Title Pro-thrombotic changes associated with exposure to ambient ultrafine particles in patients with chronic obstructive pulmonary disease: roles of lipid peroxidation and systemic inflammation
Authors Wang, Teng
Chen, Xi
Li, Haonan
Chen, Wu
Xu, Yifan
Yao, Yuan
Zhang, Hanxiyue
Han, Yiqun
Zhang, Lina
Que, Chengli
Gong, Jicheng
Qiu, Xinghua
Zhu, Tong
Affiliation Peking Univ, Coll Environm Sci & Engn, BIC ESAT, Beijing, Peoples R China
Peking Univ, Coll Environm Sci & Engn, SKL ESPC, Beijing, Peoples R China
Shenzhen Inst Bldg Res Co Ltd, Hebei Technol Innovat Ctr Human Settlement Green, Xiongan, Peoples R China
Imperial Coll London, MRC Ctr Environm & Hlth, Environm Res Grp, London, England
Shi Cha Hai Community Hlth Serv Ctr, Beijing, Peoples R China
Peking Univ, Peking Univ First Hosp, Beijing, Peoples R China
Keywords DIESEL-EXHAUST INHALATION
AIR-POLLUTION
PLATELET ACTIVATION
CARDIOVASCULAR-DISEASE
COPD
12-LIPOXYGENASE
BIOMARKERS
MECHANISMS
MORTALITY
RISK
Issue Date 24-Oct-2022
Publisher PARTICLE AND FIBRE TOXICOLOGY
Abstract Background: Exposure to particulate matter air pollution is associated with an increased risk of cardiovascular mortality in patients with chronic obstructive pulmonary disease (COPD), but the underlying mechanisms are not yet understood. Enhanced platelet and pro-thrombotic activity in COPD patients may explain their increased cardiovascular risk. We aim to explore whether short-term exposure to ambient particulate matter is associated with pro-thrombotic changes in adults with and without COPD, and investigate the underlying biological mechanisms in a longitudinal panel study. Serum concentration of thromboxane (Tx)B2 was measured to reflect platelet and pro-thrombotic activity. Lipoxygenase-mediated lipid peroxidation products (hydroxyeicosatetraenoic acids [HETEs]) and inflammatory biomarkers (interleukins [ILs], monocyte chemoattractant protein-1 [MCP-1], tumour necrosis factor alpha [TNF-alpha], and macrophage inflammatory proteins [MIPs]) were measured as potential mediating determinants of particle-associated pro-thrombotic changes. Results: 53 COPD and 82 non-COPD individuals were followed-up on a maximum of four visits conducted from August 2016 to September 2017 in Beijing, China. Compared to non-COPD individuals, the association between exposure to ambient ultrafine particles (UFPs) during the 3-8 days preceding clinical visits and the TxB2 serum concentration was significantly stronger in COPD patients. For example, a 10(3)/cm(3) increase in the 6-day average UFP level was associated with a 25.4% increase in the TxB2 level in the COPD group but only an 11.2% increase in the non-COPD group. The association in the COPD group remained robust after adjustment for the levels of fine particulate matter and gaseous pollutants. Compared to the non-COPD group, the COPD group also showed greater increases in the serum concentrations of 12-HETE (16.6% vs. 6.5%) and 15-HETE (9.3% vs. 4.5%) per 10(3)/cm(3) increase in the 6-day UFP average. The two lipid peroxidation products mediated 35% and 33% of the UFP-associated increase in the TxB2 level of COPD patients. UFP exposure was also associated with the increased levels of IL-8, MCP-1, MIP-1 alpha, MIP-1 beta, TNF-alpha, and IL-1 beta in COPD patients, but these inflammatory biomarkers did not mediate the TxB2 increase. Conclusions: Short-term exposure to ambient UFPs was associated with a greater pro-thrombotic change among patients with COPD, at least partially driven by lipoxygenase-mediated pathways following exposure.
URI http://hdl.handle.net/20.500.11897/657509
ISSN 1743-8977
DOI 10.1186/s12989-022-00503-9
Indexed SCI(E)
Appears in Collections: 环境科学与工程学院
第一医院

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