Respiratory morbidity and lung function in two Aboriginal communities in Western Australia

OBJECTIVE: To examine differences in the rates of respiratory symptoms, asthma and levels of lung function in two remote Aboriginal communities. METHODOLOGY: Respiratory symptoms, smoking history, skin prick test responses to common allergens, serum IgE, lung function, airway responsiveness to methacholine and white blood cell counts were compared in two Aboriginal communities, one from the central desert (n = 84) and another from the tropical north (n = 209) of Western Australia. RESULTS: Compared with the tropical community, chest tightness and dyspnoea were more frequent and forced expiratory volume in 1 s and forced vital capacity were lower in the desert community, despite similar levels of wheeze, doctor-diagnosed asthma and skin prick test responses and lower levels of airway responsiveness and smoking. The total white cell and neutrophil counts were greater in the desert community. Serum IgE was very high and similar in both communities. CONCLUSIONS: Our findings show a low prevalence of asthma in children, a high prevalence of respiratory symptoms and low levels of lung function in remote Aboriginal communities. The greater prevalence of respiratory morbidity in the desert community was not explained by diagnosed asthma, airway hyperresponsiveness or cigarette smoking. The role of infection requires further investigation. The results suggest that the lower lung function observed in Aboriginal communities (compared with non-Aboriginal communities) results at least partly from environmental factors.     

Psychological aspects of emotional regulation in smoking dependency

We reviewed the literature on the relationships between smoking and affect regulation. There is strong evidence that vulnerability to smoking dependence is a function of a high initial sensitivity to nicotine, which produces reinforcing consequences that lead to chronic use. These strong reinforcers of tobacco dependence include regulation of mood and modulation of arousal. We focused on studies concerned with the subjective component of arousal and emotional experience. We discuss first the models and classifications used to differentiate types of smoking as related to the management of emotions and studies evaluating the stimulant and subjective effects of smoking behavior, questioning the paradoxical tranquilizing and anxiety-reducing effects of nicotine. We also looked into the mood regulation effects that may explain the strong relationships observed between depression and smoking and finally focus on some of the personality risk factors that may make individuals more susceptible to these rewarding properties of smoking.     

男性医生吸烟现状调查及肺功能检测分析

目的 调查咸宁市男性医生的吸烟状况及控烟知识掌握情况,探讨吸烟对肺功能的影响.方法 采用自行设计的调查问卷于2013年6月对我市30家医院的男性医生进行吸烟状况调查及肺功能检测.结果 共发放问卷1200份,有效问卷1123份,有效回收率为93.6％（1123/1200）,男医生的吸烟率为31.0％,其中市属医院、区县医院、乡镇医院吸烟率分别为21.1％（80/380）、28.4％（101/356）和43.2％（167/387）,不同医院、年龄、文化程度、职称的医务人员吸烟率比较差异有统计学意义（P＜0.01）.医务人员对烟草所造成的心肺系统危害知晓率高,有72.1％的吸烟者尝试过戒烟或有戒烟计划,58.6％的医生在医院会劝阻患者吸烟.吸烟者的肺功能指标低于非吸烟者.结论 咸宁市男性医生吸烟率较高,吸烟者肺功能与非吸烟者比较有不同程度下降.     

Effects of smoking cessation on lung function and airway inflammation in smokers with asthma

RATIONALE: Active smoking in asthma is associated with worsening of symptoms, accelerated decline in lung function, and impaired response to corticosteroids. OBJECTIVES: To examine the short-term effects of smoking cessation on lung function, airway inflammation, and corticosteroid responsiveness in smokers with asthma. METHODS AND MEASUREMENTS: Smokers with asthma were given the option to quit or continue smoking. Both groups underwent spirometry and induced sputum at baseline and at 1, 3, and 6 wk. Cutaneous vasoconstrictor response to topical beclometasone, airway response to oral prednisolone, and sensitivity of peripheral blood lymphocytes to corticosteroids were measured before smoking cessation and at 6 wk. MAIN RESULTS: Of 32 subjects recruited, 11 opted to continue smoking (smoking control group). Of 21 subjects who opted for smoking cessation, 10 quit smoking for 6 wk (quit group). In the comparison of quitters with smokers at 6 wk, the mean (confidence interval [CI]) difference in FEV(1) was 407 ml (21, 793), p = 0.040, and the proportion of sputum neutrophils was reduced by 29 (51, 8), p = 0.039. Total cutaneous vasoconstrictor response score to topical beclometasone improved after smoking cessation with a mean (CI) difference of 3.56 (0.84, 6.28), p = 0.042, between quitters and smokers. There was no change in airway corticosteroid responses after smoking cessation. CONCLUSIONS: By 6 wk after smoking cessation, subjects who quit smoking had achieved considerable improvement in lung function and a fall in sputum neutrophil count compared with subjects who continued to smoke. These findings highlight the importance of smoking cessation in asthma.     

慢性肺病住院患者戒烟成功影响因素研究

目的研究住院慢性肺病患者相对于其他住院患者吸烟行为特征的特点及戒烟成功相关影响因素。方法在2014年6月至2015年6期间肺病科连续的慢性肺病住院患者,配对抽取同期于其他科室住院的非慢性肺病患者,填写调查表进行数据分析。结果本调查中吸烟患者均以控制不住烟瘾为继续吸烟主要原因;在慢性肺病患者分组中主要以经济原因为主要戒烟原因,而在非慢性肺病分组中主要以防未病为主;吸烟人群中,大家对戒烟行为的认知是一致的,在戒烟过程中不仅取决于本人的态度是否坚决,还与其对整个过程的信心及外界环境息息相关;在戒烟过程中,戒烟持续时间在很大程度上决定戒烟是否成功。多因素Logistic回归分析发现年龄、月经济收入、饮酒、是否患有其他慢性病、自觉健康状况、尼古丁依赖均影响是否戒烟成功。结论目前慢性肺病患者戒烟能够成功很大程度上是因为随着年龄增大及疾病的进行性加重及经济条件不佳所"被迫"成功的,提示我们在今后的戒烟治疗中,应早期干预,变被动戒烟为主动戒烟。     

Heritability of longitudinal change in lung function. The Framingham study.

There have been multiple reports of heritability of lung function in cross-sectional analysis, but no prior reports of heritability of rate of change in lung function. We examined heritability of rate of change of lung function in families participating in the Framingham Heart Study. Spirometric measures from two time points were used to calculate annualized rate of change in FEV(1), FVC, and FEV(1)/FVC ratio, adjusting for the effects of age, height, and weight using multiple linear regression models. Standardized residuals from these models were used as phenotypic variables in variance components analysis to assess effects of smoking and heritable factors on rate of change in lung function. Heritable factors explained a modest proportion of the population variance, with heritability estimates for change in FEV(1), FVC, and ratio of 0.05, 0.18, and 0.13, respectively. Restricting the analysis to subjects concordant for smoking status during the interval over which lung function was measured, the heritability estimates increased to 0.18, 0.39, and 0.14, respectively, among interim smokers. These data suggest that in middle-aged and older persons in the general population, genetic factors contribute modestly to the overall population variance in rate of lung function decline, and further suggest the importance of gene-environment interactions.     

"Physiologic" aging in 5 years of pulmonary function in 140 iron miners

Ageing of the lung function in 5 years was studied in a group of 140 iron-ore miners, aged initially from 36 to 55 years. These men had no respiratory symptom and no pulmonary radiological abnormality. The sample was stratified on age and smoking. These factors were studied by a two-way analysis of variance. Lung function testing was performed twice, at 5 years of interval, in the same conditions. It consisted in: spirometry (for measuring FVC, FEV1, FEV1/FVC); a bronchial challenge test with acetylcholine (measurement of the fall of FEV1 after the test); measurement of total lung capacity (TLC) and residual volume (RV) by the open-circuit helium dilution method, and measurement of the transfer factor of the lung for CO, by the steady-state method (TCO/V). The only indices, whose values significantly changed in 5 years were: FVC, FEV1 and TCO/V. Their decrease rate did not appear to be significantly linked to age nor to smoking. According to these results, it seems that the decline of the pulmonary function is relatively constant during the middle period of life and that it is not strongly influenced by smoking, but only among subjects who remain without any respiratory symptom.     

Cigarette smoking and pulmonary diffusion defects in rheumatoid arthritis

The pathogenesis of lung disease in rheumatoid arthritis (RA) has still to be defined. Risk factors associated with lung involvement in RA were investigated by means of pulmonary function studies in 40 RA patients without apparent lung disease. A decreased carbon monoxide (CO) diffusion capacity indicative of interstitial lung disease (ILD) was the main pulmonary function defect found in the first 20 patients. The occurrence was associated with current cigarette smoking. This association was confirmed in a case control study performed subsequently. These data suggest that ILD in RA is stimulated by smoking and provide an additional argument that modification of smoking behaviour in RA patients might lead to less severe complications. Received: 15 January 1998 / Accepted: 12 March 1998     

Trends in passive smoking in cystic fibrosis, 1993-1998

We set out to study trends in exposure to passive smoking in children with cystic fibrosis over a 5-year period. We also evaluated the effects of this exposure on lung function. Cross-sectional data were collected on 52 children in 1998 and compared with similar data collected on 56 children in 1993. Within these two groups, there were 34 children who were studied on both occasions. Data collected included: questionnaire information about family smoking habits; forced expiratory volume in 1 sec (FEV1); forced vital capacity (FVC); and measurements of urinary and salivary cotinine levels. Salivary cotinine was more closely related to family smoking behavior than urinary cotinine concentrations (r for salivary cotinine = 0.54, P < 0.001; r for urinary cotinine = 0.37, P = 0.008). In 1993, 26/56 (46%) households contained at least one smoker (smoking households) compared with 23/52 (44%) in 1998. In 1993, a median of 15 cigarettes was smoked/day in smoking households compared to 20 cigarettes/day in 1998. In the longitudinal group, there was a small, nonsignificant reduction in mean urinary cotinine levels (geometric mean, 1993 = 5.03 ng/mL; 1998 = 4.76 ng/mL; P = 0.4). There was no significant difference between the smoking and nonsmoking households in change in lung function over 5 years (fall in FEV1 in smoking households, 10.3% vs. 11.2% in nonsmoking households; P = 0.87). We conclude that in a group of children with cystic fibrosis followed over 5 years, there was little reduction in passive smoking exposure. We did not show a relationship between such exposure and decline in lung function. A larger study will be necessary to determine whether such an effect is present. .     

Epidemiology, etiology, and prevention of lung cancer

Over the past century, lung cancer has gone from an obscure disease to the leading cause of cancer death worldwide. Initially an epidemic disease among men in industrialized nations, lung cancer now has become the leading cancer killer in both sexes in the United States and an increasingly common disease of both sexes in developing countries. Lung cancer incidence largely mirrors smoking prevalence, with a latency period of several decades. Other important risk factors for the development of lung cancer include environmental exposure to tobacco smoke, radon, occupational carcinogens, and pre-existing nonmalignant lung disease. Studies in molecular biology have elucidated the role that genetic factors play in modifying an individual's risk for lung cancer. Although chemopreventive agents may be developed to prevent lung cancer, prevention of smoking initiation and promotion of smoking cessation are currently the best weapons to fight lung cancer. No other malignancy has been shown to have such a strong epidemiologic relation between a preventable behavior and incidence of disease. Despite this knowledge, more than 20% of all Americans smoke, and tobacco use is exploding in developing countries. Based on current and projected smoking patterns, it is anticipated that lung cancer will remain the leading cause of cancer death in the world for decades to come.     

Smoking cessation improves both direct and indirect airway hyperresponsiveness in COPD.

Smoking induces chronic obstructive pulmonary disease (COPD) and is associated with airway inflammation and airway hyperresponsiveness (AHR). It has not been studied in COPD whether direct (methacholine) and indirect (adenosine-5'-monophosphate (AMP)) stimuli are associated with airway inflammation and neither whether smoking cessation improves these features. The current authors cross-sectionally investigated the relationship of AHR to methacholine and AMP with lung function and inflammatory cells in the sputum of 33 smokers with COPD. In addition, changes in these parameters were prospectively assessed in 14 smokers who successfully quit smoking for 1 yr. The presence of AHR to both methacholine and AMP was associated with lower lung function, but not with sputum inflammation. AHR to methacholine and AMP improved significantly after a 1-yr smoking cessation, yet this was unrelated to changes in sputum cell counts. The numbers of neutrophils and epithelial cells significantly increased with smoking cessation. Both direct and indirect airway hyperresponsiveness are associated with lower lung function, but not with sputum inflammation in chronic obstructive pulmonary disease. Interestingly, 1-yr smoking cessation improved both direct and indirect airway hyperresponsiveness, yet without a significant association with changes in lung function or sputum inflammation. Thus, other factors are likely to induce these improvements, e.g. a reduction in stimulation of irritant receptors, airway wall changes or mucus hypersecretion.     

吸烟对不同性别AECOPD患者气道炎症影响

目的 通过比较不同性别COPD急性发作期(AECOPD)患者的肺功能、血清细胞因子差异,研究性别差异对COPD患者气道炎症的影响.方法 将AECOPD患者分为四组,其中1组为既往无吸烟史男性,2组为吸烟指数>200支年男性,3组为既往无吸烟史女性,4组为吸烟指数>200支年女性,每组25例.检测所有患者入院时肺功能、血浆IL-8、TNF-α值.结果 非吸烟男性和女性血清炎症因子IL-8、TNF-α和肺功能比较无显著性差异(P>0.05),而在长期吸烟患者中,男性和女性患者的炎症因子、肺功能与无吸烟男性和女性比较均有显著性差异(P<0.05),同时吸烟女性与吸烟男性比较炎症因子更高(P<0.05)和肺功能更差(P<0.05).结论 吸烟的COPD女性患者在急性发作期炎症因子释放高于不吸烟女性及吸烟男性.     

Relevance of Birth Cohorts to Assessment of Asthma Persistence

The definition of persistent asthma in longitudinal studies reflects symptoms reported at every assessment with no substantive asymptomatic periods. Early-childhood wheezing may be transient, especially if it is of viral etiology. Longitudinal studies provide greater opportunity to confirm the diagnosis by variability of symptoms, objective measurements, and therapeutic responses. Several clinical phenotypes of childhood asthma have been identified, with general consistency between cohorts. Persistent wheezing is often associated with loss of lung function, which is evident from early-childhood and related to persistent inflammation and airway hyperresponsiveness. Female sex, atopy, airway responsiveness, and personal smoking, but not exposure to environmental tobacco smoke, are risk factors for persistence of childhood asthma into adulthood. The effect of breastfeeding remains controversial, but gene–environment interactions may partly explain outcomes. Understanding the natural history and underlying causes of asthma may lead to development of strategies for primary prevention.     

Longitudinal effects of passive smoking on pulmonary function in New Zealand children.

In this study we examined the longitudinal effects of smoke exposure on lung function in a cohort of New Zealand children observed from 9 to 15 yr of age. Possible exposures included in utero exposure from mothers smoking during pregnancy, passive smoke from parents, and active smoking by the children. Lung function measures of forced expiratory volume in one second (FEV1) and vital capacity (VC) were measured biennially and ratios (FEV1/VC) were computed. The data were analyzed using longitudinal methodology, and all subjects with at least one pulmonary function test and responses to the questions concerning smoke exposures were included (n = 634). Subjects reporting wheeze or asthma were examined as a separate subgroup. In the whole cohort, no significant detrimental effects were detected for absolute FEV1 or VC in either sex, related to active or passive smoke exposures. Parental smoking was, however, associated with persistent but mild and nonprogressive impairment of the FEV1/VC ratio in males, an effect that was present at the time lung function measurements were first made. This effect was not seen in females. In children with reported wheeze or asthma, parental smoking had progressive, more serious, and clinically significant effects on the FEV1/VC ratio among adolescents of both sexes, causing a mean reduction in FEV1/VC ratios by age 15 of 3.9% in males and 2.3% in females, in contrast to the observed increase in FEV1/VC ratios with age seen in nonexposed wheezing children. We conclude that passive smoking is a major contributing factor to the development and persistence of airflow limitation in wheezing children.     

Effect of smoking on pulmonary function among patients with pneumoconiosis

To clarify the effect of cigarette smoking on pulmonary function among patients with pneumoconiosis, we studied the relationship between the smoking index (number of cigarettes smoked per day X number of years of continued smoking) and lung function tests. The value of V25/Ht was significantly decreased with an increase of the smoking index, but there were no difference between %VC, FEV1.0%, AaDO2 and smoking index. Moreover, there was no relationship between pulmonary function and duration of dust exposure. These results show that antismoking campaigns are important among workers in a dusty work environment.     

Comparison of lung function in infants exposed to maternal smoking and in infants with a family history of asthma.

STUDY OBJECTIVE: To compare lung function in infants exposed to maternal smoking with lung function in infants with a family history of asthma. There are no published studies comparing lung function in both groups. DESIGN: Cross-sectional study. SETTING: A tertiary pulmonary care center at a children's hospital. PATIENTS: One hundred five infants with daily wheezing. Thirty-five infants had persistent exposure to maternal smoking, and 70 had a family history of asthma in parents or siblings. MEASUREMENTS: Infant pulmonary function tests were compared between the two groups. The ratio of terminal to peak expiratory flow at tidal breathing at 25% of the previous expiration remaining and the ratio of terminal to peak expiratory flow with forced expiration at 25% of the previous expiration remaining (FEF25/PFEF) were used to evaluate peripheral airflow. A > 25% improvement in FEF25/PFEF after a bronchodilator challenge test was considered a positive response. RESULTS: Most infants in both groups had evidence of peripheral airflow obstruction with forced expiration. In infants exposed to maternal smoking, only 4 of 35 (11.4%) responded to a bronchodilator, compared to 51 of 70 (72.9%) in the group with a family history of asthma (p < 0.0005). There was no statistically significant difference in total respiratory system compliance, total respiratory system resistance, tidal volume, and degree of peripheral airflow obstruction at tidal breathing or after forced expiration in both groups. CONCLUSION: Infants with exposure to maternal smoking and infants with a family history of asthma have altered lung function, and a positive response to a bronchodilator is one variable that seems to differentiate the two groups.     

Cigarette smoke augments the expression and responses of toll-like receptor 3 in human macrophages

Background and objective: Cigarette smoking is the main risk factor for the development of chronic obstructive pulmonary disease (COPD). Recently, toll‐like receptor 3 (TLR3) was shown to recognize pathogen‐associated molecular patterns, especially viral‐derived double‐stranded RNA, and to be involved in immune responses. However, the effects of cigarette smoke on TLR3 remain unclear. In this study, it was examined whether cigarette smoke affects the expression and responses of TLR3 in human macrophages. Methods: The expression of TLR3 in alveolar macrophages from human lung tissues was analysed by immunohistochemistry, and the correlation of TLR3 expression with smoking history and lung function was evaluated. In addition, the effect of cigarette smoke on the expression and responses of TLR3 in macrophage lineage cells was investigated. Results: TLR3‐positive alveolar macrophage numbers were significantly increased in smokers and COPD patients compared with non‐smoking control subjects, but there was no difference between smokers and COPD patients. TLR3‐positive macrophage numbers were positively correlated with smoking history and inversely correlated with corrected carbon monoxide diffusing capacity, but were not correlated with % predicted forced expiratory volume in 1 s. Furthermore, cigarette smoke extract potentiated the expression of TLR3 in monocyte‐derived macrophages and significantly augmented the release of interleukin‐8, as well as total matrix metalloproteinase‐9 activity, in cells treated with TLR3 ligand. Conclusions: These data suggest that cigarette smoke augments the expression and responses of TLR3 in human macrophages, and this may contribute to neutrophilic airway inflammation and parenchymal destruction in the lungs of smokers and patients with COPD.     

Personality type and neural circulatory control

Psychosocial factors, including type A personality, anger, hostility, and anxiety, have been implicated in the pathogenesis of cardiovascular disease. Abnormal sympathetic responses to stress may help explain the link between certain behavior patterns and cardiovascular disease. We tested the hypothesis that in normal humans, type A personality characteristics are associated with exaggerated heart rate, pressor, and sympathetic nerve responses to mental and physical stress. We measured heart rate, blood pressure, and muscle sympathetic nerve activity (obtained with direct intraneural recordings) at rest and during stress in 45 healthy subjects (19 men and 26 women, age 29.2+/-8.7 years) who had no chronic diseases and were taking no medications. Subjects were divided into tertiles based on type A scores. There were no significant differences in sympathetic or hemodynamic reactivity among the 3 different intensity levels of type A characteristics. Baseline measures and responses to stress tests were similar across the 3 groups. Sympathetic and hemodynamic changes during stress tests were also similar in subject groups stratified according to anger scale and cynicism scale. Sympathetic nerve and hemodynamic measurements at rest and during stress were not different in normal subjects with type A characteristics. Abnormalities in sympathetic or cardiovascular reactivity are unlikely to be implicated in any excess of cardiovascular disease in people with type A personality characteristics.     

Pulmonary function in patients with reduced left ventricular function: influence of smoking and cardiac surgery.

STUDY OBJECTIVE: The impact of stable, chronic heart failure on baseline pulmonary function remains controversial. Confounding influences include previous coronary artery bypass or valve surgery (CABG), history of obesity, stability of disease, and smoking history. DESIGN: To control for some of the variables affecting pulmonary function in patients with chronic heart failure, we analyzed data in four patient groups, all with left ventricular (LV) dysfunction (LV ejection fraction [LVEF] < or =35%): (1) chronic heart failure, nonsmokers, no CABG (n = 78); (2) chronic heart failure, nonsmokers, CABG (n = 46); (3) chronic heart failure, smokers, no CABG (n = 40); and (4) chronic heart failure, smokers, CABG (n = 48). Comparisons were made with age- and gender-matched patients with a history of coronary disease but no LV dysfunction or smoking history (control subjects, n = 112) and to age-predicted norms. RESULTS: Relative to control subjects and percent-predicted values, all groups with chronic heart failure had reduced lung volumes (total lung capacity [TLC] and vital capacity [VC]) and expiratory flows (p < 0.05). CABG had no influence on lung volumes and expiratory flows in smokers, but resulted in a tendency toward a reduced TLC and VC in nonsmokers. Smokers with chronic heart failure had reduced expiratory flows compared to nonsmokers (p < 0.05), indicating an additive effect of smoking. Diffusion capacity of the lung for carbon monoxide (DLCO) was reduced in smokers and in subjects who underwent CABG, but not in patients with chronic heart failure alone. There was no relationship between LV size and pulmonary function in this population, although LV function (cardiac index and stroke volume) was weakly associated with lung volumes and DLCO. CONCLUSIONS: We conclude that patients with chronic heart failure have primarily restrictive lung changes with smoking causing a further reduction in expiratory flows.     

Evidence for a Positive Association Between Pulmonary Function and Wine Intake in a Population-Based Study

Background: Lung function is a strong predictor of cardiovascular and all-cause mortality. Previous studies suggest that alcohol exposure may be linked to impaired pulmonary function through oxidant-antioxidant mechanisms. Alcoholic beverages may be an important source of oxidants and antioxidants. We analyzed the relation of beverage-specific alcohol intake with forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) in a random sample of 1555 residents of Western New York, USA. Methods: We expressed pulmonary function as percent of predicted normal FEV1 (FEV1%) and FVC (FVC%) after adjustment for height, age, gender, and race. To obtain information on alcohol intake we used a questionnaire that reliably queries total alcohol and beverage-specific recent (past 30 days) and lifetime alcohol consumption. Results: Using multiple linear regression analysis after adjustment for covariates (pack-years of smoking, weight, smoking status, education, nutritional factors, and for FEV1%, in addition, eosinophil count), we observed no significant correlation between total alcohol intake and lung function. However, we found positive associations of recent and lifetime wine intake with FEV1% and FVC%. When we analyzed white and red wine intake separately, the association of lung function with red wine was weaker than with white wine. Conclusion: While total alcohol intake was not related to lung function, wine intake showed a positive association with lung function. Although we cannot exclude residual confounding by healthier lifestyle in wine drinkers, differential effects of alcoholic beverages on lung health may exist.