scholarly journals Air pollution exposure of lung models: focus on inflammation, oxidative stress and cyclic AMP signaling

2021 ◽  
Author(s):  
◽  
Isabella Cattani Pinto Cavalieri
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Cyclic Amp ◽  
Air Pollution Exposure ◽  
Pollution Exposure ◽  
Cyclic Amp Signaling

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 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.

Oxidative stress and air pollution exposure during pregnancy

2014 ◽  
Vol 34 (8) ◽  
pp. 838-847 ◽  
Author(s):  
S Nagiah ◽  
A Phulukdaree ◽  
D Naidoo ◽  
K Ramcharan ◽  
RN Naidoo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Stress Response ◽  
Oxidative Stress Response ◽  
Air Pollutant ◽  
Dna Integrity ◽  
Mitochondrial Depolarization ◽  
Air Pollution Exposure ◽  
Exposure During Pregnancy ◽  
Pollution Exposure

Chronic air pollution exposure during pregnancy can cause oxidative stress leading to adverse birth outcomes. The aim of this study was to assess and compare oxidative stress response in peripheral lymphocytes isolated from pregnant women from a highly industrialized locale (south Durban (SD); n = 50) and a control with lower air pollutant levels (north Durban (ND); n = 50). Oxidative stress response was measured by quantifying malondialdehyde (MDA) levels and a SuperArray gene panel. Mitochondrial function (adenosine triphosphate (ATP) levels and mitochondrial depolarization), DNA integrity (comet assay and mitochondrial DNA (mtDNA) viability) and DNA repair (OGG1) were assessed. Antioxidant response was assessed by quantification of glutathione (GSH) and SOD2, nuclear factor erythroid 2-related factor 2 (Nrf2) and uncoupling protein 2 (UCP2) protein and messenger RNA (mRNA) expression. Levels of MDA ( p = 0.9), mitochondrial depolarization ( p = 0.88), ATP (1.89-fold), SOD2 (1.23-fold) and UCP2 (1.58-fold) gene expression were elevated in the SD group with significantly higher UCP2 protein levels ( p = 0.05) and longer comet tail length ( p = 0.0004). The expression of Nrf2 protein ( p = 0.03) and mRNA levels (−1.37-fold), GSH concentration ( p < 0.0001), mtDNA amplification (−2.04-fold) and OGG1 mRNA (−2.78-fold) activity were decreased in the SD group. Of the 84 oxidative stress-related genes evaluated, 26 were differentially regulated. Pregnant women exposed to higher air pollutant levels showed increased markers for oxidative stress and compromised DNA integrity and repair.

scholarly journals Oxidative Stress and Air Pollution Exposure

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Maura Lodovici ◽  
Elisabetta Bigagli
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Health Impact ◽  
Target Organ ◽  
Biological Processes ◽  
Vehicular Traffic ◽  
Oxygen Species ◽  
Air Pollution Exposure ◽  
Pollution Exposure ◽  
Qualitative Characteristics

Air pollution is associated with increased cardiovascular and pulmonary morbidity and mortality. The mechanisms of air pollution-induced health effects involve oxidative stress and inflammation. As a matter of fact, particulate matter (PM), especially fine (PM2.5, PM < 2.5 μm) and ultrafine (PM0.1, PM < 0.1 μm) particles, ozone, nitrogen oxides, and transition metals, are potent oxidants or able to generate reactive oxygen species (ROS). Oxidative stress can trigger redox-sensitive pathways that lead to different biological processes such as inflammation and cell death. However, it does appear that the susceptibility of target organ to oxidative injury also depends upon its ability to upregulate protective scavenging systems. As vehicular traffic is known to importantly contribute to PM exposure, its intensity and quality must be strongly relevant determinants of the qualitative characteristics of PM spread in the atmosphere. Change in the composition of this PM is likely to modify its health impact.

scholarly journals The impact of urban air pollution exposure on the development of alterations on oxidative stress and behavioral parameters in adult mice

2008 ◽  
Vol 7 (S1) ◽  
Author(s):  
Karina Karina Abe ◽  
Leticia de Campos Brandao ◽  
Sergio Tufik ◽  
Paulo Hilario do Nascimento Saldiva ◽  
Vania D'Almeida
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Urban Air Pollution ◽  
Urban Air ◽  
Adult Mice ◽  
Air Pollution Exposure ◽  
Behavioral Parameters ◽  
Pollution Exposure ◽  
The Impact

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 Inflammation response, oxidative stress and DNA damage caused by urban air pollution exposure increase in the lack of DNA repair XPC protein

2020 ◽  
Vol 145 ◽  
pp. 106150
Author(s):  
Nilmara de Oliveira Alves ◽  
Guilherme Martins Pereira ◽  
Marlise Di Domenico ◽  
Giovanna Costanzo ◽  
Sarah Benevenuto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Dna Damage ◽  
Dna Repair ◽  
Urban Air Pollution ◽  
Urban Air ◽  
Inflammation Response ◽  
Air Pollution Exposure ◽  
Pollution Exposure

scholarly journals Human Serum Albumin Cys34 Adducts in Newborn Dried Blood Spots: Associations With Air Pollution Exposure During Pregnancy

2021 ◽  
Vol 9 ◽  
Author(s):  
William E. Funk ◽  
Nathan Montgomery ◽  
Yeunook Bae ◽  
Jiexi Chen ◽  
Ting Chow ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Human Serum Albumin ◽  
Serum Albumin ◽  
Human Serum ◽  
Dried Blood Spots ◽  
Air Pollution Exposure ◽  
Exposure During Pregnancy ◽  
Pollution Exposure ◽  
In Pregnancy

Background: Increasing evidence suggests that exposure to air pollution during pregnancy is associated with adverse pregnancy outcomes. However, biomarkers associated with air pollution exposure are widely lacking and often transient. In addition, ascertaining biospecimens during pregnacy to assess the prenatal environment remains largely infeasible.Objectives: To address these challenges, we investigated relationships between air pollution exposure during pregnancy and human serum albumin Cys34 (HSA-Cys34) adducts in newborn dried blood spots (DBS) samples, which captures an integration of perinatal exposures to small reactive molecules in circulating blood.Methods: Newborn DBS were obtained from a state archive for a cohort of 120 children born at one Kaiser Permanente Southern California (KPSC) hospitals in 2007. These children were selected to maximize the range of residential air pollution exposure during the entire pregnancy to PM2.5, PM10, NO2, O3, based on monthly estimates interpolated from regulatory monitoring sites. HSA-Cys34 adducts were selected based on previously reported relationships with air pollution exposure and oxidative stress.Results: Six adducts measured in newborn DBS samples were associated with air pollution exposures during pregnancy; these included direct oxidation products, adducts formed with small thiol compounds, and adducts formed with reactive aldehydes. Two general trends were identified: Exposure to air pollution late in pregnancy (i.e., in the last 30 days) was associated with increased oxidative stress, and exposure to air pollution earlier in pregnancy (i.e., not in the last 30 days) was associated with decreased oxidative stress around the time of birth.Discussion: Air pollution exposure occurring during pregnancy can alter biology and leave measurable impacts on the developing infant captured in the newborn DBS adductome, which represents a promising tool for investigating adverse birth outcomes in population-based studies.

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