Correlation of Clinical Symptoms and Sputum Inflammatory Markers with Air Pollutants in Stable COPD Patients in Beijing Area

Abstract

Short-term exposure to major air pollutants can increase the risk of acute exacerbation in chronic obstructive pulmonary disease (COPD) patients. However, evidence on the mechanism of acute exacerbation of COPD (AECOPD) caused by air pollutants is still limited. A total of 78 patients with stable COPD and 58 healthy controls were recruited in Peking University Third Hospital in China from December 2014 to January 2015. The correlation and lag effect over 7 days (lag1–7) of 6 air pollutants with clinical symptoms and inflammatory markers in induced sputum were analyzed. PM_2.5, NO₂ and CO were positively correlated with the COPD assessment test (CAT) score at lag 5, PM₁₀ was positively correlated with the CAT score at lag 3, MMP-9 and IL-8 were positively correlated with PM_2.5, PM₁₀ and NO₂ at lag 2, and CO was positively correlated with each other marker at lag 4. Short-term exposure to PM_2.5, PM₁₀, NO₂, and CO can cause a neutrophil-mediated airway inflammatory response, followed by increased clinical symptoms. If the PM_2.5, PM₁₀, NO₂ and CO exposure levels increase during air pollution monitoring, the early usage of medication or reduction of exposure to pollutants can effectively reduce the clinical symptoms of patients.

Keywords:

• chronic obstructive pulmonary disease
• air pollution
• matrix metalloproteinase 9
• interleukin 8
• induced sputum

Acknowledgments

The present study was funded by the National Natural Science Foundation of China (Grant Nos: 81270097; 81470235; 81670034) and National Key R & D Program of China (2018YFC1311900).Thanks to Yi Zhang from the School Public Health at Peking University for providing the air pollution data.

Abbreviations

COPD, chronic obstructive pulmonary disease; AECOPD, acute exacerbation of COPD; BMI, body mass index; HRCT, high resolution computed tomography; LAA, low attenuation area; GOLD, global Initiative for chronic obstructive lung disease; FEV₁, forced expiratory volume in the first second; FEV₁/FVC, the ratio of the forced expiratory volume in one second to the forced vital capacity; RV/TLC, the ratio of residual volume to total lung capacity; DLCO%, the diffusing capacity of the lungs for carbon monoxide; CAT, COPD assessment test; WBC, white blood cell; Fib, fibrinogen; CRP, C-reactive protein; IL-8, interleukin 8; CXCL10, CXC chemokine 10; CCL18, chemokine ligand 18; sRAGE, soluble advanced glycation end products; MMP-3, matrix metalloproteinase 3; MMP-9, matrix metalloproteinase 9; SP-D, pulmonary surfactant protein D; CC16, Clara cell protein 16.

Data Sharing Statement

The data used to support the findings of this study are included within the article. No additional data are available.

Ethics Approval and Informed Consent

This study (IRB #00001052-13083) was approved by the ethics committee of Peking University third hospital, andwritten informed consent was acquired from all subjects before enrollment into the study in accordance with the principles of the Declaration of Helsinki. This study was registered at http://www.clinicaltrials.gov(NCT2964117).

Author Contributions

C Guo directed the execution of the study, participated in the assaying of the samples, conducted statistical analyses and interpretation and wrote the manuscript; X Sun and W Diao enrolled subjects; B He and N Shen were involved in study design and final approval of the version to be published. All authors made substantial contributions to conception and design, acquisition of data, or analysis and interpretation of data; took part in drafting the article or revising it critically for important intellectual content; gave final approval of the version to be published; and agree to be accountable for all aspects of the work.

Disclosure

The authors report no conflicts of interest in this work.