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Original Research |

Patterns of Retention of Particulate Matter in Lung Tissues of Patients With COPDParticulate Matter Retention in Lungs With COPD: Potential Role in Disease Progression

Sean H. Ling, MSc; John E. McDonough, PhD; John V. Gosselink, BSc; W. Mark Elliott, PhD; Shizu Hayashi, PhD; James C. Hogg, MD, PhD; Stephan F. van Eeden, MD, PhD
Author and Funding Information

From the UBC James Hogg Research Centre, Heart and Lung Institute, St. Paul’s Hospital, University of British Columbia, Vancouver, BC, Canada.

Correspondence to: Stephan F. van Eeden, MD, PhD, the UBC James Hogg Research Centre, Heart and Lung Institute, St. Paul’s Hospital, University of British Columbia, 1081 Burrard St, Vancouver, BC, Canada, V6Z1Y6; e-mail: stephan.vaneeden@hli.ubc.ca

Values are average ± SEM unless otherwise noted. GOLD = Global Initiative for Obstructive Lung Disease; NS = No significant difference in gender between different GOLD categories (analysis of variance).

a

Data based on those individuals in this group (n = 13) for whom smoking history was available for calculation of mean and SEM.

b

Data based on those individuals in this group (n = 6) for whom smoking history was available for calculation of mean and SEM.

Airways thickness given for airways < 2 mm in diameter. Lm = mean linear intercept (measure of alveolar size).

Funding/Support: This work was supported by the British Columbia Lung Association, the Heart and Stroke Foundation of Canada, and the Canadian Institutes of Health Research. Dr van Eeden was supported by a scholarship from the Michael Smith Foundation for Health Research and the Canadian Institute for Health Research. He is a senior scholar with the Michael Smith Foundation for Health Research and CIHR/GSK professor in Chronic Obstructive Pulmonary Disease.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


Funding/Support: This work was supported by the British Columbia Lung Association, the Heart and Stroke Foundation of Canada, and the Canadian Institutes of Health Research. Dr van Eeden was supported by a scholarship from the Michael Smith Foundation for Health Research and the Canadian Institute for Health Research. He is a senior scholar with the Michael Smith Foundation for Health Research and CIHR/GSK professor in Chronic Obstructive Pulmonary Disease.

Funding/Support: This work was supported by the British Columbia Lung Association, the Heart and Stroke Foundation of Canada, and the Canadian Institutes of Health Research. Dr van Eeden was supported by a scholarship from the Michael Smith Foundation for Health Research and the Canadian Institute for Health Research. He is a senior scholar with the Michael Smith Foundation for Health Research and CIHR/GSK professor in Chronic Obstructive Pulmonary Disease.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


Chest. 2011;140(6):1540-1549. doi:10.1378/chest.10-2281
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Background:  Particulate matter (PM) is present in lung tissues of smokers and urban dwellers. This study was designed to quantify the burden of PM in different lung tissues of subjects with COPD and determine its relationship to disease severity.

Methods:  Surgical lung tissue samples from nonsmokers (control subjects) were compared with those from smokers with normal spirometry and subjects in the four other categories of the GOLD (Global Initiative for Obstructive Lung Disease) classification of COPD severity using quantitative histologic techniques.

Results:  PM was present in the lung parenchyma, blood vessel walls, airways, lymphoid follicles, and alveolar macrophages. The total burden of PM (volume fraction [Vv]) in all tissues of the lung was higher in smokers than nonsmokers (P < .001) and also in smokers with airflow obstruction compared with the smokers with normal spirometry (P < .01). There was an incremental increase in total PM burden with increased COPD severity that peaked in GOLD II and then trended downward in GOLD III and IV COPD. This same pattern of PM retention was also observed in alveolar walls. The total burden of PM in lung tissues correlated with a decline in FEV1/FVC as well as pack-years smoking. mRNA expression of fibrinogen (γ chain) correlated with total lung burden of PM and burden of PM in lung parenchyma (r2 = 0.22, P < .001).

Conclusions:  We conclude that retained PM is widely distributed in lung tissues of subjects with COPD and that cigarette smoke exposure and airflow obstruction are associated with retention of PM in lung tissues. We attribute the downward trend in PM burden in severe COPD to either less deposition and retention or selective removal of PM containing tissues by emphysematous destruction.

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