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 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.

Association between lung function of school age children and short-term exposure to air pollution and pollen: the PARIS cohort

Thorax ◽  
2021 ◽  
pp. thoraxjnl-2020-215515
Author(s):  
Hélène Amazouz ◽  
Nicolas Bougas ◽  
Michel Thibaudon ◽  
Guillaume Lezmi ◽  
Nicole Beydon ◽  
...  
Keyword(s):  
Air Pollution ◽  
Lung Function ◽  
School Age Children ◽  
School Age ◽  
Short Term ◽  
Short Term Exposure ◽  
Air Pollution Exposure ◽  
Total Pollen ◽  
Pollution Exposure ◽  
Cluster 2

BackgroundDaily levels of ambient air pollution and pollen may affect lung function but have rarely been studied together. We investigated short-term exposure to pollen and air pollution in relation to lung function in school-age children from a French population-based birth cohort.MethodsThis study included 1063 children from the PARIS (Pollution and Asthma Risk: an Infant Study) cohort whose lung function and FeNO measurements were performed at age 8 years old. Exposure data were collected up to 4 days before testing. We estimated daily total pollen concentration, daily allergenic risk indices for nine pollen taxa, as well as daily concentrations of three air pollutants (particulate matter less than 10 µm (PM10), nitrogen dioxide (NO2), ozone (O3)). Children with similar pollen and air pollution exposure were grouped using multidimensional longitudinal cluster analysis. Associations between clusters of pollen and air pollution exposure and respiratory indices (FEV1, FVC, FeNO) were studied using multivariable linear and logistic regression models adjusted for potential confounders.ResultsFour clusters of exposure were identified: no pollen and low air pollution (Cluster 1), grass pollen (Cluster 2), PM10 (Cluster 3) and birch/plane-tree pollen with high total pollen count (Cluster 4). Compared with children in Cluster 1, children in Cluster 2 had significantly lower FEV1 and FVC levels, and children from Cluster 3 had higher FeNO levels. For FEV1 and FVC, the associations appeared stronger in children with current asthma. Additional analysis suggested a joint effect of grass pollen and air pollution on lung function.ConclusionDaily ambient chemical and biological air quality could adversely influence lung function in children.

scholarly journals Short-term effects of air pollution on blood pressure

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
You-Jung Choi ◽  
Sun-Hwa Kim ◽  
Si-Hyuck Kang ◽  
Sun-Young Kim ◽  
Ok-Jin Kim ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Air Pollution ◽  
Air Pollutants ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Pathophysiological Mechanism ◽  
Short Term ◽  
Mortality And Morbidity ◽  
Short Term Exposure ◽  
Increased Risk

AbstractElevated blood pressure (BP) has been proposed as a possible pathophysiological mechanism linking exposure to ambient air pollution and the increased risk of cardiovascular mortality and morbidity. In this study, we investigated the hourly relationship between ambient air pollutants and BP. BP measurements were extracted from the electronic health record database of the Seoul National University Bundang Hospital from February 2015 to June 2017. A total of 98,577 individual BP measurements were matched to the hourly levels of air pollutants. A generalized additive model was constructed for hour lags of 0–8 of air pollutants adjusting for age, sex, meteorological variables, and time trend. Systolic BP was shown to be significantly lower at 2–4 hours and 3–5 hours after increased levels of SO2 and CO, respectively (0.24 mmHg and 0.26 mmHg for an interquartile range, respectively). In contrast, O3 and NO2 were associated with significantly increased systolic BP at 3–5 lag hours and at 0–2 lag hours, respectively. BP elevation in association with O3 and NO2 was shown to be significantly greater in hypertensive patients than normotensive subjects. Our findings suggest that short-term exposure to air pollution may be associated with elevated BP.

SHORT-TERM EXPOSURE TO AMBIENT AIR POLLUTION AND BLOOD PRESSURE IN THE FRAMINGHAM HEART STUDY

2011 ◽  
Vol 2011 (1) ◽  
Author(s):  
Joshua I Rosenbloom ◽  
Elissa H Wilker ◽  
Gary F Mitchell ◽  
Brent Coull ◽  
Naomi A Hamberg ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Air Pollution ◽  
Framingham Heart Study ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Short Term ◽  
Heart Study ◽  
Short Term Exposure

scholarly journals Ambient air pollution exposure and blood pressure changes during pregnancy

2012 ◽  
Vol 117 ◽  
pp. 46-53 ◽  
Author(s):  
Pei-Chen Lee ◽  
Evelyn O. Talbott ◽  
James M. Roberts ◽  
Janet M. Catov ◽  
Richard A. Bilonick ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Air Pollution ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Air Pollution Exposure ◽  
Pressure Changes ◽  
Pollution Exposure

scholarly journals Potential Short-Term Air Pollution Effects on Rheumatoid Arthritis Activity in Metropolitan Areas in the North of Italy: A Cross-Sectional Study

2021 ◽  
Vol 18 (16) ◽  
pp. 8490
Author(s):  
Francesca Ingegnoli ◽  
Tania Ubiali ◽  
Tommaso Schioppo ◽  
Valentina Longo ◽  
Antonella Murgo ◽  
...  
Keyword(s):  
Air Pollution ◽  
Disease Activity ◽  
Cross Sectional Study ◽  
Short Term ◽  
Cross Sectional ◽  
Short Term Exposure ◽  
Air Pollution Exposure ◽  
Synthetic Dmards ◽  
Pollution Exposure ◽  
The Impact

Rheumatoid arthritis (RA) flare is related to increased joint damage, disability, and healthcare use. The impact of short-term air pollution exposure on RA disease activity is still a matter of debate. In this cross-sectional study, we investigated whether short-term exposure to particulate matter (PM)10, PM2.5, nitrogen dioxide (NO2), and ozone (O3) affected RA disease activity (DAS28 and SDAI) in 422 consecutive RA residents in Lombardy, North of Italy. Air pollutant concentrations, estimated by Regional Environmental Protection Agency (Lombardy—Italy) at the municipality level, were used to assign short-term exposure from the day of enrolment, back to seven days. Some significant negative associations emerged between RA disease activity, PM10, and NO2, whereas some positive associations were observed for O3. Patients were also stratified according to their ongoing Disease-Modifying anti-Rheumatic Drugs (DMARDs) treatment: no DMARDs (n = 25), conventional synthetic DMARDs (n = 108), and biological or targeted synthetic DMARDs (n = 289). Therapy interaction seemed partially able to influence the relationship between short-term air pollution exposure and RA disease activity (PM2.5 levels and DAS28 at the day of the visit-O3 levels and disease activity scores for the seven days before the evaluation). According to our results, the impact of short-term air pollution exposure (seven days) minimally impacts disease activity. Moreover, our study suggests therapy could alter the response to environmental factors. Further evidence is needed to elucidate determinants of RA flare and its management.

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