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Background: Although secondhand smoke (SHS) has been linked with various respiratory conditions and symptoms, its association with health-related quality of life (HRQOL) is unknown., Methods: A cross-sectional study was performed of 2500 never smokers in Switzerland who participated in the Swiss Cohort Study on Air Pollution and Lung Diseases in Adults and completed a 36-Item Short Form Health Survey (SF-36) in 2002. Using linear regression models adjusting for confounders, we measured the association between HRQOL and moderate or high SHS exposure (< or =3 h/d or >3 h/d) compared with no SHS exposure. Data from men and women were analyzed separately and further stratified by source of SHS (home, workplace, and public spaces)., Results: After adjustments, SHS was associated with reduced scores in all SF-36 domains. High SHS exposure predicted a greater reduction in HRQOL. Compared with nonexposed women, those with high SHS exposure at home had significantly lower scores on the physical functioning (-7.8, P < .001), role physical (-10.5, P = .02), bodily pain (-9.2, P = .01), and social functioning (-8.1, P = .007) domains. Exposed men had lower scores for the role physical domain (-20.0, P < .001) and a trend toward lower scores in other domains. In women, exposure to SHS at home was associated with a stronger negative effect on HRQOL than at work and in public spaces., Conclusions: Secondhand smoke is associated with reduced HRQOL, more significantly so in women. Exposure to SHS at home and high levels of exposure are associated with lower SF-36 scores, suggesting a dose-response relationship.

Background: The aim was to determine if effects from smoking on lung function measured over 11 years differ between men and women., Methods: In a prospective population based cohort study (Swiss Study on Air Pollution and Lung Diseases in Adults) current smokers in 1991 (18-60 yrs) were reassessed in 2002 (n = 1792). Multiple linear regression was used to estimate effects from pack-years of cigarettes smoked to 1991 and mean packs of cigarettes smoked per day between 1991 and 2002 on change in lung volume and flows over the 11 years., Results: In both sexes, packs smoked between assessments were related to lung function decline but pack-years smoked before 1991 were not. Mean annual decline in FEV1 was -10.4 mL(95%CI -15.3, -5.5) per pack per day between assessments in men and -13.8 mL(95%CI-19.5,-8.1) in women. Decline per pack per day between 1991 and 2002 was lower in women who smoked in 1991 but quit before 2002 compared to persistent smokers (-6.4 vs -11.6 mL, p = 0.05) but this was not seen in men (-14.3 vs -8.8 mL p = 0.49). Smoking related decline was accelerated in men and women with airway obstruction, particularly in women where decline in FEV1 was three fold higher in participants with FEV1/FVC<0.70 compared to other women (-39.4 vs -12.2 mL/yr per pack per day, p < 0.002)., Conclusion: There are differences in effects from smoking on lung function between men and women. Lung function recovers faster in women quitters than in men. Women current smokers with airway obstruction experience a greater smoking related decline in lung function than men.

Background: Reproductive characteristics play an aetiological role for many diseases, including reproductive cancers. They have been shown to vary internationally and nationally, but have not yet been described for the whole Swiss population. Aim: The study investigated the variability of reproductive characteristics, their patterns, and main determinants across a population-based female study population in Switzerland. Methods: Reproductive characteristics obtained from 3119 women (28-72 years) participating in the SAPALDIA cohort survey in 2001-2003 are described across birth cohorts, study areas, language regions, and levels of urbanization. Determinants of age at menopause were analysed by Cox regression. Results: Reported median age at menarche was 13 years and median age at natural menopause was 52 years. The prevalence of nulliparity was 27%, and the fertility rate 1.6. Across birth cohorts there was a decline of menarcheal age and fertility rates, and an increase of nulliparity and age at last pregnancy. All characteristics varied across study areas, language regions, and levels of urbanization. Smoking, parity, and physical exercise were stronger predictors of earlier (<52 years) than older (>52 years) menopausal age. Conclusion: Reproductive events show secular and geographic variation within Switzerland. Smoking, parity and physical activity significantly predict age at natural menopause, particularly before age 52. The secular trend of earlier menarche and increased nulliparity may result in a higher risk of reproductive cancers in younger generations. [ABSTRACT FROM AUTHOR]

Cigarette smoking is known to be the leading cause of chronic obstructive pulmonary disease (COPD). However, the detailed mechanisms have not been elucidated. PAF (platelet-activating factor), a potent inflammatory mediator, is involved in the pathogenesis of various respiratory diseases such as bronchial asthma and COPD. We focused on LPLAT9 (lysophospholipid acyltransferase 9), a biosynthetic enzyme of PAF, in the pathogenesis of COPD. LPLAT9 gene expression was observed in excised COPD lungs and single-cell RNA sequencing data of alveolar macrophages (AMs). LPLAT9 was predominant and upregulated in AMs, particularly monocyte-derived AMs, in patients with COPD. To identify the function of LPLAT9/PAF in AMs in the pathogenesis of COPD, we exposed systemic LPLAT9-knockout (LPALT9−/−) mice to cigarette smoke (CS). CS increased the number of AMs, especially the monocyte-derived fraction, which secreted MMP12 (matrix metalloprotease 12). Also, CS augmented LPLAT9 phosphorylation/activation on macrophages and, subsequently, PAF synthesis in the lung. The LPLAT9−/− mouse lung showed reduced PAF production after CS exposure. Intratracheal PAF administration accumulated AMs by increasing MCP1 (monocyte chemoattractant protein-1). After CS exposure, AM accumulation and subsequent pulmonary emphysema, a primary pathologic change of COPD, were reduced in LPALT9−/− mice compared with LPLAT9+/+ mice. Notably, these phenotypes were again worsened by LPLAT9+/+ bone marrow transplantation in LPALT9−/− mice. Thus, CS-induced LPLAT9 activation in monocyte-derived AMs aggravated pulmonary emphysema via PAF-induced further accumulation of AMs. These results suggest that PAF synthesized by LPLAT9 has an important role in the pathogenesis of COPD. [ABSTRACT FROM AUTHOR]

An individual's experience of COPD is determined by many factors in addition to the pathological features of chronic bronchitis and emphysema and the symptoms that derive directly from them. Multimorbidity is the norm rather than the exception, so most people with COPD are living with a range of other medical problems which can decrease overall quality of life. COPD is caused by the inhalation of noxious particles or gases, in particular tobacco smoke, but also by early life disadvantage impairing lung development and by occupations where inhaled exposures are common (e.g. industrial, farming and cleaning work). Wealthy people are therefore relatively protected from developing COPD and people who do develop the condition may have reduced resources to cope. COPD is also no longer a condition that predominantly affects men. The prevalence of COPD among women has equalled that of men since 2008 in many high‐income countries, due to increased exposure to tobacco, and in low‐income countries due to biomass fuels. COPD is one of the leading causes of death in women in the USA, and death rates attributed to COPD in women in some countries are predicted to overtake those of men in the next decade. Many factors contribute to this phenomenon, but in addition to socioeconomic and occupational factors, there is increasing evidence of a higher susceptibility of females to smoking and pollutants. Quality of life is also more significantly impaired in women. Although most medications (bronchodilators and inhaled corticosteroids) used to treat COPD demonstrate similar trends for exacerbation prevention and lung function improvement in men and women, this is an understudied area and clinical trials frequently have a preponderance of males. A better understanding of gender‐based predictors of efficacy of all therapeutic interventions is crucial for comprehensive patient care. There is an urgent need to recognize the increasing burden of COPD in women and to facilitate global improvements in disease prevention and management in this specific population. Many individuals with COPD follow a trajectory of both lung function decline and also multimorbidity. Unfavourable lung function trajectories throughout life have implications for later development of other chronic diseases. An enhanced understanding of the temporal associations underlying the development of coexisting diseases is a crucial first step in unravelling potential common disease pathways. Lessons can be learned from exploring disease trajectories of other NCD as well as multimorbidity development. Further research will be essential to explain how early life risk factors commonly influence trajectories of COPD and other diseases, how different diseases develop in relation to each other in a temporal way and how this ultimately leads to different multimorbidity patterns in COPD. This review integrates new knowledge and ideas pertaining to three broad themes (i) the overall burden of disease in COPD, (ii) an unappreciated high burden in women and (iii) the contrast of COPD trajectories and different multimorbidity patterns with trajectories of other NCD. The underlying pathology of COPD is largely irreversible, but many factors noted in the review are potentially amenable to intervention. Health and social care systems need to ensure that effective treatment is accessible to all people with the condition. Preventive strategies and treatments that alter the course of disease are crucial, particularly for patients with COPD as one of many problems. [ABSTRACT FROM AUTHOR]

Rationale: The association between airborne occupational exposures and lung function level is inconsistent in the general population. Moreover, little is known about the association between occupational exposures and annual lung function decline.Objectives: We investigated the association between occupational exposures and lung function level and annual lung function decline in the population-based Lifelines cohort study.Methods: We included 55,631 adults with baseline spirometry and reliable job code-13,759 of these subjects were aged ≥30 years and underwent spirometry again after 4.5 years of follow-up. Occupational exposures in the current or last-held job at baseline were estimated with the ALOHA+ job-exposure matrix. Linear regression analyses adjusted for covariates were used to test the association between each occupational exposure-biological dust, mineral dust, gases and fumes, pesticides, solvents, and metals-and lung function level and annual lung function decline. Interactions were used to test effect modification by sex or smoking.Results: Exposures to biological dust, mineral dust, gases and fumes, insecticides, fungicides, and aromatic solvents were associated with a lower lung function level at baseline. The effects were larger in males and smokers compared with females and nonsmokers, respectively. However, no association between occupational exposures and the rate of annual lung function decline was found between baseline and follow-up.Conclusions: In this study, airborne occupational exposures are associated with lower lung function level but not with a faster lung function decline. These negative effects are more pronounced among males and smokers. [ABSTRACT FROM AUTHOR]

In this cross‐sectional study, the prevalences of tooth loss, prosthetic dental restorations, and probing pocket depths (PPD) ≥4 mm, and their relationship to sociodemographic factors, were investigated in older Swiss adults. There were up to 1,673 participants aged ≥55 yr in the fourth survey of the Swiss Cohort Study on Air Pollution And Lung And Heart Disease In Adults (SAPALDIA4). Missing teeth, prosthetic dental restorations, and PPD ≥4 mm were recorded in clinical examinations conducted by field workers and compared with self‐reported information from questionnaires. Examination data showed that participants were missing five teeth on average, 74.8% had a prosthetic dental restoration, and 21.1% had PPD of ≥4 mm. The mean number of missing teeth and the prevalences of tooth loss, fixed dental prostheses, and removable dental prostheses were associated with age, education level, smoking status, and time since last visit to a dentist. Comparison of data obtained by field workers and that from self‐reports show a high level of agreement for the number of missing teeth and the prevalence of removable dental prostheses, but a lower level of agreement for self‐reports of fixed dental prostheses and periodontitis. [ABSTRACT FROM AUTHOR]

Background: Chronic obstructive pulmonary disease (COPD) is not restricted to smokers. Dietary habits may contribute to the disease occurrence. Epidemiological studies point to a protective effect of fruit and vegetable intake against COPD.Objective: To investigate the associations between dietary patterns and parameters of lung function related to COPD in the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA). Methods: Data were included from the second follow-up assessment of the SAPALDIA cohort in 2010–2011 using a food frequency questionnaire. Principal component factor analysis was used to derive dietary patterns, whose association with FEV1, FEV1/FVC, FEF2575, and COPD was investigated by applying multivariate regression analyses. Results: After adjustment for potential confounders, the “prudent dietary pattern” characterised by the predominant food groups vegetables, fruits, water, tea and coffee, fish, and nuts was positively associated with FEV1 (increase of 40 mL per SD, p < 0.001). Also for factor 3 (“high-carbohydrate diet”), we found a significant positive association with FEV1 (with an increase per SD of 36 mL, p = 0.006). Conclusions: The main results are consistent with a protective effect of a diet rich in fruits, vegetables, fish, and nuts against age-related chronic respiratory disease. If confirmed in prospective cohorts, our results may guide nutritional counselling towards respiratory health promotion. [ABSTRACT FROM AUTHOR]

Introduction: The aim of this study was to assess respiratory health and airway and systemic inflammation in professional forest firefighters post firefighting. Methods: A total of 60 firefighters who participated in forest firefighting operations in Greece during 2008 were included in the study. A questionnaire consisting of symptoms and exposure, pulmonary function, atopy, bronchial hyperresponsiveness, and markers of inflammation in induced sputum, serum, and bronchoalveolar lavage (BAL) fluid was assessed. Results: A measurable eosinophilic and neutrophilic inflammation was shown to be induced in the bronchial airways after acute exposure during forest firefighting. This was associated with increased respiratory symptoms from the upper and lower respiratory tract and pulmonary function impairment. Additionally, a measurable systemic inflammatory response was demonstrated. This study showed that acute exposure during forest firefighting significantly augments the intensity of airway and systemic inflammation in relation to the baseline inflammatory background due to chronic exposure. Conclusion: The repeated acute exposures during firefighting augment the burden of chronic airway and systemic inflammation and may eventually lead to allergic sensitization of the airways and increased incidence of rhinitis and asthma after prolonged exposure. [ABSTRACT FROM AUTHOR]

Purpose:Previous studies showed inconsistent results concerning the relationship between chronic smoking and blood pressure. Most of the studies involved self-reported smoking status. This study was performed to evaluate the association of urinary cotinine or self-reported smoking status with hypertension and blood pressure in Korean adults. Materials and methods:Among individuals enrolled in the Kangbuk Samsung Health Study and Kangbuk Samsung Cohort Study, 167,868 participants (men, 55.7%; age, 37.5 ± 6.9 years) between 2011 and 2013 who had urinary cotinine measurements were included. Individuals with urinary cotinine levels ≥50 ng/mL were defined as cotinine-verified current smokers. Results:The prevalence of hypertension and cotinine-verified current smokers in the overall population was 6.8% and 22.7%, respectively (10.0% in men and 2.8% in women for hypertension: 37.7% in men and 3.9% in women for cotinine-verified current smokers). In a multivariate regression analysis adjusted for age, sex, body mass index, waist circumference, alcohol drinking, vigorous exercise, and diabetes, cotinine-verified current smoking was associated with lower prevalence of hypertension compared with cotinine-verified never smoking (OR[95% CI], 0.79 [0.75, 0.84]). Log-transformed cotinine levels and unobserved smoking were negatively associated with hypertension, respectively (0.96 [0.96, 0.97] and 0.55 [0.39, 0.79]). In a multivariate linear regression analysis, the cotinine-verified current smoking was inversely associated with systolic and diastolic blood pressure (BP) (regression coefficient[95% CI], −1.23[−1.39, −1.07] for systolic BP and −0.71 [−0.84, −0.58] for diastolic BP). In subgroup analyses according to sex, the inverse associations between cotinine-verified current smoking and hypertension were observed only in men. Conclusions:This large observational study showed that cotinine-verified current smoking and unobserved smoking were inversely associated with hypertension in Korean adults, especially only in men. [ABSTRACT FROM AUTHOR]

Background: Studies aiming to assess genetic susceptibility for impaired lung function levels upon exposure to environmental tobacco smoke (ETS) have thus far focused on candidate-genes selected based on a-priori knowledge of potentially relevant biological pathways, such as glutathione S-transferases and ADAM33. By using a hypothesis-free approach, we aimed to identify novel susceptibility loci, and additionally explored biological pathways potentially underlying this susceptibility to impaired lung function in the context of ETS exposure.Methods: Genome-wide interactions of single nucleotide polymorphism (SNP) by ETS exposure (0 versus ≥1 h/day) in relation to the level of forced expiratory volume in one second (FEV1) were investigated in 10,817 subjects from the Dutch LifeLines cohort study, and verified in subjects from the Swiss SAPALDIA study (n = 1276) and the Dutch Rotterdam Study (n = 1156). SNP-by-ETS exposure p-values obtained from the identification analysis were used to perform a pathway analysis.Results: Fourty Five SNP-by-ETS exposure interactions with p-values <10-4 were identified in the LifeLines study, two being replicated with nominally significant p-values (<0.05) in at least one of the replication cohorts. Three pathways were enriched in the pathway-level analysis performed in the identification cohort LifeLines, i.E. the apoptosis, p38 MAPK and TNF pathways.Conclusion: This unique, first genome-wide gene-by-ETS interaction study on the level of FEV1 showed that pathways previously implicated in chronic obstructive pulmonary disease (COPD), a disease characterized by airflow obstruction, may also underlie susceptibility to impaired lung function in the context of ETS exposure. [ABSTRACT FROM AUTHOR]

Background: Both airflow limitation and smoking are established cardiovascular risk factors. However, their interaction as risk factors for the development of atherosclerosis in coronary artery disease patients remains unclear. Objectives: To evaluate the effect of the interaction between airflow limitation and smoking status on the severity of carotid atherosclerosis. Methods: We categorized the 234 enrolled patients with coronary artery disease into four groups: never-smokers with normal pulmonary function (group A), never-smokers with airflow limitation (group B), ever-smokers with normal pulmonary function (group C), and ever-smokers with airflow limitation (group D). Results: The prevalence of airflow limitation in the enrolled patients was 23.1% (ever-smokers: 15.8%, never-smokers: 7.3%). The prevalence of severe carotid atherosclerosis was 28.2, 29.4, 41.3, and 45.9%, respectively, in the four groups (group D vs. group A, p = 0.035). Even after multivariate adjusting for confounding factors, ever-smokers with airflow limitation were independently associated with severe carotid atherosclerosis (odds ratio 2.89, 95% confidence interval, 1.19-7.00, p = 0.019). Conclusions: Ever-smokers with airflow limitation were significantly associated with severe carotid atherosclerosis among patients with coronary artery disease. These findings also provide additional insight into the correlation between airflow limitation and poor cardiovascular clinical outcomes. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Tobacco use and exposure are preventable causes of morbidity and mortality. Whereas the impact of this public health issue is well described in adults with kidney disease, its role in the pediatric chronic kidney disease (CKD) population is largely unknown. This review discusses the prevalence of tobacco use and exposure in children with CKD, updates the reader on how tobacco affects the kidney, and presents intervention strategies relevant to this patient population. [ABSTRACT FROM AUTHOR]

Background and Objectives Smoking tobacco is the leading cause of preventable illness in the United States and around the world. However, much remains unknown about the factors that motivate individuals to smoke. Quality of life (QoL) has become an important measure of outcomes across all medical specialties, in both research and clinical settings. To date, there has not been a critical review of the research relevant to QoL in smokers. In this review, we describe which scales are used to quantify the QoL of smokers, the relationship between smoking and QoL and the positive impact of smoking cessation. Methods Fifty-four relevant studies are included in our review. Results Low QoL and depression are associated with higher odds of smoking initiation and lower odds of successful smoking cessation. There is a negative relationship between smoking and QoL and the magnitude of this association is related to the number of cigarettes smoked. Secondhand smoke also appears to be negatively associated with QoL. Smoking cessation significantly improves QoL. These findings have been replicated across populations with diverse socioeconomic and cultural groups around the world. Discussion and Conclusions QoL data promotes smokers and practitioners to become more sensitive to the sub-clinical adverse effects of cigarette smoking, thereby improving motivation to quit, cessation rates, and treatment outcomes. Scientific Significance Understanding the relationship between QoL and tobacco smoking is important for patients, clinicians, and researchers. (Am J Addict 2014;23:540-562) [ABSTRACT FROM AUTHOR]

Aim: In this study, the effects of cigarette smoking on maximal aerobic capacity, anaerobic capacity, and heart rate variability among female university students were investigated. Materials and methods: Twelve smokers and 21 nonsmokers participated in this study. All participants performed an intermittent sprint test (IST) and a 20 m shuttle run test to measure their anaerobic capacity and maximal aerobic capacity. The IST was comprised of 6 × 10-second sprints with a 60-second active recovery between each sprint. Heart rate variability was recorded while the participants were in a supine position 20 minutes before and 30 minutes after the IST. Results: The total work, peak power, and heart rate of the smokers and nonsmokers did not differ significantly. However, the smokers' average power declined significantly during sprints 4 to 6 (smokers versus nonsmokers, respectively: 95% confidence interval =6.2-7.2 joule/kg versus 6.8-7.6 joule/kg; P<0.05), and their fatigue index increased (smokers versus nonsmokers, respectively: 35.8% ± 2.3% versus 24.5% ± 1.76%; P<0.05) during the IST. The maximal oxygen uptake of nonsmokers was significantly higher than that of the smokers (P<0.05). The standard deviation of the normal to normal intervals and the root mean square successive difference did not differ significantly between nonsmokers and smokers. However, the nonsmokers exhibited a significantly higher normalized high frequency (HF), and significantly lower normalized low frequency (LF), LF/HF ratio, and natural logarithm of the LF/HF when compared with those of the smokers (P<0.05). Conclusion: Smoking may increase female smokers' exercise fatigue and decrease their average performance during an IST, while reducing their maximal aerobic capacity. Furthermore, smoking reduces parasympathetic nerve activity and activates sympathetic cardiac control. [ABSTRACT FROM AUTHOR]

Chronic Obstructive Pulmonary Disease (COPD) is one of the foremost causes of death worldwide. It is primarily caused by tobacco smoke, making it an easily preventable disease, but facilitated by genetic α-1 antitrypsin deficiency. In addition to active smokers, health problems also occur in people involuntarily exposed to second hand smoke (SHS). Currently, the relationship between SHS and COPD is not well established. Knowledge of pathogenic mechanisms is limited, thereby halting the advancement of new treatments for this socially and economically detrimental disease. Here, we attempt to summarize tobacco smoke studies undertaken in animal models, applying both mainstream (direct, nose only) and side stream (indirect, whole body) smoke exposures. This overview of 155 studies compares cellular and molecular mechanisms as well as proteolytic, inflammatory, and vasoreactive responses underlying COPD development. This is a difficult task, as listing of exposure parameters is limited for most experiments. We show that both mainstream and SHS studies largely present similar inflammatory cell populations dominated by macrophages as well as elevated chemokine/cytokine levels, such as TNF-α. Additionally, SHS, like mainstream smoke, has been shown to cause vascular remodeling and neutrophil elastase-mediated proteolytic matrix breakdown with failure to repair. Disease mechanisms and therapeutic interventions appear to coincide in both exposure scenarios. One of the more widely applied interventions, the anti-oxidant therapy, is successful for both mainstream and SHS. The comparison of direct with indirect smoke exposure studies in this review emphasizes that, even though there are many overlapping pathways, it is not conclusive that SHS is using exactly the same mechanisms as direct smoke in COPD pathogenesis, but should be considered a preventable health risk. Some characteristics and therapeutic alternatives uniquely exist in SHS-related COPD. [ABSTRACT FROM AUTHOR]

Background: No study has been carried out on the time trend in the prevalence of chronic bronchitis (CB) in recent years, despite its clinical and epidemiological relevance. We evaluated the trend in CB prevalence during the past decade among young Italian adults. Methods: A screening questionnaire was mailed to general population samples of 20-44 year-old subjects in two cross-sectional surveys: the Italian Study on Asthma in Young Adults (ISAYA) (1998/2000; n = 18,873, 9 centres) and the screening stage of the Gene Environment Interactions in Respiratory Diseases (GEIRD) study (2007/2010; n = 10,494, 7 centres). CB was defined as having cough and phlegm on most days for a minimum of 3 months a year and for at least 2 successive years. The prevalence rates and the risk ratios (RRs) for the association between CB and each potential predictor were adjusted for gender, age, season of response, type of contact, cumulative response rate, and centre. Results: CB prevalence was 12.5% (95% CI: 12.1-12.9%) in 1998/2000 and 12.6% (95% CI: 11.7-13.7%) in 2007/2010; it increased among never smokers (from 7.6 to 9.1%, p = 0.003), current light smokers (<15 pack-years; from 15.1 to 18.6%, p < 0.001), and unemployed/retired subjects (from 14.3 to 19.1%, p = 0.001). In this decade, the prevalence of current smoking decreased (from 33.6 to 26.9%, p < 0.001), whereas the prevalence of unemployment/premature retirement (from 5.3 to 6.0%, p = 0.005), asthma (from 5.0 to 6.2%, p = 0.003), and allergic rhinitis (from 19.5 to 24.5%, p < 0.001) increased. In both 1998/2000 and 2007/2010, the likelihood of having CB was significantly higher for women, current smokers, asthmatic patients, and subjects with allergic rhinitis. During this period, the strength of the association between CB and current heavy smoking (⩾15 pack-years) decreased (RR: from 4.82 to 3.57, p = 0.018), whereas it increased for unemployment/premature retirement (from 1.11 to 1.53, p = 0.019); no change was observed for gender, asthma, and allergic rhinitis. Conclusions: Despite the significant reduction in current smoking, CB prevalence did not vary among young Italian adults. The temporal pattern of CB prevalence can only be partly explained by the increase of unemployment/ premature retirement, asthma and allergic rhinitis, and suggests that other factors could have played a role. [ABSTRACT FROM AUTHOR]

Background: Up to 60% of chronic obstructive pulmonary disease (COPD) patients can present airway hyperresponsiveness. However, it is not known whether the peripheral lung tissue also shows an exaggerated response to agonists in COPD. Objectives: To investigate the in vitro mechanical behavior and the structural and inflammatory changes of peripheral lung tissue in COPD patients and compare to nonsmoking controls. Methods: We measured resistance and elastance at baseline and after acetylcholine (ACh) challenge of lung strips obtained from 10 COPD patients and 10 control subjects. We also assessed the alveolar tissue density of neutrophils, eosinophils, macrophages, mast cells and CD8+ and CD4+ cells, as well as the content of α-smooth muscle actin-positive cells and elastic and collagen fibers. We further investigated whether changes in in vitro parenchymal mechanics correlated to structural and inflammatory parameters and to in vivo pulmonary function. Results: Values of resistance after ACh treatment and the percent increase in tissue resistance (%R) were higher in the COPD group (p ≤ 0.03). There was a higher density of macrophages and CD8+ cells (p < 0.05) and a lower elastic content (p = 0.003) in the COPD group. We observed a positive correlation between %R and eosinophil and CD8+ cell density (r = 0.608, p = 0.002, and r = 0.581, p = 0.001, respectively) and a negative correlation between %R and the ratio of forced expiratory volume in 1 s to forced vital capacity (r = -0.451, p < 0.05). Conclusions: The cholinergic responsiveness of parenchymal lung strips is increased in COPD patients and seems to be related to alveolar tissue eosinophilic and CD8 lymphocytic inflammation and to the degree of airway obstruction on the pulmonary function test. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Recent surveys report a surprisingly high prevalence of chronic obstructive pulmonary disease (COPD) worldwide. However, there is evidence that the application of a fixed ratio of forced expiratory volume in 1 s (FEV1) to forced vital capacity (FVC) may result in a relevant misclassification of airflow limitation. Objectives: The definition of airflow limitation does have a significant impact on its prevalence. Methods: Individual values of lung volumes were assessed in comparison to a reference population by applying either a fixed ratio below 0.7 or the fifth percentile of FEV1 in relation to FVC. Based on a large-scale population-based survey, reference equations for lung volumes were derived by quantile regression analysis based on 1,809 subjects aged 25–85 years. Both functional definitions were applied to calculate the prevalence of airflow limitation. Results: The prevalence of airflow limitation was significantly higher when applying the fifth percentile compared to the fixed ratio of 0.7 for all age groups and both sexes (all 6.7 vs. 1.9%; women 6.7 vs. 1.3%; men 6.6 vs. 2.6%). Almost 26% of the subjects with airflow limitation complained of dyspnea, whereas COPD had not been previously diagnosed by a physician in 87%. Conclusion: The definition of airflow limitation has a major impact on the observed prevalence rates. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: The rate of forced expiratory volume in 1 second (FEV1) decline ("beta") is a marker of chronic obstructive pulmonary disease risk. The reduction in beta after quitting smoking is an upper limit for the reduction achievable from switching to novel nicotine delivery products. We review available evidence to estimate this reduction and quantify the relationship of smoking to beta. Methods: Studies were identified, in healthy individuals or patients with respiratory disease, that provided data on beta over at least 2 years of follow-up, separately for those who gave up smoking and other smoking groups. Publications to June 2010 were considered. Independent beta estimates were derived for four main smoking groups: never smokers, ex-smokers (before baseline), quitters (during follow-up) and continuing smokers. Unweighted and inverse variance-weighted regression analyses compared betas in the smoking groups, and in continuing smokers by amount smoked, and estimated whether beta or beta differences between smoking groups varied by age, sex and other factors. Results: Forty-seven studies had relevant data, 28 for both sexes and 19 for males. Sixteen studies started before 1970. Mean follow-up was 11 years. On the basis of weighted analysis of 303 betas for the four smoking groups, never smokers had a beta 10.8 mL/yr (95% confidence interval (CI), 8.9 to 12.8) less than continuing smokers. Betas for ex-smokers were 12.4 mL/yr (95% CI, 10.1 to 14.7) less than for continuing smokers, and for quitters, 8.5 mL/yr (95% CI, 5.6 to 11.4) less. These betas were similar to that for never smokers. In continuing smokers, beta increased 0.33 mL/yr per cigarette/day. Beta differences between continuing smokers and those who gave up were greater in patients with respiratory disease or with reduced baseline lung function, but were not clearly related to age or sex. Conclusion: The available data have numerous limitations, but clearly show that continuing smokers have a beta that is dose-related and over 10 mL/yr greater than in never smokers, ex-smokers or quitters. The greater decline in those with respiratory disease or reduced lung function is consistent with some smokers having a more rapid rate of FEV1 decline. These results help in designing studies comparing continuing smokers of conventional cigarettes and switchers to novel products. [ABSTRACT FROM AUTHOR]

Approximately 15% of cases of COPD occur in non-smokers. Among the potential risk factors for COPD in non-smokers is second-hand smoke (SHS) exposure. However, the Surgeon General reported in 2006 that the evidence linking second hand smoke and COPD is insufficient to infer a causal relationship, largely because current evidence does not establish a biological link. The goal of this study was to determine whether SHS exposure can induce alveolar macrophage recruitment and expression of activation markers that we have previously demonstrated in human smokers and in mouse models of emphysema. To achieve these goals, we studied mice exposed to an ambient mixture of predominantly [89%] sidestream smoke at increasing doses over 3 months. We found that second hand smoke exposure induced a dose-dependent increase in alveolar macrophage recruitment (mean ± sd; 224,511 ± 52,330 vs 166,152 ± 47,989 macrophages/ml of bronchoalveolar lavage in smoke-exposed vs air-exposed controls at 3 months, p = 0.003). We also found increased expression of several markers of alveolar macrophage activation (PLA2g7, dkfzp434l142, Trem-2, and pirin, all p < 0.01 at 3 months) and increased lavage levels of two inflammatory mediators associated with COPD (CCL2 [MCP-1], 58 ± 12 vs. 43 ± 22 pg/ml, p = 0.03; and TNFα, 138 ± 43 vs 88 ± 78 pg/ml, p = 0.04 at 3 months). These findings indicate that second smoke exposure can cause macrophage recruitment and activation, providing a biological link between second-hand smoke exposure and the development of inflammatory processes linked to COPD. [ABSTRACT FROM AUTHOR]

Background: Little is known about the long-term outcomes of individuals with mild chronic obstructive pulmonary disease (COPD) as defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD). Methods: A population cohort of 6671 randomly selected adults without asthma was stratified into categories of modified GOLD-defined COPD (prebronchodilator spirometry). Further stratification was based on the presence or absence of respiratory symptoms. After 11 years, associations between baseline categories of COPD and decline in forced expiratory volume in 1 s (FEV1), respiratory care utilisation and quality of life as measured by the SF-36 questionnaire were examined after controlling for age, sex, smoking and educational status. Results: At baseline, modified GOLD criteria were met by 610 (9.1%) participants, 519 (85.1%) of whom had stage 1 COPD. At follow-up, individuals with symptomatic stage 1 COPD (n = 224) had a faster decline in FEV1 (-9 ml/year (95% CI -13 to -5)), increased respiratory care utilisation (OR 1.6 (95% Cl 1.0 to 2.6)) and a lower quality of life than asymptomatic subjects with normal lung function (n = 3627, reference group). In contrast, individuals with asymptomatic stage 1 COPD (n = 295) had no significant differences in FEV1 decline (-3 mI/year (95% CI -7 to +1)), respiratory care utilisation (OR 1.05 (95% CI 0.63 to 1.73)) or quality of life scores compared with the reference group. Conclusions: In population-based studies, respiratory symptoms are of major importance for predicting long-term clinical outcomes in subjects with COPD with mild obstruction. Population studies based on spirometry only may misestimate the prevalence of clinically relevant COPD. [ABSTRACT FROM AUTHOR]

Background: Exposure to environmental tobacco smoke (ETS) increases the risk of respiratory illness in children but data are inconclusive regarding the risk of IgE sensitisation. Objective: To elucidate whether exposure to smoking prenatally and/or postnatally is related to IgE sensitisation in children at 4 years of age. Methods: As part of a prospective birth cohort study (BAMSE), a total of 4089 families with children answered questionnaires when the child was 2 months, 1, 2 and 4 years old on environmental factors and symptoms of allergic disease. Blood collected at age 4 years from 2614 children was analysed for IgE antibodies to common inhalant and food allergens. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using logistic regression with adjustments for potential confounders. Results: There was no evident association between maternal smoking during pregnancy and risk of IgE sensitisation. In contrast, a dose-response effect was found for exposure to ETS from parental smoking during the first few months of life and IgE sensitisation. There was an increased risk of sensitisation to inhalant and/or food allergens (ORadj 1.28 (95% CI 1.01 to 1.62)) among children exposed to ETS at 2 months of age. The risk appeared particularly elevated for indoor inhalant allergens, such as cat (ORadj 1.96 (95% CI 1.28 to 2.99)) and for food allergens (ORadj 1.46 (95% CI 1.11 to 1.93)). The IgE sensitising effect of ETS seemed to be confined to infants of parents without allergic diseases and to ETS exposure during early infancy. Conclusions: Our data indicate that exposure in early infancy to ETS increases the risk of IgE sensitisation to indoor inhalant and food allergens. [ABSTRACT FROM AUTHOR]

Background: Severe alpha1-antitrypsin (AAT) deficiency associated with low AAT blood concentrations is an established genetic COPD risk factor. Less is known about the respiratory health impact of variation in AAT serum concentrations in the general population. We crosssectionally investigated correlates of circulating AAT concentrations and its association with FEV1. Methods: In 5187 adults (2669 females) with high-sensitive c-reactive protein (CRP) levels ≤ 10 mg/l from the population-based Swiss SAPALDIA cohort, blood was collected at the time of follow-up examination for measuring serum AAT and CRP. Results: Female gender, hormone intake, systolic blood pressure, age in men and in postmenopausal women, as well as active and passive smoking were positively, whereas alcohol intake and BMI inversely correlated with serum AAT levels, independent of CRP adjustment. We observed an inverse association of AAT with FEV1 in the total study population (p < 0.001), that disappeared after adjustment for CRP (p = 0.28). In addition, the AAT and FEV1 association was modified by gender, menopausal status in women, and smoking. Conclusion: The results of this population-based study reflect a complex interrelationship between tobacco exposure, gender related factors, circulating AAT, systemic inflammatory status and lung function. [ABSTRACT FROM AUTHOR]

Background: Socio-economic status, smoking, and exposure to increased levels of environmental air pollution are associated with adverse effects on respiratory health. We assessed the contribution of occupational exposures, smoking and outdoor air pollution as competing factors for the association between socio-economic status and respiratory health indicators in a cohort of women from the Ruhr area aged 55 at the time of investigation between 1985 and 1990. Methods: Data of 1251 women with spirometry and complete questionnaire information about respiratory diseases, smoking and potential confounders were used in the analyses. Exposure to large-scale air pollution was assessed with data from monitoring stations. Exposure to small-scale air pollution was assessed as traffic-related exposure by distance to the nearest major road. Socio-economic status was defined by educational level. Multiple regression models were used to estimate the contribution of occupational exposures, smoking and outdoor air pollution to social differences in respiratory health. Results: Women with less than 10 years of school education in comparison to more than 10 years of school education were more often occupationally exposed (16.4% vs. 10.1%), smoked more often (20.3% vs. 13.9%), and lived more often close to major roads (26.0% vs. 22.9%). Long-term exposure to increased levels of PM10 was significantly associated with lower school education. Women with low school education were more likely to suffer from respiratory symptoms and had reduced lung function. In the multivariate analysis the associations between education and respiratory health attenuated after adjusting for occupational exposure, smoking and outdoor air pollution. The crude odds ratio for the association between the lung function indicator FEV1 less than 80% of predicted value and educational level (<10 years vs. >10 years of school education) was 1.83 (95% CI: 1.22-2.74). This changed to 1.56 (95% CI: 1.03-2.37) after adjusting for occupational exposure, smoking and outdoor air pollution. Conclusion: We found an association between socio-economic status and respiratory health. This can partly be explained by living conditions indicated by occupational exposure, smoking behaviour and ambient air pollution. A relevant part of the social differences in respiratory health, however, remained unexplained. [ABSTRACT FROM AUTHOR]

Exposure to environmental tobacco smoke (ETS) and active tobacco smoking has been shown to increase symptoms of bronchial asthma such as bronchoconstriction but effects on other respiratory symptoms remain poorly assessed. Current levels of exposure to tobacco smoke may also be responsible for the development of chronic cough in both children and adults. The present study analyses the effects of tobacco smoke exposure as potential causes of chronic cough. A panel of PubMed-based searches was performed relating the symptom of cough to various forms of tobacco smoke exposure. It was found that especially prenatal and postnatal exposures to ETS have an important influence on children's respiratory health including the symptom of cough. These effects may be prevented if children and pregnant women are protected from exposure to ETS. Whereas the total number of studies addressing the relationship between cough and ETS exposure is relatively small, the present study demonstrated that there is a critical amount of data pointing to a causative role of environmental ETS exposure for the respiratory symptom of cough. Since research efforts have only targeted this effect to a minor extent, future epidemiological and experimental studies are needed to further unravel the relation between ETS and cough. [ABSTRACT FROM AUTHOR]

Background: Little is known about long-term adverse health consequences experienced by flight attendants exposed to secondhand smoke (SHS) during the time smoking was allowed on airplanes. We undertook this study to evaluate the association between accumulated flight time in smoky airplane cabins and respiratory tract diseases in a cohort of never smoking flight attendants. Methods: We conducted a mailed survey in a cohort of flight attendants. Of 15,000 mailed questionnaires, 2053 (14%) were completed and returned. We excluded respondents with a personal history of smoking (n = 748) and non smokers with a history of respiratory tract diseases before the age of 18 years (n = 298). The remaining 1007 respondents form the study sample. Results: The overall study sample was predominantly white (86%) and female (89%), with a mean age of 54 years. Overall, 69.7% of the respondents were diagnosed with at least one respiratory tract disease. Among these respondents, 43.4% reported a diagnosis of sinusitis, 40.3% allergies, 30.8% bronchitis, 23.2% middle ear infections, 13.6% asthma, 13.4% hay fever, 12.5% pneumonia, and 2.0% chronic obstructive pulmonary disease. More hours in a smoky cabin were observed to be significantly associated with sinusitis (OR = 1.21; p = 0.024), middle ear infections (OR = 1.30; p = 0.006), and asthma (OR = 1.26; p = 0.042). Conclusion: We observed a significant association between hours of smoky cabin exposure and self-reported reported sinusitis, middle ear infections, and asthma. Our findings suggest a doseresponse between duration of SHS exposure and diseases of the respiratory tract. Our findings add additional evidence to the growing body of knowledge supporting the need for widespread implementation of clean indoor air policies to decrease the risk of adverse health consequences experienced by never smokers exposed to SHS. [ABSTRACT FROM AUTHOR]

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% < 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. [ABSTRACT FROM AUTHOR]

Background: The distribution of airway responsiveness in a general population of non-smokers without respiratory symptoms has not been established, limiting its use in clinical and epidemiological practice. We derived reference equations depending on individual characteristics (i.e., sex, age, baseline lung function) for relevant percentiles of the methacholine two-point dose-response slope. Methods: In a reference sample of 1567 adults of the SAPALDIA cross-sectional survey (1991), defined by excluding subjects with respiratory conditions, responsiveness during methacholine challenge was quantified by calculating the two-point dose-response slope (O'Connor). Weighted L1-regression was used to estimate reference equations for the 95th, 90th, 75th and 50th percentiles of the two-point slope. Results: Reference equations for the 95th, 90th, 75th and 50th percentiles of the two-point slope were estimated using a model of the form a + b* Age + c* FEV1 + d* (FEV1)² , where FEV1 corresponds to the pre-test (or baseline) level of FEV1. For the central half of the FEV1 distribution, we used a quadratic model to describe the dependence of methacholine slope on baseline FEV1. For the first and last quartiles of FEV1, a linear relation with FEV1 was assumed (i.e., d was set to 0). Sex was not a predictor term in this model. A negative linear association with slope was found for age. We provide an Excel file allowing calculation of the percentile of methacholine slope of a subject after introducing age - pre-test FEV1 - and results of methacholine challenge of the subject. Conclusion: The present study provides equations for four relevant percentiles of methacholine two-point slope depending on age and baseline FEV1 as basic predictors in an adult reference population of non-obstructive and non-atopic persons. These equations may help clinicians and epidemiologists to better characterize individual or population airway responsiveness. [ABSTRACT FROM AUTHOR]

Background: There is a dearth of standardized studies examining exposure to environmental tobacco smoke (ETS) and its relationship to respiratory health among adults in developing countries. Methods: In 2004, the Syrian Center for Tobacco Studies (SCTS) conducted a population-based survey using stratified cluster sampling to look at issues related to environmental health of adults aged 18-65 years in Aleppo (2,500,000 inhabitants). Exposure to ETS was assessed from multiple self-reported indices combined into a composite score (maximum 22), while outcomes included both self-report (symptoms/diagnosis of asthma, bronchitis, and hay fever), and objective indices (spirometric assessment of FEV1 and FVC). Logistic and linear regression analyses were conducted to study the relation between ETS score and studied outcomes, whereby categorical (tertiles) and continuous scores were used respectively, to evaluate the association between ETS exposure and respiratory health, and explore the dose-response relationship of the association. Results: Of 2038 participants, 1118 were current non-smokers with breath CO levels ≤ 10 ppm (27.1% men, mean age 34.7 years) and were included in the current analysis. The vast majority of study participants were exposed to ETS, whereby only 3.6% had ETS score levels ≤ 2. In general, there was a significant dose-response pattern in the relationship of ETS score with symptoms of asthma, hay fever, and bronchitis, but not with diagnoses of these outcomes. The magnitude of the effect was in the range of two-fold increases in the frequency of symptoms reported in the high exposure group compared to the low exposure group. Severity of specific respiratory problems, as indicated by frequency of symptoms and health care utilization for respiratory problems, was not associated with ETS exposure. Exposure to ETS was associated with impaired lung function, indicative of airflow limitation, among women only. Conclusions: This study provides evidence for the alarming extent of exposure to ETS among adult nonsmokers in Syria, and its dose-response relationship with respiratory symptoms of infectious and noninfectious nature. It calls for concerted efforts to increase awareness of this public health problem and to enforce regulations aimed at protecting non-smokers. [ABSTRACT FROM AUTHOR]

In air pollution epidemiology, estimates of long term exposure are often based on measurements made at one fixed site monitor per area. This may lead to exposure misclassification. The present paper validates a questionnaire-based indicator of ambient air pollution levels and its applicability to assess their within-area variability. Within the framework of the SAPALDIA (Swiss Study on Air Pollution and Lung Diseases in Adults) cross-sectional study (1991), 9,651 participants reported their level of annoyance caused by air pollution on an 11-point scale. This subjective measure was compared with annual mean concentrations of particulate matter less than 10 μm in diameter (PM10) and nitrogen dioxide. The impact of individual factors on reported scores was evaluated. Nitrogen dioxide concentrations at home outdoors (measured in 1993), smoking, workplace dust exposure, and respiratory symptoms were found to be predictors of individual annoyance scores. Regression of population mean annoyance scores against annual mean PM10 and nitrogen dioxide concentrations (measured in 1993 and 1991, respectively) across areas showed a linear relation and strong correlations (r > 0.85). Analysis within areas yielded consistent results. The observed associations between subjective and objective air pollution exposure estimates suggest that population mean scores, but not individual scores, may serve as a simple tool for grading air quality within areas. Reported annoyance due to air pollution should be considered an indicator for a complex environmental condition and thus might be used for evaluating the implementation of environmental policies. [ABSTRACT FROM PUBLISHER]

Incompletely documented symptom episodes pose methodological problems in the analysis of diary data. The aim of this study was to develop a method of estimating the average durations of symptomatic and nonsymptomatic episodes, respectively, coping with the problem of bias due to undocumented days and censored episodes that is found in most diary studies. The authors derived their outcome variables from a Markov model using transition probabilities. To evaluate this method, the authors assessed the impact of active smoking on the duration of episodes of bronchitis symptoms and the corresponding nonsymptomatic periods, respectively, using diary data (1992–1993) obtained from 801 participants in the Swiss Study on Air Pollution and Lung Diseases in Adults. Covariate-adjusted distribution curves for the mean durations of individual episodes were estimated by Cox regression. Median values for light smokers (<10 cigarettes/day) were 60.0 sympton-free days (95% confidence interval (CI) 42.0–78.5) and 4.0 symptomatic days (95% CI 3.0–6.0), respectively, compared with medians of only 21.0 days 95% CI 16.2–29.8) for periods without bronchitis symptoms and 6.0 days (95% CI 4.9–9.0) for episodes of bronchitis symptoms in heavy smokers(≥30 cigarettes/day). The authors suggest that the Markov method is a feasible approach to the assessment of long term effects of smoking and environmental risk factors on the average duration of symptomatic and nonsymptomatic respiratory episodes. Am J Epidemiol 1998;148:600–8. [ABSTRACT FROM AUTHOR]

Both smoking and air pollution impair lung function, but little information is available regarding the combined effects on the pulmonary system. The potential effects of smoking and sulfur dioxide (SO2) were examined on lung function. Data were collected from family health examinations of 867 subjects, aged 20-86 yr, in a Korean community. The subjects responded to a questionnaire interview and completed lung function tests. Data on SO2 exposure were obtained from the Environmental Management Corporation. Studies sshowed that exposure to SO2 induced a short, marked decrease in forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) in smokers compared with nonsmokers. The effect lasted up to 30 h after exposure. Consequently, preventive efforts are necessary to reduce the risks that air pollution and smoking pose to the respiratory system. [ABSTRACT FROM AUTHOR]

No study has reported the relationship between secondhand smoke (SHS) exposure and hypertension in self-reported never-smokers verified by nicotine metabolite. The aim of this study is to determine the relationship between SHS exposure and hypertension in self-reported and cotinine-verified never-smokers. A total of 106,268 self-reported never-smokers, verified as nonsmokers by urinary cotinine, who participated in Kangbuk Samsung Cohort study (KSCS) between 2012 and 2016 were included. Cotinine-verified nonsmokers were defined as individuals having urinary cotinine <50 ng/mL. SHS exposure was defined as current exposure to passive smoke indoors at home or the workplace. The multivariate regression model revealed that SHS exposure was associated with hypertension (odds ratio (OR) (95% confidence interval (CI)), 1.16 (1.08, 1.24)). Current SHS exposure that has been exposed to home SHS (1.22 (1.11, 1.33)) as well as current SHS exposure only at the workplace (1.15 (1.02, 1.29)) significantly increased the ORs for hypertension compared to no SHS exposure. There was no significant gender interaction for the relationships between SHS exposure and hypertension. This study showed that SHS exposure was significantly associated with hypertension in self-reported never-smokers verified as nonsmokers by urinary cotinine, suggesting necessity of health program and stricter smoking regulation to reduce the risk of hypertension. [ABSTRACT FROM AUTHOR]

Background: Traffic-related pollution is associated with the onset of asthma in children. Its effect on adult-onset asthma is poorly investigated. The SAPALDIA cohort study was used to investigate associations between the 11-year change (1991-2002) in home outdoor traffic-related particulate matter up to 10 μm in diameter (TPM10) and the incidence of asthma. Methods: Never-smokers without asthma at baseline aged 18-60 years in 1991 were eligible for inclusion in the study. Subjects reporting doctor-diagnosed asthma at follow-up were considered incident cases. TPM10 at baseline and follow-up was predicted and interpolated to subjects' place of residence by dispersion models using emission and meteorological data. Cox proportional hazard models for time to asthma onset were adjusted (age, gender, baseline atopy, body mass index, bronchial reactivity, maternal allergies). Results: Of 2725 never-smokers, 41 reported asthma onset in 2002. Home outdoor TPM10 concentrations improved during the interval (mean -0.6; range -9 to +7.2; IQR 0.6 μg/m3). The incidence of asthma was associated with a change in TPM10. The hazard ratio (1.30; 95% CI 1.05 to 1.61) per 1 μg/m3 change in TPM10 (IQR) was not sensitive to further adjustments (education, workplace exposure, passive smoking, parental asthma or allergies, random area effects, lung function or co-pollutants such as regional, secondary, total PM10 or proximity to busy roads). Conclusion: The data suggest a role for traffic-related pollution in adult-onset asthma. Space, time and source-specific individual assignment of exposure to traffic-related pollution is a key strength of SAPALDIA. It may explain why findings were statistically significant despite the limited number of new cases. As traffic-related pollution prevails, the finding may be of substantial public health relevance. [ABSTRACT FROM AUTHOR]