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UBC Theses and Dissertations

The relationship of particulate matter retention in the lung to the severity of chronic obstructive pulmonary disease Ling, Sean Hilton


Particulate matter (PM) deposited into the lung is removed predominantly by ciliary action of epithelial cells in the airways and by macrophages that phagocytose these particles in the peripheral air space. We hypothesize that the particle load or burden in the lungs’ of patients with Chronic Obstructive Pulmonary Disease (COPD) are responsible for perpetuating the chronic inflammatory response in the lung of subjects with COPD (even after smoking cessation). Samples were selected to cover the whole range of severity of COPD. Quantitative histological methods were used to quantify and characterize the particle burden in the lung tissue. The volume fraction (Vv) of PM in the lung tissue, including the parenchyma, airways, alveolar macrophages, blood vessels, and lymphoid follicles was determined using the aforementioned methods. To determine the chemical composition of the PM, Raman spectroscopy was used to analyze samples in situ. PM could be found in virtually all compartments of the lung: the parenchyma, blood vessels, airways, lymphoid follicles, and alveolar macrophages. The total burden of PM in all tissues of the lung was higher in subjects with COPD compared to controls (p<O.OO1) as well as in smokers with normal lung function (p<O.O1). There was an incremental increase in PM with increased COPD severity that peaks at GOLD 2 and then falls off in the GOLD 3/4 group. These findings were very similar in analysis to the lung parenchyma, but the same relationship was not found in the blood vessels and lymphoid follicles. An increase in lung PM burden correlated with a decline in FEV ₁/FVC and pack years smoking. The PM in the lung tissue was found to have a similar Raman spectrum to that of carbonaceous soot. We conclude that PM is retained in the lung of COPD subjects. Whether just the burden of exposure or whether poor clearance of PM from the lungs is responsible, remains unclear from our data. We speculate that this retained PM could perpetuate the chronic inflammatory response in the lung and contribute to the progression of COPD.

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