Effect of treatment for nicotine dependence in patients with COPD

Stopping smoking is the only known method to slow down the inevitable progression of COPD. Early detection of the disease in smokers at risk of COPD gives a unique opportunity to prevent the disease progression. The aim of the study was to evaluate the effects of smoking intervention in a group of subjects with newly diagnosed airflow limitation (AL). Of 558 current smokers participating in population spirometric screening for COPD combined with smoking cessation advice, 297 were diagnosed to have AL (FEV1/FVC < 0.7). After one year 193 presented for follow-up visit. Thirty subjects (10.1%) quit smoking. Remaining 163 smokers were invited to smokers' clinic. Attendees (n = 70), 40 males, and 30 females, mean age 56 years, were randomized at visit 1 to treatment with nicotine patch (n = 38) or bupropion SR (n = 32). Follow-up was scheduled at 2 weeks, at the end of treatment, 6 months and 12 months. After 12 months a phone call assessed the smoking status. Non smoking was validated with carbon monoxide measurements in exhaled air. Patients who did not attend the follow-up visits were considered smokers. The number of participants at follow-up decreased significantly: from 70 subjects at visit one to 57 after 2 weeks, 34 at end of treatment and 14 subjects at months. Almost all (n = 69) were reached at 12 month by the phone. The validated quit rate after 12 months was 18.5% (13/70), 8 in group treated with nicotine patch and 5 in the group treated with bupropion SR (NS). When total group of smokers with newly diagnosed COPD was considered 10% quit smoking as result of minimal intervention with another 4.5% after pharmacological treatment.     

Predictors of success in smoking cessation among participants of spirometric screening for COPD

The aim of the study was to evaluate factors that could predict smoking cessation after a minimal antismoking counseling during spirometric screening for COPD. Every subject filled-in a simple questionnaire on clinical signs of COPD and tobacco habit, had a spirometry performed according to ATS standards and received a short antitobacco counseling together with a booklet on how to quit smoking. Out of 800 smokers over 40 years of age, smoking history of more than 10 packyears, screened for COPD in 1999, four hundred were invited a year later for a follow-up spirometry and evaluation of anti-smoking intervention. Of 383 patients, who responded to the invitation (208 M and 175 F, mean age 56.6 +/- 10.7 yrs), 52 (13.6%) quit smoking for one year and another 48 (12.5%) quit smoking temporarily and than resumed smoking. Smokers who permanently succeeded in quitting smoking were older (60.5 vs 55.9 years p < 0.01), started smoking later (age at starting smoking 22 vs 19.5 years p < 0.001), had a shorter tobacco exposition (28.8 vs 34.3 packyears p < 0.05), had lower lung function (FEV1%pred 80.5 vs 89.2% p < 0.05) and were less nicotine dependent (FTQ score 1 vs 4.8 p < 0.00001).     

Effects of spirometric screening in the community on smoking cessation

In the years 1998-2000 in the Centre of COPD and Respiratory Failure in Bydgoszcz a group of tobacco smokers at risk of COPD (over 40 years of age, with smoking history of more than 10 packyears) were studied. Every patient filled-in a simple questionnaire on clinical signs of COPD and tobacco habit, had a spirometry performed according to ATS standards and received a short antitobacco counseling together with a booklet on how to quit smoking. Out of 1072 patients studied in 1998, airway obstruction was found in 200. Eighty seven of these were current smokers (studied group-S). Another 90 current smokers with normal spirometry served as a control group-C. Both groups of smokers were invited in 1999 and 2000 to perform spirometry. Changes in smoking habit were recorded at each yearly visit. After one year 13 patients (15%) from the S group and 4 (4.5%) from the C group permanently stopped smoking. In 2000 24 patients (28%) in S group and 13 (14.7%) in C group permanently quit smoking. CONCLUSION: Spirometric screening in smokers at risk of COPD together with a minimal antismoking intervention seems to be a promising method of smoking cessation.     

Effect of occupational exposure and smoking on spirometric tests and symptoms of chronic bronchitis

The importance of occupational exposure to airborne agents in the development of obstructive lung disease is uncertain. The aim of the study was to evaluate the effects of smoking and of occupational exposure on the lung function and chronic respiratory symptoms. I studied a group of 1239 adults (766 men and 473 women; mean age 44.9 +/- 8.6 yrs; current smokers 42.1%, lifetime nonsmokers 41.6%) working in 5 factories in the Bielsko-Biala area. Simple spirometric test (FEV1, FVC, FEV1%FVC) and a questionnaire on chronic respiratory symptoms, smoking habits and occupational exposures were applied. Respiratory symptoms and lung function were studied in relation to years of occupational exposure and adjusted for smoking habit. Occupational exposure was reported by 35.7% (n = 442) participants (dust 20.6%; gases or fumes 27.6%; mixed exposure 51.8%), with a mean duration of 20.9 +/- 9.2 years. In all cases concentrations of noxious agents did not exceed allowed levels. The symptoms of chronic bronchitis (cough and phlegm) were present in 12.3% and airflow limitation (FEV1% FVC < 0.7) in 6.9% of subjects. The significant relation of respiratory symptoms and bronchial obstruction to smoking was confirmed. No significant association between occupational exposure and ventilatory function or respiratory symptoms was found in a whole group. Smoking--specific analysis showed that current smokers appeared to be more susceptible to the effects of professional exposure. It was expressed in lower lung function indices and significantly higher odds ratios for airflow limitation or chronic respiratory symptoms for smokers exposed compared to nonexposed. Sufficient evidence of health selection processes known as a "healthy smoker" and a "healthy worker" effects were revealed.     

Effects of smoking cessation on airflow obstruction and quality of life in asthmatic smokers

Purpose

Smoking elicits airway inflammation and airflow obstruction in patients with asthma, even after smoking cessation. The aim of this study was to examine the effects of smoking cessation on lung function and quality of life (QOL) in asthmatic patients.

Methods

Thirty-two patients with asthma who were active smokers were recruited. After education on the effects of smoking on asthma, 22 patients continued to smoke, and 10 quit smoking. All patients were treated with inhaled fluticasone propionate (1 mg/day) for 3 months. We compared forced expiratory volume in 1 s (FEV1), FEV1/forced vital capacity (FVC), forced expiratory flow between 25 and 75% FVC (FEF_25-75%), and scores on a QOL questionnaire at baseline, 1, 2, and 3 months.

Results

Quitters showed a greater percent change in FEV1 (19.1±6.3 vs. 7.9±2.4%, P=0.024) and FEV1/FVC (6.5±4.14 vs. 3.5±1.5%, P=0.05) than smokers. Both quitters and smokers showed improved QOL scores after 1, 2, and 3 months of fluticasone treatment.

Conclusions

Patients with asthma who quit smoking showed less airway obstruction, suggesting that smoking cessation is crucial in the management of asthma.     

Incidence and determinants of moderate COPD (GOLD II) in male smokers aged 40–65 years: 5-year follow up

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a major health problem with an estimated prevalence of 10-15% among smokers. The incidence of moderate COPD, as defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD), is largely unknown. AIM: To determine the cumulative incidence of moderate COPD (forced expiratory volume in 1 second/forced vital capacity ratio [FEV1/FVC] <0.7 and FEV1 <80% predicted) and its association with patient characteristics in a cohort of male smokers. DESIGN: Prospective cohort study. SETTING: The city of IJsselstein, a small town in the Netherlands. METHOD: Smokers aged 40-65 years who were registered with local GPs, participated in a study to identify undetected COPD. Baseline measurements were taken in 1998 of 399 smokers with normal spirometry (n = 292) or mild COPD (FEV1/FVC <0.7 and FEV1 >or=80% predicted, n = 107) and follow-up measurements were conducted in 2003. RESULTS: After a mean follow-up of 5.2 years, 33 participants developed moderate COPD (GOLD II). This showed an estimated cumulative incidence of 8.3% (95% CI = 5.8 to 11.4) and a mean annual incidence of 1.6%. No participant developed severe airflow obstruction. The risk of developing moderate COPD in smokers with baseline mild COPD (GOLD I) was five times higher than in those with baseline normal spirometry (one in five versus one in 25). CONCLUSIONS: In a cohort of middle-aged male smokers, the estimated cumulative incidence of moderate COPD (GOLD II) over 5 years was relatively high (8.3%). Age, childhood smoking, cough, and one or more GP contacts for lower respiratory tract problems were independently associated with incident moderate COPD.     

Lung matrix metalloproteinase-9 correlates with cigarette smoking and obstruction of airflow

Cigarette smoking is the most important risk factor for obstruction of airflow in chronic obstructive pulmonary disease (COPD). Matrix metalloproteinases (MMPs) or an imbalance between MMPs and their inhibitors, the tissue inhibitors of MMP (TIMPs), is considered to play a role in the pathogenesis of COPD. We investigated whether the MMPs expression or the imbalance between MMPs and TIMP-1 is associated with the amount of cigarette smoking and the FEV1 value, in the lung parenchyma of 26 subjects (6 non-smokers and 20 cigarette smokers). First, we performed zymographic analysis to identify the profile of the MMPs, which revealed gelatinolytic bands mainly equivalent to MMP-9 in the smokers. We then measured, using enzyme immunoassay, the concentrations of MMP-9 and its inhibitor, TIMP-1. Correlation analysis revealed that both the MMP-9 concentrations and the molar ratios of MMP-9 to TIMP-1 (MMP-9/TIMP-1) were correlated with the amount of cigarette smoking. Furthermore, MMP-9 concentrations were inversely correlated with FEV1. In conclusion, this study shows that MMP-9 expression in human lung parenchyma is associated with cigarette smoking and also with the obstruction of airflow, suggesting that MMP-9 may play a role in the pathogenesis of the cigarette smoke-induced obstruction of airflow known as the characteristic of COPD.     

Clinical examinations for COPD

The natural history of COPD such as pulmonary emphysema demonstrates that FEV1 rapidly declines in smokers who are susceptible to cigarette smoke. The susceptible smokers who quit smoking do not regain only a little, but the rate of the FEV1 decline is no longer steep. These have been interpreted that early detection of this obstructive impairment is the most important issue to prevent the progression to severe emphysema. Pulmonary function tests, at least a measure of FEV1, in the all middle-aged smokers have been particularly recommended. The smokers with abnormal FEV1 defect should be advised to quit smoking. In moderate and severe cases, after staging of the disease by pulmonary function and exercise tests, assessments of complicated factors such as eosinophilic bronchitis are clinically important for constructing therapeutic strategies. Asthmatic component can be assessed by eosinophil count in the sputum and/or reversibility of the pulmonary function after challenging of bronchodilater inhalations. In the severe stage of the disease, examinations such as arterial blood gas analysis and pulse oxymetric measure are critical because oxygen therapy for the patients with respiratory failure has been known to improve survival prognosis. Portable devices which can assess arterial oxygen saturation during daily activity will be useful to decide its indication or to titrate oxygen. In conclusion, clinical examination in COPD, particularly in pulmonary emphysema in this paper, should appropriately be planned in each stage of the disease, or in each clinical purpose.     

Early detection of COPD by high risk population spirometric screening

COPD is the most frequent chronic lung disease in Poland. The disease is however under-diagnosed, especially at the early stages. The aim of the study was to assess the efficacy of spirometric screening for COPD in middle aged smokers. Informations on causes and symptoms of COPD were disseminated in mass media in 14 large cities. Subject aged over 39 and with smoking history of > 10 packyears were invited for a free spirometry in local chest clinic. However, everyone attending had the spirometry performed. Spirometry was performed according to ATS recommendations. Airway obstruction (AO) was diagnosed when FEV1/FVC < 85% of N and categorised as mild (FEV1 > 70% of N), moderate (FEV1 50-69% of N) or severe (FEV1 < 50% of N). Spirometry was accompanied by an antismoking advice. RESULTS: 12.781 subjects were screened (mean age 52 +/- 12 years, 57% males). In 8.269 subjects who complied with inclusion criteria AO was diagnosed in 29.8% (mild in 10.9%, moderate in 12% and severe in 6.9%). In smokers < 40 years of age and a history of < 10 packyears AO was found in 8.8% (mild in 6.0%, moderate in 1.8% and severe in 1.0%). CONCLUSION: Mass spirometry is an effective and easy method for early detection of COPD.     

Evaluation of the influence of tobacco smoking on pulmonary function in youg men

According to WHO estimates in the early 1990s there were around 1.100 million smokers in the world, about one third of the global population over 15 years of age. The aim of the study was to evaluate tobacco influence on pulmonary function tests in young healthy men. The study was performed on 3004 subjects 18-23 years old. The subjects were divided into two groups, smokers (S n = 1726) and non-smokers (NS n = 1278). Each subject had spirometry and body pletysmography done. The analysis of influence of smoking on pulmonary function tests showed statistically significant decrease of TLC, FEV1, FEV1%/VC, PEF and FEF50 in the smokers' group. Percentage of people with airflow limitation (FEV1%VC < 85% N, FEV1 < 80% N, FEF50 < 70% N) was two times higher than in the non-smokers' group. In conclusion: smoking significantly increases the number of subjects with airflow limitation among healthy young males in Poland.     

Genome-wide linkage analysis of severe, early-onset chronic obstructive pulmonary disease: airflow obstruction and chronic bronchitis phenotypes

Familial aggregation of chronic obstructive pulmonary disease (COPD) has been demonstrated, but linkage analysis of COPD-related phenotypes has not been reported previously. An autosomal 10 cM genome-wide scan of short tandem repeat (STR) polymorphic markers was analyzed for linkage to COPD-related phenotypes in 585 members of 72 pedigrees ascertained through severe, early-onset COPD probands without severe alpha1-antitrypsin deficiency. Multipoint non-parametric linkage analysis (using the ALLEGRO program) was performed for qualitative phenotypes including moderate airflow obstruction [forced expiratory volume at one second (FEV(1)) < 60% predicted, FEV(1)/FVC < 90% predicted], mild airflow obstruction (FEV(1) < 80% predicted, FEV(1)/FVC < 90% predicted) and chronic bronchitis. The strongest evidence for linkage in all subjects was observed at chromosomes 12 (LOD = 1.70) and 19 (LOD = 1.54) for moderate airflow obstruction, chromosomes 8 (LOD = 1.36) and 19 (LOD = 1.09) for mild airflow obstruction and chromosomes 19 (LOD = 1.21) and 22 (LOD = 1.37) for chronic bronchitis. Restricting analysis to cigarette smokers only provided increased evidence for linkage of mild airflow obstruction and chronic bronchitis to several genomic regions; for mild airflow obstruction in smokers only, the maximum LOD was 1.64 at chromosome 19, whereas for chronic bronchitis in smokers only, the maximum LOD was 2.08 at chromosome 22. On chromosome 12p, 12 additional STR markers were genotyped, which provided additional support for an airflow obstruction locus in that region with a non-parametric multipoint approach for moderate airflow obstruction (LOD = 2.13) and mild airflow obstruction (LOD = 1.43). Using a dominant model with the STR markers on 12p, two point parametric linkage analysis of all subjects demonstrated a maximum LOD score of 2.09 for moderate airflow obstruction and 2.61 for mild airflow obstruction. In smokers only, the maximum two point LOD score for mild airflow obstruction was 3.14. These observations provide suggestive evidence that there is a locus on chromosome 12p which contributes to susceptibility to early-onset COPD.     

Early detection of COPD in smokers from Warsaw using spirometric screening

COPD is the fourth leading cause of death in Poland. The disease is diagnosed not early enough. The aim of the study was to establish prevalence of COPD in smokers, inhabitants of Warsaw. Therefore, using local mass media, smokers with at least 10 pack-years history of smoking, over 40 years of age, were invited for a free spirometry. The spirometries were performed during 33 weekends. 3340 subjects (51.8% M and 48.2% F) mean age 57 +/- 13.2 years were examined. Most of them were current smokers (57.8%) or ex-smokers (27%) with a history of 31.9 +/- 18.8 packyears, the remaining subjects (15.2%) declared themselves as a life non-smokers. From all screened 1520 (45.6%) presented airflow limitation (AL). Following ERS recommendations, AL was classified as mild in 27.7%, moderate in 11.1% and severe in 6.8% subjects. One third of examined declared morning cough (36.9%) or sputum production (34.8%), or both symptoms (26.7%). Morning cough (p < 0.05) or cough together with sputum production (p < 0.01) were related to result of spirometry. Subjects aged > or = 40 years with a history of > or = 10 packyears had AL diagnosed in 50.1%, in contrast to younger than 40 years and smoking < 10 packyears in whom AL was detected in 14.3%. In life non-smokers AL was diagnosed in 35.9%. The majority of non-smokers were females (70%), 7.5% declared history of bronchial asthma. The great efficacy of AL detection in targeted population (50%) should be an incentive to perform routine spirometric examination in smokers aged 40+ with a history of 10+ packyears of smoking.     

Characteristics of patients with COPD in three motivational stages related to smoking cessation

OBJECTIVE: To characterize patients with chronic obstructive pulmonary disease (COPD) in different motivational stages related to smoking cessation. METHODS: 633 smoking COPD patients from 67 general practices participated in a cross-sectional study. The patients were compared with respect to health indicators, demographics, self-efficacy, nicotine dependence, attitudes, and action plans. RESULTS: In line with previous Dutch results, smokers in precontemplation associated significantly fewer advantages with smoking cessation than smokers contemplating quitting and preparing to quit. Preparers had significantly higher self-efficacy expectations about quitting than the other smokers. Patients preparing to quit suffered from more COPD complaints than precontemplators. Smokers contemplating quitting and preparing to quit developed more plans to turn intentions to quit into action. CONCLUSION: More than 50% of the smokers with COPD are amenable to smoking cessation support. Preparers and contemplators did not differ as much as previous studies found. It would be advantageous to tailor COPD counseling to two distinct groups (unmotivated smokers and smokers motivated to quit), to discuss the advantages of quitting with unmotivated smokers, and to increase self-efficacy, and action planning for smokers motivated to quit. PRACTICE IMPLICATIONS: COPD patients are amenable to counseling to quit smoking. Addressing COPD complaints may contribute to greater motivation.     

Quality of life in smokers: focus on functional limitations rather than on lung function?

BACKGROUND: The Global Initiative for Chronic Obstructive Lung Disease (GOLD) classification of severity of chronic obstructive pulmonary disease (COPD) is based solely on obstruction and does not capture physical functioning. The hypothesis that the Medical Research Council (MRC) dyspnoea scale would correlate better with quality of life than the level of airflow limitation was examined. AIM: To study the associations between quality of life in smokers and limitations in physical functioning (MRC dyspnoea scale) and, quality of life and airflow limitation (GOLD COPD stages). DESIGN: Cross-sectional study. SETTING: The city of IJsselstein, a small town in the centre of The Netherlands. METHOD: Male smokers aged 40-65 years without a prior diagnosis of COPD and enlisted with a general practice, participated in this study. Quality of life was assessed by means of a generic (SF-36) and a disease-specific, questionnaire (QOLRIQ). RESULTS: A total of 395 subjects (mean age 55.4 years, pack years 27.1) performed adequate spirometry and completed the questionnaires. Limitations of physical functioning according to the MRC dyspnoea scale were found in 25.1% (99/395) of the participants and airflow limitation in 40.2% (159/395). The correlations of limitations of physical functioning with all quality-of-life components were stronger than the correlations of all quality-of-life subscales with the severity of airflow limitation. CONCLUSION: In middle-aged smokers the correlation of limitations of physical functioning (MRC dyspnoea scale) with quality of life was stronger than the correlation of the severity of airflow limitation with quality of life. Future staging systems of severity of COPD should capture this and not rely on forced expiratory volume in one second (FEV1) alone.     

Monocyte chemoattractant protein 1, interleukin 8, and chronic airways inflammation in COPD

Chronic obstructive pulmonary disease (COPD) is one of the most common causes of death, with cigarette smoking among the main risk factors. Hallmarks of COPD include chronic airflow obstruction and chronic inflammation in the airway walls or alveolar septa. An earlier study reported elevated numbers of macrophages and mast cells within the bronchiolar epithelium in smokers with COPD, compared with smokers without. Since specific chemokines may be involved in this influx, the in situ protein and mRNA expression of monocyte chemoattractant protein 1 (MCP-1) and of interleukin 8 (IL-8) were studied in tumour-free peripheral lung tissue resected for lung cancer of current or ex-smokers with COPD (FEV(1)<75%; n=14) and without COPD (FEV(1)>84; n=14). MCP-1 was expressed by macrophages, T cells, and endothelial and epithelial cells. Its receptor, CCR2, is expressed by macrophages, mast cells, and epithelial cells. IL-8 was found in neutrophils, epithelial cells, and macrophages. In subjects with COPD, semi-quantitative analysis revealed 1.5-fold higher levels of MCP-1 mRNA and IL-8 mRNA and protein in bronchiolar epithelium (p<0.01) and 1.4-fold higher levels of CCR2 in macrophages (p=0.014) than in subjects without COPD. The bronchiolar epithelial MCP-1 mRNA expression correlated with both CCR2 expression on macrophages and mast cells (p<0.05) and the numbers of intra-epithelial macrophages and mast cells (p<0.04). The epithelial IL-8 expression did not correlate with the numbers of neutrophils, macrophages, CD45RO+, CD8+, or mast cells. These data suggest that MCP-1 and CCR2 are involved in the recruitment of macrophages and mast cells into the airway epithelium in COPD.     

Early, targeted population based screening for COPD. Preliminary study

COPD is the fourth leading cause of death in Poland, unfortunately diagnosed not early enough. The aim of the study was to establish prevalence of COPD in chronic smokers. Therefore, using daily press and TV, smokers with at least 10 year history of smoking, over 40 years of age, were invited for a free spirometry. 263 subjects (177 M and 86 F) mean age 54 +/- 0.6 years were examined. Most of them (97.7%) were smokers with a history of 32.2 +/- 0.9 pack-years, 6 persons (2.3%) were passive smokers. 110 persons (41.8%) presented bronchial obstruction, the remaining (58.2%) had normal spirometric values. Following recommendations of the Polish Society of Physio-pneumonology bronchial obstruction was classified as mild in 25.1%,- moderate in 12.1% and severe in 4.6% subjects. Majority of examined subjects presented with COPD symptoms, cough (62.7%), expectoration (68.8%) and dyspnoea (50.2%). The presence of those symptoms did not differ among groups with different severity of bronchial obstruction. However, there were significant differences in age (p < 0.05) and years of smoking habit (p < 0.01). The great efficacy of targeted screening for COPD (40%) should be an incentive to perform routine spirometric examination in smokers with more than 20 years of smoking history.     

Decreased T lymphocyte infiltration in bronchial biopsies of subjects with severe chronic obstructive pulmonary disease

BACKGROUND: Studies on the inflammatory process in the large airways of patients with mild/moderate COPD have shown a prevalent T lymphocyte and macrophage infiltration of the bronchial mucosa. However, bronchial inflammation in more severe disease has not been extensively studied. OBJECTIVE: The aim of the present study was to characterize the lymphocyte infiltration in the bronchial mucosa of subjects with severe, compared to mild, COPD, and to examine the relationship between airflow limitation and T lymphocyte numbers in the bronchial mucosa. METHODS: We examined bronchial biopsies obtained from nine smokers with severe airflow limitation, nine smokers with mild/moderate airflow limitation and 14 smokers with normal lung function. Immunohistochemical methods on cryostat sections were used to assess the number of CD3+, CD4+, CD8+ cells and the number of CD3+ cells coexpressing the chemokine receptor CCR5 (CCR5+CD3+) in the subepithelium. RESULTS: Subjects with severe COPD had lower numbers of CD3+, CD8+ and CCR5+CD3+ cells than mild/moderate COPD (P < 0.012, P < 0.02 and P < 0.02, respectively) and control smokers (P < 0.015, P < 0.005 and P < 0.015, respectively). In subjects with airflow limitation the number of CD3+ and CD8+ cells was inversely correlated with the degree of airway obstruction (r = 0.59, P < 0.015 and r = 0.52, P < 0.032, respectively). CONCLUSIONS: Bronchial inflammation in severe COPD is characterized by lower numbers of CD3+ and CD8+ cells and decreased numbers of CD3+ cells coexpressing the chemokine receptor CCR5. T lymphocyte infiltration is inversely correlated with the degree of airflow limitation.     

Prevalence and Frequency of mHealth and eHealth Use Among US and UK Smokers and Differences by Motivation to Quit

BackgroundBoth mHealth and eHealth interventions for smoking cessation are rapidly being developed and tested. There are no data on use of mHealth and eHealth technologies by smokers in general or by smokers who are not motivated to quit smoking.ObjectiveThe aims of our study were to (1) assess technology use (eg, texting, social media, Internet) among smokers in the United States and United Kingdom, (2) examine whether technology use differs between smokers who are motivated to quit and smokers who are not motivated to quit, (3) examine previous use of technology to assist with smoking cessation, and (4) examine future intentions to use technology to assist with smoking cessation.MethodsParticipants were 1000 adult smokers (54.90%, 549/1000 female; mean age 43.9, SD 15.5 years; US: n=500, UK: n=500) who were recruited via online representative sampling strategies. Data were collected online and included demographics, smoking history, and frequency and patterns of technology use.ResultsAmong smokers in general, there was a high prevalence of mobile and smartphone ownership, sending and receiving texts, downloading and using apps, using Facebook, and visiting health-related websites. Smokers who were unmotivated to quit were significantly less likely to own a smartphone or handheld device that connects to the Internet than smokers motivated to quit. There was a significantly lower prevalence of sending text messages among US smokers unmotivated to quit (78.2%, 179/229) versus smokers motivated to quit (95.0%, 229/241), but no significant differences between the UK groups (motivated: 96.4%, 239/248; unmotivated: 94.9%, 223/235). Smokers unmotivated to quit in both countries were significantly less likely to use a handheld device to read email, play games, browse the Web, or visit health-related websites versus smokers motivated to quit. US smokers had a high prevalence of app downloads regardless of motivation to quit, but UK smokers who were motivated to quit had greater prevalence of app downloads than smokers unmotivated to quit. US smokers were significantly more likely to have a Facebook account (87.0%, 435/500) than UK smokers (76.4%, 382/500), but smokers unmotivated to quit in both countries used Facebook less frequently than smokers motivated to quit. Smokers who were unmotivated to quit were less likely to have used eHealth or mHealth platforms to help them quit smoking in the past and less likely to say that they would use them for smoking cessation in the future.ConclusionsAlthough smokers unmotivated to quit make less use of technology than smokers motivated to quit, there is sufficient prevalence to make it worthwhile to develop eHealth and mHealth interventions to encourage cessation. Short and low-effort communications, such as text messaging, might be better for smokers who are less motivated to quit. Multiple channels may be required to reach unmotivated smokers.     

Chronic obstructive pulmonary disease: role of bronchiolar mast cells and macrophages.

Chronic obstructive pulmonary disease (COPD) is considered to be caused in part by smoking-induced inflammation, but it is unknown which inflammatory cells within the small airways are associated with the obstruction. We investigated the inflammatory infiltrate in the small airways of 16 current or ex-smokers with COPD (FEV1 < or = 75% predicted) and 15 without COPD (FEV1 > or = 85% predicted) in pneumectomy specimens that were removed for lung cancer. Mast cells, macrophages, neutrophils, eosinophils, T cells, and B cells were identified using immunohistochemistry on formalin-fixed, paraffin-embedded specimens. These cells were quantified in the epithelium and the remainder of the airway wall. The number of mast cells and macrophages in the epithelium, but not in the remainder of the airway wall, was significantly increased in patients with COPD. Neutrophil and T cell numbers did not differ between the groups. Only few B cells and eosinophils were present in both groups. Smoking history, perioperative steroid usage, tumor localization, or reversibility in the FEV1 to salbutamol could not account for the observed differences. We conclude that the number of epithelial mast cells and macrophages is increased in the bronchioli in smokers with airflow limitation, suggesting a role in development of COPD.