期刊论文详细信息
Environmental Health
Immune biomarkers link air pollution exposure to blood pressure in adolescents
Juyong Brian Kim1  Joseph C. Wu1  Francois Haddad1  Holden Maecker2  Nicholas Cauwenberghs3  Tatiana Kuznetsova3  Jennifer Arthur Ataam4  Hesam Movassagh5  Mary Prunicki5  Kari Nadeau5 
[1] Division of Cardiovascular Medicine, Department of Medicine, Stanford University, Stanford, USA;Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, USA;Institute for Immunity, Transplantation, and Infection, Stanford University, Stanford, USA;Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium;Research and Innovation Unit, INSERM U999, DHU TORINO, Paris Sud University, Marie Lannelongue Hospital, Le Plessis Robinson, France;Institute for Immunity, Transplantation, and Infection, Stanford University, Stanford, USA;Sean N Parker Center for Allergy and Asthma Research, Stanford University, Stanford, USA;
关键词: Adolescent;    Blood pressure;    Immune;    Inflammation;    Air pollution;    Cardiovascular disease;   
DOI  :  10.1186/s12940-020-00662-2
来源: Springer
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【 摘 要 】

BackgroundChildhood exposure to air pollution contributes to cardiovascular disease in adulthood. Immune and oxidative stress disturbances might mediate the effects of air pollution on the cardiovascular system, but the underlying mechanisms are poorly understood in adolescents. Therefore, we aimed to identify immune biomarkers linking air pollution exposure and blood pressure levels in adolescents.MethodsWe randomly recruited 100 adolescents (mean age, 16 years) from Fresno, California. Using central-site data, spatial-temporal modeling, and distance weighting exposures to the participant’s home, we estimated average pollutant levels [particulate matter (PM), polyaromatic hydrocarbons (PAH), ozone (O3), carbon monoxide (CO) and nitrogen oxides (NOx)]. We collected blood samples and vital signs on health visits. Using proteomic platforms, we quantitated markers of inflammation, oxidative stress, coagulation, and endothelial function. Immune cellular characterization was performed via mass cytometry (CyTOF). We investigated associations between pollutant levels, cytokines, immune cell types, and blood pressure (BP) using partial least squares (PLS) and linear regression, while adjusting for important confounders.ResultsUsing PLS, biomarkers explaining most of the variance in air pollution exposure included markers of oxidative stress (GDF-15 and myeloperoxidase), acute inflammation (C-reactive protein), hemostasis (ADAMTS, D-dimer) and immune cell types such as monocytes. Most of these biomarkers were independently associated with the air pollution levels in fully adjusted regression models. In CyTOF analyses, monocytes were enriched in participants with the highest versus the lowest PM2.5 exposure. In both PLS and linear regression, diastolic BP was independently associated with PM2.5, NO, NO2, CO and PAH456 pollution levels (P ≤ 0.009). Moreover, monocyte levels were independently related to both air pollution and diastolic BP levels (P ≤ 0.010). In in vitro cell assays, plasma of participants with high PM2.5 exposure induced endothelial dysfunction as evaluated by eNOS and ICAM-1 expression and tube formation.ConclusionsFor the first time in adolescents, we found that ambient air pollution levels were associated with oxidative stress, acute inflammation, altered hemostasis, endothelial dysfunction, monocyte enrichment and diastolic blood pressure. Our findings provide new insights on pollution-related immunological and cardiovascular disturbances and advocate preventative measures of air pollution exposure.

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