ArticleEnvironmental health perspectives2009
Direct impairment of vascular function by diesel exhaust particulate through reduced bioavailability of endothelium-derived nitric oxide induced by superoxide free radicals.
Article in Environmental health perspectives, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.
- Particulates induced lung inflammation and its consequences in the development of restrictive and obstructive lung diseases: a systematic review.Environmental science and pollution research international · 2021Pooled it
- Acute cardiovascular effects of controlled exposure to dilute Petrodiesel and biodiesel exhaust in healthy volunteers: a crossover study.Particle and fibre toxicology · 2021Trial
- Controlled exposure to particulate matter from urban street air is associated with decreased vasodilation and heart rate variability in overweight and older adults.Particle and fibre toxicology · 2015Trial
- Altered nitric oxide bioavailability contributes to diesel exhaust inhalation-induced cardiovascular dysfunction in man.Journal of the American Heart Association · 2013Trial
- Reducing personal exposure to particulate air pollution improves cardiovascular health in patients with coronary heart disease.Environmental health perspectives · 2012Trial
- Combustion-derived nanoparticulate induces the adverse vascular effects of diesel exhaust inhalation.European heart journal · 2011Trial
- Acute decreases in proteasome pathway activity after inhalation of fresh diesel exhaust or secondary organic aerosol.Environmental health perspectives · 2011Trial
- Review
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- Association between residential proximity to major roadways and nonfatal cardiovascular disease in Chinese older adults: a nationwide study.Scientific reports · 2025Article
- Environmentally Not So Friendly: Global Warming, Air Pollution, and Wildfires: JACC Focus Seminar, Part 1.Journal of the American College of Cardiology · 2024Review
- Impact of Airborne Exposure to PMInternational journal of environmental research and public health · 2024Article
- Coronary Spasm Testing with Acetylcholine: A Powerful Tool for a Personalized Therapy of Coronary Vasomotor Disorders.Life (Basel, Switzerland) · 2024Review
- Exposure to urban nanoparticles at low PM[Formula: see text] concentrations as a source of oxidative stress and inflammation.Scientific reports · 2023Article
- PMFrontiers in cellular and infection microbiology · 2023Article
- Cigarette smoking and air pollution exposure and their effects on cardiovascular diseases.Frontiers in public health · 2023Review
- The cardiovascular effects of air pollution: Prevention and reversal by pharmacological agents.Pharmacology & therapeutics · 2022Review
- Controlled human exposure to diesel exhaust: results illuminate health effects of traffic-related air pollution and inform future directions.Particle and fibre toxicology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundDiesel exhaust particulate (DEP) is a key arbiter of the adverse cardiovascular effects of air pollution.
objectivesWe assessed the in vitro effects of DEP on vascular function, nitric oxide (NO) availability, and the generation of oxygen-centered free radicals.
methodsWe assessed the direct vascular effects of DEP (10-100 microg/mL) in isolated rat aortic rings using myography. We investigated NO scavenging and oxygen-centered free radical generation using an NO electrode and electron paramagnetic resonance (EPR) with the Tempone-H (1-hydroxyl-2,2,6,6-tetramethyl-4-oxo-piperidine) spin trap, respectively.
resultsAcetylcholine-induced relaxation was attenuated by DEP (maximum relaxation reduced from 91 +/- 4% to 49 +/- 6% with 100 microg/mL DEP; p < 0.001) but was restored by superoxide dismutase (SOD; maximum relaxation, 73 +/- 6%; p < 0.001). DEP caused a modest inhibition of relaxation to NO donor drugs, an effect that could be reversed by SOD (p < 0.01). At 10 microg/mL, DEP did not affect verapamil-induced relaxation (p = 0.73), but at 100 microg/mL DEP inhibited relaxation (p < 0.001) by a mechanism independent of SOD. NO concentrations generated by 2-(N,N-diethylamino)-diazenolate-2-oxide (DEA/NO; 10 microM) were reduced by DEP (100 microg/mL; from 5.2 +/- 0.4 to 3.3 +/- 0.4 microM; p = 0.002). Free radical generation was increased by DEP (10 microg/mL; 9-fold increase in EPR spectra; p = 0.004) in a manner that could be attenuated by SOD (p = 0.015).
conclusionsDEP caused oxidative stress through the generation of oxygen-centered free radicals that reduced the bioavailability of endothelium-derived NO without prior interaction with the lung or vascular tissue. These findings provide a mechanism for the adverse cardiovascular effects of particulate air pollution.
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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.