Traffic-related air pollution associated pulmonary pathophysiologic changes and cardiac injury in elderly patients with COPD
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Traffic-related air pollution associated pulmonary pathophysiologic changes and cardiac injury in elderly patients with COPD. / Wang, Tong; Xu, Hongbing; Zhu, Yutong; Sun, Xiaoyan; Chen, Jie; Liu, Beibei; Zhao, Qian; Zhang, Yi; Liu, Lingyan; Fang, Jiakun; Xie, Yunfei; Liu, Shuo; Wu, Rongshan; Song, Xiaoming; He, Bei; Huang, Wei.
In: Journal of Hazardous Materials, Vol. 424, No. Part B, 12763, 2022.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Traffic-related air pollution associated pulmonary pathophysiologic changes and cardiac injury in elderly patients with COPD
AU - Wang, Tong
AU - Xu, Hongbing
AU - Zhu, Yutong
AU - Sun, Xiaoyan
AU - Chen, Jie
AU - Liu, Beibei
AU - Zhao, Qian
AU - Zhang, Yi
AU - Liu, Lingyan
AU - Fang, Jiakun
AU - Xie, Yunfei
AU - Liu, Shuo
AU - Wu, Rongshan
AU - Song, Xiaoming
AU - He, Bei
AU - Huang, Wei
PY - 2022
Y1 - 2022
N2 - Traffic-related air pollution (TRAP) has shown enormous environmental toxicity, but its cardiorespiratory health impact on chronic obstructive pulmonary disease (COPD) has been less studied. We followed a panel of 45 COPD patients with 4 repeated clinical visits across 14 months in a traffic-predominated urban area of Beijing, China, with concurrent measurements of TRAP metrics (fine particulate matter, black carbon, oxides of nitrogen and carbon monoxide). Linear mixed-effect models were performed to evaluate the associations and potential pathways linking traffic pollution to indicators of spirometry, cardiac injury, inflammation and oxidative stress. We observed that interquartile range increases in moving averages of TRAP exposures at prior up to 7 days were associated with significant reductions in large and small airway functions, namely decreases in forced vital capacity of 3.1–9.3% and forced expiratory flow 25–75% of 5.9–16.4%. Higher TRAP levels were also associated with worsening of biomarkers relevant to lung injury (hepatocyte growth factor and surfactant protein D) and cardiac injury (high-sensitivity cardiac troponin I, B-type natriuretic peptide and soluble ST2), as well as enhanced airway/systemic inflammation and oxidative stress. Mediation analyses showed that TRAP exposures may prompt cardiac injury, possibly via worsening pulmonary pathophysiology. These findings highlight the importance of traffic pollution control priority in urban areas.
AB - Traffic-related air pollution (TRAP) has shown enormous environmental toxicity, but its cardiorespiratory health impact on chronic obstructive pulmonary disease (COPD) has been less studied. We followed a panel of 45 COPD patients with 4 repeated clinical visits across 14 months in a traffic-predominated urban area of Beijing, China, with concurrent measurements of TRAP metrics (fine particulate matter, black carbon, oxides of nitrogen and carbon monoxide). Linear mixed-effect models were performed to evaluate the associations and potential pathways linking traffic pollution to indicators of spirometry, cardiac injury, inflammation and oxidative stress. We observed that interquartile range increases in moving averages of TRAP exposures at prior up to 7 days were associated with significant reductions in large and small airway functions, namely decreases in forced vital capacity of 3.1–9.3% and forced expiratory flow 25–75% of 5.9–16.4%. Higher TRAP levels were also associated with worsening of biomarkers relevant to lung injury (hepatocyte growth factor and surfactant protein D) and cardiac injury (high-sensitivity cardiac troponin I, B-type natriuretic peptide and soluble ST2), as well as enhanced airway/systemic inflammation and oxidative stress. Mediation analyses showed that TRAP exposures may prompt cardiac injury, possibly via worsening pulmonary pathophysiology. These findings highlight the importance of traffic pollution control priority in urban areas.
KW - Traffic-related air pollution
KW - Pulmonary dysfunction
KW - Cardiac injury
KW - Biomarker
KW - COPD
U2 - 10.1016/j.jhazmat.2021.127463
DO - 10.1016/j.jhazmat.2021.127463
M3 - Journal article
C2 - 34687998
VL - 424
JO - Journal of Hazardous Materials
JF - Journal of Hazardous Materials
SN - 0304-3894
IS - Part B
M1 - 12763
ER -
ID: 285711478