Title:
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Studies of markers of inflammation and oxidative stress in a newly developed exhaled breath condensate collecting system
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Exhaled breath condensate (EBC) collection, is a non-invasive method of measuring airways inflammation. This thesis records the development of a portable and reusable EBC collection
system and its use in health and disease to determine ranges of EBC nitrate and nitrite (NOx) and glutathione (GSH) concentration; additionally the effect of direct and ambient air
pollution exposure on NOx and GSH in EBC and nasal lavage NALF) was examined. Preliminary experiments revealed a collection time of 15 minutes with a system employing Teflon® tubes provided mean EBC volumes of 1.94±0.58m1. EBC NOx found in >90% of samples, was reproducible within healthy subjects over 6 collections; whilst EBC GSH was consistently below the limit of detection. EBC NOx levels were higher in asthma and COPD,
suggestive of increased airways inflammation when compared to healthy subjects (8.1±7.7;9.0±7.5μmoVL respectively vs. 4.8±2.3μmoVL), whilst salbutamol inhalation in-between
EBC collections caused a decrease in EBC NOx in COPD but not in asthma. Exposure to 200ppb sulphur dioxide (SO2) in healthy subjects elicited an immediate oxidative stress response evident by depletion of GSH in NALF which was absent in
coronary artery disease (CAD); whilst an increase in NALF NOx was seen at 4 hours post SO2 in the CAD group only. Evidence for lower airways inflammation was supported by an
increase in EBC NOx in both groups at 24 hours post SO2. Exposure to carbon particles failed to elicit a response in either group. Chronic lung disease patients exposed to ambient
levels of pollution at homes in Athens, Amsterdam, Helsinki and Birmingham, displayed increases in EBC NOx in line with increases in pollution indices; in particular with PMIO and
coarse particles measured at a central site and PM2.5 inside the home, particularly in subjects from Athens, where EBC NOx was greater. EBC was reliably collected in this thesis and
changes in the inflammatory marker NOx may be detected in response to oxidative stress in the airways due to disease, drug administration and direct and ambient air pollution exposure
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