ArticleEnvironmental health perspectives2011
TRPA1 and sympathetic activation contribute to increased risk of triggered cardiac arrhythmias in hypertensive rats exposed to diesel exhaust.
Article in Environmental health perspectives, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.
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Who cites it
86 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A systematic review of the health effects associated with the inhalation of particle-filtered and whole diesel exhaust.Inhalation toxicology · 2020Pooled it
- Modulation of TRPV-1 by prostaglandin-EScientific reports · 2020Trial
- Sympathomimetic Effects of Acute E-Cigarette Use: Role of Nicotine and Non-Nicotine Constituents.Journal of the American Heart Association · 2017Trial
- The characteristics of coarse particulate matter air pollution associated with alterations in blood pressure and heart rate during controlled exposures.Journal of exposure science & environmental epidemiologyTrial
- Sleep disruption from inhalation of biomass smoke: a basis for coincident hypertension?Particle and fibre toxicology · 2025Article
- Air Pollution and Stroke: An Emerging Challenge From Cardio-Cerebrovascular Multimorbidity.Journal of the American Heart Association · 2025Review
- Role of the Transient Receptor Potential Ankyrin-1 in the Pulmonary, Vascular, and Systemic Effects of Short-Term Acrolein Inhalation in Mice: Implications for the Toxicity of Electronic Nicotine Delivery Systems.Cardiovascular toxicology · 2025Article
- Smoking-associated electrocardiographic abnormalities predict cardiovascular mortality.Scientific reports · 2024Article
- Formaldehyde and the transient receptor potential ankyrin-1 contribute to electronic cigarette aerosol-induced endothelial dysfunction in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Unveiling the role of TRPA1 in cardiovascular health and disease: a mini review.Frontiers in cardiovascular medicine · 2024Review
- E-cigarettes and arrhythmogenesis: a comprehensive review of pre-clinical studies and their clinical implications.Cardiovascular research · 2023Review
- Noise and Air Pollution as Risk Factors for Hypertension: Part II-Pathophysiologic Insight.Hypertension (Dallas, Tex. : 1979) · 2023Review
- Expression of Trpa1 and Trpv1 Genes in the Hypothalamus and Blood Pressure in Normotensive and Hypertensive Rats. Effect of Losartan and Captopril.Bulletin of experimental biology and medicine · 2023Article
- Cigarette smoking and air pollution exposure and their effects on cardiovascular diseases.Frontiers in public health · 2023Review
- The Impact of Fine Particulate Matter 2.5 on the Cardiovascular System: A Review of the Invisible Killer.Nanomaterials (Basel, Switzerland) · 2022Review
- RETRACTED: Effect Comparison of E-Cigarette and Traditional Smoking and Association with Stroke-A Cross-Sectional Study of NHANES.Neurology international · 2022Article
- Key Characteristics of Cardiovascular Toxicants.Environmental health perspectives · 2021Article
- Particulate matter air pollutants and cardiovascular disease: Strategies for intervention.Pharmacology & therapeutics · 2021Review
- Biological Toxicity of the Compositions in Electronic-Cigarette on Cardiovascular System.Journal of cardiovascular translational research · 2021Review
- Atrial proarrhythmic effect of lead as one of the PM10 metal components of air pollution. An in-silico study.PloS one · 2021Article
26 more citing papers are in PubMed but not listed here.
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7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundDiesel exhaust (DE), which is emitted from on- and off-road sources, is a complex mixture of toxic gaseous and particulate components that leads to triggered adverse cardiovascular effects such as arrhythmias.
objectiveWe hypothesized that increased risk of triggered arrhythmias 1 day after DE exposure is mediated by airway sensory nerves bearing transient receptor potential (TRP) channels [e.g., transient receptor potential cation channel, member A1 (TRPA1)] that, when activated by noxious chemicals, can cause a centrally mediated autonomic imbalance and heightened risk of arrhythmia.
methodsSpontaneously hypertensive rats implanted with radiotelemeters were whole-body exposed to either 500 μg/m³ (high) or 150 μg/m³ (low) whole DE (wDE) or filtered DE (fDE), or to filtered air (controls), for 4 hr. Arrhythmogenesis was assessed 24 hr later by continuous intravenous infusion of aconitine, an arrhythmogenic drug, while heart rate (HR) and electrocardiogram (ECG) were monitored.
resultsRats exposed to wDE or fDE had slightly higher HRs and increased low-frequency:high-frequency ratios (sympathetic modulation) than did controls; ECG showed prolonged ventricular depolarization and shortened repolarization periods. Rats exposed to wDE developed arrhythmia at lower doses of aconitine than did controls; the dose was even lower in rats exposed to fDE. Pretreatment of low wDE-exposed rats with a TRPA1 antagonist or sympathetic blockade prevented the heightened sensitivity to arrhythmia.
conclusionsThese findings suggest that a single exposure to DE increases the sensitivity of the heart to triggered arrhythmias. The gaseous components appear to play an important role in the proarrhythmic response, which may be mediated by activation of TRPA1, and subsequent sympathetic modulation. As such, toxic inhalants may partly exhibit their toxicity by lowering the threshold for secondary triggers, complicating assessment of their risk.
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