The Influence of Airborne Particulate Matter on Biomarkers and Biological Pathways

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Human Toxicology and Epidemiology".

Deadline for manuscript submissions: closed (15 November 2023) | Viewed by 9954

Special Issue Editors


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Guest Editor
Department of Public Health Sciences, University of Connecticut School of Medicine, Farmington, CT 06030, USA
Interests: air pollution; cardiovascular disease; transportation; environmental epidemiology
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Guest Editor
Division of Nutrition Epidemiology and Data Science of the Friedman School of Nutrition Science and Policy, Tufts University, Boston, MA 02111, USA
Interests: epidemiological research methods; evidence-synthesis methods; epigenetics and chronic disease risks; cardiovascular disease risks

Special Issue Information

Dear Colleagues,

Fine particulate matter, PM < 2.5 microns, is an established global public health problem on a par with other leading health risks. Other fractions of PM, including ultrafine particles (UFPs) and black carbon (BC), are also potential health hazards. While causal inference is strong for PM2.5, it is not as well-established for UFPs and BC. Improving confidence in biological pathways, as well as establishing dose–response relationships, especially those related to inflammation, can strengthen causal inference. The aim of this Special Issue is to publish papers that explore the ways that particulate matter enters and travels through biological systems, affects biomarkers of effect and exposure, and influences biological pathways.

We are pleased to invite you to contribute to this Special Issue, which aims to publish original research, systematic reviews (with or without meta-analyses), narrative reviews, theoretical commentaries, and reports on methods as well as on the need for future research. Research areas may include (but are not limited to) the following:

  • Epidemiology studies that measure associations between PM and blood pressure, blood biomarkers (inflammation, coagulation, and others), neurological/cognitive function tests, gene expression/regulation, epigenetics, and any other biological measures.
  • Measurement of PM components, including PAHs and nanoparticles, in tissues.
  • Toxicology studies that measure biological effects in animals, tissues, or cells.
  • Reports on new research or statistical modeling methods that can be used to study the influence of PM on biomarkers and biological pathways or on clinical outcomes.
  • Description of research needs for better understanding the effects of PM on biomarkers and biological pathways.

We look forward to receiving your contributions.

Prof. Dr. Doug Brugge
Prof. Dr. Mei Chung
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • particulate matter
  • air pollution
  • biomarkers
  • biological pathways
  • biological plausibility

Published Papers (6 papers)

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16 pages, 4255 KiB  
Article
Short-Term Effects of Primary and Secondary Particulate Matter on Ceramide Metabolism, Pro-Inflammatory Response, and Blood Coagulation
by Bin Zhang, Hongbing Xu, Xinghou He, Tong Wang, Mengyao Li, Xuyang Shan, Yutong Zhu, Changjie Liu, Qian Zhao, Xiaoming Song, Yele Sun, Lemin Zheng and Wei Huang
Toxics 2024, 12(3), 225; https://doi.org/10.3390/toxics12030225 - 19 Mar 2024
Viewed by 1053
Abstract
Evidence of the precise biological pathway responsible for acute cardiovascular events triggered by particulate matter (PM) exposure from anthropogenic emissions is sparse. We investigated the associations of biomarkers relevant to the pathophysiology of atherothrombosis (ceramide metabolism, pro-inflammatory response, and blood coagulation) with primary [...] Read more.
Evidence of the precise biological pathway responsible for acute cardiovascular events triggered by particulate matter (PM) exposure from anthropogenic emissions is sparse. We investigated the associations of biomarkers relevant to the pathophysiology of atherothrombosis (ceramide metabolism, pro-inflammatory response, and blood coagulation) with primary and secondary components in particulate matter with aerodynamic diameters less than 2.5 μm (PM2.5). A total of 152 healthy participants were followed with four repeated clinical visits between September 2019 and January 2020 in Beijing. Exposure to ambient inorganic aerosols (sulfate, nitrate, ammonium, and chloride), as well as organic aerosols (OA) in PM2.5, was measured by a real-time aerosol chemical speciation monitor, and sources of OA were performed by positive matrix factorization. We found significant increases of 101.9–397.9% in ceramide indicators associated with interquartile-range increases in inorganic aerosols and OA prior to 72 h of exposure. Higher levels of organic and inorganic aerosols in PM2.5 were associated with increases of 3.1–6.0% in normal T cells regulated upon activation and expressed and secreted relevant to the pro-inflammatory response; increases of 276.9–541.5% were observed in D-dimers relevant to coagulation. Detrimental effects were further observed following OA exposure from fossil fuel combustion. Mediation analyses indicated that ceramide metabolism could mediate the associations of PM2.5 components with pro-inflammatory responses. Our findings expand upon the current understanding of potential pathophysiological pathways of cardiovascular events posed by ambient particulates and highlight the importance of reducing primary and secondary PM from anthropogenic combustions. Full article
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22 pages, 4631 KiB  
Article
The Exposure Peaks of Traffic-Related Ultrafine Particles Associated with Inflammatory Biomarkers and Blood Lipid Profiles
by Cheng Lin, Kevin J. Lane, Virginia R. Chomitz, Jeffrey K. Griffiths and Doug Brugge
Toxics 2024, 12(2), 147; https://doi.org/10.3390/toxics12020147 - 13 Feb 2024
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Abstract
In this article, we explored the effects of ultrafine particle (UFP) peak exposure on inflammatory biomarkers and blood lipids using two novel metrics—the intensity of peaks and the frequency of peaks. We used data previously collected by the Community Assessment of Freeway Exposure [...] Read more.
In this article, we explored the effects of ultrafine particle (UFP) peak exposure on inflammatory biomarkers and blood lipids using two novel metrics—the intensity of peaks and the frequency of peaks. We used data previously collected by the Community Assessment of Freeway Exposure and Health project from participants in the Greater Boston Area. The UFP exposure data were time-activity-adjusted hourly average concentration, estimated using land use regression models based on mobile-monitored ambient concentrations. The outcome data included C-reactive protein, interleukin-6 (IL-6), tumor necrosis factor-alpha receptor 2 (TNF-RII), low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglycerides and total cholesterol. For each health indicator, multivariate regression models were used to assess their associations with UFP peaks (N = 364–411). After adjusting for age, sex, body mass index, smoking status and education level, an increase in UFP peak exposure was significantly (p < 0.05) associated with an increase in TNF-RII and a decrease in HDL and triglycerides. Increases in UFP peaks were also significantly associated with increased IL-6 and decreased total cholesterol, while the same associations were not significant when annual average exposure was used. Our work suggests that analysis using peak exposure metrics could reveal more details about the effect of environmental exposures than the annual average metric. Full article
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24 pages, 5041 KiB  
Article
Erythrocyte Vulnerability to Airborne Nanopollutants
by Cristina Hermosillo-Abundis, Aracely Angulo-Molina and Miguel A. Méndez-Rojas
Toxics 2024, 12(1), 92; https://doi.org/10.3390/toxics12010092 - 21 Jan 2024
Cited by 2 | Viewed by 2483
Abstract
The toxicological impact of airborne polluting ultrafine particles (UFPs, also classified as nanoparticles with average sizes of less than 100 nm) is an emerging area of research pursuing a better understanding of the health hazards they pose to humans and other organisms. Hemolytic [...] Read more.
The toxicological impact of airborne polluting ultrafine particles (UFPs, also classified as nanoparticles with average sizes of less than 100 nm) is an emerging area of research pursuing a better understanding of the health hazards they pose to humans and other organisms. Hemolytic activity is a toxicity parameter that can be assessed quickly and easily to establish part of a nanoparticle’s behavior once it reaches our circulatory system. However, it is exceedingly difficult to determine to what extent each of the nanoparticles present in the air is responsible for the detrimental effects exhibited. At the same time, current hemolytic assessment methodologies pose a series of limitations for the interpretation of results. An alternative is to synthesize nanoparticles that model selected typical types of UFPs in air pollution and evaluate their individual contributions to adverse health effects under a clinical assay of osmotic fragility. Here, we discuss evidence pointing out that the absence of hemolysis is not always a synonym for safety; exposure to model nanopollutants, even at low concentrations, is enough to increase erythrocyte susceptibility and dysfunction. A modified osmotic fragility assay in combination with a morphological inspection of the nanopollutant–erythrocyte interaction allows a richer interpretation of the exposure outcomes. Membrane–nanoparticle interplay has a leading role in the vulnerability observed. Therefore, future research in this line of work should pay special attention to the evaluation of the mechanisms that cause membrane damage. Full article
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17 pages, 2828 KiB  
Article
The Influence of Airborne Particulate Matter on the Risk of Gestational Diabetes Mellitus: A Large Retrospective Study in Chongqing, China
by Xiaoling Zeng, Yu Zhan, Wei Zhou, Zhimei Qiu, Tong Wang, Qing Chen, Dandan Qu, Qiao Huang, Jia Cao and Niya Zhou
Toxics 2024, 12(1), 19; https://doi.org/10.3390/toxics12010019 - 24 Dec 2023
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Abstract
Emerging research findings suggest that airborne particulate matter might be a risk factor for gestational diabetes mellitus (GDM). However, the concentration–response relationships and the susceptible time windows for different types of particulate matter may vary. In this retrospective analysis, we employ a novel [...] Read more.
Emerging research findings suggest that airborne particulate matter might be a risk factor for gestational diabetes mellitus (GDM). However, the concentration–response relationships and the susceptible time windows for different types of particulate matter may vary. In this retrospective analysis, we employ a novel robust approach to assess the crucial time windows regarding the prevalence of GDM and to distinguish the susceptibility of three GDM subtypes to air pollution exposure. This study included 16,303 pregnant women who received routine antenatal care in 2018–2021 at the Maternal and Child Health Hospital in Chongqing, China. In total, 2482 women (15.2%) were diagnosed with GDM. We assessed the individual daily average exposure to air pollution, including PM2.5, PM10, O3, NO2, SO2, and CO based on the volunteers’ addresses. We used high-accuracy gridded air pollution data generated by machine learning models to assess particulate matter per maternal exposure levels. We further analyzed the association of pre-pregnancy, early, and mid-pregnancy exposure to environmental pollutants using a generalized additive model (GAM) and distributed lag nonlinear models (DLNMs) to analyze the association between exposure at specific gestational weeks and the risk of GDM. We observed that, during the first trimester, per IQR increases for PM10 and PM2.5 exposure were associated with increased GDM risk (PM10: OR = 1.19, 95%CI: 1.07~1.33; PM2.5: OR = 1.32, 95%CI: 1.15~1.50) and isolated post-load hyperglycemia (GDM-IPH) risk (PM10: OR = 1.23, 95%CI: 1.09~1.39; PM2.5: OR = 1.38, 95%CI: 1.18~1.61). Second-trimester O3 exposure was positively correlated with the associated risk of GDM, while pre-pregnancy and first-trimester exposure was negatively associated with the risk of GDM-IPH. Exposure to SO2 in the second trimester was negatively associated with the risk of GDM-IPH. However, there were no observed associations between NO2 and CO exposure and the risk of GDM and its subgroups. Our results suggest that maternal exposure to particulate matter during early pregnancy and exposure to O3 in the second trimester might increase the risk of GDM, and GDM-IPH is the susceptible GDM subtype to airborne particulate matter exposure. Full article
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14 pages, 8132 KiB  
Article
Association between Residential Exposure to Air Pollution and Incident Coronary Heart Disease Is Not Mediated by Leukocyte Telomere Length: A UK Biobank Study
by Chia-Ling Kuo, Rui Liu, Lucas da Cunha Godoy, Luke C. Pilling, Richard H. Fortinsky and Doug Brugge
Toxics 2023, 11(6), 489; https://doi.org/10.3390/toxics11060489 - 28 May 2023
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Abstract
Higher air pollution exposure and shorter leukocyte telomere length (LTL) are both associated with increased risk of coronary heart disease (CHD), and share plausible mechanisms, including inflammation. LTL may serve as a biomarker of air pollution exposure and may be intervened with to [...] Read more.
Higher air pollution exposure and shorter leukocyte telomere length (LTL) are both associated with increased risk of coronary heart disease (CHD), and share plausible mechanisms, including inflammation. LTL may serve as a biomarker of air pollution exposure and may be intervened with to reduce the risk of CHD. To the best of our knowledge, we are the first to test the mediation effect of LTL in the relationship between air pollution exposure and incident CHD. Using the UK Biobank (UKB) data (n = 317,601), we conducted a prospective study linking residential air pollution exposure (PM2.5, PM10, NO2, NOx) and LTL to incident CHD during a mean follow-up of 12.6 years. Cox proportional hazards models and generalized additive models with penalized spline functions were used to model the associations of pollutant concentrations and LTL with incident CHD. We found non-linear associations of air pollution exposure with LTL and CHD. Pollutant concentrations in the lower range were decreasingly associated with longer LTL and reduced risk of CHD. The associations between lower pollutant concentrations and reduced risk of CHD, however, were minimally mediated by LTL (<3%). Our findings suggest that air pollution influences CHD through pathways that do not involve LTL. Replication is needed with improved measurements of air pollution that more accurately assesses personal exposure. Full article
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5 pages, 885 KiB  
Commentary
On the Need for Human Studies of PM Exposure Activation of the NLRP3 Inflammasome
by Doug Brugge, Jianghong Li and Wig Zamore
Toxics 2023, 11(3), 202; https://doi.org/10.3390/toxics11030202 - 21 Feb 2023
Viewed by 1128
Abstract
Particulate matter air pollution is associated with blood inflammatory biomarkers, however, the biological pathways from exposure to periferal inflammation are not well understood. We propose that the NLRP3 inflammasome is likely stimulated by ambient particulate matter, as it is by some other particles [...] Read more.
Particulate matter air pollution is associated with blood inflammatory biomarkers, however, the biological pathways from exposure to periferal inflammation are not well understood. We propose that the NLRP3 inflammasome is likely stimulated by ambient particulate matter, as it is by some other particles and call for more research into this pathway. Full article
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