scholarly journals Immune biomarkers link air pollution exposure to blood pressure in adolescents

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Mary Prunicki ◽  
Nicholas Cauwenberghs ◽  
Jennifer Arthur Ataam ◽  
Hesam Movassagh ◽  
Juyong Brian Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Air Pollution ◽  
Acute Inflammation ◽  
Immune Cell ◽  
Cell Types ◽  
Pollution Levels ◽  
Immune Biomarkers ◽  
Air Pollution Exposure ◽  
Pollution Exposure

Abstract Background Childhood 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. Methods We 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. Results Using 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. Conclusions For 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.

scholarly journals Air pollution exposure is linked with methylation of immunoregulatory genes, altered immune cell profiles, and increased blood pressure in children

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mary Prunicki ◽  
Nicholas Cauwenberghs ◽  
Justin Lee ◽  
Xiaoying Zhou ◽  
Hesam Movassagh ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Air Pollution ◽  
Immune Regulation ◽  
Immune Cell ◽  
Ambient Air ◽  
Cell Types ◽  
Short Term ◽  
Short Term Exposure ◽  
Air Pollution Exposure ◽  
Pollution Exposure

AbstractAmbient air pollution exposure is associated with cardiovascular dysregulation and immune system alterations, yet no study has investigated both simultaneously in children. Understanding the multifaceted impacts may provide early clues for clinical intervention prior to actual disease presentation. We therefore determined the associations between exposure to multiple air pollutants and both immunological outcomes (methylation and protein expression of immune cell types associated with immune regulation) and cardiovascular outcomes (blood pressure) in a cohort of school-aged children (6–8 years; n = 221) living in a city with known elevated pollution levels. Exposure to fine particular matter (PM2.5), carbon monoxide (CO), and ozone (O3) was linked to altered methylation of most CpG sites for genes Foxp3, IL-4, IL-10 and IFN-g, all involved in immune regulation (e.g. higher PM2.5 exposure 1 month prior to the study visit was independently associated with methylation of the IL-4 CpG24 site (est = 0.16; P = 0.0095). Also, immune T helper cell types (Th1, Th2 and Th17) were associated with short-term exposure to PM2.5, O3 and CO (e.g. Th1 cells associated with PM2.5 at 30 days: est = − 0.34, P < 0.0001). Both B cells (est = − 0.19) and CD4+ cells (est = 0.16) were associated with 1 day NO2 exposure (P ≤ 0.031), whereas CD4+ and CD8+ cells were associated with chronic exposure to PAH456, NOx and/or NO2 (P ≤ 0.038 for all). Finally, diastolic BP (DBP) was inversely associated with long-term exposures to both CO and PAH456, and both systolic and pulse pressure were associated with short-term NO2 and chronic NOx exposure. Our findings demonstrate links between air pollution exposure and methylation of immunoregulatory genes, immune cell profiles and blood pressure, suggesting that even at a young age, the immune and cardiovascular systems are negatively impacted by exposure to air pollution.

scholarly journals Fine particulate matter (PM2.5) inhalation-induced alterations in the plasma lipidome as promoters of vascular inflammation and insulin resistance

2021 ◽  
Author(s):  
Bradford G. Hill ◽  
Benjamin Rood ◽  
Amanda Ribble ◽  
Petra Haberzettl
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Air Pollution ◽  
Vascular Inflammation ◽  
Fine Particulate Matter ◽  
Cvd Risk ◽  
Vegf Signaling ◽  
Fine Particulate ◽  
Air Pollution Exposure ◽  
Pollution Exposure

Fine particulate matter (PM2.5) air pollution exposure increases the risk of developing cardiovascular disease (CVD). Although the precise mechanisms by which air pollution exposure increases CVD risk remain uncertain, research indicates that PM2.5-induced endothelial dysfunction contributes to the CVD risk. Previous studies demonstrate that concentrated PM2.5 (CAP) exposure induces vascular inflammation and impairs insulin and VEGF signaling dependent upon pulmonary oxidative stress. To assess whether CAP exposure induces these vascular effects via plasmatic factors, we incubated aortas from naïve mice with plasma isolated from mice exposed to HEPA-filtered air or CAP (9 d) and examined vascular inflammation and insulin and VEGF signaling. We found that treatment of naïve aortas with plasma from CAP-exposed mice activates NF-κBα and induces insulin and VEGF resistance, indicating transmission by plasmatic factor(s). To identify putative factors, we exposed lung-specific ecSOD-transgenic (ecSOD-Tg) mice and wildtype (WT) littermates to CAP at concentrations of either ~60 µg/m3 (CAP60) or ~100 µg/m3 (CAP100) and measured the abundance of plasma metabolites by mass spectrometry. In WT mice, both CAP concentrations increased levels of fatty acids such as palmitate, myristate, and palmitoleate and decreased numerous phospholipid species; however, these CAP-induced changes in the plasma lipidome were prevented in ecSOD-Tg mice. Consistent with the literature, we found that fatty acids such as palmitate are sufficient to promote endothelial inflammation. Collectively, our findings suggest that PM2.5 exposure, by inducing pulmonary oxidative stress, promotes unique lipidomic changes characterized by high levels of circulating fatty acids, which are sufficient to trigger vascular pathology.

scholarly journals Prenatal Air Pollution Exposure and Newborn Blood Pressure

2015 ◽  
Vol 123 (4) ◽  
pp. 353-359 ◽  
Author(s):  
Lenie van Rossem ◽  
Sheryl L. Rifas-Shiman ◽  
Steven J. Melly ◽  
Itai Kloog ◽  
Heike Luttmann-Gibson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Air Pollution ◽  
Air Pollution Exposure ◽  
Pollution Exposure

scholarly journals Neonatal blood pressure in association with prenatal air pollution exposure, traffic, and land use indicators: An ENVIRONAGE birth cohort study

2019 ◽  
Vol 130 ◽  
pp. 104853 ◽  
Author(s):  
Narjes Madhloum ◽  
Tim S. Nawrot ◽  
Wilfried Gyselaers ◽  
Harry A. Roels ◽  
Esmée Bijnens ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Land Use ◽  
Air Pollution ◽  
Cohort Study ◽  
Birth Cohort ◽  
Birth Cohort Study ◽  
Air Pollution Exposure ◽  
Neonatal Blood ◽  
Pollution Exposure

scholarly journals Air pollution-induced placental alterations: an interplay of oxidative stress, epigenetics, and the aging phenotype?

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
N. D. Saenen ◽  
D. S. Martens ◽  
K. Y. Neven ◽  
R. Alfano ◽  
H. Bové ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Energy Metabolism ◽  
Early Life ◽  
Nitrosative Stress ◽  
Later Life ◽  
Modes Of Action ◽  
Air Pollution Exposure ◽  
Exposure During Pregnancy ◽  
Pollution Exposure

Abstract According to the “Developmental Origins of Health and Disease” (DOHaD) concept, the early-life environment is a critical period for fetal programming. Given the epidemiological evidence that air pollution exposure during pregnancy adversely affects newborn outcomes such as birth weight and preterm birth, there is a need to pay attention to underlying modes of action to better understand not only these air pollution-induced early health effects but also its later-life consequences. In this review, we give an overview of air pollution-induced placental molecular alterations observed in the ENVIRONAGE birth cohort and evaluate the existing evidence. In general, we showed that prenatal exposure to air pollution is associated with nitrosative stress and epigenetic alterations in the placenta. Adversely affected CpG targets were involved in cellular processes including DNA repair, circadian rhythm, and energy metabolism. For miRNA expression, specific air pollution exposure windows were associated with altered miR-20a, miR-21, miR-146a, and miR-222 expression. Early-life aging markers including telomere length and mitochondrial DNA content are associated with air pollution exposure during pregnancy. Previously, we proposed the air pollution-induced telomere-mitochondrial aging hypothesis with a direct link between telomeres and mitochondria. Here, we extend this view with a potential co-interaction of different biological mechanisms on the level of placental oxidative stress, epigenetics, aging, and energy metabolism. Investigating the placenta is an opportunity for future research as it may help to understand the fundamental biology underpinning the DOHaD concept through the interactions between the underlying modes of action, prenatal environment, and disease risk in later life. To prevent lasting consequences from early-life exposures of air pollution, policy makers should get a basic understanding of biomolecular consequences and transgenerational risks.

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