Abstract

PurposeAcute exacerbation of chronic obstructive pulmonary disease (AECOPD) is an important event in the course of chronic obstructive pulmonary disease that negatively affects patients’ quality of life and leads to higher socioeconomic costs. While previous studies have demonstrated a significant association between urban air pollution and hospitalization for AECOPD, there is a lack of research on the impact of particulate matter (PM) on inflammation and coagulation in AECOPD inpatients. Therefore, this study investigated the association of changes in coagulation function and C-reactive protein (CRP) with PM levels in the days preceding hospitalization.Patients and methodsWe reviewed the medical records of AECOPD patients admitted to Putuo Hospital, Shanghai University of Traditional Chinese Medicine, between March 2017 and September 2019. We analyzed the association of coagulation function and CRP level in AECOPD patients with PM levels in the days before hospitalization. Multivariate unconditional logistic regression analyses were used to evaluate the adjusted odds ratio (OR) and 95% confidence interval (CI) for the association of CRP data with hospitalization day. Kruskal–Wallis tests were used to evaluate mean aerodynamic diameter of ≥ 2.5 μm (PM2.5) exposure on the day before hospitalization; we assessed its association with changes in prothrombin time (PT) in AECOPD inpatients with different Global Initiative for Chronic Obstructive Lung Disease (GOLD) classes.ResultsThe peripheral blood PT of AECOPD patients with PM2.5 ≥ 25 mg/L on the day before hospitalization were lower than those of patients with PM2.5 < 25 mg/L (t = 2.052, p = 0.041). Patients with severe GOLD class exposed to greater than 25 mg/L of PM2.5on the day before hospitalization showed significant differences in PT (F = 9.683, p = 0.008). Peripheral blood CRP levels of AECOPD patients exposed to PM2.5 ≥ 25 mg/L and PM10 ≥ 50 mg/L on the day before hospitalization were higher than those of patients exposed to PM2.5 < 25 mg/L and PM10 < 50 mg/L (t = 2.008, p = 0.046; t = 2.637, p = 0.009). Exposure to < 25 mg/L of PM2.5 on the day before hospitalization was significantly associated with CRP levels (adjusted OR 1.91; 95% CI 1.101, 3.315; p = 0.024).ConclusionExposure of patients with AECOPD to high PM levels on the day before hospitalization was associated with an increased CRP level and shortened PT. Moreover, PM2.5 had a greater effect on CRP level and PT than mean aerodynamic diameter of ≥ 10 μm (PM10). AECOPD patients with severe GOLD class were more sensitive to PM2.5-induced shortening of PT than those with other GOLD classes.

Highlights

  • Chronic obstructive pulmonary disease (COPD) is considered a heterogeneous syndrome and has been associated with abnormal inflammatory immune responses in the lungs to particulate air pollution [1]

  • PM2.5, Particulate matter smaller than 2.5 μm in diameter; ­PM10, Particulate matter smaller than 10 μm in diameter; thrombin time (TT), Thrombin Time; prothrombin time (PT), Prothrombin Time; FIB, Fibrinogen; activated partial thromboplastin time (APTT), Activated Partial Thromboplastin Time; CRP, C-reactive protein p-values are shown for the Pearson’s correlation analysis

  • PM10, Particulate matter smaller than 10 μm in diameter; TT, Thrombin Time; PT, Prothrombin Time; FIB, Fibrinogen; APTT, Activated Partial Thromboplastin Time; CRP,C-reactive protein p-values are shown for the Student’s t-tests

Read more

Summary

Introduction

Chronic obstructive pulmonary disease (COPD) is considered a heterogeneous syndrome and has been associated with abnormal inflammatory immune responses in the lungs to particulate air pollution [1]. Exposure to ambient PM increases the incidence of AECOPD events, and a higher median of fine P­ M2.5 at 48 h before the onset of symptoms has been reported [2, 3]. It is estimated that the burden of death caused by air pollution is annually as high as 40,000 people in the UK. From the perspective of public health and policy, as well as in the context of disease and environmental pollution prevention, it is crucial to understand how the pathophysiologic mechanisms induced by ambient air pollutants might induce adverse AECOPD

Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call