ArticleOccupational and environmental medicine2005
The procoagulant potential of environmental particles (PM10).
Article in Occupational and environmental medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 73 citations in OpenAlex.
- Article
- Long-term exposure to air pollution and the risks of venous thromboembolism: a nationwide population-based retrospective cohort study.Clinical research in cardiology : official journal of the German Cardiac Society · 2026Article
- Long-Term Exposure to Air Pollution and Incidence of Venous Thromboembolism in the General Population: A Population-Based Retrospective Cohort Study.Journal of clinical medicine · 2022Article
- Cumulative Lifetime Burden of Cardiovascular Disease From Early Exposure to Air Pollution.Journal of the American Heart Association · 2020Review
- Air Pollution and Other Environmental Modulators of Cardiac Function.Comprehensive Physiology · 2017Review
- Estimating Causal Effects of Local Air Pollution on Daily Deaths: Effect of Low Levels.Environmental health perspectives · 2017Article
- Placental Pathology Associated with Household Air Pollution in a Cohort of Pregnant Women from Dar es Salaam, Tanzania.Environmental health perspectives · 2017Article
- Platelet activation independent of pulmonary inflammation contributes to diesel exhaust particulate-induced promotion of arterial thrombosis.Particle and fibre toxicology · 2016Article
- Kinetics of lung tissue factor expression and procoagulant activity in bleomycin induced acute lung injury.Clinical and translational medicine · 2015Article
- Air pollution, inflammation and preterm birth: a potential mechanistic link.Medical hypotheses · 2014Article
- Evaluation of consequences of dust positioned in southwest of iran on coagulant factors.Iranian journal of medical sciences · 2013Article
- Air pollution and markers of coagulation, inflammation, and endothelial function: associations and epigene-environment interactions in an elderly cohort.Epidemiology (Cambridge, Mass.) · 2012Article
- Article
- The relationship of air pollution and surrogate markers of endothelial dysfunction in a population-based sample of children.BMC public health · 2011Article
- Nanoparticles, human health hazard and regulation.Journal of the Royal Society, Interface · 2010Article
- The limits of testing particle-mediated oxidative stress in vitro in predicting diverse pathologies; relevance for testing of nanoparticles.Particle and fibre toxicology · 2009Article
- Adverse cardiovascular effects of air pollution.Nature clinical practice. Cardiovascular medicine · 2009Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsEpidemiology studies have shown that cardiovascular (CV) disease is primarily responsible for the mortality associated with increased pulmonary environmental particle (PM10) exposure. The mechanisms involved in PM10 mediated CV effects are unknown although changes in plasma viscosity and in the homoeostasis of blood coagulation have been implicated. It was hypothesised that PM10 exposure would result in an inflammatory response and enhance the activation of the extrinsic coagulation mechanisms in pulmonary and vascular cells in culture.
methodsPrimary human monocyte derived macrophages and human umbilical cord vein endothelial, human alveolar type II epithelial (A549), and human bronchial epithelial (16HBE) cells were tested for their inflammatory and procoagulant response to PM10 exposure. IL-8, tissue factor (TF), and tissue plasminogen activator (tPA) gene expression and protein release, and coagulation enhancing ability of culture media were determined 6 and 24 hours following exposure.
resultsThe culture media from macrophages and 16HBE bronchial epithelial cells, but not A549 cells, exposed to PM10 had an enhanced ability to cause clotting. Furthermore, H2O2 also increased the clotting activity. Apoptosis was significantly increased in macrophages exposed to PM10 and LPS as shown by annexin V binding. TF gene expression was enhanced in macrophages exposed to PM10, and HUVEC tissue factor and tPA gene and protein expression were inhibited.
conclusionsThese data indicate that PM10 has the ability to alter macrophage, epithelial, and endothelial cell function to favour blood coagulation via activation of the extrinsic pathway and inhibition of fibrinolysis pathways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.