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  • 1. Adam, Martin
    et al.
    Schikowski, Tamara
    Carsin, Anne Elie
    Cai, Yutong
    Jacquemin, Benedicte
    Sanchez, Margaux
    Vierkötter, Andrea
    Marcon, Alessandro
    Keidel, Dirk
    Sugiri, Dorothee
    Al Kanani, Zaina
    Nadif, Rachel
    Siroux, Valérie
    Hardy, Rebecca
    Kuh, Diana
    Rochat, Thierry
    Bridevaux, Pierre-Olivier
    Eeftens, Marloes
    Tsai, Ming-Yi
    Villani, Simona
    Phuleria, Harish Chandra
    Birk, Matthias
    Cyrys, Josef
    Cirach, Marta
    de Nazelle, Audrey
    Nieuwenhuijsen, Mark J
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    de Hoogh, Kees
    Declerq, Christophe
    Bono, Roberto
    Piccioni, Pavilio
    Quass, Ulrich
    Heinrich, Joachim
    Jarvis, Deborah
    Pin, Isabelle
    Beelen, Rob
    Hoek, Gerard
    Brunekreef, Bert
    Schindler, Christian
    Sunyer, Jordi
    Krämer, Ursula
    Kauffmann, Francine
    Hansell, Anna L
    Künzli, Nino
    Probst-Hensch, Nicole
    Adult lung function and long-term air pollution exposure. ESCAPE: a multicentre cohort study and meta-analysis2015In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 41, no 5, p. 38-50Article in journal (Refereed)
    Abstract [en]

    The chronic impact of ambient air pollutants on lung function in adults is not fully understood. The objective of this study was to investigate the association of long-term exposure to ambient air pollution with lung function in adult participants from five cohorts in the European Study of Cohorts for Air Pollution Effects (ESCAPE). Residential exposure to nitrogen oxides (NO2, NOx) and particulate matter (PM) was modelled and traffic indicators were assessed in a standardised manner. The spirometric parameters forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) from 7613 subjects were considered as outcomes. Cohort-specific results were combined using meta-analysis. We did not observe an association of air pollution with longitudinal change in lung function, but we observed that a 10 μg·m(-3) increase in NO2 exposure was associated with lower levels of FEV1 (-14.0 mL, 95%CI -25.8- -2.1) and FVC (-14.9 mL, 95% CI -28.7- -1.1). An increase of 10 μg·m(-3) in PM10, but not other PM metrics (PM2.5, coarse fraction of PM, PM absorbance), was associated with a lower level of FEV1 (-44.6 mL, 95% CI -85.4- -3.8) and FVC (-59.0 mL, 95% CI -112.3- -5.6). The associations were particularly strong in obese persons. This study adds to the evidence for an adverse association of ambient air pollution with lung function in adults at very low levels in Europe.

  • 2. Andersson, E
    et al.
    Knutsson, A
    Hagberg, S
    Nilsson, T
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Karlsson, B
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Alfredsson, L
    Torén, K
    Incidence of asthma among workers exposed to sulphur dioxide and other irritant gases.2006In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 27, no 4, p. 720-725Article in journal (Refereed)
    Abstract [en]

    The aim of the present study was to investigate whether repeated peak exposure (gassings) to sulphur dioxide (SO2) and other irritant gases increases the risk of new-onset asthma. A questionnaire was sent to 4,112 sulphite workers, of whom 1,919 completed the questionnaire and 396 completed the short-form questionnaire, which was sent out as a last reminder. A sample of 130 nonrespondents completed a telephone interview using the short-form questionnaire. The incidence of adult-onset, physician-diagnosed asthma during employment duration was analysed in relation to exposure to SO2 and gassings giving rise to respiratory symptoms. Incidence rates, as well as incidence rate ratios with 95% confidence interval (CI), were calculated. Further Cox regression models were used allowing assessment of hazard ratios (HR) stratified for sex and adjusted for atopy, smoking habits and age. The incidence rate for asthma among sulphite mill workers reporting gassings of SO2 was 6.2 out of 1,000 person-yrs, compared with 1.9 out of 1,000 person-yrs among subjects unexposed to SO2 and any gassings (HR (95% CI) 4.0 (2.1-7.7)). Among males reporting gassings to SO2, the HR (95% CI) for asthma was 5.8 (2.6-13) compared with unexposed males. In conclusion, repeated peak exposure to sulphur dioxide increased the incidence of asthma during work in sulphite pulp mills, which supports the hypothesis of irritant-induced asthma.

  • 3. Ayres, JG
    et al.
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Annesi-Maesano, I
    Dey, R
    Ebi, KL
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Helms, PJ
    Medina-Ramón, M
    Windt, M
    Forastiere, F
    Climate change and respiratory disease: European Respiratory Society position statement2009In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 34, no 2, p. 295-302Article in journal (Refereed)
    Abstract [en]

    Climate change will affect individuals with pre-existing respiratory disease, but the extent of the effect remains unclear. The present position statement was developed on behalf of the European Respiratory Society in order to identify areas of concern arising from climate change for individuals with respiratory disease, healthcare workers in the respiratory sector and policy makers. The statement was developed following a 2-day workshop held in Leuven (Belgium) in March 2008. Key areas of concern for the respiratory community arising from climate change are discussed and recommendations made to address gaps in knowledge. The most important recommendation was the development of more accurate predictive models for predicting the impact of climate change on respiratory health. Respiratory healthcare workers also have an advocatory role in persuading governments and the European Union to maintain awareness and appropriate actions with respect to climate change, and these areas are also discussed in the position statement.

  • 4. Bakke, PS
    et al.
    Rönnmark, Eva
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Eagan, T
    Pistelli, F
    Annesi-Maesano, I
    Maly, M
    Meren, M
    Vermeire, P
    Vestbo, J
    Viegi, G
    Zielinski, J
    Lundbäck, B
    Recommendations for epidemiological studies on COPD2011In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 38, no 6, p. 1261-1277Article in journal (Refereed)
    Abstract [en]

    The prevalence of chronic obstructive pulmonary disease (COPD) has been extensively studied, especially in Western Europe and North America. Few of these data are directly comparable because of differences between the surveys regarding composition of study populations, diagnostic criteria of the disease and definitions of the risk factors. Few community studies have examined phenotypes of COPD and included other ways of characterising the disease beyond that of spirometry. The objective of the present Task Force report is to present recommendations for the performance of general population studies in COPD in order to facilitate comparable and valid estimates on COPD prevalence by various risk factors. Diagnostic criteria in epidemiological settings, and standardised methods to examine the disease and its potential risk factors are discussed. The paper also offers practical advice for planning and performing an epidemiological study on COPD. The main message of the paper is that thorough planning is worth half the study. It is crucial to stick to standardised methods and good quality control during sampling. We recommend collecting biological markers, depending on the specific objectives of the study. Finally, studies of COPD in the population at large should assess various phenotypes of the disease.

  • 5.
    Behndig, Annelie
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Mudway, IS
    Brown, JL
    Stenfors, Nikolai
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Helleday, Ragnberth
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Duggan, ST
    Wilson, SJ
    Boman, C
    Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics, Energy Technology and Thermal Process Chemistry.
    Cassee, FR
    Frew, AJ
    Kelly, FJ
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Airway antioxidant and inflammatory responses to diesel exhaust exposure in healthy humans.2006In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 27, no 2, p. 359-365Article in journal (Refereed)
    Abstract [sv]

    Pulmonary cells exposed to diesel exhaust (DE) particles in vitro respond in a hierarchical fashion with protective antioxidant responses predominating at low doses and inflammation and injury only occurring at higher concentrations. In the present study, the authors examined whether similar responses occurred in vivo, specifically whether antioxidants were upregulated following a low-dose DE challenge and investigated how these responses related to the development of airway inflammation at different levels of the respiratory tract where particle dose varies markedly. A total of 15 volunteers were exposed to DE (100 microg x m(-3) airborne particulate matter with a diameter of <10 microm for 2 h) and air in a double-blinded, randomised fashion. At 18 h post-exposure, bronchoscopy was performed with lavage and mucosal biopsies taken to assess airway redox and inflammatory status. Following DE exposure, the current authors observed an increase in bronchial mucosa neutrophil and mast cell numbers, as well as increased neutrophil numbers, interleukin-8 and myeloperoxidase concentrations in bronchial lavage. No inflammatory responses were seen in the alveolar compartment, but both reduced glutathione and urate concentrations were increased following diesel exposure. In conclusion, the lung inflammatory response to diesel exhaust is compartmentalised, related to differing antioxidant responses in the conducting airway and alveolar regions.

  • 6.
    Behndig, Annelie
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Mudway, IS
    Brown, JL
    Stenfors, Nikolai
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Helleday, Ragnberth
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Duggan, ST
    Wilson, SJ
    Boman, Christoffer
    Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics, Energy Technology and Thermal Process Chemistry.
    Cassee, FR
    Frew, AJ
    Kelly, FJ
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Airway antioxidant and inflammatory responses to diesel exhaust exposure in healthy humans.2006In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 27, no 2, p. 359-365Article in journal (Refereed)
    Abstract [sv]

    Pulmonary cells exposed to diesel exhaust (DE) particles in vitro respond in a hierarchical fashion with protective antioxidant responses predominating at low doses and inflammation and injury only occurring at higher concentrations. In the present study, the authors examined whether similar responses occurred in vivo, specifically whether antioxidants were upregulated following a low-dose DE challenge and investigated how these responses related to the development of airway inflammation at different levels of the respiratory tract where particle dose varies markedly. A total of 15 volunteers were exposed to DE (100 microg x m(-3) airborne particulate matter with a diameter of <10 microm for 2 h) and air in a double-blinded, randomised fashion. At 18 h post-exposure, bronchoscopy was performed with lavage and mucosal biopsies taken to assess airway redox and inflammatory status. Following DE exposure, the current authors observed an increase in bronchial mucosa neutrophil and mast cell numbers, as well as increased neutrophil numbers, interleukin-8 and myeloperoxidase concentrations in bronchial lavage. No inflammatory responses were seen in the alveolar compartment, but both reduced glutathione and urate concentrations were increased following diesel exposure. In conclusion, the lung inflammatory response to diesel exhaust is compartmentalised, related to differing antioxidant responses in the conducting airway and alveolar regions.

  • 7.
    Bergdahl, I A
    et al.
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Torén, K
    Eriksson, K
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Hedlund, U
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Nilsson, T
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Flodin, R
    Järvholm, B
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Increased mortality in COPD among construction workers exposed to inorganic dust.2004In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 23, no 3, p. 402-406Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to find out if occupational exposure to dust, fumes or gases, especially among never-smokers, increased the mortality from chronic obstructive pulmonary disease (COPD). A cohort of 317,629 Swedish male construction workers was followed from 1971 to 1999. Exposure to inorganic dust (asbestos, man-made mineral fibres, dust from cement, concrete and quartz), gases and irritants (epoxy resins, isocyanates and organic solvents), fumes (asphalt fumes, diesel exhaust and metal fumes), and wood dust was based on a job-exposure matrix. An internal control group with "unexposed" construction workers was used, and the analyses were adjusted for age and smoking. When all subjects were analysed, there was an increased mortality from COPD among those with any airborne exposure (relative risk 1.12 (95% confidence interval (CI) 1.03-1.22)). In a Poisson regression model, including smoking, age and the major exposure groups, exposure to inorganic dust was associated with an increased risk (hazard ratio (HR) 1.10 (95% CI 1.06-1.14)), especially among never-smokers (HR 2.30 (95% CI 1.07-4.96)). The fraction of COPD among the exposed attributable to any airborne exposure was estimated as 10.7% overall and 52.6% among never-smokers. In conclusion, occupational exposure among construction workers increases mortality due to chronic obstructive pulmonary disease, even among never-smokers.

  • 8.
    Bergdahl, Ingvar
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Torén, K
    Nilsson, Tohr
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Eriksson, Kåre
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Hedlund, U
    Flodin, R
    Järvholm, Bengt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Increased mortality in COPD among construction workers exposed to inorganic dust: from the authors2004In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 24, no 3, p. 512-512Article in journal (Refereed)
  • 9.
    Bosson, Jenny
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Barath, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Pourazar, Jamshid
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Behndig, Annelie F
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Ädelroth, Ellinor
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Diesel exhaust exposure enhances the ozone-induced airway inflammation in healthy humans2008In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 31, no 6, p. 1234-1240Article in journal (Refereed)
    Abstract [en]

    Exposure to particulate matter and ozone cause adverse airway reactions. Individual pollutant effects are often addressed separately, despite coexisting in ambient air. The present investigation was performed to study the effects of sequential exposures to diesel exhaust (DE) and ozone on airway inflammation in human subjects. Healthy subjects underwent bronchoscopy with bronchoalveolar lavage (BAL) and bronchial wash (BW) sampling on two occasions. Once following a DE exposure (with 300 mug.m(-3) particles with a 50% cut-off aerodynamic diameter of 10 mum) with subsequent exposure to O(3) (0.2 ppm) 5 h later. The other bronchoscopy was performed after a filtered air exposure followed by an ozone exposure, using an identical protocol. Bronchoscopy was performed 24 h after the start of the initial exposure. Significant increases in neutrophil and macrophage numbers were found in BW after DE followed by ozone exposure versus air followed by ozone exposure. DE pre-exposure also raised eosinophil protein X levels in BAL compared with air. The present study indicates additive effects of diesel exhaust on the ozone-induced airway inflammation. Together with similar results from a recent study with sequential diesel exhaust and ozone exposures, the present data stress a need to consider the interaction and cumulative effects of different air pollutants.

  • 10. Brunekreef, B
    et al.
    Annesi-Maesano, I
    Ayres, JG
    Forastiere, F
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Kuenzli, N
    Pekkanen, J
    Sigsgaard, T
    Ten principles for clean air2012In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 39, no 3, p. 525-528Article in journal (Refereed)
  • 11. Brunekreef, Bert
    et al.
    Künzli, Nino
    Pekkanen, Juha
    Annesi-Maesano, Isabella
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Sigsgaard, Torben
    Keuken, Menno
    Forastiere, Francesco
    Barry, Maeve
    Querol, Xavier
    Harrison, Roy M
    Clean air in Europe: beyond the horizon?2015In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 45, no 1, p. 7-10Article in journal (Other academic)
  • 12. Castro-Giner, F
    et al.
    Kogevinas, M
    Imboden, M
    de Cid, R
    Jarvis, D
    Mächler, M
    Berger, W
    Burney, P
    Franklin, Karl A
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery.
    Gonzalez, J R
    Heinrich, J
    Janson, C
    Omenaas, E
    Pin, I
    Rochat, T
    Sunyer, J
    Wjst, M
    Antó, J-M
    Estivill, X
    Probst-Hensch, N M
    Joint effect of obesity and TNFA variability on asthma: two international cohort studies.2009In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 33, no 5, p. 1003-1009Article in journal (Refereed)
    Abstract [en]

    Obesity is a risk factor for asthma. Adipose tissue expresses pro-inflammatory molecules including tumour necrosis factor (TNF), and levels of TNF are also related to polymorphisms in the TNF-alpha (TNFA) gene. The current authors examined the joint effect of obesity and TNFA variability on asthma in adults by combining two population-based studies. The European Community Respiratory Health Survey and the Swiss Cohort Study on Air Pollution and Lung and Heart Disease in Adults used comparable protocols, questionnaires and measures of lung function and atopy. DNA samples from 9,167 participants were genotyped for TNFA -308 and lymphotoxin-alpha (LTA) +252 gene variants. Obesity and TNFA were associated with asthma when mutually adjusting for their independent effects (odds ratio (OR) for obesity 2.4, 95% confidence interval (CI) 1.7-3.2; OR for TNFA -308 polymorphism 1.3, 95% CI 1.1-1.6). The association of obesity with asthma was stronger for subjects carrying the G/A and A/A TNFA -308 genotypes compared with the more common G/G genotype, particularly among nonatopics (OR for G/A and A/A genotypes 6.1, 95% CI 2.5-14.4; OR for G/G genotype 1.7, 95% CI 0.8-3.3). The present findings provide, for the first time, evidence for a complex pattern of interaction between obesity, a pro-inflammatory genetic factor and asthma.

  • 13. Castro-Giner, F
    et al.
    Kogevinas, M
    Mächler, M
    de Cid, R
    Van Steen, K
    Imboden, M
    Schindler, C
    Berger, W
    Gonzalez, J R
    Franklin, Karl A
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Janson, C
    Jarvis, D
    Omenaas, E
    Burney, P
    Rochat, T
    Estivill, X
    Antó, J M
    Wjst, M
    Probst-Hensch, N M
    TNFA -308G>A in two international population-based cohorts and risk of asthma2008In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 32, no 2, p. 350-361Article in journal (Refereed)
    Abstract [en]

    Genetic association studies have related the tumour necrosis factor-alpha gene (TNFA) guanine to adenine substitution of nucleotide -308 (-308G>A) polymorphism to increased risk of asthma, but results are inconsistent. The aim of the present study was to test whether two single-nucleotide polymorphisms, of TNFA and of the lymphotoxin-alpha gene (LTA), are associated with asthma, bronchial hyperresponsiveness and atopy in adults, by combining the results of two large population-based multicentric studies and conducting a meta-analysis of previously published studies. The European Community Respiratory Health Survey (ECRHS) and Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) used comparable protocols, including questionnaires for respiratory symptoms and measures of lung function and atopy. DNA samples from 11,136 participants were genotyped at TNFA -308 and LTA 252. Logistic regression employing fixed and random effects models and nonparametric techniques were used. The prevalence of asthma was 6%. The TNFA -308G>A polymorphism was associated with increased asthma prevalence and with bronchial hyperresponsiveness. No consistent association was found for atopy. The LTA 252A>G polymorphism was not associated with any of the outcomes. A meta-analysis of 17 studies showed an increased asthma risk for the TNFA -308 adenine allele. The tumour necrosis factor-alpha gene nucleotide -308 polymorphism is associated with a moderately increased risk of asthma and bronchial hyperresponsiveness, but not with atopy. These results are supported by a meta-analysis of previously published studies.

  • 14.
    Ekerljung, Linda
    et al.
    Krefting Research Centre, Department of Internal Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Bossios, Apostolos
    Krefting Research Centre, Department of Internal Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Lötvall, Jan
    Krefting Research Centre, Department of Internal Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Olin, Anna-Carin
    Department of Public Health and Community Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Rönmark, Eva
    Obstructive Lung Disease in Northern Sweden (OLIN), Dept of Medicine, Sunderby Central Hospital of Norrbotten, Luleå, Sweden.
    Wennergren, Göran
    Department of Paediatrics, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Torén, Kjell
    Department of Environmental & Occupational Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Lundbäck, Bo
    Obstructive Lung Disease In Northern Sweden (OLIN) studies, Department of Medicine, Sunderby Central Hospital of Norrbotten, Luleå, Sweden.
    Multi-symptom asthma as an indication of disease severity in epidemiology2011In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 38, no 4, p. 825-832Article in journal (Refereed)
    Abstract [en]

    Epidemiological questionnaires have failed to identify individuals with severe asthma. The extent of symptoms of asthma can, however, be easily established in epidemiology, by identification of multiple symptoms. We hypothesise that reporting of multiple symptoms of asthma reflects uncontrolled disease and is a sign of more severe asthma. The aims of the current study were, therefore, to determine the prevalence and determinants of multi-symptom asthma.

    A postal questionnaire was sent to 30,000 randomly selected individuals aged 16–75 yrs. A subgroup underwent clinical examinations. Multi-symptom asthma was defined as reported physician-diagnosed asthma, use of asthma medication, recurrent wheeze, attacks of shortness of breath and at least one additional respiratory symptom.

    The prevalence of multi-symptom asthma was 2.0%, and it was more common among females (2.4 versus 1.5%; p<0.001) and those with a body mass index >30 kg·m-2. Multi-symptom asthmatics had lower forced expiratory volume in 1 s, higher exhaled nitric oxide fraction and more pronounced hyperresponsiveness. Family history of both asthma and allergy (OR 7.3), and occupational exposure to gas dust or fumes (OR 2.0) were also significant risk factors.

    Multi-symptom asthmatics comprise 2% of the general population; multi-symptom asthma is related to signs of more severe disease and could be used as an epidemiological marker of disease severity.

  • 15. Ekström, Magnus
    et al.
    Schiöler, Linus
    Grønseth, Rune
    Johannessen, Ane
    Svanes, Cecilie
    Leynaert, Benedicte
    Jarvis, Deborah
    Gislason, Thorarinn
    Demoly, Pascal
    Probst-Hensch, Nicole
    Pin, Isabelle
    Corsico, Angelo G
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Heinrich, Joachim
    Nowak, Dennis
    Raherison-Semjen, Chantal
    Dharmage, Shyamali C
    Trucco, Giulia
    Urrutia, Isabel
    Martinez-Moratalla Rovira, Jesús
    Sánchez-Ramos, José Luis
    Janson, Christer
    Torén, Kjell
    Absolute values of lung function explain the sex difference in breathlessness in the general population2017In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 49, no 5, article id 1602047Article in journal (Refereed)
    Abstract [en]

    Activity-related breathlessness is twice as common among females as males in the general population and is associated with adverse health outcomes. We tested whether this sex difference is explained by the lower absolute forced expiratory volume in 1 s (FEV1) or forced vital capacity (FVC) in females.This was a cross-sectional analysis of 3250 subjects (51% female) aged 38-67 years across 13 countries in the population-based third European Community Respiratory Health Survey. Activity-related breathlessness was measured using the modified Medical Research Council (mMRC) scale. Associations with mMRC were analysed using ordered logistic regression clustering on centre, adjusting for post-bronchodilator spirometry, body mass index, pack-years smoking, cardiopulmonary diseases, depression and level of exercise.Activity-related breathlessness (mMRC ≥1) was twice as common in females (27%) as in males (14%) (odds ratio (OR) 2.21, 95% CI 1.79-2.72). The sex difference was not reduced when controlling for FEV1 % predicted (OR 2.33), but disappeared when controlling for absolute FEV1 (OR 0.89, 95% CI 0.69-1.14). Absolute FEV1 explained 98-100% of the sex difference adjusting for confounders. The effect was similar within males and females, when using FVC instead of FEV1 and in healthy never-smokers.The markedly more severe activity-related breathlessness among females in the general population is explained by their smaller spirometric lung volumes.

  • 16.
    Emilsson, Ossur I.
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Bengtsson, Anna
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Franklin, Karl A.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Toren, Kjell
    Benediktsdottir, Bryndis
    Farkhooy, Amir
    Weyler, Joost
    Dom, Sandra
    De Backer, Wilfried
    Gislason, Thorarinn
    Janson, Christer
    Nocturnal gastro-oesophageal reflux, asthma and symptoms of OSA: a longitudinal, general population study2013In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 41, no 6, p. 1347-1354Article in journal (Refereed)
    Abstract [en]

    Nocturnal gastro-oesophageal reflux (nGOR) is associated with asthma and obstructive sleep apnoea (OSA). Our aim was to investigate whether nGOR is a risk factor for onset of asthma and onset of respiratory and OSA symptoms in a prospective population-based study. We invited 2640 subjects from Iceland, Sweden and Belgium for two evaluations over a 9-year interval. They participated in structured interviews, answered questionnaires, and underwent spirometries and methacholine challenge testing. nGOR was defined by reported symptoms. Subjects with persistent nGOR (n=123) had an independent increased risk of new asthma at follow-up (OR 2.3, 95% CI 1.1-4.9). Persistent nGOR was independently related to onset of respiratory symptoms (OR 3.0, 95% CI 1.6-5.6). The risk of developing symptoms of OSA was increased in subjects with new and persistent nGOR (OR 2.2, 95% CI 1.3-1.6, and OR 2.0, 95% CI 1.0-3.7, respectively). No significant association was found between nGOR and lung function or bronchial responsiveness. Persistent symptoms of nGOR contribute to the development of asthma and respiratory symptoms. New onset of OSA symptoms is higher among subjects with symptoms of nGOR. These findings provide evidence that nGOR may play a role in the genesis of respiratory symptoms and diseases.

  • 17.
    Forsberg, Bertil
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Stjernberg, Nils
    Falk, M
    Lundbäck, B
    Wall, Stig
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Air pollution levels, meteorological conditions and asthma symptoms1993In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 6, no 8, p. 1109-1115Article in journal (Refereed)
    Abstract [en]

    We wanted to assess relations between the daily occurrence of asthma symptoms and fluctuations of air pollution concentrations and meteorological conditions. In a panel of 31 asthmatic patients residing in the town of Piteå in northern Sweden, severe symptoms of shortness of breath, wheeze, cough and phlegm were recorded in an asthma diary together with suspected causes. Sulphur dioxide, nitrogen dioxide, black smoke, relative humidity and temperature were used to evaluate the relationship to the environment. By using multivariate analyses, we found that daily variations in the particulate pollution levels, indicated by black smoke levels below the criteria limits, had significant effects on the risk of developing severe symptoms of shortness of breath. This association was stronger among 10 subjects, who had at least five incident days with severe shortness of breath. Meteorological conditions were not significant in the multivariate models. Cough and phlegm did not show significant relationships to any environmental condition that was evaluated. Only one-third of the subjects reported, at least once during the study, symptoms believed to be related to air pollutants, although we found significant correlations between the pollution levels and the frequency of pollution-related symptoms. We conclude that an association has been established for black smoke as pollutant and shortness of breath as respiratory symptom, and that in certain asthmatics, effects were occurring at lower particulate levels than suggested previously.

  • 18.
    Forsberg, Bertil
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Stjernberg, Nils
    National Institute for Working Life, Umeå, Sweden.
    Linné, R
    Landskrona Hospital, Landskrona, Sweden.
    Segerstedt, Bo
    Umeå University, Faculty of Social Sciences, Umeå School of Business and Economics (USBE).
    Wall, Stig
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Daily air pollution levels and acute asthma in southern Sweden1998In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 12, no 4, p. 900-905Article in journal (Refereed)
    Abstract [en]

    This study aimed to investigate the association between daily air pollution levels and the occurrence of acute respiratory signs and symptoms among people with asthma or asthma-like problems.

    Thirty eight subjects in the southern Swedish city of Landskrona kept a daily diary for 10 weeks. The daily prevalence of symptoms, supplementary bronchodilator use and peak flow deviations were compared with measurements of environmental nitrogen dioxide (NO2), sulphur dioxide, temperature and humidity in the city.

    The occurrence of severe asthma, both during the day and during the evening, was significantly positively associated with the concurrent 24 h average concentration of NO2, which never exceeded 72 microg x m(-3). A correlation of borderline significance was found between the use of on-demand medication and the NO2 level. However, peak flow deviations were not associated with air pollution or weather conditions, which may be explained by the beneficial effect of bronchodilators used by 28 of the subjects.

    The results of this study confirm those of some earlier studies and suggest that aggravation of asthma is related to daily variations in air quality, as indicated by relatively low ambient concentrations of nitrogen dioxide. These results also indicate that it may be appropriate to examine severe asthma symptoms separately.

  • 19.
    Franklin, Karl
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine. Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Pulmonary Medicine.
    From the author2007In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 30, no 5, p. 1023-1024Article in journal (Other academic)
  • 20.
    Franklin, Karl
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine. Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery.
    Sleep apnoea screening in heart failure? Not until benefit is proven!2007In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 29, no 6, p. 1073-1074Article in journal (Refereed)
  • 21.
    Franklin, Karl A.
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Surgery.
    Sahlin, Carin
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Stenlund, Hans
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health.
    Lindberg, Eva
    Sleep apnoea is a common occurrence in females2013In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 41, no 3, p. 610-615Article in journal (Refereed)
    Abstract [en]

    Obstructive sleep apnoea (OSA) is primarily regarded as a male disorder, presenting with snoring, daytime sleepiness and cardiovascular disease. We aimed to determine the frequency of sleep apnoea among females in the general population. We investigated 400 females from a population-based random sample of 10,000 females aged 20-70 yrs. They answered a questionnaire and performed overnight polysomnography. OSA (apnoea/hypopnoea index (AHI) >= 5) was found in 50% (95% CI 45-55%) of females aged 20-70 yrs. Sleep apnoea was related to age, obesity and hypertension, but not to daytime sleepiness. Severe sleep apnoea (AHI >= 30) was present in 14% (95% CI 8.1-21%) of females aged 55-70 yrs and in 31% (95% CI 12-50%) of obese females with a body mass index of >= 30 kg.m(-2) aged 55-70 yrs. Sleep apnoea with daytime sleepiness and sleep apnoea with hypertension were observed as two different phenotypes of OSA. OSA occurs in 50% of females aged 20-70 yrs. 20% of females have moderate and 6% severe sleep apnoea. Sleep apnoea in females is related to age, obesity and hypertension, but not to daytime sleepiness. When searching for sleep apnoea in females, females with hypertension or obesity should be investigated.

  • 22.
    Hedlund, Ulf
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Eriksson, Kåre
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Rönmark, Eva
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Socio-economic status is related to incidence of asthma and respiratory symptoms in adults.2006In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 28, no 2, p. 303-310Article in journal (Refereed)
  • 23. Heikkila, Katriina
    et al.
    Madsen, Ida E. H.
    Nyberg, Solja T.
    Fransson, Eleonor I.
    Ahola, Kirsi
    Alfredsson, Lars
    Bjorner, Jakob B.
    Borritz, Marianne
    Burr, Hermann
    Knutsson, Anders
    Koskenvuo, Markku
    Koskinen, Aki
    Nielsen, Martin L.
    Nordin, Maria
    Umeå University, Faculty of Social Sciences, Department of Psychology.
    Pahkin, Krista
    Pentti, Jaana
    Rugulies, Reiner
    Salo, Paula
    Shipley, Martin J.
    Suominen, Sakari B.
    Theorell, Tores
    Vaananen, Ari
    Vahtera, Jussi
    Virtanen, Marianna
    Westerholm, Peter J. M.
    Batty, G. David
    Singh-Manoux, Archana
    Kivimaki, Mika
    Job strain and COPD exacerbations: an individual-participant meta-analysis2014In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 44, no 1, p. 247-251Article in journal (Refereed)
  • 24.
    Inghammar, M
    et al.
    Dept of Clinical Sciences Lund, Lund University.
    Löfdahl, C-G
    Dept of Clinical Sciences Lund, Lund University.
    Winqvist, N
    Dept of Clinical Sciences Malmö , Lund University.
    Ljungberg, Börje
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Egesten, A
    Dept of Clinical Sciences Lund, Lund University.
    Engström, G
    Dept of Clinical Sciences Malmo¨ , Lund University.
    Impaired pulmonary function and the risk of tuberculosis: a population-based cohort study2011In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 37, no 5, p. 1285-1287Article in journal (Refereed)
  • 25. Jacquemin, B
    et al.
    Sunyer, J
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Aguilera, I
    Bouso, L
    Briggs, D
    de Marco, R
    García-Esteban, R
    Heinrich, J
    Jarvis, D
    Maldonado, J A
    Payo, F
    Rage, E
    Vienneau, D
    Künzli, N
    Association between modelled traffic related air pollution (NO2) and asthma score in ECHRS.2009In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 34, no 4, p. 834-842Article in journal (Refereed)
    Abstract [en]

    The aim of this analysis is to study the association between air pollution and asthma among adults. For this goal, a previously developed "asthma score" was used.Persons aged 25-44 years were randomly selected (1991-1993) and followed up (2000-2002) within the European Community Respiratory Health Survey (ECRHS-I and II). The asthma score was defined from 0 to 5, based on positive answers to symptoms reported for the last 12 months: wheeze/breathlessness, chest tightness, dyspnoea at rest, dyspnoea after exercise, and woken by dyspnoea. Participants' home addresses were linked to outdoor modelled NO2 estimates for 2001. Negative binomial regression was used to model the asthma score.The score from ECRHS-II was positively associated with NO2 (Ratio of the Mean asthma Score (RMS) 1.23, 95% Confidence Intervals (CI): 1.09-1.38 for an increase of 10 microg.m(-3)). After excluding participants with asthma and symptoms at baseline, the association remained (RMS 1.25, 95%CI: 1.05-1.51) and was particularly high among those reporting a high score in ECRHS-II. The latter probably reflects incident cases of asthma.Our results suggest that traffic-related pollution causes asthma symptoms and possibly asthma incidence in adults. The asthma score offers an alternative to investigate the course and aetiology of asthma in adults.

  • 26. Jansson, Sven-Arne
    et al.
    Backman, Helena
    Stenling, Anna
    AstraZeneca Nordic.
    Lindberg, Anne
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Rönmark, Eva
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Lundbäck, Bo
    Costs of COPD by disease severity2011In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 38, no Suppl 55Article in journal (Refereed)
    Abstract [en]

    Background: Chronic obstructive pulmonary disease (COPD) is one of the most common chronic and disabling diseases worldwide, and the societal costs are high.

    Aim: To estimate the societal costs of COPD in Sweden and to examine the relationship between disease severity and costs.

    Methods: The study sample was identified in earlier clinical examinations of general population cohorts within the OLIN (Obstructive Lung Disease in Northern Sweden) studies. The cohort consisted initially of 993 subjects fulfilling COPD spirometric criteria (GOLD). In 2009-2010, telephone interviews on resource utilization were made to a sample of 244 subjects, stratified by disease severity. Interviews were performed quarterly to minimize the risk of recall bias. A non-parametric Mann-Whitney U-test was used to test cost differences between groups; p-values adjusted by Bonferroni correction. Unit costs from 2010 were applied.

    Results: A highly significant relationship was found between disease severity and costs. The mean annual total cost per patient in relation to disease severity (GOLD) was: stage I €811; II €2,660; III €7,068; and IV €20,665. Indirect costs were higher than direct costs in all severity stages. For direct costs, main cost drivers were hospitalizations in stage III and IV, and drugs in stage I and II, respectively. The main cost driver in indirect costs was productivity loss due to early retirement, except in stage I where the driver was sick-leave. In comparison with a similar study performed in 1999 a numerical increase in mean annual total costs per patient was observed (ns).

    Conclusions: The results indicate that the societal costs of COPD in Sweden are substantial, and the costs increase considerably by disease severity.

  • 27. Juusela, Maria
    et al.
    Pallasaho, Paula
    Rönmark, Eva
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine. Sunderby Central Hospital of Norrbotten, Luleå.
    Sarna, Seppo
    Sovijarvi, Anssi
    Lundback, Bo
    Dose-dependent association of smoking and bronchial hyperresponsiveness2013In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 42, no 6, p. 1503-1512Article in journal (Refereed)
    Abstract [en]

    Our aim was to study the association of smoking habits and environmental tobacco smoke (ETS) exposure with bronchial hyperresponsiveness (BHR). A random sample of 292 adults was examined using a structured interview, spirometry, skin prick tests, exhaled nitric oxide fraction (FeNO) and bronchial histamine challenge. A large majority of subjects with BHR were smokers or ex-smokers. Starting to smoke before 20 years of age was significantly associated with BHR, as was current smoking, quantity of smoking and ETS exposure. The severity of BHR increased significantly with increasing pack-years of exposure (p<0.001). Current smokers with decreased lung function were at a particularly high risk of BHR. Impaired forced expiratory volume in 1 s and mean maximal expiratory flow were independent determinants for more severe BHR, regardless of age. In multivariate analysis, smoking remained an independent determinant for BHR after adjustment for impaired lung function and other covariates: >= 15 pack-years yielded an odds ratio of 3.00 (95% CI 1.33-6.76) for BHR. The association between BHR and FeNO was dependent on smoking habits. The results indicate that smoking is a significant risk factor for BHR, with a dose-dependent pattern, and that the severity of BHR increases with pack-years. The findings strongly suggest assessment of smoking habits in subjects with BHR.

  • 28. Juusela, Maria
    et al.
    Pallasaho, Paula
    Rönmark, Eva
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Sarna, Seppo
    Sovijarvi, Anssi
    Lundbäck, Bo
    Can overweight/obesity and smoking have combined effects on bronchial hyperresponsiveness?2014In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 43, no 2, p. 653-654Article in journal (Refereed)
  • 29.
    Larsson, B-M
    et al.
    Dept of Public Health Sciences, Division of Occupational Medicine, Karolinska institutet, Stockholm.
    Sehlstedt, Maria
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Grunewald, J
    Dept of Medicine, Division of Respiratory Medicine, Karolinska Institutet, Stockholm.
    Sköld, C M
    Dept of Medicine, Division of Respiratory Medicine, Karolinska Institutet, Stockholm.
    Lundin, A
    Dept of Occupational and Environmental Health, Stockholm Centre for Public Health, Stockholm County Council, Stockholm.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Eklund, A
    Dept of Medicine, Division of Respiratory Medicine, Karolinska Institutet, Stockholm.
    Svartengren, M
    Dept of Public Health Sciences, Division of Occupational Medicine, Karolinska institutet, Stockholm.
    Road tunnel air pollution induces bronchoalveolar inflammation in healthy subjects2007In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 29, no 4, p. 699-705Article in journal (Refereed)
    Abstract [en]

    Traffic-related air pollution is associated with adverse respiratory effects. The aim of the present study was to investigate whether exposure to air pollution in a road tunnel causes airway inflammatory and blood coagulation responses.

    A total of 16 healthy subjects underwent bronchoscopy with bronchial mucosal biopsies and bronchoalveolar lavage (BAL) on two occasions, in random order: once at 14 h after a 2-h exposure to air pollution in a busy road tunnel, and once after a control day with subjects exposed to urban air during normal activities. Peripheral blood was sampled prior to bronchoscopy.

    The road tunnel exposures included particulate matter with a 50% cut-off aerodynamic diameter of 2.5 μm, particulate matter with a 50% cut-off aerodynamic diameter of 10 μm and nitrogen dioxide which had median concentrations of 64, 176 and 230 µg·m−3, respectively. Significantly higher numbers of BAL fluid total cell number, lymphocytes and alveolar macrophages were present after road tunnel exposure versus control. Significantly higher nuclear expression of the transcription factor component c-Jun was found in the bronchial epithelium after exposure. No upregulation of adhesion molecules or cellular infiltration was present and blood coagulation factors were unaffected.

    In conclusion, exposure of healthy subjects to traffic-related air pollution resulted in a lower airway inflammatory response with cell migration, together with signs of an initiated signal transduction in the bronchial epithelium.

  • 30.
    Larsson, Nirina
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Lundström, Susanna
    Pinto, Rui
    Rankin, Greg
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Karimpour, Masoumeh
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Pourazar, Jamshid
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Trygg, Johan
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Behndig, Annelie
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Wheelock, Craig
    Nording, Malin
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Lipid mediator profiles differ between lung compartments in asthmatic and healthy humans2014In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 43, no 2, p. 453-463Article in journal (Refereed)
    Abstract [en]

    Oxylipins are oxidised fatty acids that can exert lipid mediator functions in inflammation, and several oxylipins derived from arachidonic acid are linked to asthma. This study quantified oxylipin profiles in different regions of the lung to obtain a broad-scale characterisation of the allergic asthmatic inflammation in relation to healthy individuals. Bronchoalveolar lavage fluid (BALF), bronchial wash fluid and endobronchial mucosal biopsies were collected from 16 healthy and 16 mildly allergic asthmatic individuals. Inflammatory cell counts, immunohistochemical staining and oxylipin profiling were performed. Univariate and multivariate statistics were employed to evaluate compartment-dependent and diagnosis-dependent oxylipin profiles in relation to other measured parameters. Multivariate modelling showed significantly different bronchial wash fluid and BALF oxylipin profiles in both groups ((RY)-Y-2[cum]=0.822 and Q(2)[cum]=0.759). Total oxylipin concentrations and five individual oxylipins, primarily from the lipoxygenase (LOX) pathway of arachidonic and linoleic acid, were elevated in bronchial wash fluid from asthmatics compared to that from healthy controls, supported by immunohistochemical staining of 15-LOX-1 in the bronchial epithelium. No difference between the groups was found among BALF oxylipins. In conclusion, bronchial wash fluid and BALF contain distinct oxylipin profiles, which may have ramifications for the study of respiratory diseases. Specific protocols for sampling proximal and distal airways separately should be employed for lipid mediator studies.

  • 31. Lietzen, R.
    et al.
    Virtanen, Pekka
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Kivimaki, M.
    Sillanmaki, L.
    Vahtera, J.
    Koskenvuoe, M.
    Stressful life events and the onset of asthma2011In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 37, no 6, p. 1360-1365Article in journal (Refereed)
    Abstract [en]

    The status of stressful life events as a risk factor for asthma is unclear and may be dependent on pre-existing allergic rhinitis. This study examined whether exposure to stressful life events predicted the onset of asthma in adults. This is a prospective, population-based cohort study of 16,881 males and females, aged 20-54 yrs and free of diagnosed asthma at the beginning of the follow-up (January 1, 2004). Data about stressful life events were gathered with a postal survey. The onset of asthma was ascertained through national registers until December 31, 2005. During the follow-up period, 192 incident cases of asthma were identified. High total exposure to stressful life events, as indicated by a cumulative severity score, predicted the onset of asthma (hazard ratio 1.96, 95% CI 1.22-3.13). This association was robust to adjustment for demographics, smoking and having a cat/dog at home and it was observed both among those with and without allergic rhinitis at baseline. Of the 10 most stressful life events, the illness of a family member, marital problems, divorce or separation and conflicts with a supervisor were associated with the onset of asthma. Our study suggests that stressful life events may increase the onset of asthma.

  • 32.
    Marklund, Marie
    et al.
    Umeå University, Faculty of Medicine, Department of Odontology, Ortodontics.
    Verbraecken, Johan
    Randerath, Winfried
    Non-CPAP therapies in obstructive sleep apnoea: mandibular advancement device therapy2012In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 39, no 5, p. 1241-1247Article in journal (Refereed)
    Abstract [en]

    Mandibular advancement devices (MADs) represent the main non-continuous positive airway pressure (non-CPAP) therapy for patients with obstructive sleep apnoea (OSA). The aim of the European Respiratory Society Task Force was to review the evidence in favour of MAD therapy . Effects of tongue-retaining devices are not included in this report.

     Custom-made MADs reduce apnoea/hypopnoea index (AHI) and daytime sleepness compared with placebo devices. CPAP more effectively dIminishes AHI, while increasing data suggest fairly similar outcomes in relation to symptoms and cardiovascular health from these treatments. Patients often prefer MADs to CPAP. Milder  cases and patients with a proven increase in upper airway size as a result of mandibular advancement are most likely to experience treatment success with MADs. A custom-made device titrated from an initial 50% of  maximum mandibular  advancement has been recommended. More research is needed to define the patients who will benefit from MAD treatment compared with CPAP, in terms of the effects on sleep—disordered breathing and on other diseases related to OSA.

     In conclusion,  MADs are recommended for patients with mild to moderate OSA (Recommendation Level A) and for those who do not tolerate CPAP. The treatment must be followed up and the device adjusted or exchanged in relation to the outcome.

  • 33. Melén, Erik
    et al.
    Barouki, Robert
    Barry, Maeve
    Boezen, H. Marike
    Hoffmann, Barbara
    Krauss-Etschmann, Susanne
    Koppelman, Gerard H.
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Promoting respiratory public health through epigenetics research: an ERS Environment Health Committee workshop report2018In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 51, no 4, article id 1702410Article in journal (Refereed)
  • 34. Miravitlles, Marc
    et al.
    Vogelmeier, Claus
    Roche, Nicolas
    Halpin, David
    Cardoso, Joao
    Chuchalin, Alexander G.
    Kankaanranta, Hannu
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Sliwinski, Pawel
    Zatloukal, Jaromir
    Blasi, Francesco
    A review of national guidelines for management of COPD in Europe2016In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 47, no 2, p. 625-637Article, review/survey (Refereed)
    Abstract [en]

    The quality of care can be improved by the development and implementation of evidence-based treatment guidelines. Different national guidelines for chronic obstructive pulmonary disease (COPD) exist in Europe and relevant differences may exist among them. This was an evaluation of COPD treatment guidelines published in Europe and Russia in the past 7 years. Each guideline was reviewed in detail and information about the most important aspects of patient diagnosis, risk stratification and pharmacotherapy was extracted following a standardised process. Guidelines were available from the Czech Republic, England and Wales, Finland, France, Germany, Italy, Poland, Portugal, Russia, Spain and Sweden. The treatment goals, criteria for COPD diagnosis, consideration of comorbidities in treatment selection and support for use of long-acting bronchodilators, were similar across treatment guidelines. There were differences in measures used for stratification of disease severity, consideration of patient phenotypes, criteria for the use of inhaled corticosteroids and recommendations for other medications (e.g. theophylline and mucolytics) in addition to bronchodilators. There is generally good agreement on treatment goals, criteria for diagnosis of COPD and use of long-acting bronchodilators as the cornerstone of treatment among guidelines for COPD management in Europe and Russia. However, there are differences in the definitions of patient subgroups and other recommended treatments.

  • 35.
    Modig, Lars
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Järvholm, Bengt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Rönnmark, Eva
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Nyström, Lennart
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Lundbäck, B
    Andersson, C
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Vehicle exhaust exposure in an incident case-control study of adult asthma2006In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 28, no 1, p. 75-81Article in journal (Refereed)
    Abstract [en]

    The objective of this case–control study was to evaluate whether traffic-related air pollution exposure at home increases the risk of asthma in adults and to compare two commonly used exposure variables and differences between urban and rural living. Incident cases of asthma and matched controls of subjects aged 20–60 yrs were recruited in Luleå, Sweden. In total 203 cases and 203 controls were enrolled in the study. Exposure was estimated by traffic flow and measured levels of outdoor nitrogen dioxide (NO2) in the surrounding environment of each home, respectively. The relationship between measured levels of NO2 and traffic flow was studied using linear regression. The results indicated a nonsignificant tendency between living in a home close to a high traffic flow and an increased risk of asthma. The association between asthma and measured NO2 was weak and not significant, but the skin-prick test result acted as an effect modifier with a borderline significant association among positives. The correlation between traffic flow and outdoor NO2 was low. The results suggest that living close to high traffic flows might increase the asthma incidence in adults, while the tendency for nitrogen dioxide was only seen among atopics. Traffic flow and nitrogen dioxide had a lower than expected correlation.

  • 36.
    Modig, Lars
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Torén, K
    Janson, C
    Jarvholm, B
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Forsberg, B
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Vehicle exhaust outside the home and onset of asthma among adults2009In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 33, no 6, p. 1261-7Article in journal (Refereed)
    Abstract [en]

    Few studies have investigated the relationship between vehicle exhaust and new onset of asthma among adults. The aim of this prospective cohort study was to investigate the relationship between the cumulative incidence of asthma and onset asthma among adults and vehicle exhaust concentrations at home.Participants from three Swedish cities included in the RHINE (Respiratory Health in Northern Europe) Cohort constituted the study population. Exposure at each participant's home was calculated using dispersion models. We also used less than 50 meter distance to nearest major road as a more simple indicator of exposure. The adjusted model included 3609 participants of which 107 were classified as onset cases and 55 as true incident cases of asthma.There was a positive association between asthma onset (Odds Ratio, OR per 10 microg.m(-3) = 1.46, 95% Confidence Interval (CI) 1.07-1.99) and incident asthma (OR per 10 microg.m(-3) = 1.54, 95% CI 1.00-2.36) and the levels of NO2 which remained statistically significant after adjusting for potential confounders. The relationship between asthma and NO2 was not significantly modified by sex, hay fever or wheeze.This study suggests that elevated levels of vehicle exhaust outside the home increase the risk of onset and incident asthma among adults.

  • 37.
    Nordenhäll, C
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Pourazar, Jamshid
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Levin, Jan-Olof
    Dept of Occupational Chemistry, Institute for Working Life, Umeå.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Ädelroth, Ellinor
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Airway inflammation following exposure to diesel exhaust: a study of time kinetics using induced sputum2000In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 15, no 6, p. 1046-1051Article in journal (Refereed)
    Abstract [en]

    The adverse health effects of particulate matter pollution are of increasing concern. In a recent bronchoscopic study in healthy volunteers, pronounced airway inflammation was detected following exposure to diesel exhaust (DE). The present study was conducted in order to evaluate the time kinetics of the inflammatory response following exposure to DE using induced sputum from healthy volunteers. Fifteen healthy nonsmoking volunteers were exposed to DE particles with a 50% cut-off aerodynamic diameter of 10 microm 300 microg x m(-3) and air for 1 h on two separate occasions. Sputum induction with hypertonic saline was performed 6 and 24 h after each exposure. Analyses of sputum differential cell counts and soluble protein concentrations were performed. Six hours after exposure to DE, a significant increase was found in the percentage of sputum neutrophils (37.7 versus 26.2% p=0.002) together with increases in the concentrations of interleukin-6 (12.0 versus 6.3 pg x mL(-1), p=0.006) and methylhistamine (0.11 versus 0.12 microg x L(-1), p=0.024). Irrespective of exposure, a significant increase was found in the percentage of sputum neutrophils at 24 as compared to 6 h, indicating that the procedure of sputum induction itself may change the composition of sputum. This study demonstrates that exposure to diesel exhaust induces inflammatory response in healthy human airways, represented by an early increase in interleukin-6 and methylhistamine concentration and the percentage of neutrophils. Induced sputum provides a safe tool for the investigation of the inflammatory effects of diesel exhaust, but care must be taken when interpreting results from repeated sputum inductions.

  • 38.
    Nordenhäll, C
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Pourazar, Jamshid
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Ledin, M-C
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Levin, Jan-Olof
    Institute for Working Life, Dept of Occupational Chemistry, Umeå.
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Ädelroth, Ellinor
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Diesel exhaust enhances airway responsiveness in asthmatic subjects2001In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 17, no 5, p. 909-915Article in journal (Refereed)
    Abstract [en]

    Particulate matter (PM) pollution has been associated with negative health effects, including exacerbations of asthma following exposure to PM peaks. The aim of the present study was to investigate the effects of short-term exposure to diesel exhaust (DE) in asthmatics, by specifically addressing the effects on airway hyperresponsiveness, lung function and airway inflammation. Fourteen nonsmoking, atopic asthmatics with stable disease, on continuous treatment with inhaled corticosteroids, were included. All were hyperresponsive to methacholine. Each subject was exposed to DE (particles with a 50% cut-off aerodynamic diameter of 10 microm (PM10) 300 microg x m(-3)) and air during 1 h on two separate occasions. Lung function was measured before and immediately after the exposures. Sputum induction was performed 6 h, and methacholine inhalation test 24 h, after each exposure. Exposure to DE was associated with a significant increase in the degree of hyperresponsiveness, as compared to after air, of 0.97 doubling concentrations at 24 h after exposure (p < 0.001). DE also induced a significant increase in airway resistance (p=0.004) and in sputum levels of interleukin (IL)-6 (p=0.048). No changes were detected in sputum levels of methyl-histamine, eosinophil cationic protein, myeloperoxidase and IL-8. This study indicated that short-term exposure to diesel exhaust, equal to high ambient levels of particulate matter, is associated with adverse effects in asthmatic airways, even in the presence of inhaled corticosteroid therapy. The increase in airway responsiveness may provide an important link to epidemiological findings of exacerbations of asthma following exposure to particulate matter.

  • 39.
    Orru, Hans
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Andersson, Camilla
    Swedish Meteorological and Hydrological Institute, Norrköping, Sweden.
    Ebi, Kristie L
    ClimAdapt, Los Altos, California, USA.
    Langner, Joakim
    Swedish Meteorological and Hydrological Institute, Norrköping, Sweden.
    Åström, Christofer
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Impact of climate change on ozone-related mortality and morbidity in Europe2013In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 41, no 2, p. 285-294Article in journal (Refereed)
    Abstract [en]

    Ozone is a highly oxidative pollutant formed from precursors in the presence of sunlight, associated with respiratory morbidity and mortality. All else being equal, concentrations of ground-level ozone are expected to increase due to climate change.Ozone-related health impacts under a changing climate are projected using emission scenarios, models and epidemiological data. European ozone concentrations are modelled with MATCH-RCA3 (50×50 km). Projections from two climate models, ECHAM4 and HadCM3, are applied, under greenhouse gas emission scenarios A2 and A1B respectively. We apply a European-wide exposure-response function to gridded population data and country-specific baseline mortality and morbidity.Comparing the current situation (1990-2009) with the baseline period (1961-1990), the largest increase in ozone-associated mortality and morbidity due to climate change (4-5%) have occurred in Belgium, Ireland, Netherlands and UK. Comparing the baseline period and the future periods (2021-2050 and 2041-2060), much larger increase in ozone-related mortality and morbidity are projected for Belgium, France, Spain and Portugal with the impact being stronger using the climate projection from ECHAM4 (A2). However, in Nordic and Baltic countries the same magnitude of decrease is projected.The current study suggests that projected effects of climate change on ozone concentrations could differentially influence mortality and morbidity across Europe.

  • 40. Pekkanen, Juha
    et al.
    Valkonen, Maria
    Täubel, Martin
    Tischer, Christina
    Leppänen, Hanna
    Kärkkäinen, Päivi M
    Rintala, Helena
    Zock, Jan-Paul
    Casas, Lidia
    Probst-Hensch, Nicole
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Holm, Mathias
    Janson, Christer
    Pin, Isabelle
    Gislason, Thorarinn
    Jarvis, Debbie
    Heinrich, Joachim
    Hyvärinen, Anne
    Indoor bacteria and asthma in adults: a multicentre case-control study within ECRHS II2018In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 51, no 2, article id 1701241Article in journal (Refereed)
    Abstract [en]

    Both protective and adverse effects of indoor microbial exposure on asthma have been reported, but mostly in children. To date, no study in adults has used non-targeted methods for detection of indoor bacteria followed by quantitative confirmation. A cross-sectional study of 198 asthmatic and 199 controls was conducted within the European Community Respiratory Health Survey (ECRHS) II. DNA was extracted from mattress dust for bacterial analysis using denaturing gradient gel electrophoresis (DGGE). Selected bands were sequenced and associations with asthma confirmed with four quantitative PCR (qPCR) assays. 15 out of 37 bands detected with DGGE, which had at least a suggestive association (p<0.25) with asthma, were sequenced. Of the four targeted qPCRs, Clostridium cluster XI confirmed the protective association with asthma. The association was dose dependent (aOR 0.43 (95% CI 0.22-0.84) for the fourth versus first quartile, p for trend 0.009) and independent of other microbial markers. Few significant associations were observed for the three other qPCRs used. In this large international study, the level of Clostridium cluster XI was independently associated with a lower risk of prevalent asthma. Results suggest the importance of environmental bacteria also in adult asthma, but need to be confirmed in future studies.

  • 41. Perez, Laura
    et al.
    Declercq, Christophe
    Iñiguez, Carmen
    Aguilera, Inmaculada
    Badaloni, Chiara
    Ballester, Ferran
    Bouland, Catherine
    Chanel, Olivier
    Cirarda, Fb
    Forastiere, Francesco
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Haluza, Daniela
    Hedlund, Britta
    Cambra, Koldo
    Lacasaña, Marina
    Moshammer, Hanns
    Otorepec, Peter
    Rodríguez-Barranco, Miguel
    Medina, Sylvia
    Künzli, Nino
    Chronic burden of near-roadway traffic pollution in 10 European cities (APHEKOM network)2013In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 42, no 3, p. 594-605Article in journal (Refereed)
    Abstract [en]

    Recent epidemiological research suggests that near road traffic-related pollution may cause chronic disease, as well as exacerbate related pathologies, implying that the entire "chronic disease progression" should be attributed to air pollution, no matter what the proximate cause was. We estimated the burden of childhood asthma attributable to air pollution in 10 European cities by calculating the number of cases of 1) asthma caused by near road traffic-related pollution, and 2) acute asthma events related to urban air pollution levels. We then expanded our approach to include coronary heart diseases in adults.Derivation of attributable cases required combining concentration-response function (CRF) between exposures and the respective health outcome of interest (obtained from published literature), an estimate of the distribution of selected exposures in the target population, and information about the frequency of the assessed morbidities.Exposure to roads with high vehicle traffic, a proxy for near road traffic-related pollution, accounted for 14% of all asthma cases. When a causal relationship between near road traffic-related pollution and asthma is assumed, 15% of all episodes of asthma symptoms were attributable to air pollution. Without this assumption, only 2% of asthma symptoms were attributable to air pollution. Similar patterns were found for coronary heart diseases in older adults.Pollutants along busy roads are responsible for a large and preventable share of chronic disease and related acute exacerbation in European urban areas.

  • 42. Randerath, W J
    et al.
    Verbraecken, J
    Andreas, S
    Bettega, G
    Boudewyns, A
    Hamans, E
    Jalbert, F
    Paoli, J R
    Sanner, B
    Smith, I
    Stuck, B A
    Lacassagne, L
    Marklund, Marie
    Umeå University, Faculty of Medicine, Department of Odontology.
    Maurer, J T
    Pepin, J L
    Valipour, A
    Verse, T
    Fietze, I
    Non-CPAP therapies in obstructive sleep apnoea2011In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 37, no 5, p. 1000-1028Article in journal (Refereed)
    Abstract [en]

    In view of the high prevalence and the relevant impairment of patients with obstructive sleep apnoea syndrome (OSAS) lots of methods are offered which promise definitive cures for or relevant improvement of OSAS. This report summarises the efficacy of alternative treatment options in OSAS. An interdisciplinary European Respiratory Society task force evaluated the scientific literature according to the standards of evidence-based medicine. Evidence supports the use of mandibular advancement devices in mild to moderate OSAS. Maxillomandibular osteotomy seems to be as efficient as continuous positive airway pressure (CPAP) in patients who refuse conservative treatment. Distraction osteogenesis is usefully applied in congenital micrognathia or midface hypoplasia. There is a trend towards improvment after weight reduction. Positional therapy is clearly inferior to CPAP and long-term compliance is poor. Drugs, nasal dilators and apnoea triggered muscle stimulation cannot be recommended as effective treatments of OSAS at the moment. Nasal surgery, radiofrequency tonsil reduction, tongue base surgery, uvulopalatal flap, laser midline glossectomy, tongue suspension and genioglossus advancement cannot be recommended as single interventions. Uvulopalatopharyngoplasty, pillar implants and hyoid suspension should only be considered in selected patients and potential benefits should be weighed against the risk of long-term side-effects. Multilevel surgery is only a salvage procedure for OSA patients.

  • 43.
    Rocklöv, Joacim
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Meister, Kadri
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Winter mortality modifies the heat-mortality association the following summer2009In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 33, no 2, p. 245-251Article in journal (Refereed)
    Abstract [en]

    The present study aimed to investigate how the heat-related increase in deaths in summer and the extent of mortality displacement depend on influenza and other categories of mortality in the previous winter, which when low leaves a greater pool of susceptible individuals. Mortality data from Stockholm, Sweden, from 1990-2002 were stratified into a summer period and a winter period. A Poisson regression model was established for the daily mortality in the summer, with temperature and confounders as explanatory variables. In addition, indicators of total, respiratory, cardiovascular and influenza mortality of the winter period were incorporated as effect modifiers in the summer model, and lagged effects in strata defined by indicators were studied. A high rate of respiratory as well as cardiovascular mortality in winter reduced the heat effect the following summer, and influenza mortality tended to do so as well. The cumulative effect per degrees C increase was 0.95% below and 0.89% above a threshold (21.3 degrees C) after a winter with low cardiovascular and respiratory mortality, but -0.23% below and 0.21% above the threshold after a winter with high cardiovascular and respiratory mortality. The current study shows that high respiratory, cardiovascular and influenza mortality in winter leads to lower temperature effects in the following summer. It also suggests that persons for whom influenza may be fatal are often also susceptible to heat and this subgroup might, therefore, not benefit as much as expected from influenza vaccinations.

  • 44.
    Sahlin, Carin
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Svanborg, Eva
    Stenlund, Hans
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health.
    Franklin, Karl
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Cheyne-Stokes respiration and supine dependency2005In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 25, no 5, p. 829-33Article in journal (Refereed)
  • 45. Samoli, E
    et al.
    Aga, E
    Touloumi, G
    Nisiotis, K
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Lefranc, A
    Pekkanen, J
    Wojtyniak, B
    Schindler, C
    Niciu, E
    Brunstein, R
    Dodic Fikfak, M
    Schwartz, J
    Katsouyanni, K
    Short-term effects of nitrogen dioxide on mortality: an analysis within the APHEA project2006In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 27, no 6, p. 1129-1138Article in journal (Refereed)
    Abstract [en]

    The short-term effects of nitrogen dioxide (NO2) on total, cardiovascular and respiratory mortality in 30 European cities participating in the Air Pollution on Health: a European Approach (APHEA)-2 project were investigated.

    The association was examined using hierarchical models implemented in two stages. In the first stage, data from each city were analysed separately, whereas in the second stage, the city-specific air pollution estimates were regressed on city-specific covariates to obtain overall estimates and to explore sources of possible heterogeneity.

    A significant association of NO2 with total, cardiovascular and respiratory mortality was found, with stronger effects on cause-specific mortality. There was evidence of confounding in respiratory mortality with black smoke and sulphur dioxide. The effect of NO2 on total and cardiovascular mortality was observed mainly in western and southern European cities, and was larger when smoking prevalence was lower and household gas consumption was higher. The effect of NO2 on respiratory mortality was higher in cities with a larger proportion of elderly persons in the population and higher levels of particulate matter with a 50% cut-off aerodynamic diameter of 10 μm.

    The results of this large study are consistent with an independent effect of nitrogen dioxide on mortality, but the role of nitrogen dioxide as a surrogate of other unmeasured pollutants cannot be completely ruled out.

  • 46.
    Sandström, Thomas
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Lundbäck, B
    Tobacco smoke: old foe more important for asthma than commonly appreciated?2004In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 24, no 5, p. 720-721Article in journal (Refereed)
  • 47. Schikowski, Tamara
    et al.
    Adam, Martin
    Marcon, Alessandro
    Cai, Yutong
    Vierkötter, Andrea
    Carsin, Anne Elie
    Jacquemin, Benedicte
    Al Kanani, Zaina
    Beelen, Rob
    Birk, Matthias
    Bridevaux, Pierre-Olivier
    Brunekeef, Bert
    Burney, Peter
    Cirach, Marta
    Cyrys, Josef
    de Hoogh, Kees
    de Marco, Roberto
    de Nazelle, Audrey
    Declercq, Christophe
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Hardy, Rebecca
    Heinrich, Joachim
    Hoek, Gerard
    Jarvis, Debbie
    Keidel, Dirk
    Kuh, Diane
    Kuhlbusch, Thomas
    Migliore, Enrica
    Mosler, Gioia
    Nieuwenhuijsen, Mark J
    Phuleria, Harish
    Rochat, Thierry
    Schindler, Christian
    Villani, Simona
    Tsai, Ming-Yi
    Zemp, Elisabeth
    Hansell, Anna
    Kauffmann, Francine
    Sunyer, Jordi
    Probst-Hensch, Nicole
    Krämer, Ursula
    Künzli, Nino
    Association of ambient air pollution with the prevalence and incidence of COPD2014In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 44, no 3, p. 614-626Article in journal (Refereed)
    Abstract [en]

    The role of air pollution in chronic obstructive pulmonary disease (COPD) remains uncertain.The aim was to assess the impact of chronic exposure to air pollution on COPD in four cohorts using the standardised ESCAPE exposure estimates. Annual average particulate matter (PM), nitrogen oxides (NOx) and road traffic exposure were assigned to home addresses using land-use regression models. COPD was defined by NHANES reference equation (forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) less than the lower limit of normal) and the Global Initiative for Chronic Obstructive Lung Disease criterion (FEV1/FVC <0.70) and categorised by severity in non-asthmatics.We included 6550 subjects with assigned NOx and 3692 with PM measures. COPD was not associated with NO2 or PM10 in any individual cohort. In meta-analyses only NO2, NOx, PM10 and the traffic indicators were positively, although not significantly, associated with COPD. The only statistically significant associations were seen in females (COPD prevalence using GOLD: OR 1.57, 95% CI 1.11-2.23; and incidence: OR 1.79, 95% CI 1.21-2.68).None of the principal results were statistically significant, the weak positive associations of exposure with COPD and the significant subgroup findings need to be evaluated in further well standardised cohorts followed up for longer time, and with time-matched exposure assignments.

  • 48. Shaw, Dominick E.
    et al.
    Sousa, Ana R.
    Fowler, Stephen J.
    Fleming, Louise J.
    Roberts, Graham
    Corfield, Julie
    Pandis, Ioannis
    Bansal, Aruna T.
    Bel, Elisabeth H.
    Auffray, Charles
    Compton, Chris H.
    Bisgaard, Hans
    Bucchioni, Enrica
    Caruso, Massimo
    Chanez, Pascal
    Dahlen, Barbro
    Dahlen, Sven-Erik
    Dyson, Kerry
    Frey, Urs
    Geiser, Thomas
    de Verdier, Maria Gerhardsson
    Gibeon, David
    Guo, Yi-ke
    Hashimoto, Simone
    Hedlin, Gunilla
    Jeyasingham, Elizabeth
    Hekking, Pieter-Paul W.
    Higenbottam, Tim
    Horvath, Ildiko
    Knox, Alan J.
    Krug, Norbert
    Erpenbeck, Veit J.
    Larsson, Lars X.
    Lazarinis, Nikos
    Matthews, John G.
    Middelveld, Roelinde
    Montuschi, Paolo
    Musial, Jacek
    Myles, David
    Pahus, Laurie
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Seibold, Wolfgang
    Singer, Florian
    Strandberg, Karin
    Vestbo, Jorgen
    Vissing, Nadja
    von Garnier, Christophe
    Adcock, Ian M.
    Wagers, Scott
    Rowe, Anthony
    Howarth, Peter
    Wagener, Ariane H.
    Djukanovic, Ratko
    Sterk, Peter J.
    Chung, Kian Fan
    Clinical and inflammatory characteristics of the European U-BIOPRED adult severe asthma cohort2015In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 46, no 5, p. 1308-1321Article in journal (Refereed)
    Abstract [en]

    U-BIOPRED is a European Union consortium of 20 academic institutions, 11 pharmaceutical companies and six patient organisations with the objective of improving the understanding of asthma disease mechanisms using a systems biology approach. This cross-sectional assessment of adults with severe asthma, mild/moderate asthma and healthy controls from 11 European countries consisted of analyses of patient-reported outcomes, lung function, blood and airway inflammatory measurements. Patients with severe asthma (nonsmokers, n=311; smokers/ex-smokers, n=110) had more symptoms and exacerbations compared to patients with mild/moderate disease (n=88) (2.5 exacerbations versus 0.4 in the preceding 12 months; p<0.001), with worse quality of life, and higher levels of anxiety and depression. They also had a higher incidence of nasal polyps and gastro-oesophageal reflux with lower lung function. Sputum eosinophil count was higher in severe asthma compared to mild/moderate asthma (median count 2.99% versus 1.05%; p=0.004) despite treatment with higher doses of inhaled and/or oral corticosteroids. Consistent with other severe asthma cohorts, U-BIOPRED is characterised by poor symptom control, increased comorbidity and airway inflammation, despite high levels of treatment. It is well suited to identify asthma phenotypes using the array of "omic" datasets that are at the core of this systems medicine approach.

  • 49. Sigsgaard, Torben
    et al.
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Annesi-Maesano, Isabella
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Bølling, Anette
    Boman, Christoffer
    Umeå University, Faculty of Science and Technology, Department of Applied Physics and Electronics.
    Bønløkke, Jakob
    Brauer, Michael
    Bruce, Nigel
    Héroux, Marie-Eve
    Hirvonen, Maija-Riitta
    Kelly, Frank
    Künzli, Nino
    Lundbäck, Bo
    Moshammer, Hanns
    Noonan, Curtis
    Pagels, Joachim
    Sallsten, Gerd
    Sculier, Jean-Paul
    Brunekreef, Bert
    Health impacts of anthropogenic biomass burning in the developed world2015In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 46, no 6, p. 1577-1588Article in journal (Refereed)
    Abstract [en]

    Climate change policies have stimulated a shift towards renewable energy sources such as biomass. The economic crisis of 2008 has also increased the practice of household biomass burning as it is often cheaper than using oil, gas or electricity for heating. As a result, household biomass combustion is becoming an important source of air pollutants in the European Union. This position paper discusses the contribution of biomass combustion to pollution levels in Europe, and the emerging evidence on the adverse health effects of biomass combustion products. Epidemiological studies in the developed world have documented associations between indoor and outdoor exposure to biomass combustion products and a range of adverse health effects. A conservative estimate of the current contribution of biomass smoke to premature mortality in Europe amounts to at least 40 000 deaths per year. We conclude that emissions from current biomass combustion products negatively affect respiratory and, possibly, cardiovascular health in Europe. Biomass combustion emissions, in contrast to emissions from most other sources of air pollution, are increasing. More needs to be done to further document the health effects of biomass combustion in Europe, and to reduce emissions of harmful biomass combustion products to protect public health.

  • 50. Storaas, Torgeir
    et al.
    Zock, Jan-Paul
    Morano, Ana Espinosa
    Holm, Mathias
    Bjørnsson, Eythor
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Gislason, Thorarinn
    Janson, Christer
    Norback, Dan
    Omenaas, Ernst
    Schlünssen, Vivi
    Torén, Kjell
    Svanes, Cecilie
    Incidence of rhinitis and asthma related to welding in Northern Europe2015In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 46, no 5, p. 1290-1297Article in journal (Refereed)
    Abstract [en]

    Welding-related asthma is well recognised but less is known about rhinitis in relation to welding. The aim here, was to study associations between welding, rhinitis and asthma in a general population sample, and factors influencing selection into and out of a welding occupation.Adult-onset asthma and non-infectious rhinitis were investigated in the international multicentre population-based Respiratory Health in Northern Europe (RHINE) study, including 16 191 responders aged 26-54 years. Ever welding (n=2181), welding >25% of working time (n=747), and welding in stainless steel >6 months (n=173) were assessed by questionnaire. Subjects with rhinitis or asthma onset when aged <18 years were excluded. Incidence rates for asthma and rhinitis were calculated from year of disease onset, and start and end of welding job. Cox's proportional hazard models adjusting for age, sex, parental education and study centre, and Kaplan-Meier curves were used.Rhinitis incidence was higher among welders (hazard ratio (HR) 1.4, 95% CI 1.3-1.6), consistent in men and women, and across centres (pheterogeneity=0.4). In men, asthma incidence was higher among welders (HR 1.4, 95% CI 1.04-1.97). Quitting welding was indicated higher after adult-onset rhinitis (HR 1.1, 95% CI 1.0-1.3).Adult-onset rhinitis and asthma was higher among welders, consistent across population samples from Northern Europe. No pre-employment selection was found, whereas selection out of welding jobs was suggested.

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