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Fine particulate matter exposure and systemic inflammation: A potential mediating role of bioactive lipids.
Chen, Wu; Han, Yiqun; Xu, Yifan; Wang, Teng; Wang, Yanwen; Chen, Xi; Qiu, Xinghua; Li, Weiju; Li, Haonan; Fan, Yunfei; Yao, Yuan; Zhu, Tong.
Afiliación
  • Chen W; BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health, Peking University, Beijing, China; Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
  • Han Y; BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health, Peking University, Beijing, China; Environmental Research Group, MRC Centre for Environment and Health, Imperial College London, London, UK.
  • Xu Y; BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health, Peking University, Beijing, China.
  • Wang T; BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health, Peking University, Beijing, China.
  • Wang Y; BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health, Peking University, Beijing, China; National Institute of Environmental Health, Chinese Center for Disease Control and Prevention, Beijing, China.
  • Chen X; BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health, Peking University, Beijing, China; Hebei Technology Innovation Center of Human Settlement in Green Building (TCHS), Shenzhen Institute of Building Research Co., Ltd., Xiongan, Hebei, China.
  • Qiu X; BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health, Peking University, Beijing, China.
  • Li W; Peking University Hospital, Peking University, Beijing, China.
  • Li H; BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health, Peking University, Beijing, China.
  • Fan Y; BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health, Peking University, Beijing, China; China National Environmental Monitoring Centre, Beijing, China.
  • Yao Y; BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health, Peking University, Beijing, China; Department of Environmental Health Sciences, Jonathan and Karin Fielding School of Public Health, University of California Los Angeles, Los Angeles, CA, USA
  • Zhu T; BIC-ESAT and SKL-ESPC, College of Environmental Sciences and Engineering, Center for Environment and Health, Peking University, Beijing, China. Electronic address: tzhu@pku.edu.cn.
Sci Total Environ ; 931: 172993, 2024 Jun 25.
Article en En | MEDLINE | ID: mdl-38719056
ABSTRACT
Inflammation is a key mechanism underlying the adverse health effects of exposure to fine particulate matter (PM2.5). Bioactive lipids in the arachidonic acid (ARA) pathway are important in the regulation of inflammation and are reportedly altered by PM2.5 exposure. Ceramide-1-phosphate (C1P), a class of sphingolipids, is required to initiate ARA metabolism. We examined the role of C1P in the alteration of ARA metabolism after PM2.5 exposure and explored whether changes in the ARA pathway promoted systemic inflammation based on a panel study involving 112 older adults in Beijing, China. Ambient PM2.5 levels were continuously monitored at a fixed station from 2013 to 2015. Serum cytokine levels were measured to assess systemic inflammation. Multiple bioactive lipids in the ARA pathway and three subtypes of C1P were quantified in blood samples. Mediation analyses were performed to test the hypotheses. We observed that PM2.5 exposure was positively associated with inflammatory cytokines and the three subtypes of C1P. Mediation analyses showed that C1P significantly mediated the associations of ARA and 5, 6-dihydroxyeicosatrienoic acid (5, 6-DHET), an ARA metabolite, with PM2.5 exposure. ARA, 5, 6-DHET, and leukotriene B4 mediated systemic inflammatory response to PM2.5 exposure. For example, C1P C160 (a subtype of C1P) mediated a 12.9 % (95 % confidence interval 3.7 %, 32.5 %) increase in ARA associated with 3-day moving average PM2.5 exposure, and ARA mediated a 27.1 % (7.8 %, 61.2 %) change in interleukin-8 associated with 7-day moving average PM2.5 exposure. Our study indicates that bioactive lipids in the ARA and sphingolipid metabolic pathways may mediate systemic inflammation after PM2.5 exposure.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Contaminantes Atmosféricos / Material Particulado / Inflamación Límite: Aged / Female / Humans / Male / Middle aged País/Región como asunto: Asia Idioma: En Revista: Sci Total Environ Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Países Bajos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Contaminantes Atmosféricos / Material Particulado / Inflamación Límite: Aged / Female / Humans / Male / Middle aged País/Región como asunto: Asia Idioma: En Revista: Sci Total Environ Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Países Bajos