Particulate and gaseous pollutants on inflammation, thrombosis, and autonomic imbalance in subjects at risk for cardiovascular disease
Journal
Environmental Pollution
Journal Volume
223
Pages
403-408
Date Issued
2017
Author(s)
Abstract
This study examined effects of short-term urban air pollution exposures on inflammation, thrombosis, and autonomic imbalance in subjects at risk for cardiovascular disease (CVD). We enrolled 61 patients with multiple CVD risk factors and measured high sensitive C-reactive protein (hs-CRP), fibrinogen, D-dimer, and heart rate variability (HRV) indices. Two health examinations for each participant were performed during December 2002 through September 2003. Changes in inflammation and thrombotic markers and HRV indices with exposures to PM2.5, organic carbon (OC), elemental carbon (EC), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO) at 1- to 3-day lags were analyzed using mixed models. The results showed inflammatory and thrombotic markers increased with 1- to 3-day lagged PM2.5components and gaseous pollutants exposures. hs-CRP maximally increased 0.19 [95% confidence interval (CI): 0.07–0.31] and 0.15 (95% CI: 0.05–0.24) mg/L for an interquartile range (IQR) of 1-day lagged SO2(2.3 ppb) and CO (0.5 ppm), respectively. D-dimer maximally increased 1.05 (95% CI: 0.13–1.75), 0.72 (95% CI: 0.09–1.21), 0.92 (95% CI: 0.13–1.50), and 0.90 (95% CI: 0.07–1.61) mg/dL for an IQR of 1-day lagged OC (3.9 μg/m3), EC (2.0 μg/m3), SO2, and NO2(13.4 ppb), respectively. The HRV indices, including low frequency, very low frequency, and the ratio of low frequency to high frequency decreased 19.8 (95% CI: 4.4–32.7), 12.9 (95% CI: 0.8–23.4), and 17.6 (95% CI: 5.4–28.2)% for an IQR of 1-day lagged PM2.5(20.2 μg/m3), respectively. Our findings demonstrated PM2.5components and gaseous pollutants exert prolonged inflammatory and thrombotic reactions, while PM2.5exert an immediate autonomic imbalance. © 2017 Elsevier Ltd
Other Subjects
Air pollution; Blood vessels; Carbon monoxide; Cardiology; Fog; Heart; Nitrogen oxides; Organic carbon; Particles (particulate matter); Pathology; Risk assessment; Sulfur dioxide; Cardio-vascular disease; Heart rate variability; Inflammation; Particulate Matter; Thrombosis; Diseases; C reactive protein; carbon; carbon monoxide; D dimer; elemental carbon; fibrinogen; nitrogen dioxide; organic carbon; sulfur dioxide; unclassified drug; air pollutant; biological marker; carbon; carbon monoxide; nitrogen dioxide; particulate matter; sulfur dioxide; atmospheric pollution; cardiovascular disease; health risk; particulate matter; pollution effect; pollution exposure; risk factor; adult; air pollutant; air pollution; Article; autonomic dysfunction; cardiovascular disease; cardiovascular risk; disease marker; environmental exposure; exhaust gas; female; heart rate variability; human; inflammation; major clinical study; male; medical examination; risk assessment; suspended particulate matter; thrombosis; urban area; adverse effects; aged; air pollutant; air pollution; analysis; blood analysis; cardiovascular disease; chemically induced; drug effects; exposure; heart rate; inflammation; metabolism; middle aged; particulate matter; risk factor; Taiwan; thrombosis; very elderly; Aged; Aged, 80 and over; Air Pollutants; Air Pollution; Biomarkers; Blood Chemical Analysis; Carbon; Carbon Monoxide; Cardiovascular Diseases; Female; Heart Rate; Humans; Inflammation; Inhalation Exposure; Male; Middle Aged; Nitrogen Dioxide; Particulate Matter; Risk Factors; Sulfur Dioxide; Taiwan; Thrombosis
Publisher
Elsevier Ltd
Type
journal article