BackgroundSmoking cessation is the best possible way to prevent the progression of smoking related airway diseases. However, the effect and time scale of smoking cessation on airway inflammation/remodelling are largely unknown. This prospective study evaluated the effects of smoking cessation on induced sputum (IS) neutrophils, matrix metalloproteinases (MMP-7, -8, -9) and tissue inhibitor of metalloproteinase-1 (TIMP-1).MethodsA total of 61 subjects participated in the study; 17 stopped smoking for 3 months and 9 for 6 months. The proportion of IS neutrophils and the levels of MMPs and TIMP-1 by ELISA were determined at baseline and at 3 and 6 months after cessation.ResultsIn the smokers, baseline IS neutrophils, MMPs and TIMP-1 were significantly higher compared to non-smokers. Levels of MMP-7, -8 and TIMP-1 decreased nearly to those of non-smokers but the levels of MMP-9 increased significantly from the baseline of the same subjects at 3 months after cessation (p = 0.009) with no significant decline at 6 months after cessation.ConclusionsSputum MMP-9 remained elevated after 6 months of smoking cessation, which may contribute to ongoing lung damage typical of COPD.
Nitric oxide (NO) is an important biological mediator with a variety of cellular and tissue functions. Fractional exhaled (FE(NO)) and nasal NO (FN(NO)) are known to be altered in several respiratory tract disease and disorders. However, there are rather few studies into the reproducibility of FE(NO) or FN(NO) measurements in healthy subjects. The aim of this study was to examine both short- and long-term variations of FE(NO) and FN(NO). In addition to intraday, day-to-day and week-to-week variations, the seasonal variation was assessed. The data revealed that FE(NO) and FN(NO) levels were lower in the mornings compared to the afternoon values. There were clinically significant correlations in day-to-day (morning values 121.4+/-37.5 vs. 119.8+/-29.6, r=0.868, P=0.000), week-to-week (morning values 121.4+/-37.5 vs. 128.0+/-32.1, r=0.637, P=0.000) and seasonal (winter 133.5+/-29.7, summer 138.1+/-47.6, autumn 121.4+/-37.5, r=0.624, P=0.000) values of FN(NO). Day-to-day (morning values 14.6+/-6.7 vs. 14.2+/-5.1, r=0.784, P=0.000) week-to-week (morning values 14.6+/-6.7 vs. 15.4+/-7.3, r=0.738, P=0.000) and seasonal (autumn 14.6+/-7.2, winter 16.6+/-6.4, summer 17.4+/-8.0, r=0.709, P=0.000) levels of FE(NO) were also highly reproducible. Serial FE(NO) and FN(NO) measurements can be used in the monitoring of respiratory tract inflammation. Due to the diurnal variation of FE(NO) and FN(NO,) in long-term follow-up the measurements should be performed at the same time of day.
BackgroundPolyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown.ParticipantsWe challenged 10 subjects experimentally to degraded PVC products under controlled conditions. All of the subjects had previously experienced respiratory symptoms suspected to be caused by this kind of exposure in their work place. Five subjects had doctor-diagnosed asthma.MethodsThe subjects were exposed to degraded PVC material in an exposure chamber; a challenge with ceramic tile was used as the control test. We followed exhaled nitric oxide, nasal NO, lung functions, cytokines [tumor necrosis factor-α (TNF-α), interleukin-4 (IL-4), IL-6, and IL-12] and NO in nasal lavage fluid (NAL) during and after the exposures. We also measured 2-ethylhexanol in exhaled breath samples and NAL.ResultsOn the morning after the PVC exposure, subjects reported respiratory tract symptoms significantly more often than they did after the control test (50% vs. 0%, respectively; p = 0.029; n = 10). We did not detect any changes in lung functions or levels of exhaled NO, nasal NO, or NO in NAL after PVC challenge compared with the control test. Cytokine levels increased after both exposures, with no statistically significant difference between situations. All of the exhaled breath samples collected during the PVC exposure contained 2-ethylhexanol.ConclusionsPVC flooring challenge can evoke respiratory tract symptoms in exposed subjects. Our results do not support the hypothesis that PVC materials themselves evoke immediate asthmatic reactions. The chamber test used is well suited to this type of exposure study.
Background: Markers of airway inflammation and oxidative stress have been mainly investigated in moderate/severe chronic obstructive pulmonary disease (COPD) or during its exacerbation. They have not been compared in noninvasive specimens such as exhaled breath condensate (EBC) and induced sputum in healthy nonsymptomatic smokers or in those who have symptoms and are at risk for COPD development. Objectives: To compare the relative proportions of 2 potential COPD biomarkers, 8-isoprostane and interleukin- 8 (IL-8) in the induced sputum and EBC sampled from the same subjects: nonsmokers (n = 14), healthy smokers (n = 17) and symptomatic smokers (n = 9) who are considered to be at risk for COPD. COPD patients with acute exacerbation (n = 10) were employed as positive controls. Methods: The levels of the aforementioned biomarkers in induced sputum and EBC were investigated using commercial biochemical techniques. Results: In induced sputum, the levels of 8-isoprostane and IL-8 were at least 10-fold higher compared to EBC levels in all groups. Healthy nonsmokers had the lowest levels, and patients with exacerbation of COPD the highest levels of 8-isoprostane in induced sputum and EBC. The same observation held true for IL-8 in induced sputum. Inverse correlations with lung function parameters were observed for both mediators. Conclusions: The levels of both potential markers were clearly higher in the induced sputum than in EBC. The results point to an advantage of induced sputum over EBC for assessing the degree of airway oxidative stress and inflammation in smokers with a potential risk for COPD development.
Several studies have shown an association between exposure in moisture-damaged buildings and adverse health effects. There are several indicator microbes of moisture damage, but Aspergillus fumigatus is one of the best-documented molds provoking health problems in different occupational conditions. We assessed whether inhalation of a commercial A. fumigatus solution would affect cytokine levels (tumor necrosis factor [TNF]-alpha, interleukin [IL]-1beta, IL-4, IL-6, interferon [IFN]-gamma) in nasal lavage fluid (NAL) compared with that evoked by placebo challenge. Twenty-seven subjects were studied: 13 had occupational exposure in a moisture-damaged building, 4 were atopic, and 10 were considered as controls. In all the subjects, the IL-1beta levels were increased significantly both at 6 (p = 0.013) and 24 h (p = .005) after the A. fumigatus challenge compared to placebo. In subjects with previous occupational exposure in a moisture-damaged building, IL-4 concentrations were increased significantly both at 6 (p =.046) and 24 h (p =.008) after the A. fumigatus challenge compared with placebo. Furthermore, in the control group, TNF-alpha levels were significantly increased at 6 h after the A. fumigatus challenge compared to placebo (p = .028). Thus, these data show a link between markers of inflammation in NAL and experimental A. fumigatus challenge.
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