Effects of bioaerosol exposure on work-related symptoms among Swiss sawmill workers

Objective Exposure to bioaerosols in the occupational environment of sawmills could be associated with a wide range of health effects, in particular respiratory impairment, allergy and organic dust toxic syndrome. The objective of the study was to assess the frequency of medical respiratory and general symptoms and their relation to bioaerosol exposure. Method Twelve sawmills in the French part of Switzerland were investigated and the relationship between levels of bioaerosols (wood dust, airborne bacteria, airborne fungi and endotoxins), medical symptoms and impaired lung function was explored. A health questionnaire was distributed to 111 sawmill workers. Results The concentration of airborne fungi exceeded the limit recommended by the Swiss National Insurance (SUVA) in the twelve sawmills. This elevated fungi level significantly influenced the occurrence of bronchial syndrome (defined by cough and expectorations). No other health effects (irritations or respiratory effects) could be associated to the measured exposures. We observed that junior workers showed significantly more irritation syndrome (defined by itching/running nose, snoring and itching/red eyes) than senior workers. Lung function tests were not influenced by bioaerosol levels nor dust exposure levels. Conclusion Results suggest that occupational exposure to wood dust in a Swiss sawmill does not promote a clinically relevant decline in lung function. However, the occurrence of bronchial syndrome is strongly influenced by airborne fungi levels. [Authors]]]> Air Pollutants, Occupational ; Air Microbiology ; Bacteria ; Endotoxins ; Fungi ; Dust ; Environmental Monitoring ; Wood ; Occupational Exposure ; Occupational Diseases ; Respiratory Tract Diseases eng https://serval.unil.ch/resource/serval:BIB_B4AA3AA89E66.P001/REF.pdf http://nbn-resolving.org/urn/resolver.pl?urn=urn:nbn:ch:serval-BIB_B4AA3AA89E664 info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_B4AA3AA89E664 info:eu-repo/semantics/publishedVersion info:eu-repo/semantics/openAccess Copying allowed only for non-profit organizations https://serval.unil.ch/disclaimer application/pdf oai:serval.unil.ch:BIB_B4AA7325E6FA 2022-02-19T02:29:06Z openaire documents urnserval <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> https://serval.unil.ch/notice/serval:BIB_B4AA7325E6FA Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes. info:eu-repo/semantics/altIdentifier/pmid/18188003 Klionsky, D.J. Abeliovich, H. Agostinis, P. Agrawal, D.K. Aliev, G. Askew, D.S. Baba, M. Baehrecke, E.H. Bahr, B.A. Ballabio, A. Bamber, B.A. Bassham, D.C. Bergamini, E. Bi, X. Biard-Piechaczyk, M. Blum, J.S. Bredesen, D.E. Brodsky, J.L. Brumell, J.H. Brunk, U.T. Bursch, W. Camougrand, N. Cebollero, E. Cecconi, F. Chen, Y. Chin, L.S. Choi, A. Chu, C.T. Chung, J. Clarke, P.G.H et, al. info:eu-repo/semantics/review article 2008 Autophagy, vol. 4, no. 2, pp. 151-175 info:eu-repo/semantics/altIdentifier/pissn/1554-8635 <![CDATA[Research in autophagy continues to accelerate,(1) and as a result many new scientists are entering the field. Accordingly, it is important to establish a standard set of criteria for monitoring macroautophagy in different organisms. Recent reviews have described the range of assays that have been used for this purpose.(2,3) There are many useful and convenient methods that can be used to monitor macroautophagy in yeast, but relatively few in other model systems, and there is much confusion regarding acceptable methods to measure macroautophagy in higher eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers of autophagosomes versus those that measure flux through the autophagy pathway; thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from fully functional autophagy that includes delivery to, and degradation within, lysosomes (in most higher eukaryotes) or the vacuole (in plants and fungi). Here, we present a set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes. This set of guidelines is not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to verify an autophagic response

Effect of low-level CO2 on innate inflammatory protein response to organic dust from swine confinement barns

Background: Organic hog barn dust (HDE) exposure induces lung inflammation and long-term decreases in lung function in agricultural workers. While concentrations of common gasses in confined animal facilities are well characterized, few studies have been done addressing if exposure to elevated barn gasses impacts the lung immune response to organic dusts. Given the well documented effects of hypercapnia at much higher levels we hypothesized that CO2 at 8 h exposure limit levels (5000 ppm) could alter innate immune responses to HDE. Methods: Using a mouse model, C57BL/6 mice were nasally instilled with defined barn dust extracts and then housed in an exposure box maintained at one of several CO2 levels for six hours. Bronchiolar lavage (BAL) was tested for several cytokines while lung tissue was saved for mRNA purification and immunohistochemistry. Results: Exposure to elevated CO2 significantly increased the expression of pro-inflammatory markers, IL-6 and KC, in BAL fluid as compared to dust exposure alone. Expression of other pro-inflammatory markers, such as ICAM-1 and matrix metalloproteinase-9 (MMP-9), were also tested and showed similar increased expression upon HDE + CO2 exposure. A chemokine array analysis of BAL fluid revealed that MIP-1γ (CCL9) shows a similar increased response to HDE + CO2. Further testing showed CCL9 was significantly elevated by barn dust and further enhanced by CO2 co-exposure in a dose-dependent manner that was noticeable at the protein and mRNA levels. In all cases, except for ICAM-1, increases in tested markers in the presence of elevated CO2 were only significant in the presence of HDE as well. Conclusions: We show that even at mandated safe exposure limits, CO2 is capable of enhancing multiple markers of inflammation in response to HDE