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  • 1.
    Andreassen, Siw Lillevik
    et al.
    Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway.
    Liaaen, Erik Dyb
    Department of Internal Medicine, Aalesund Hospital, Aalesund, Norway.
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Henriksen, Anne H
    Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway ; Department of Thoracic- and Occupational Medicine, Trondheim University Hospital, Trondheim, Norway.
    Impact of pneumonia on hospitalizations due to acute exacerbations of COPD2014Ingår i: Clinical Respiratory Journal, ISSN 1752-6981, E-ISSN 1752-699X, Vol. 8, nr 1, s. 93-99Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND AND AIMS: Pneumonia is often diagnosed among patients hospitalized with acute exacerbations of chronic obstructive pulmonary disease (AECOPD). The aims of this study were to find the proportion of patients with pneumonia among admissions due to AECOPD and whether pneumonia has impact on the length of stay (LOS), usage of non-invasive ventilation (NIV) or the in-hospital mortality.

    METHODS: Retrospectively, all hospitalizations in 2005 due to AECOPD in the Departments of Internal and Respiratory Medicine in one Swedish and two Norwegian hospitals were analyzed. A total of 1144 admittances (731 patients) were identified from patient administrative systems. Pneumonic AECOPD (pAECOPD) was defined as pneumonic infiltrates on chest X-ray and C-reactive protein (CRP) value of ≥40 mg/L, and non-pneumonic AECOPD (npAECOPD) was defined as no pneumonic infiltrate on X-ray and CRP value of <40 at admittance.

    RESULTS: In admissions with pAECOPD (n = 237), LOS was increased (median 9 days vs 5 days, P < 0.001) and usage of NIV was more frequent (18.1% vs 12.5%, P = 0.04), but no significant increase in the in-hospital mortality (3.8% vs 3.6%) was found compared to admissions with npAECOPD. A higher proportion of those with COPD GOLD stage I-II had pAECOPD compared to those with COPD GOLD stage III-IV (28.2% vs 18.7%, P = 0.001).

    CONCLUSIONS: In-hospital morbidity, but not mortality, was increased among admissions with pAECOPD compared to npAECOPD. This may, in part, be explained by the extensive treatment with antibiotics and NIV in patients with pAECOPD.

  • 2.
    Behndig, Annelie F
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Larsson, Nirina
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Brown, Joanna L
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Helleday, Ragnberth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Duggan, Sean T
    Dove, Rosamund E
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Wilson, Susan J
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Kelly, Frank J
    Mudway, Ian S
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Proinflammatory doses of diesel exhaust in healthy subjects fail to elicit equivalent or augmented airway inflammation in subjects with asthma2011Ingår i: Thorax, ISSN 0040-6376, E-ISSN 1468-3296, Vol. 66, nr 1, s. 12-19Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Exposure to diesel exhaust at concentrations consistent with roadside levels elicited an acute and active neutrophilic inflammation in the airways of healthy subjects. This response was absent in subjects with asthma, as was evidence supporting a worsening of allergic airway inflammation.

  • 3.
    Behndig, Annelie F.
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Shanmuganathan, Karthika
    Whitmarsh, Laura
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin. Östersund Research Unit, Umeå University. .
    Brown, Joanna L.
    Frew, Anthony J.
    Kelly, Frank J.
    Mudway, Ian S.
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Wilson, Susan J.
    Effects of controlled diesel exhaust exposure on apoptosis and proliferation markers in bronchial epithelium: an in vivo bronchoscopy study on asthmatics, rhinitics and healthy subjects2015Ingår i: BMC Pulmonary Medicine, ISSN 1471-2466, E-ISSN 1471-2466, Vol. 15, artikel-id 99Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Epidemiological evidence demonstrates that exposure to traffic-derived pollution worsens respiratory symptoms in asthmatics, but controlled human exposure studies have failed to provide a mechanism for this effect. Here we investigated whether diesel exhaust (DE) would induce apoptosis or proliferation in the bronchial epithelium in vivo and thus contribute to respiratory symptoms.

    Methods: Moderate (n = 16) and mild (n = 16) asthmatics, atopic non-asthmatic controls (rhinitics) (n = 13) and healthy controls (n = 21) were exposed to filtered air or DE (100 μg/m 3 ) for 2 h, on two separate occasions. Bronchial biopsies were taken 18 h post-exposure and immunohistochemically analysed for pro-apoptotic and anti-apoptotic proteins (Bad, Bak, p85 PARP, Fas, Bcl-2) and a marker of proliferation (Ki67). Positive staining was assessed within the epithelium using computerized image analysis.

    Results: No evidence of epithelial apoptosis or proliferation was observed in healthy, allergic or asthmatic airways following DE challenge.

    Conclusion: In the present study, we investigated whether DE exposure would affect markers of proliferation and apoptosis in the bronchial epithelium of asthmatics, rhinitics and healthy controls, providing a mechanistic basis for the reported increased airway sensitivity in asthmatics to air pollutants. In this first in vivo exposure investigation, we found no evidence of diesel exhaust-induced effects on these processes in the subject groups investigated.

  • 4.
    Behndig, Annelie
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Mudway, IS
    Brown, JL
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Helleday, Ragnberth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Duggan, ST
    Wilson, SJ
    Boman, C
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för tillämpad fysik och elektronik, Energiteknik och termisk processkemi.
    Cassee, FR
    Frew, AJ
    Kelly, FJ
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Airway antioxidant and inflammatory responses to diesel exhaust exposure in healthy humans.2006Ingår i: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 27, nr 2, s. 359-365Artikel i tidskrift (Refereegranskat)
    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.

  • 5.
    Behndig, Annelie
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Mudway, IS
    Brown, JL
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Helleday, Ragnberth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Duggan, ST
    Wilson, SJ
    Boman, Christoffer
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för tillämpad fysik och elektronik, Energiteknik och termisk processkemi.
    Cassee, FR
    Frew, AJ
    Kelly, FJ
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Airway antioxidant and inflammatory responses to diesel exhaust exposure in healthy humans.2006Ingår i: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 27, nr 2, s. 359-365Artikel i tidskrift (Refereegranskat)
    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.
    Bosson, Jenny A
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Helleday, Ragnberth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Kelly, Frank J.
    Behndig, Annelie F.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Mudway, Ian S.
    Peripheral blood neutrophilia as a biomarker of ozone-induced pulmonary inflammation2013Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 8, nr 12, artikel-id e81816Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Ozone concentrations are predicted to increase over the next 50 years due to global warming and the increased release of precursor chemicals. It is therefore urgent that good, reliable biomarkers are available to quantify the toxicity of this pollutant gas at the population level. Such a biomarker would need to be easily performed, reproducible, economically viable, and reflective of ongoing pathological processes occurring within the lung.

    METHODOLOGY: We examined whether blood neutrophilia occurred following a controlled ozone challenge and addressed whether this could serve as a biomarker for ozone-induced airway inflammation. Three separate groups of healthy subjects were exposed to ozone (0.2 ppm, 2h) and filtered air (FA) on two separate occasions. Peripheral blood samples were collected and bronchoscopy with biopsy sampling and lavages was performed at 1.5h post exposures in group 1 (n=13), at 6h in group 2 (n=15) and at 18h in group 3 (n=15). Total and differential cell counts were assessed in blood, bronchial tissue and airway lavages.

    RESULTS: In peripheral blood, we observed fewer neutrophils 1.5h after ozone compared with the parallel air exposure (-1.1±1.0x10(9) cells/L, p<0.01), at 6h neutrophil numbers were increased compared to FA (+1.2±1.3x10(9) cells/L, p<0.01), and at 18h this response had fully attenuated. Ozone induced a peak in neutrophil numbers at 6h post exposure in all compartments examined, with a positive correlation between the response in blood and bronchial biopsies.

    CONCLUSIONS: These data demonstrate a systemic neutrophilia in healthy subjects following an acute ozone exposure, which mirrors the inflammatory response in the lung mucosa and lumen. This relationship suggests that blood neutrophilia could be used as a relatively simple functional biomarker for the effect of ozone on the lung.

  • 7.
    Bosson, Jenny
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Bucht, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Helleday, Ragnberth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Pourazar, Jamshid
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Holgate, Stephen
    Kelly, Frank
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Wilson, Susan
    Frew, Anthony
    Ozone-induced bronchial epithelial cytokine expression differs between healthy and asthmatic subjects2003Ingår i: Clinical and Experimental Allergy, ISSN 0954-7894, E-ISSN 1365-2222, Vol. 33, nr 6, s. 777-782Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background Ozone (O3) is a common air pollutant associated with adverse health effects. Asthmatics have been suggested to be a particularly sensitive group.

    Objective This study evaluated whether bronchial epithelial cytokine expression would differ between healthy and allergic asthmatics after ozone exposure, representing an explanatory model for differences in susceptibility.

    Methods Healthy and mild allergic asthmatic subjects (using only inhaled β2-agonists prn) were exposed for 2 h in blinded and randomized sequence to 0.2 ppm of O3 and filtered air. Bronchoscopy with bronchial mucosal biopsies was performed 6 h after exposure. Biopsies were embedded in GMA and stained with mAbs for epithelial expression of IL-4, IL-5, IL-6, IL-8, IL-10, TNF-α, GRO-α, granulocyte–macrophage colony-stimulating factor (GM–CSF), fractalkine and ENA-78.

    Results When comparing the two groups at baseline, the asthmatic subjects showed a significantly higher expression of IL-4 and IL-5. After O3 exposure the epithelial expression of IL-5, GM–CSF, ENA-78 and IL-8 increased significantly in asthmatics, as compared to healthy subjects.

    Conclusion The present study confirms a difference in epithelial cytokine expression between mild atopic asthmatics and healthy controls, as well as a differential epithelial cytokine response to O3. This O3-induced upregulation of T helper type 2 (Th2)-related cytokines and neutrophil chemoattractants shown in the asthmatic group may contribute to a subsequent worsening of the airway inflammation, and help to explain their differential sensitivity to O3 pollution episodes.

  • 8.
    Eriksson, L. M.
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Irewall, Tommie
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Lindberg, Anne
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Prevalence, age at onset, and risk factors of self-reported asthma among Swedish adolescent elite cross-country skiers2018Ingår i: Scandinavian Journal of Medicine and Science in Sports, ISSN 0905-7188, E-ISSN 1600-0838, Vol. 28, nr 1, s. 180-186Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The objective of the study was to compare the prevalence of self-reported physician-diagnosed asthma and age at asthma onset between Swedish adolescent elite skiers and a reference group and to assess risk factors associated with asthma. Postal questionnaires were sent to 253 pupils at the Swedish National Elite Sport Schools for cross-country skiing, biathlon, and ski-orienteering (skiers) and a random sample of 500 adolescents aged 16-20, matched for sport school municipalities (reference). The response rate was 96% among the skiers and 48% in the reference group. The proportion of participants with self-reported physician-diagnosed asthma was higher among skiers than in the reference group (27 vs 19%, P=.046). Female skiers reported a higher prevalence of physician-diagnosed asthma compared to male skiers (34 vs 20%, P=.021). The median age at asthma onset was higher among skiers (12.0 vs 8.0years; P<.001). Female sex, family history of asthma, nasal allergy, and being a skier were risk factors associated with self-reported physician-diagnosed asthma. Swedish adolescent elite cross-country skiers have a higher asthma prevalence and later age at asthma onset compared to a reference population. Being an adolescent, elite skier is an independent risk factor associated with asthma.

  • 9.
    Eriksson, Linda
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Schagatay, Filip
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Sjöström, Rita
    Umeå universitet, Medicinska fakulteten, Institutionen för samhällsmedicin och rehabilitering.
    Soderstrom, Lars
    Hanstock, Helen
    Sandström, Thomas
    Department of Medicine, Respiratory & allergy unit, Umeå university hospital, Umeå, Sweden.
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Symptoms of moderate exercise in subzero temperatures - An experimental exposure study2018Ingår i: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 52Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    Humans react to cold with various symptoms. Previous studies enquiring about symptoms during cold exposure have for the most part been population based studies using questionnaries and have focused on a narrow spectrum of symptoms. The purpose of this study was to study the effect of cold air and physical exercise on a wide range of symptoms in healthy individuals.

    A total of 31 healthy subjects were experimentally exposed to +10 °C and -10 °C in an environmental chamber for one hour, on two separate occasions. During each exposure, subjects performed an intermittent moderate-intensity running protocol between 62-78% of maximal oxygen consumption (VO2 max). At five timepoints, before, during and after the exposures, subjects were asked about 18 symptoms and their intensity. The Borg CR10 scale was used to rate the intensity from 0 to 11, where 0 meant "none" and 11 meant "maximal". The sum of all five Borg CR10-scores were added together to form a single score for each exposure. Paired Wilcoxon signed-rank test was used for analysis. Data are presented as medians.

    Symptoms of cough, eye irritation, physical discomfort, and cold extremities were present only at -10 °C. Compared to exercise in +10 °C, exercise in -10 °C induced significantly higher summed symptom scores for eye irritation 2.0 vs 0.5 (p=0.011), rhinitis 12.0 vs 8.0 (p=0.000), nasal irritation 3.5 vs 0.5 (p=0.001), cold face 7.0 vs 1.0 (p=0.000), physical discomfort 6.5 vs 0.0 (p=0.000), and cold extremities 10.0 vs 0.5 (p=0.000).

    In healthy subjects, moderate-intensity exercise in -10 °C can induce and enhance the intensity of a wide range of symptoms. Symptoms of the lower airways were infrequent and mild.

  • 10. Holgate, Stephen T
    et al.
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Frew, Anthony J
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Nördenhall, Charlotta
    Salvi, Sundeep
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Helleday, Ragnberth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Söderberg, Margaretha
    Health effects of acute exposure to air pollution. Part I: Healthy and asthmatic subjects exposed to diesel exhaust2003Ingår i: Research report (Health Effects Institute), ISSN 1041-5505, nr 112, s. 1-30; discussion 51Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The purpose of this study was to assess the impact of short-term exposure to diluted diesel exhaust on inflammatory parameters in human airways. We previously exposed control subjects for 1 hour to a high ambient concentration of diesel exhaust (particle concentration 300 pg/m3--a level comparable with that found in North Sea ferries, highway underpasses, etc). Although these exposures did not have any measurable effect on standard indices of lung function, there was a marked neutrophilic inflammatory response in the airways accompanied by increases in blood neutrophil and platelet counts. Endothelial adhesion molecules were upregulated, and the expression of interleukin 8 messenger RNA (IL-8 mRNA*) was increased in a pattern consistent with neutrophilia. Individuals with asthma have inflamed airways and are clinically more sensitive to air pollutants than are control subjects. The present study was designed to assess whether this clinical sensitivity can be explained by acute neutrophilic inflammation or an increase in allergic airway inflammation resulting from diesel exhaust exposure. For this study, we used a lower concentration of diesel exhaust (100 microg/m3 PM10) for a 2-hour exposure. At this concentration, both the control subjects and those with asthma demonstrated a modest but statistically significant increase in airway resistance following exposure to diesel exhaust. This increase in airway resistance was associated with an increased number of neutrophils in the bronchial wash (BW) fluid obtained from control subjects (median after diesel exhaust 22.0 vs median after air 17.2; P = 0.015), as well as an increase in lymphocytes obtained through bronchoalveolar lavage (BAL) (15.0% after diesel exhaust vs 12.3% after air; P = 0.017). Upregulation of the endothelial adhesion molecule P-selectin was noted in bronchial biopsy tissues from control subjects (65.4% of vessels after diesel exhaust vs 52.5% after air). There was also a significant increase in IL-8 protein concentrations in BAL fluid and IL-8 mRNA gene expression in the bronchial biopsy tissues obtained from control subjects after diesel exhaust exposure (median IL-8 expression 65.7% of adenine phosphoribosyl transferase [APRT] gene expression value after diesel exhaust vs 51.0% after air; P = 0.007). There were no significant changes in total protein, albumin, or other soluble inflammatory markers in the BW or BAL fluids. Red and white blood cell counts in peripheral blood were unaffected by diesel exhaust exposure. Airway mucosal biopsy tissues from subjects with mild asthma (defined as forced expiratory volume in 1 second [FEV1] greater than or equal to 70% of the predicted value) showed eosinophilic airway inflammation after air exposure compared with the airways of the corresponding control subjects. However, among the subjects with mild asthma, diesel exhaust did not induce any significant change in airway neutrophils, eosinophils, or other inflammatory cells; cytokines; or mediators of inflammation. The only clear effect of diesel exhaust on the airways of subjects with asthma was a significant increase in IL-10 staining in the biopsy tissues. This study demonstrated that modest concentrations of diesel exhaust have clear-cut inflammatory effects on the airways of nonasthmatic (or control) subjects. The data suggest a direct effect of diesel exhaust on IL-8 production leading to upregulation of endothelial adhesion molecules and neutrophil recruitment. Despite clinical reports of increased susceptibility of patients with asthma to diesel exhaust and other forms of air pollution, it does not appear that this susceptibility is caused either directly by induction of neutrophilic inflammation or indirectly by worsening of preexisting asthmatic airway inflammation. The increased level of IL-10 after diesel exhaust exposure in airways of subjects with asthma suggests that this pollutant may induce subtle changes in airway immunobiology. This is an important topic for further investigation. Other possible explanations for the apparent lack of response to diesel exhaust among subjects with asthma include (1) the time course of the response to diesel may differ from the response to allergens, which peaks 6 to 8 hours after exposure; (2) a different type of inflammation may occur that was not detectable by the standard methods used in this study; and (3) the increased sensitivity of patients with asthma to particulate air pollution may reflect the underlying bronchial hyperresponsiveness found in asthma rather than any specific increase in inflammatory responses.

  • 11.
    Huber, Daniel
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Henriksson, Robin
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Jakobsson, Stina
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Mooe, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Implementation of a telephone-based secondary preventive intervention after acute coronary syndrome (ACS): participation rate, reasons for non-participation and 1-year survival2016Ingår i: Trials, ISSN 1745-6215, E-ISSN 1745-6215, Vol. 17, artikel-id 85Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Acute coronary syndrome (ACS) is a major cause of death from a non-communicable disease. Secondary prevention is effective for reducing morbidity and mortality, but evidence-based targets are seldom reached and new interventional methods are needed. The present study is a feasibility study of a telephone-based secondary preventive programme in an unselected ACS cohort. Methods: The NAILED (Nurse-based Age-independent Intervention to Limit Evolution of Disease) ACS trial is a prospective randomized controlled trial. All eligible patients admitted for ACS were randomized to usual follow-up by a general practitioner or telephone follow-up by study nurses. The intervention was made by continuous telephone contact, with counseling on healthy living and titration of medicines to reach target values for blood pressure and blood lipids. Exclusion criteria were limited to physical inability to follow the study design or participation in another study. Results: A total of 907 patients were assessed for inclusion. Of these, 661 (72.9 %) were included and randomized, 100 (11 %) declined participation, and 146 (16.1 %) were excluded. The main reasons for exclusion were participation in another trial, dementia, and advanced disease. "Excluded" and "declining" patients were significantly older with more co-morbidity, decreased functional status, and had more seldom received education above compulsory school level than "included" patients. Non-participants had a higher 1-year mortality than participants. Conclusions: Nurse-led telephone-based follow-up after ACS can be applied to a large proportion in an unselected clinical setting. Reasons for non-participation, which were associated with increased mortality, include older age, multiple co-morbidities, decreased functional status and low level of education.

  • 12.
    Larsson, Nirina
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Brown, Joanna
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Wilson, Susan
    Mudway, Ian S
    Pourazar, Jamshid
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Behndig, Annelie F
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Airway inflammatory responses to diesel exhaust in allergic rhinitics2013Ingår i: Inhalation Toxicology, ISSN 0895-8378, E-ISSN 1091-7691, Vol. 25, nr 3, s. 160-167Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Context: Proximity to traffic, particularly to diesel-powered vehicles, has been associated with inducing and enhancing allergies. To investigate the basis for this association, we performed controlled exposures of allergic rhinitics to diesel exhaust (DE) at a dose known to be pro-inflammatory in healthy individuals.

    Objective: We hypothesized that diesel-exhaust exposure would augment lower airway inflammation in allergic rhinitics.

    Materials and methods: Fourteen allergic rhinitics were exposed in a double-blinded, randomized trial to DE (100 mu g/m(3) PM10) and filtered air for 2 h on separate occasions. Bronchoscopy with endobronchial mucosal biopsies and airway lavage was performed 18 h post-exposure, and inflammatory markers were assessed.

    Results: No evidence of neutrophilic airway inflammation was observed post-diesel, however, a small increase in myeloperoxidase was found in bronchoalveolar lavage (p = 0.032). We found no increases in allergic inflammatory cells. Reduced mast cell immunoreactivity for tryptase was observed in the epithelium (p = 0.013) parallel to a small decrease in bronchial wash stem cell factor (p = 0.033). Discussion and conclusion: DE, at a dose previously shown to cause neutrophilic inflammation in healthy individuals, induced no neutrophilic inflammation in the lower airways of allergic rhinitics, consistent with previous reports in asthmatics. Although there was no increase in allergic inflammatory cell numbers, the reduction in tryptase in the epithelium may indicate mast cell degranulation. However, this occurred in the absence of allergic symptoms. These data do not provide a simplistic explanation of the sensitivity in rhinitics to traffic-related air pollution. The role of mast cells requires further investigation.

  • 13. Liaaen, Erik Dyb
    et al.
    Henriksen, Anne H
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    A Scandinavian audit of hospitalizations for chronic obstructive pulmonary disease2010Ingår i: Respiratory Medicine, ISSN 0954-6111, E-ISSN 1532-3064, Vol. 104, nr 9, s. 1304-1309Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    In Scandinavia no large audits of hospitalizations for chronic obstructive pulmonary disease (COPD) have been performed, and data on adherence to national guidelines are scarce. The aims of the present study were to audit hospitalizations for COPD exacerbations in three Scandinavian hospitals with respect to incidence, patient population and standards of hospital care. Retrospectively all hospitalizations in the Departments of Internal and Respiratory Medicine in Ostersund Hospital (Sweden), Aalesund Hospital (Norway) and Trondheim University Hospital (Norway) from Jan 1 to Dec 31, 2005, with discharge ICD-10 diagnoses J43-J44, J96 + J44 or J13-18 + j44 were registered. A total of 1144 admissions (731 patients) were identified from patient administrative systems and medical charts. Among the admitted patients 27% were >80 years old, >50% had COPD stage III or IV, and 14% had respiratory acidosis at admittance. Patients with 3 or more admissions (13%) during 2005 accounted for 36% of all hospitalizations. One third of the patients were current smokers. Non-invasive ventilation was used in 14% of the admissions, with large variation between centres. In-hospital mortality was 3.7%. In this first large Scandinavian audit of COPD-hospitalizations, all centres had low in-hospital mortality. We consider this as an indication of good clinical practice in the three studied centres and possibly due to the frequent use of non-invasive ventilation.

  • 14. Mudway, I S
    et al.
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Department of Respiratory Medicine and Allergy, University Hospital, Umeå.
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Department of Respiratory Medicine and Allergy, University Hospital, Umeå.
    Helleday, Ragnberth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Department of Respiratory Medicine and Allergy, University Hospital, Umeå.
    Dunster, C
    Marklund, S L
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Klinisk kemi.
    Frew, A J
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Department of Respiratory Medicine and Allergy, University Hospital, Umeå.
    Kelly, F J
    Differences in basal airway antioxidant concentrations are not predictive of individual responsiveness to ozone: a comparison of healthy and mild asthmatic subjects2001Ingår i: Free Radical Biology & Medicine, ISSN 0891-5849, E-ISSN 1873-4596, Vol. 31, nr 8, s. 962-974Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The air pollutant ozone induces both airway inflammation and restrictions in lung function. These responses have been proposed to arise as a consequence of the oxidizing nature of ozone, depleting endogenous antioxidant defenses with ensuing tissue injury. In this study we examined the impact of an environmentally relevant ozone challenge on the antioxidant defenses present at the surface of the lung in two groups known to have profound differences in their antioxidant defense network: healthy control (HC) and mild asthmatic (MA) subjects. We hypothesized that baseline differences in antioxidant concentrations within the respiratory tract lining fluid (RTLF), as well as induced responses, would predict the magnitude of individual responsiveness. We observed a significant loss of ascorbate (ASC) from proximal (-45.1%, p <.01) and distal RTLFs (-11.7%, p <.05) in healthy subjects 6 h after the end of the ozone challenge. This was associated (Rs, -0.71, p <.01) with increased glutathione disulphide (GSSG) in these compartments (p =.01 and p <.05). Corresponding responses were not seen in asthmatics, where basal ASC concentrations were significantly lower (p <.01) and associated with elevated concentrations of GSSG (p <.05). In neither group was any evidence of lipid oxidation seen following ozone. Despite differences in antioxidant levels and response, the magnitude of ozone-induced neutrophilia (+20.6%, p <.01 [HC] vs. +15.2%, p =.01 [MA]) and decrements in FEV(1) (-8.0%, p <.01 [HC] vs. -3.2%, p <.05 [MA]) did not differ between the two groups. These data demonstrate significant differences between the interaction of ozone with RTLF antioxidants in MA and HC subjects. These responses and variations in basal antioxidant defense were not, however, useful predictive markers of group or individual responsiveness to ozone.

  • 15. Mudway, Ian S
    et al.
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Duggan, Sean T
    Roxborough, Heather
    Zielinski, Hendrick
    Marklund, Stephan L
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Klinisk kemi.
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Frew, Anthony J
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Kelly, Frank J
    An in vitro and in vivo investigation of the effects of diesel exhaust on human airway lining fluid antioxidants.2004Ingår i: Arch Biochem Biophys, ISSN 0003-9861, Vol. 423, nr 1, s. 200-12Artikel i tidskrift (Refereegranskat)
  • 16. Norqvist, Johan
    et al.
    Eriksson, Linda
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Söderström, Lars
    Unit of Research , Education and Development - Östersund, Umeå University.
    Lindberg, Anne
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin. Unit of Research , Education and Development - Sunderbyn, Umeå University.
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin. Unit of Research , Education and Development - Östersund, Umeå University.
    Self-reported physician-diagnosed asthma among Swedish adolescent, adult and former elite endurance athletes2015Ingår i: Journal of Asthma, ISSN 0277-0903, E-ISSN 1532-4303, Vol. 52, nr 10Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVE: Asthma is common among elite endurance athletes. Since the first published Swedish studies in 1993, awareness of "skiers' asthma" has increased. The current prevalence of asthma among Swedish skiers is unknown. This paper aims to present the design of a 5-year prospective annual questionnaire study on asthma among Swedish current and former elite endurance athletes, the first cross-sectional results on prevalence, age of onset, and predictors of self-reported physician-diagnosed asthma in the study population.

    METHODS: An annual postal questionnaire is sent to Swedish elite skiers and orienteers during 2011-2015. In 2013, former Swedish Olympic skiers were similarly invited. We present cross-sectional data obtained in 2011 from the adolescents and adults and in 2013 from former skiers. A total of 491 athletes were invited. The results are presented by age, sex and sport. Chi-square test was used for group comparisons. Predictors of asthma were identified using logistic regression.

    RESULTS: Response rate was 82%. Among athletes aged 15-19, 29% of the skiers (38% of the female skiers), and 17% of the orienteers reported asthma (p = 0.071). Among the athletes aged 20-34, 35% of the skiers and 16% of the orienteers reported asthma (p = 0.029). Among the former skiers aged 40-94, 22% reported asthma. Among the active athletes, the onset of asthma was in early adolescence. Logistic regression found increasing age, female sex, allergy, family history of allergy/asthma and being skier predictors of self-reported physician-diagnosed asthma.

    CONCLUSIONS: The prevalence of physician-diagnosed asthma is high among Swedish endurance athletes, especially female adolescent skiers.

  • 17.
    Näsman, Amanda
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Irewall, Tommie
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Hållmarker, Ulf
    Lindberg, Anne
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Asthma and Asthma Medication Are Common among Recreational Athletes Participating in Endurance Sport Competitions2018Ingår i: Canadian Respiratory Journal, ISSN 1198-2241, Vol. 2018, artikel-id 3238546Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Asthma prevalence is high among elite endurance athletes, but little is known about its prevalence among competitive recreational athletes. The aim of this study was to determine the prevalence of self-reported asthma and asthma medication use among competitive recreational endurance athletes and their association with training.

    Methods: A web survey on asthma and medication was conducted among 38,603 adult participants of three Swedish endurance competitions (cross-country running, cross-country skiing, and swimming).

    Results: The overall response rate was 29%. The prevalence of self-reported asthma (physician-diagnosed asthma and use of asthma medication in the last 12 months) was 12%. Among those reporting asthma, 23% used inhaled corticosteroids and long-acting beta-agonists daily. We found no association between training volume and daily use of asthma medication, except a trend in relation to short-acting beta-agonists. Independent predictors of self-reported asthma were female sex, allergic rhinitis, previous eczema, family history of asthma, cycling, and training for >5 h 50 min/week.

    Conclusions: The prevalence of self-reported asthma among Swedish competitive recreational endurance athletes appears to be higher than that in the general Swedish population. A large proportion of recreational athletes were reported with asthma use medications, indicating an association between high physical activity and self-reported asthma among competitive recreational athletes.

  • 18. Olin, A C
    et al.
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Department for Respiratory Medicine and Allergy, University Hospital and Medical Division, National Institute for Working Life, Umeå.
    Torén, K
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Department for Respiratory Medicine and Allergy, University Hospital and Medical Division, National Institute for Working Life, Umeå.
    Helleday, Ragnberth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Department for Respiratory Medicine and Allergy, University Hospital and Medical Division, National Institute for Working Life, Umeå.
    Ledin, M C
    Ljungkvist, G
    Ekman, A
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Department for Respiratory Medicine and Allergy, University Hospital and Medical Division, National Institute for Working Life, Umeå.
    Nitric oxide (NO) in exhaled air after experimental ozone exposure in humans2001Ingår i: Respiratory Medicine, ISSN 0954-6111, E-ISSN 1532-3064, Vol. 95, nr 6, s. 491-495Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We hypothesized that ozone, a common air pollutant, potent in producing airway inflammation, would increase the production of exhaled nitric oxide (NO). If so, measurement of exhaled NO could potentially be a valuable tool in population studies of air pollution effects. Eleven healthy non-smoking volunteers were exposed to 0.2 ppm ozone (O3) and filtered air for 2h on two separate occasions. Exhaled NO and nasal NO were measured before and on five occasions following the exposures. Changes in exhaled and nasal NO after ozone exposure were adjusted for changes after air exposure. There was a slight decrease in exhaled NO (-0.6; -3.1-1.2 ppb) (median and 95% confidence interval) and of nasal NO (-57; -173-75 ppb) directly after the ozone exposure. No significant changes in exhaled or nasal NO were however found 6 or 24 h after the exposure. Within the examined group, an O3 exposure level proven to induce an airway inflammation caused no significant changes in exhaled or nasal NO levels. Hence, the current study did not yield support for exhaled NO as a useful marker of ozone-induced oxidative stress and airway inflammation after a single exposure. This contrasts with data for workers exposed to repeated high peaks of ozone. The potential for exhaled NO as a marker of oxidative stress therefore deserves to be further elucidated.

  • 19.
    Persson, Hampus
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Lindberg, Anne
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Asthma Control and Asthma Medication Use among Swedish Elite Endurance Athletes2018Ingår i: Canadian Respiratory Journal, ISSN 1198-2241, artikel-id 4646852Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. Asthma is common in elite athletes. In this study, we examined the use of asthma medication and asthma control in endurance athletes in Sweden and compared the findings with those in a reference group of patients with asthma. Methods. The Asthma Control Test (ACT) and a questionnaire on asthma, respiratory symptoms, and medication use were posted to endurance athletes (n = 711) and the reference group of patients with asthma (n = 1026). Four hundred and sixty-nine athletes (66%) responded, of whom 141 (20%) reported physician-diagnosed asthma. In the reference group, 397 (39%) responded. Results. Seventy-seven percent of the athletes with asthma reported using asthma medication during the previous year; 39% used short/long-acting β2-agonists, 31% used inhaled corticosteroids, and 31% used both daily. According to the ACT scores, 19%, 24%, and 58% of athletes with asthma had uncontrolled, partially controlled, or well-controlled asthma, respectively. After adjustment, there was no difference in ACT scores or daily use of asthma medication between the study groups. Conclusions. Many endurance athletes had uncontrolled or partially controlled asthma, and one-third used inhaled corticosteroids and long-acting β2-agonists daily. Their adjusted ACT scores and use of asthma medication were similar to the values in the reference population.

  • 20.
    Sawalha, Sami
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Hedman, Linnea
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Backman, Helena
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Rönmark, Eva
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Lundbäck, Bo
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Lindberg, Anne
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    The impact of comorbidities on mortality in COPD, report from the OLIN COPD study.2018Ingår i: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 52Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    Comorbidities contribute to the increased mortality observed among subjects with COPD, but the prognostic impact and possible sex differences have rarely been evaluated in population-based studies.

    Aim: To evaluate the impact of common comorbidities; cardiovascular disease (CVD), diabetes mellitus (DM) and anxiety/depression (A/D), on mortality in a population-based study of subjects with (COPD) and without airway obstruction.

    Methods: All subjects with airway obstruction (FEV1/(F)VC<0.70, n=993), were, together with age- and sex matched referents, identified after examinations of population-based cohorts in 2002-04. Spirometric groups: Normal Lung Function (NLF), COPD; post- bronchodilator fixed ratio (GOLD) and lower limit of normal (LLN). Mortality data were collected until December 2015.

    Results: The cumulative mortality was significantly higher in GOLD-COPD than NLF, and higher in men than women in both groups. CVD, DM and A/D independently increased the risk for death (Hazard Ratio; 95% CI, 1.50-1.59; 1.07-2.11) in GOLD-COPD when adjusted for age, sex, smoking habits, BMI and FEV1% predicted, while in NLF A/D (1.54; 1.03-2.30) but not CVD (1.20; 0.87-1.65) or DM (1.46; 0.95-2.26). Among women with GOLD-COPD, CVD and A/D but not DM increased the risk for death, while among men DM and A/D, but not CVD. When the LLN-criterion was applied, the significantly increased risk for death associated with comorbidities remained among men, but not among women.

    Conclusion: CVD, DM and A/D increased the risk for death in GOLD-COPD, but there seems to be sex-dependent differences in prognosis associated with comorbidities, also in relation to different spirometric criteria for COPD.

  • 21.
    Stenfors, Nikolai
    Department of Respiratory Medicine & Allergy, Östersund Hospital, Östersund, Sweden.
    Physician-diagnosed COPD global initiative for chronic obstructive lung disease stage IV in Östersund, Sweden: patient characteristics and estimated prevalence2006Ingår i: Chest, ISSN 0012-3692, E-ISSN 1931-3543, Vol. 130, nr 3, s. 666-671Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: The prevalence of COPD is estimated to 4 to 14%. According to the Global Initiative for Chronic Obstructive Lung Disease guidelines, COPD is divided into four stages. Patients with stage IV disease (very severe) have FEV1 < 30% of predicted values and/or respiratory insufficiency. The few studies that exist have reported a stage IV disease prevalence of 0.1 to 0.2% but provide limited additional patient characteristics. The present study estimated the prevalence of physician-diagnosed stage IV COPD in the city of Ostersund, Sweden, and characterized the patients.

    METHODS: Due to the regional integrated care pathway, patients in whom severe COPD is diagnosed are under surveillance by the Respiratory Department at Ostersund Hospital. Among these patients and all others in whom COPD has been diagnosed at Ostersund Hospital from 2000 to 2004, all those with an FEV1 of < 40% predicted were examined.

    RESULTS: A total of 76 patients fulfilled the criteria for stage IV COPD. The mean age was 71 years, 59% were women, and 40% were receiving long-term oxygen therapy. Sixty-five percent of the patients lived independently at home, 9% were present smokers, and 75% used inhaled corticosteroids daily. Sixty-seven percent of the patients had received vaccination against influenza the previous year. During 2004, 48% of the patients had at least one COPD-related hospitalization, and 11% had made at least one visit to the hospital for emergency care.

    CONCLUSIONS: The present study indicated that 0.13% of the population in Ostersund in 2004 had physician-diagnosed stage IV COPD. This is probably an underestimation of the true prevalence. Patients with stage IV COPD appear to require periods of hospitalization more often than intermittent emergency department visits.

  • 22.
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Self-reported symptoms and bronchial hyperresponsiveness in elite cross-country skiers.2010Ingår i: Respiratory Medicine, ISSN 0954-6111, E-ISSN 1532-3064, Vol. 104, nr 11, s. 1760-1763Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    INTRODUCTION: Respiratory symptoms in relationship to exercise, bronchial hyperresponsiveness (BHR), and exercise-induced asthma (EIA) are very common in elite winter athletes. Symptom-based screening for BHR would facilitate selection of athletes with possible EIA. OBJECTIVES: The aim of the present study was to evaluate the diagnostic accuracy of self-reported symptoms as predictors of BHR in an unselected population of adult elite cross-country skiers. METHODS: Forty-six Swedish adult skiers competing at national or international level were included. They had a mean (SD) training volume in the past 12 months of 593 (122) hours. Twenty-four subjects had previous physician-diagnosed asthma. The European Community Respiratory Health Survey questionnaire was used to evaluate the presence of respiratory symptoms. BHR was defined as bronchoconstriction to either eucapnic voluntary hyperventilation, dry powder mannitol or methacholine provocation. RESULTS: The "classical" EIA symptom of shortness of breath post-exercise was reported by 17% of all skiers. Eight subjects (17%) had BHR. None of the self-reported respiratory symptoms had high positive predictive values. However, symptoms caused by grass or pollen had high negative predictive values. DISCUSSION: EIA in elite winter athletes cannot accurately be based only on self-reported symptoms but requires verification with objective testing of BHR. Bronchoprovocation of elite winter athletes reporting respiratory symptoms in rest or because of exercise will probably reveal a high proportion of athletes without BHR. CLINICAL TRIAL: EUDRA-CT number 2006-005822-21.

  • 23.
    Stenfors, Nikolai
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Bosson, Jenny
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Helleday, Ragnberth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Behndig, Annelie F
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Pourazar, Jamshid
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Törnqvist, Håkan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Kelly, F J
    Frew, A J
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Mudway, I S
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Ozone exposure enhances mast-cell inflammation in asthmatic airways despite inhaled corticosteroid therapy.2010Ingår i: Inhalation Toxicology, ISSN 0895-8378, E-ISSN 1091-7691, Vol. 22, nr 2, s. 133-139Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Asthmatics are recognised to be more susceptible than healthy individuals to adverse health effects caused by exposure to the common air pollutant ozone. Ozone has been reported to induce airway neutrophilia in mild asthmatics, but little is known about how it affects the airways of asthmatic subjects on inhaled corticosteroids. We hypothesised that ozone exposure would exacerbate the pre-existent asthmatic airway inflammation despite regular inhaled corticosteroid treatment. Therefore, we exposed subjects with persistent asthma on inhaled corticosteroid therapy to 0.2 ppm ozone or filtered air for 2 h, on 2 separate occasions. Lung function was evaluated before and immediately after exposure, while bronchoscopy was performed 18 h post exposure. Compared to filtered air, ozone exposure increased airway resistance. Ozone significantly enhanced neutrophil numbers and myeloperoxidase levels in airway lavages, and induced a fourfold increase in bronchial mucosal mast cell numbers. The present findings indicate that ozone worsened asthmatic airway inflammation and offer a possible biological explanation for the epidemiological findings of increased need for rescue medication and hospitalisation in asthmatic people following exposure to ambient ozone.

  • 24.
    Stenfors, Nikolai
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Liaaen, Erik Dyb
    Henriksen, Anne H.
    No difference in long term survival in patients hospitalized for pneumonic versus non-pneumonic acute exacerbations of COPD2018Ingår i: Clinical Respiratory Journal, ISSN 1752-6981, E-ISSN 1752-699X, Vol. 12, nr 3, s. 1305-1306Artikel i tidskrift (Refereegranskat)
  • 25.
    Stenfors, Nikolai
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Mooe, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    The Prevalence of COPD in Individuals with Acute Coronary Syndrome: A Spirometry-Based Screening Study2015Ingår i: COPD: Journal of Chronic Obstructive Pulmonary Disease, ISSN 1541-2555, E-ISSN 1541-2563, Vol. 12, nr 4, s. 453-461Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The prevalence of COPD among individuals with acute coronary syndrome (ACS) is estimated at 5% to 18%, and COPD appears to be a predictor of poor outcome. Diagnosis of COPD has mostly been based on medical records without spirometry. As COPD is largely undiagnosed and misdiagnosed, the prevalence and clinical significance of COPD in the ACS population has not been reliably assessed. The present study aimed to estimate the prevalence of COPD in patients with ACS and evaluate the accuracy of medical record-based COPD diagnoses. Methods: This was a single-centre spirometry screening study for COPD in patients admitted for ACS in the county of Jämtland, Sweden. Patient medical records were reviewed to register previous medical history. Spirometry was performed prior to discharge or at the first follow-up outpatient visit after discharge. COPD was defined as a post-bronchodilator FEV1/FVC of <0.7 or below lower limit of normal. Results: Of 743 eligible patients, 407 performed spirometry. Five percent had COPD according to medical records; 11% and 5% fulfilled spirometric criteria of COPD according to FEV1/FVC of < 0.7 (p = 0.002) and below lower limit of normal definitions, respectively. “COPD according to medical history” had a sensitivity of 23%, specificity of 98%, positive predictive value of 53%, and negative predictive value of 91% compared with spirometric COPD FEV1/FVC of < 0.7 Conclusions: In patients with ACS, COPD is underdiagnosed and misdiagnosed. We raise concerns regarding the validity of medical record-based COPD in evaluating the biological and clinical association between COPD and coronary disease. ­Clinical Trial Registration: ISRCTN number 05697808 (www.controlled-trials.com)

  • 26.
    Stenfors, Nikolai
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Nordenhäll, Charlotta
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Salvi, S S
    Mudway, I
    Söderberg, Margareta
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Helleday, Ragnberth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Levin, Jan-Olof
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Kemiska institutionen.
    Holgate, S T
    Kelly, F J
    Frew, A J
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
    Different airway inflammatory responses in asthmatic and healthy humans exposed to diesel.2004Ingår i: Eur Respir J, ISSN 0903-1936, Vol. 23, nr 1, s. 82-6Artikel i tidskrift (Refereegranskat)
  • 27.
    Stenfors, Nikolai
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Department of Respiratory Medicine and Allergy, University Hospital, Umeå.
    Pourazar, Jamshid
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Department of Respiratory Medicine and Allergy, University Hospital, Umeå.
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Department of Respiratory Medicine and Allergy, University Hospital, Umeå.
    Krishna, M T
    Mudway, I
    Helleday, Ragnberth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Department of Respiratory Medicine and Allergy, University Hospital, Umeå.
    Kelly, F J
    Frew, A J
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Department of Respiratory Medicine and Allergy, University Hospital, Umeå.
    Effect of ozone on bronchial mucosal inflammation in asthmatic and healthy subjects2002Ingår i: Respiratory Medicine, ISSN 0954-6111, E-ISSN 1532-3064, Vol. 96, nr 5, s. 352-358Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Epidemiological studies suggestthat asthmatics are more affected by ozone than healthy people. This study tested three hypotheses (1) that short-term exposure to ozone induces inflammatory cell increases and up-regulation of vascular adhesion molecules in airway lavages and bronchial tissue 6 h after ozone exposure in healthy subjects; (2) these responses are exaggerated in subjects with mild allergic asthma; (3) ozone exacerbates pre-existent allergic airways inflammation. We exposed 15 mild asthmatic and 15 healthy subjects to 0.2 ppm of ozone or filtered air for 2 h on two separate occasions. Airway lavages and bronchial biopsies were obtained 6 h post-challenge. We found that ozone induced similar increases in bronchial wash neutrophils in both groups, although the neutrophil increase in the asthmatic group was on top of an elevated baseline. In healthy subjects, ozone exposure increased the expression of the vascular endothelial adhesion molecules P-selectin and ICAM- 1, as well as increasing tissue neutrophil and mast cell numbers. The asthmatics showed allergic airways inflammation at baseline but ozone did not aggravate this at the investigated time point. At 6 h post-ozone-exposure, we found no evidence that mild asthmatics were more responsive than healthy to ozone in terms of exaggerated neutrophil recruitment or exacerbation of pre-existing allergic inflammation. Further work is needed to assess the possibility of a difference in time kinetics between healthy and asthmatic subjects in their response to ozone.

  • 28. Sydbom, A
    et al.
    Blomberg, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Dept of Respiratory Medicine and Allergy, University Hospital, Umeå.
    Parnia, S
    Dept of Respiratory Medicine and Allergy, University Hospital, Umeå and Respiratory Cell and Molecular Biology Research Division, Southampton General Hospital, Tremona Road, Southampton, UK.
    Stenfors, Nikolai
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Dept of Respiratory Medicine and Allergy, University Hospital, Umeå.
    Sandström, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin. Dept of Respiratory Medicine and Allergy, University Hospital, Umeå.
    Dahlén, S E
    Health effects of diesel exhaust emissions2001Ingår i: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 17, nr 4, s. 733-746Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Epidemiological studies have demonstrated an association between different levels of air pollution and various health outcomes including mortality, exacerbation of asthma, chronic bronchitis, respiratory tract infections, ischaemic heart disease and stroke. Of the motor vehicle generated air pollutants, diesel exhaust particles account for a highly significant percentage of the particles emitted in many towns and cities. This review is therefore focused on the health effects of diesel exhaust, and especially the particular matter components. Acute effects of diesel exhaust exposure include irritation of the nose and eyes, lung function changes, respiratory changes, headache, fatigue and nausea. Chronic exposures are associated with cough, sputum production and lung function decrements. In addition to symptoms, exposure studies in healthy humans have documented a number of profound inflammatory changes in the airways, notably, before changes in pulmonary function can be detected. It is likely that such effects may be even more detrimental in asthmatics and other subjects with compromised pulmonary function. There are also observations supporting the hypothesis that diesel exhaust is one important factor contributing to the allergy pandemic. For example, in many experimental systems, diesel exhaust particles can be shown to act as adjuvants to allergen and hence increase the sensitization response. Much of the research on adverse effects of diesel exhaust, both in vivo and in vitro, has however been conducted in animals. Questions remain concerning the relevance of exposure levels and whether findings in such models can be extrapolated into humans. It is therefore imperative to further assess acute and chronic effects of diesel exhaust in mechanistic studies with careful consideration of exposure levels. Whenever possible and ethically justified, studies should be carried out in humans.

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