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  • 1.
    Behndig, Annelie F
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Larsson, Nirina
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Brown, Joanna L
    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, Sean T
    Dove, Rosamund E
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Wilson, Susan J
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Kelly, Frank J
    Mudway, Ian S
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Proinflammatory doses of diesel exhaust in healthy subjects fail to elicit equivalent or augmented airway inflammation in subjects with asthma2011In: Thorax, ISSN 0040-6376, E-ISSN 1468-3296, Vol. 66, no 1, p. 12-19Article in journal (Refereed)
    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.

  • 2. Cai, Yutong
    et al.
    Schikowski, Tamara
    Adam, Martin
    Buschka, Anna
    Carsin, Anne-Elie
    Jacquemin, Benedicte
    Marcon, Alessandro
    Sanchez, Margaux
    Vierkötter, Andrea
    Al-Kanaani, Zaina
    Beelen, Rob
    Birk, Matthias
    Brunekreef, Bert
    Cirach, Marta
    Clavel-Chapelon, Françoise
    Declercq, Christophe
    de Hoogh, Kees
    de Nazelle, Audrey
    Ducret-Stich, Regina E.
    Valeria Ferretti, Virginia
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Gerbase, Margaret W.
    Hardy, Rebecca
    Heinrich, Joachim
    Hoek, Gerard
    Jarvis, Debbie
    Keidel, Dirk
    Kuh, Diana
    Nieuwenhuijsen, Mark J.
    Ragettli, Martina S.
    Ranzi, Andrea
    Rochat, Thierry
    Schindler, Christian
    Sugiri, Dorothea
    Temam, Sofia
    Tsai, Ming-Yi
    Varraso, Raphaëlle
    Kauffmann, Francine
    Krämer, Ursula
    Sunyer, Jordi
    Künzli, Nino
    Probst-Hensch, Nicole
    Hansell, Anna L.
    Cross-sectional associations between air pollution and chronic bronchitis: an ESCAPE meta-analysis across five cohorts2014In: Thorax, ISSN 0040-6376, E-ISSN 1468-3296, Vol. 69, no 11, p. 1005-1014Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: This study aimed to assess associations of outdoor air pollution on prevalence of chronic bronchitis symptoms in adults in five cohort studies (Asthma-E3N, ECRHS, NSHD, SALIA, SAPALDIA) participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE) project.

    METHODS: Annual average particulate matter (PM10, PM2.5, PMabsorbance, PMcoarse), NO2, nitrogen oxides (NOx) and road traffic measures modelled from ESCAPE measurement campaigns 2008-2011 were assigned to home address at most recent assessments (1998-2011). Symptoms examined were chronic bronchitis (cough and phlegm for ≥3 months of the year for ≥2 years), chronic cough (with/without phlegm) and chronic phlegm (with/without cough). Cohort-specific cross-sectional multivariable logistic regression analyses were conducted using common confounder sets (age, sex, smoking, interview season, education), followed by meta-analysis.

    RESULTS: 15 279 and 10 537 participants respectively were included in the main NO2 and PM analyses at assessments in 1998-2011. Overall, there were no statistically significant associations with any air pollutant or traffic exposure. Sensitivity analyses including in asthmatics only, females only or using back-extrapolated NO2 and PM10 for assessments in 1985-2002 (ECRHS, NSHD, SALIA, SAPALDIA) did not alter conclusions. In never-smokers, all associations were positive, but reached statistical significance only for chronic phlegm with PMcoarse OR 1.31 (1.05 to 1.64) per 5 µg/m(3) increase and PM10 with similar effect size. Sensitivity analyses of older cohorts showed increased risk of chronic cough with PM2.5abs (black carbon) exposures.

    CONCLUSIONS: Results do not show consistent associations between chronic bronchitis symptoms and current traffic-related air pollution in adult European populations.

  • 3. Carlsten, Chris
    et al.
    Blomberg, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Pui, Mandy
    Sandström, Thomas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Wong, Sze Wing
    Alexis, Neil
    Hirota, Jeremy
    Diesel exhaust augments allergen-induced lower airway inflammation in allergic individuals: a controlled human exposure study2016In: Thorax, ISSN 0040-6376, E-ISSN 1468-3296, Vol. 71, no 1, p. 35-44Article in journal (Refereed)
    Abstract [en]

    Rationale Traffic-related air pollution has been shown to augment allergy and airway disease. However, the enhancement of allergenic effects by diesel exhaust in particular is unproven in vivo in the human lung, and underlying details of this apparent synergy are poorly understood. Objective To test the hypothesis that a 2 h inhalation of diesel exhaust augments lower airway inflammation and immune cell activation following segmental allergen challenge in atopic subjects. Methods 18 blinded atopic volunteers were exposed to filtered air or 300 mg PM2.5/m(3) of diesel exhaust in random fashion. 1 h post-exposure, diluent-controlled segmental allergen challenge was performed; 2 days later, samples from the challenged segments were obtained by bronchoscopic lavage. Samples were analysed for markers and modifiers of allergic inflammation (eosinophils, Th2 cytokines) and adaptive immune cell activation. Mixed effects models with ordinal contrasts compared effects of single and combined exposures on these end points. Results Diesel exhaust augmented the allergen-induced increase in airway eosinophils, interleukin 5 (IL-5) and eosinophil cationic protein (ECP) and the GSTT1 null genotype was significantly associated with the augmented IL-5 response. Diesel exhaust alone also augmented markers of non-allergic inflammation and monocyte chemotactic protein (MCP)-1 and suppressed activity of macrophages and myeloid dendritic cells. Conclusion Inhalation of diesel exhaust at environmentally relevant concentrations augments allergen-induced allergic inflammation in the lower airways of atopic individuals and the GSTT1 genotype enhances this response. Allergic individuals are a susceptible population to the deleterious airway effects of diesel exhaust.

  • 4. Ekström, Magnus Pär
    et al.
    Blomberg, Anders
    Bergström, Göran
    Brandberg, John
    Caidahl, Kenneth
    Engström, Gunnar
    Engvall, Jan
    Eriksson, Maria
    Gränsbo, Klas
    Hansen, Tomas
    Jernberg, Tomas
    Nilsson, Lars
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Nilsson, Ulf
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Olin, Anna-Carin
    Persson, Lennart
    Rosengren, Annika
    Sandelin, Martin
    Sköld, Magnus
    Sundström, Johan
    Swahn, Eva
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Tanash, Hanan A.
    Torén, Kjell
    Östgren, Carl Johan
    Lindberg, Eva
    The association of body mass index, weight gain and central obesity with activity-related breathlessness: the Swedish Cardiopulmonary Bioimage Study2019In: Thorax, ISSN 0040-6376, E-ISSN 1468-3296, Vol. 74, no 10, p. 958-964Article in journal (Refereed)
    Abstract [en]

    Introduction: Breathlessness is common in the population, especially in women and associated with adverse health outcomes. Obesity (body mass index (BMI) >30 kg/m(2)) is rapidly increasing globally and its impact on breathlessness is unclear.

    Methods: This population-based study aimed primarily to evaluate the association of current BMI and self-reported change in BMI since age 20 with breathlessness (modified Research Council score >= 1) in the middle-aged population. Secondary aims were to evaluate factors that contribute to breathlessness in obesity, including the interaction with spirometric lung volume and sex.

    Results: We included 13 437 individuals; mean age 57.5 years; 52.5% women; mean BMI 26.8 (SD 4.3); mean BMI increase since age 20 was 5.0 kg/m(2); and 1283 (9.6%) reported breathlessness. Obesity was strongly associated with increased breathlessness, OR 3.54 (95% CI, 3.03 to 4.13) independent of age, sex, smoking, airflow obstruction, exercise level and the presence of comorbidities. The association between BMI and breathlessness was modified by lung volume; the increase in breathlessness prevalence with higher BMI was steeper for individuals with lower forced vital capacity (FVC). The higher breathlessness prevalence in obese women than men (27.4% vs 12.5%; p<0.001) was related to their lower FVC. Irrespective of current BMI and confounders, individuals who had increased in BMI since age 20 had more breathlessness.

    Conclusion: Breathlessness is independently associated with obesity and with weight gain in adult life, and the association is stronger for individuals with lower lung volumes.

  • 5. Fuertes, Elaine
    et al.
    Carsin, Anne-Elie
    Antó, Josep M.
    Bono, Roberto
    Corsico, Angelo Guido
    Demoly, Pascal
    Gislason, Thorarinn
    Gullón, José-Antonio
    Janson, Christer
    Jarvis, Deborah
    Heinrich, Joachim
    Holm, Mathias
    Leynaert, Bénédicte
    Marcon, Alessandro
    Martinez-Moratalla, Jesús
    Nowak, Dennis
    Erquicia, Silvia Pascual
    Probst-Hensch, Nicole M.
    Raherison, Chantal
    Raza, Wasif
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Real, Francisco Gómez
    Russell, Melissa
    Sánchez-Ramos, José Luis
    Weyler, Joost
    Aymerich, Judith Garcia
    Leisure-time vigorous physical activity is associated with better lung function: the prospective ECRHS study2018In: Thorax, ISSN 0040-6376, E-ISSN 1468-3296, Vol. 73, no 4, p. 376-384Article in journal (Refereed)
    Abstract [en]

    Objective: We assessed associations between physical activity and lung function, and its decline, in the prospective population-based European Community Respiratory Health Survey cohort. Methods: FEV1 and FVC were measured in 3912 participants at 27-57 years and 39-67 years (mean time between examinations= 11.1 years). Physical activity frequency and duration were assessed using questionnaires and used to identify active individuals (physical activity >= 2 times and >= 1 hour per week) at each examination. Adjusted mixed linear regression models assessed associations of regular physical activity with FEV1 and FVC. Results: Physical activity frequency and duration increased over the study period. In adjusted models, active individuals at the first examination had higher FEV1 (43.6 mL (95% CI 12.0 to 75.1)) and FVC (53.9 mL (95% CI 17.8 to 89.9)) at both examinations than their non-active counterparts. These associations appeared restricted to current smokers. In the whole population, FEV1 and FVC were higher among those who changed from inactive to active during the follow-up (38.0 mL (95% CI 15.8 to 60.3) and 54.2 mL (95% CI 25.1 to 83.3), respectively) and who were consistently active, compared with those consistently non-active. No associations were found for lung function decline. Conclusion: Leisure-time vigorous physical activity was associated with higher FEV1 and FVC over a 10-year period among current smokers, but not with FEV1 and FVC decline.

  • 6.
    Hedman, Linnéa
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Bjerg, Anders
    Sundberg, Sigrid
    Forsberg, Bertil
    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.
    Both environmental tobacco smoke and personal smoking is related to asthma and wheeze in teenagers2011In: Thorax, ISSN 0040-6376, E-ISSN 1468-3296, Vol. 66, no 1, p. 20-25Article in journal (Refereed)
    Abstract [en]

    Background: Environmental tobacco smoke (ETS) has been reported as a significant risk factor for childhood asthma. Among adults, personal smoking is a major cause of respiratory symptoms and diseases. The effects of these exposures on the prevalence of asthma and wheeze among teenagers are less well known.

    Objective: The aim was to study the independent and combined effects of ETS and personal smoking on the prevalence of asthma and wheeze in teenagers.

    Methods: A longitudinal study of asthma and allergic diseases in schoolchildren has been in progress in Northern Sweden since 1996. All children aged 7–8 years in three municipalities were invited and 3430 (97%) participants have been followed by annual questionnaires. At the age 16–17 years, 82% of the initial participants took part in the 2005 survey.

    Results: Prevalence of physician-diagnosed asthma, ever wheeze and current wheeze was significantly higher among those exposed to maternal ETS and among daily smokers. In multivariate analyses, maternal ETS was a significant risk factor for physician-diagnosed asthma and ever wheeze (OR 1.3–1.5) and personal daily smoking for current wheeze (OR 2.0). ORs for asthma and ever wheeze were highest among daily smokers who were also exposed to maternal ETS with ORs of 1.7 and 2.5, respectively. A significant dose–response association between number of cigarettes/day and the prevalence of wheeze was also found.

    Conclusions: Both ETS and personal smoking were significantly related to asthma and wheeze in teenagers. Maternal ETS exposure was associated with lifetime symptoms, but daily smoking among the teenagers was more strongly related to current symptoms.

  • 7.
    Hind, M
    et al.
    Department of Respiratory Medicine, Royal Brompton Hospital and National Heart and Lung Institute, Imperial College London, London, UK.
    Gilthorpe, Åsa
    MRC Centre for Developmental Neurobiology, King’s College London, London, UK.
    Stinchcombe, S
    MRC Centre for Developmental Neurobiology, King’s College London, London, UK.
    Maden, M
    MRC Centre for Developmental Neurobiology, King’s College London, London, UK.
    Retinoid induction of alveolar regeneration: from mice to man?2009In: Thorax, ISSN 0040-6376, E-ISSN 1468-3296, Vol. 64, no 5, p. 451-457Article in journal (Refereed)
    Abstract [en]

    The use of retinoids to induce human lung regeneration is under investigation in a number of studies in patients with chronic obstructive pulmonary disease (COPD). Retinoic acid (RA) has complex pleiotropic functions during vertebrate patterning and development and can induce regeneration in a number of different organ systems. Studies of retinoid signalling during lung development might provide a molecular basis to explain pharmacological induction of alveolar regeneration in adult models of lung disease. In this review the role of endogenous RA signalling during alveologenesis is explored and data suggesting that a number of exogenous retinoids can induce regeneration in the adult lung are discussed. Current controversies in this area are highlighted and a hypothesis of lung regeneration is put forward. Understanding the cellular and molecular mechanisms of induction of regeneration will be central for effective translation into patients with lung disease and may reveal novel insights into the pathogenesis of alveolar disease and senescence.

  • 8. Jarvis, Debbie
    et al.
    Newson, Roger
    Janson, Christer
    Corsico, Angelo
    Heinrich, Joachim
    Anto, Josep M
    Abramson, Michael J
    Kirsten, Anne-Marie
    Zock, Jan Paul
    Bono, Roberto
    Demoly, Pascal
    Leynaert, Bénédicte
    Raherison, Chantal
    Pin, Isabelle
    Gislason, Thorarinn
    Jogi, Rain
    Schlunssen, Vivi
    Svanes, Cecilie
    Watkins, John
    Weyler, Joost
    Pereira-Vega, Antonio
    Urrutia, Isabel
    Gullón, Jose A
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Probst-Hensch, Nicole
    Boezen, H Marike
    Martinez-Moratalla Rovira, Jesús
    Accordini, Simone
    de Marco, Roberto
    Burney, Peter
    Prevalence of asthma-like symptoms with ageing2018In: Thorax, ISSN 0040-6376, E-ISSN 1468-3296, Vol. 73, no 1, p. 37-48Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Change in the prevalence of asthma-like symptoms in populations of ageing adults is likely to be influenced by smoking, asthma treatment and atopy.

    METHODS: The European Community Respiratory Health Survey collected information on prevalent asthma-like symptoms from representative samples of adults aged 20-44 years (29 centres in 13 European countries and Australia) at baseline and 10 and 20 years later (n=7844). Net changes in symptom prevalence were determined using generalised estimating equations (accounting for non-response through inverse probability weighting), followed by meta-analysis of centre level estimates.

    FINDINGS: Over 20 years the prevalence of 'wheeze' and 'wheeze in the absence of a cold' decreased (-2.4%, 95% CI -3.5 to -1.3%; -1.5%, 95% CI -2.4 to -0.6%, respectively) but the prevalence of asthma attacks, use of asthma medication and hay fever/nasal allergies increased (0.6%, 95% CI 0.1 to 1.11; 3.6%, 95% CI 3.0 to 4.2; 2.7%, 95% CI 1.7 to 3.7). Changes were similar in the first 10 years compared with the second 10 years, except for hay fever/nasal allergies (increase seen in the first 10 years only). Decreases in these wheeze-related symptoms were largely seen in the group who gave up smoking, and were seen in those who reported hay fever/nasal allergies at baseline.

    INTERPRETATION: European adults born between 1946 and 1970 have, over the last 20 years, experienced less wheeze, although they were more likely to report asthma attacks, use of asthma medication and hay fever. Decrease in wheeze is largely attributable to smoking cessation, rather than improved treatment of asthma. It may also be influenced by reductions in atopy with ageing.

  • 9. Lytras, Theodore
    et al.
    Kogevinas, Manolis
    Kromhout, Hans
    Carsin, Anne-Elie
    Antó, Josep M
    Bentouhami, Hayat
    Weyler, Joost
    Heinrich, Joachim
    Nowak, Dennis
    Urrutia, Isabel
    Martinez-Moratalla, Jesús
    Gullón, José Antonio
    Pereira-Vega, Antonio
    Raherison-Semjen, Chantal
    Pin, Isabelle
    Demoly, Pascal
    Leynaert, Bénédicte
    Villani, Simona
    Gislason, Thorarinn
    Svanes, Cecilie
    Holm, Mathias
    Forsberg, Bertil
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Norbäck, Dan
    Mehta, Amar J
    Probst-Hensch, Nicole
    Benke, Geza
    Jogi, Rain
    Torén, Kjell
    Sigsgaard, Torben
    Schlünssen, Vivi
    Olivieri, Mario
    Blanc, Paul D
    Vermeulen, Roel
    Garcia-Aymerich, Judith
    Jarvis, Deborah
    Zock, Jan-Paul
    Occupational exposures and 20-year incidence of COPD: the European Community Respiratory Health Survey.2018In: Thorax, ISSN 0040-6376, E-ISSN 1468-3296, Vol. 73, no 11, p. 1008-1015Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Occupational exposures have been associated with an increased risk of COPD. However, few studies have related objectively assessed occupational exposures to prospectively assessed incidence of COPD, using postbronchodilator lung function tests. Our objective was to examine the effect of occupational exposures on COPD incidence in the European Community Respiratory Health Survey.

    METHODS: General population samples aged 20-44 were randomly selected in 1991-1993 and followed up 20 years later (2010-2012). Spirometry was performed at baseline and at follow-up, with incident COPD defined using a lower limit of normal criterion for postbronchodilator FEV1/FVC. Only participants without COPD and without current asthma at baseline were included. Coded job histories during follow-up were linked to a Job-Exposure Matrix, generating occupational exposure estimates to 12 categories of agents. Their association with COPD incidence was examined in log-binomial models fitted in a Bayesian framework.

    FINDINGS: 3343 participants fulfilled the inclusion criteria; 89 of them had COPD at follow-up (1.4 cases/1000 person-years). Participants exposed to biological dust had a higher incidence of COPD compared with those unexposed (relative risk (RR) 1.6, 95% CI 1.1 to 2.3), as did those exposed to gases and fumes (RR 1.5, 95% CI 1.0 to 2.2) and pesticides (RR 2.2, 95% CI 1.1 to 3.8). The combined population attributable fraction for these exposures was 21.0%.

    INTERPRETATION: These results substantially strengthen the evidence base for occupational exposures as an important risk factor for COPD.

  • 10. Purdue, Mark P
    et al.
    Gold, Laura
    Järvholm, Bengt
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Occupational and Enviromental Medicine.
    Alavanja, Michael C R
    Ward, Mary H
    Vermeulen, Roel
    Impaired lung function and lung cancer incidence in a cohort of Swedish construction workers.2007In: Thorax, ISSN 0040-6376, E-ISSN 1468-3296, Vol. 62, no 1, p. 51-6Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Although impaired lung function in general has been associated with an increased risk of lung cancer, past studies typically have not attempted to investigate separately the obstructive and restrictive components of respiratory impairment. To deal with this question further, data from a large (n = 176 997) cohort of male Swedish construction workers, for whom spirometry measurements before follow-up were available, were analysed. METHODS: Cancer incidence for 1971-2001 was obtained through linkage with the national cancer registry. Using a modification of the Global Initiative for Chronic Obstructive Lung Disease criteria for chronic obstructive pulmonary disease (COPD), subjects were classified into five categories of lung function: normal, mild COPD, moderate COPD, severe COPD and restrictive lung disease (RLD). Rate ratios (RR) and 95% confidence intervals (CI) for lung cancer across lung function categories were calculated using Poisson regression, adjusted for age and smoking. Other end points (histological types of lung cancer, non-lung tobacco-related cancers, other cancers, total mortality) were also investigated. RESULTS: 834 incident cases of lung cancer were identified. Increased rates of lung cancer were observed for both COPD (mild: RR 1.5, 95% CI 1.2 to 1.9; moderate/severe: RR 2.2, 95% CI 1.8 to 2.7) and RLD (RR 2.0, 95% CI 1.6 to 2.5) relative to normal lung function. These associations did not meaningfully change on applying follow-up lag times of 5, 10 and 15 years after spirometry. When analysed by histological type, associations with both COPD and RLD were stronger for squamous cell carcinoma and small cell carcinoma, and weaker for adenocarcinoma. Both COPD and RLD were associated with increased rates of total mortality. CONCLUSIONS: Obstructive and restrictive impairments in lung function are associated with increased lung cancer risk.

  • 11. Toren, Kjell
    et al.
    Qvarfordt, Ingemar
    Bergdahl, Ingvar A.
    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.
    Increased mortality from infectious pneumonia after occupational exposure to inorganic dust, metal fumes and chemicals2011In: Thorax, ISSN 0040-6376, E-ISSN 1468-3296, Vol. 66, no 11, p. 992-996Article in journal (Refereed)
    Abstract [en]

    Objectives: There are epidemiological studies indicating that exposure to metal fumes is a risk factor for infectious pneumonia. Whether occupational exposure to other agents, such as inorganic dust or chemicals, also increases the risk for infectious pneumonia is not clear. The aim of the present study was to elucidate whether occupational exposure to respiratory pollutants and irritants increases the risk for infectious pneumonia.

    Design: Prospective cohort study. Setting Swedish male construction workers. Participants 320 143 male construction workers exposed to inorganic dust (asbestos, man-made mineral fibres, dust from cement, concrete and quartz), wood dust, metal fumes and chemicals (organic solvents, diisocyanates and epoxi resins) or unexposed.

    Main outcome measures: The cohort was followed from 1971 to 2003 and the main outcome measures were mortality to infectious pneumonia, lobar pneumonia or pneumococcal pneumonia. RRs were obtained by the person-years method and from Poisson regression models, adjusting for baseline values of age and smoking habits.

    Results: Among men aged 20e64 years there was increased mortality from infectious pneumonias among construction workers exposed to metal fumes (RR 2.31, 95% CI 1.35 to 3.95), inorganic dust (RR 1.87, 95% CI 1.22 to 2.87) and chemicals (RR 1.91, 95% CI 1.37 to 3.22). The mortality was also increased from both lobar pneumonia and pneumococcal pneumonia. Among men aged 65-84 years the occupational exposure to inorganic dust and chemicals was associated with slightly increased mortality from infectious pneumonia. Among groups with mutually exclusive exposures there was increased mortality from infectious pneumonias among construction workers exposed to inorganic dust, but not among those exposed to wood dust or chemicals. There were no cases among workers exposed only to metal fumes.

    Conclusions: Our findings indicate that exposure to inorganic dust increases the mortality from infectious pneumonias, especially lobar pneumonia and pneumococcal pneumonia. The mechanism is unclear, but the effect may be mediated through induced airways inflammation.

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