.</p> <p>Methods</p> <p>Based on MEDLINE searches and other sources we obtained papers published to 2006 describing epidemiological studies relating incidence or prevalence of these outcomes to smoking. Studies in children or adolescents, or in populations at high respiratory disease risk or with co-existing diseases were excluded. Study-specific data were extracted on design, exposures and outcomes considered, and confounder adjustment. For each outcome RRs/ORs and 95% CIs were extracted for ever, current and ex smoking and various dose response indices, and meta-analyses and meta-regressions conducted to determine how relationships were modified by various study and RR characteristics.</p> <p>Results</p> <p>Of 218 studies identified, 133 provide data for COPD, 101 for CB and 28 for emphysema. RR estimates are markedly heterogeneous. Based on random-effects meta-analyses of most-adjusted RR/ORs, estimates are elevated for ever smoking (COPD 2.89, CI 2.63-3.17, n = 129 RRs; CB 2.69, 2.50-2.90, n = 114; emphysema 4.51, 3.38-6.02, n = 28), current smoking (COPD 3.51, 3.08-3.99; CB 3.41, 3.13-3.72; emphysema 4.87, 2.83-8.41) and ex smoking (COPD 2.35, 2.11-2.63; CB 1.63, 1.50-1.78; emphysema 3.52, 2.51-4.94). For COPD, RRs are higher for males, for studies conducted in North America, for cigarette smoking rather than any product smoking, and where the unexposed base is never smoking any product, and are markedly lower when asthma is included in the COPD definition. Variations by sex, continent, smoking product and unexposed group are in the same direction for CB, but less clearly demonstrated. For all outcomes RRs are higher when based on mortality, and for COPD are markedly lower when based on lung function. For all outcomes, risk increases with amount smoked and pack-years. Limited data show risk decreases with increasing starting age for COPD and CB and with increasing quitting duration for COPD. No clear relationship is seen with duration of smoking.</p> <p>Conclusions</p> <p>The results confirm and quantify the causal relationships with smoking.</p

Beta 2-agonists administered by a dry powder inhaler can be used in acute asthma

Patients with acute asthma attending the emergency room were included in a double-blind, double-dummy and parallel group study to investigate whether a dry powder inhaler (Turbuhaler) can be used in acute asthma. If so, the aim was to establish the potency relationship between a beta 2-agonist (salbutamol) administered by the dry powder inhaler and the pressurized metered-dose inhaler (pMDI). Eighty-six patients with a mean age of 38 years and forced expiratory volume in 1 s (FEV1) of 37% of predicted normal value were randomized at Siriraj Hospital in Bangkok to either Turbuhaler (50 micrograms dose -1) or pMDI (100 micrograms dose -1) with spacer (Volumatic). Doses of 100 + 300 + 300 + 300 micrograms salbutamol were given at 0, 15, 30 and 45 min via Turbuhaler and repeated at 90, 105, 120 and 135 min (total dose 2000 micrograms). The same inhalation schedule with identical number of doses was used for the pMDI with spacer but in double doses (total 4000 micrograms), assuming a dose-potency ratio of salbutamol administered via Turbuhaler compared with the pMDI of 2:1. At 85 min after the first dose, 60 mg prednisolone was given orally. FEV1 was measured 10 min after each dosing. Peak inspiratory flow (PIF) through Turbuhaler was measured on each dosing occasion. Plasma (P)-salbutamol, serum (S)-potassium concentrations, pulse rate, blood pressure and adverse events were recorded. No statistically significant differences were observed in the increase in FEV1 between the groups: 55 min (165 min) after the first dose, the increase was 0.47 l and 47% (0.64 l and 63%) in the Turbuhaler group, and 0.46 l and 42% (0.68 l and 65%) in the pMDI group. Mean PIF though Turbuhaler was 49 l min -1 (range 26-68) at first inhalation and increased to 60 l min -1 (range 38-86). There was no correlation between the initial PIF through Turbuhaler and the initial FEV1 response. P-salbutamol and S-potassium values correlated well. A larger decrease in S-potassium was noticed after 75 min in the pMDI group (0.38 mmol l -1) compared with the Turbuhaler group (0.23 mmol l -1) (P = 0.02). In conclusion, the use of a dry powder inhaler, Turbuhaler, was investigated in the emergency room treatment of acute asthma, and was as effective as a pMDI with spacer. Half the dose of salbutamol administered via Turbuhaler was as effective as the full dose given via a pMDI with spacer