Effect of urban air pollution on CRP and coagulation: a study on inpatients with acute exacerbation of chronic obstructive pulmonary disease

Abstract

Purpose Acute 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 methods We 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. Results The 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). Conclusion Exposure 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.

Biomarkers of the relationship of particulate matter exposure with the progression of chronic respiratory diseases

“…CRP, a marker of the systemic inflammatory response, has been proposed as a biomarker of COPD. Tang et al measured the blood CRP level and PT in 317 patients with acute COPD exacerbation (AECOPD) 1 day before admission; the CRP level was increased during COPD exacerbation and PM elevation [ 38 ]. Of the subjects, 13.25% were smokers, and their occupational histories were not evaluated.…”

C-Reactive Protein: Pathophysiology, Diagnosis, False Test Results and a Novel Diagnostic Algorithm for Clinicians

“…such micro- or nanoparticles can be a constituent of environmental toxicity, which can also lead to low-grade inflammation, and except for smoking/passive smokers and smoke inhalation, which was previously discussed to increased CRP levels, air pollution has already been attributed to systemic inflammation and possibly increased CRP concentrations (i.e., exposed to PM2.5, fumes, home fireplaces/indoor pets/toxic metals, and other occupational-related exposures, such as wood dust, cotton, silica, asbestos, etc.) [ 1086 , 1087 , 1088 , 1089 , 1090 , 1091 , 1092 , 1093 , 1094 , 1095 , 1096 , 1097 , 1098 , 1099 , 1100 , 1101 , 1102 , 1103 , 1104 , 1105 ]. Finally, radiation from both the medical and the industrial field as well as through accidentally exposure can result into inflammation, and some data highlight an acute phase response caused by radiotherapy/radiochemotherapy, yet evidence toward CRP behavior in the extensive use of mobile phones, related devices, and other Wi-Fi wireless technologies seem sparse; nevertheless, some data on UV radiation indicate risks for possible systemic inflammation [ 1106 , 1107 , 1108 , 1109 , 1110 , 1111 , 1112 , 1113 , 1114 ].…”

Modern Concepts of the Role of Fine Particles (PM 2.5) in the Genesis of Atherosclerosis and Myocardial Damage: Clinical and Epidemiological Data, the Main Pathophysiological Mechanisms

“…Experimental studies are consistent with the results of clinical studies. Under the exposure of a healthy human body to PM 2.5, there can be observed a reduction of prothrombin time, activated partial thromboplastin time and an increase in plasma levels of fibrinogen and D-dimers which indicates a hypercoagulable state [ 120 - 122 ]. Some researchers report the effect of individual components of PM 2.5 on the hemostasis system parameters [ 29 ].…”