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Objectives Occupational exposure to soft paper dust is associated with impaired lung function. Whether there is an increased risk for asthma or chronic obstructive pulmonary disease (COPD) is unclear. Methods We studied 7870 workers from three Swedish soft paper mills, and defined high-exposed workers, as having been exposed to soft paper dust exceeding 5 mg/m3 for at least 5 years. The remaining workers were classified as ‘low exposed’. Person-years at risk were calculated and stratified according to gender, age and calendar-year. The follow-up time was from 1960 to 2013. The expected numbers of deaths were calculated using the Swedish population as reference and standardised mortality ratios (SMRs) with 95% CIs were assessed. Results There was an increased mortality due to obstructive lung disease (asthma and COPD), among high-exposed workers, SMR 1.89, 95% CI 1.20 to 2.83, based on 23 observed cases. High-exposed workers had an increased mortality from asthma, SMR 4.13, 95% CI 1.78 to 8.14, based on eight observed cases. The increased asthma mortality was also observed among high-exposed men, SMR 4.38, 95% CI 1.42 to 10.2, based on five observed cases. The asthma mortality among low-exposed workers, both men and women, was not increased. The COPD mortality was not clearly increased among high-exposed workers (SMR 1.52, 95% CI 0.85 to 2.50). Conclusion High occupational exposure to soft paper dust increases the mortality due to asthma, and the results suggest that soft paper dust levels in workplaces should be below 5 mg/m3.

BackgroundDifficult asthma is a severe subgroup of asthma in which the main feature is uncontrollability of symptoms. Psychopathology is suggested to be prominent in patients with difficult asthma and considered important in its treatment; however, the evidence is scarce.AimsTo describe psychopathology in difficult asthma, both major mental and personality disorders, based on diagnostic interviews.MethodThis study was conducted in a specialised asthma care centre. A total of 51 patients with difficult asthma were diagnosed at the start of the treatment programme using two structured clinical interviews for both major mental (SCID-I) and personality disorders (SCID-II) according to DSM-IV-TR.ResultsAbout 55% of the patients with difficult asthma had a psychiatric disorder of which 89% was undiagnosed and untreated before being interviewed. About 49% had a minimum of one major mental disorder of which the cluster of anxiety disorders was the most common cluster of major mental disorders, followed by somatoform disorders. About 20% were diagnosed with a personality disorder. Of the 10 patients with a personality disorder, 9 had an obsessive-compulsive personality disorder.ConclusionsThis study demonstrates that more than half of patients with difficult asthma had a psychiatric disorder of which 89% was unrecognised. This study highlights the importance of offering patients with difficult asthma a psychiatric diagnostic interview and/or a psychiatric consultation as part of their routine medical examination and provision of appropriate psychiatric treatment. Moreover, it highlights the urgency of further research into the role of psychopathology in the development of difficult asthma.

Background: Industrial plants emit air pollutants like fine particles (PM2.5), sulfur dioxide (SO2) and nitrogen dioxide (NO2) that may affect the health of individuals living nearby. Objective: To assess the effects of community exposure to air emissions of PM2.5, SO2, and NO2 from pulp mills, oil refineries, metal smelters, on respiratory hospital admissions in young children in Quebec (QC) and British Columbia (BC), Canada. Methods: We assessed QC, BC and pooled associations between the following estimates of exposure and hospital admissions for asthma and bronchiolitis in children aged 2–4 years for the years 2002–2010: i) Crude emission exposures at the residential postal codes of children, calculated by multiplying estimated daily emissions of PM2.5, SO2, or NO2 from all nearby (

Current techniques used to obtain lung samples have significant limitations and do not provide reproducible biomarkers of inflammation. We have developed a novel technique that allows multiple sampling methods from the same area (or multiple areas) of the lung under direct bronchoscopic vision. It allows collection of mucosal lining fluid and bronchial brushing from the same site; biopsy samples may also be taken. The novel technique takes the same time as standard procedures and can be conducted safely. Eight healthy smokers aged 40–65 years were included in this study. An absorptive filter paper was applied to the bronchial mucosa under direct vision using standard bronchoscopic techniques. Further samples were obtained from the same site using bronchial brushings. Bronchoalveolar lavage (BAL) was obtained using standard techniques. Chemokine (C-C Motif) Ligand 20 (CCL20), CCL4, CCL5, Chemokine (C-X-C Motif) Ligand 1 (CXCL1), CXCL8, CXCL9, CXCL10, CXCL11, Interleukin 1 beta (IL-1β), IL-6, Vascular endothelial growth factor (VEGF), Matrix metalloproteinase 8 (MMP-8) and MMP-9 were measured in exudate and BAL. mRNA was collected from the bronchial brushings for gene expression analysis. A greater than 10 fold concentration of all the biomarkers was detected in lung exudate in comparison to BAL. High yield of good quality RNA with RNA integrity numbers (RIN) between 7.6 and 9.3 were extracted from the bronchial brushings. The subset of genes measured were reproducible across the samples and corresponded to the inflammatory markers measured in exudate and BAL. The bronchoabsorption technique as described offers the ability to sample lung fluid direct from the site of interest without the dilution effects caused by BAL. Using this method we were able to successfully measure the concentrations of biomarkers present in the lungs as well as collect high yield mRNA samples for gene expression analysis from the same site. This technique demonstrates superior sensitivity to standard BAL for the measurement of biomarkers of inflammation. It could replace BAL as the method of choice for these measurements. This method provides a systems biology approach to studying the inflammatory markers of respiratory disease progression. NHS Health Research Authority ( 13/LO/0256 ).