The objective of this study was to investigate the evolution of pollutant concentrations generated by smoking in a controlled indoor environment. For this purpose, a small flat in the centre of Athens, Greece was equipped with NO(x), O(3) and SO(2) continuous measuring instruments and portable analysers for spot measurements of TVOCs and CO(2), while two volunteer smokers remained inside and smoked as normal inhabitants. The results indicated that when windows are kept closed and smoking takes place NO(x), CO(2) and TVOCs concentrations increase by an order of 3, 4 or 10 times, respectively, and decrease returning to initial levels after 1 or 2 h.
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http://dx.doi.org/10.1016/j.scitotenv.2004.06.014 | DOI Listing |
Physiol Rep
January 2025
Department of Environmental Medicine, University of Rochester Medical Center, Rochester, New York, USA.
The use of genetically diverse mouse models offers a more accurate reflection of human genetic variability, improving the translatability of findings to heterogeneous human populations. This approach is particularly valuable in understanding diverse immune responses to disease by environmental exposures. This study investigates the inflammatory responses to acute exposures to mainstream cigarette smoke (CS) and environmental tobacco smoke (ETS) in two genetically diverse mouse strains, CC002/UncJ (UNC) & Diversity Outbred (J:DO).
View Article and Find Full Text PDFCurr Res Toxicol
December 2024
Department of Biomechatronics Engineering, National Taiwan University, No. 1, Sec. 4, Roosevelt Road, Taipei 10617, Taiwan.
Current treatments for chronic obstructive pulmonary disease (COPD), a common respiratory condition, include oxygen therapy and steroids for temporary relief. In this study, we established a rat model of cigarette smoke (CS)-induced COPD and investigated the benefits of a hydrogen-oxygen generator in this model. CS-exposed rats were treated using either a hydrogen-oxygen generator or a steroid.
View Article and Find Full Text PDFFront Immunol
January 2025
Immunology Translational Research Programme, Yong Loo Lin School of Medicine, Department of Microbiology & Immunology, National University of Singapore, Singapore, Singapore.
Introduction: Collagen is essential for maintaining lung structure and function and its remodeling has been associated with respiratory diseases including chronic obstructive pulmonary disease (COPD). However, the cellular mechanisms driving collagen remodeling and the functional implications of this process in the pathophysiology of pulmonary diseases remain poorly understood.
Methods: To address this question, we employed ; mice with specific depletion of Lyve-1 macrophages and assessed the content, types and organization of collagen in lung compartments at steady state and after chronic exposure to cigarette smoke (CS).
bioRxiv
January 2025
Department of Immunology and Microbiology, Scripps Research, La Jolla, San Diego, USA.
Objective: The mucosal origin hypothesis in rheumatoid arthritis (RA) posits that inhalant exposures, such as cigarette smoke and crystalline silica (c-silica), trigger immune responses contributing to disease onset. Despite the established risk posed by these exposures, the mechanistic link between inhalants, lung inflammation, and inflammatory arthritis remains poorly understood, partly from the lack of a suitable experimental model. As c-silica accelerates autoimmune phenotypes in lupus models and is a recognized risk factor for several autoimmune diseases, we investigated whether c-silica exposure could induce RA-like inflammatory arthritis in mice.
View Article and Find Full Text PDFRespir Res
January 2025
UR3738 CICLY Team Inflammation and Immunity of the Respiratory Epithelium, Claude Bernard University, Lyon 1, Pierre-Bénite, France.
Background: In patients with chronic obstructive pulmonary disease (COPD), a sensitization to A. fumigatus has been related to a decline in lung function, but the role of fungal agents in the disease pathogenesis remains unclear. The main purpose of the present study was to investigate whether cell inflammation could worsen after exposure to A.
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