ArticleParticle and fibre toxicology2014
PM2.5-induced cardiovascular dysregulation in rats is associated with elemental carbon and temperature-resolved carbon subfractions.
Article in Particle and fibre toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Fine particulate matter‑induced cardiac developmental toxicity (Review).Experimental and therapeutic medicine · 2025Review
- Characterization of Mild Delayed Gestational Hypertension in Rats Following Ozone Exposure.Cardiovascular toxicology · 2024Article
- Causal relationship between particulate matter 2.5 (PMJournal of global health · 2023Article
- The Physiological Effects of Air Pollution: Particulate Matter, Physiology and Disease.Frontiers in public health · 2022Review
- Air Pollution-Induced Autonomic Modulation.Physiology (Bethesda, Md.) · 2020Review
- Exposure to fine particulate matter induces self-recovery and susceptibility of oxidative stress and inflammation in rat lungs.Environmental science and pollution research international · 2020Article
- Nociceptive pulmonary-cardiac reflexes are altered in the spontaneously hypertensive rat.The Journal of physiology · 2019Article
- Effect of PM2.5 on invasion and proliferation of HeLa cells and the expression of inflammatory cytokines IL-1 and IL-6.Oncology letters · 2018Article
- Carbonaceous PM10 and PM2.5 and secondary organic aerosol in a coastal rural site near Brindisi (Southern Italy).Environmental science and pollution research international · 2018Article
- Long-Term Exposure of Fine Particulate Matter Causes Hypertension by Impaired Renal DJournal of the American Heart Association · 2018Article
- In Utero Exposure to Fine Particulate Matter Causes Hypertension Due to Impaired Renal Dopamine D1 Receptor in Offspring.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018Article
- Ambient Air Pollution and Risk of Gestational Hypertension.American journal of epidemiology · 2017Article
- Potential Harmful Effects of PM2.5 on Occurrence and Progression of Acute Coronary Syndrome: Epidemiology, Mechanisms, and Prevention Measures.International journal of environmental research and public health · 2016Review
- Macrophages treated with particulate matter PM2.5 induce selective neurotoxicity through glutaminase-mediated glutamate generation.Journal of neurochemistry · 2015Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundWe tested the hypothesis that cardiovascular responses to PM2.5 exposure will be enhanced in hypertensive rats and linked to specific carbonaceous pollutants in an urban industrial setting.
methodsSpontaneously hypertensive rats were exposed by inhalation to concentrated PM2.5 in an industrial area of Dearborn, Michigan, for four consecutive summer days. Blood pressure (BP), heart rate (HR) and HR variability (HRV) metrics (SDNN, RMSSD) were assessed by radiotelemetry and compared to 1 h- and 8 h-averaged fluctuations in PM2.5 composition, with a focus on elemental and organic carbon (EC and OC, respectively), and temperature-resolved subfractions (EC1-EC5, PC (pyrolized carbon), and OC1-OC4), as well as other major and minor PM components.
resultsMean HR and BP were increased, while HRV was decreased over 4 days of exposure. Using 1 h averages, EC (1 μg/m3 increase) was associated with increased HR of 11-32 bpm (4-11% increase), 1.2-1.5 ms (22-27%) decreases in SDNN, 3-14 mmHg (1.5-8%) increases in systolic BP, and 5-12 mmHg (4-9%) increases in diastolic BP. By comparison, associations with OC were negligible. Using 8 h averages, EC subfractions were linked with increased heart rate (EC1: 13 bpm; EC2, EC3, PC: <5 bpm) and SDNN (EC1> > EC2 > EC3, EC4, PC), but with decreased RMSSD (EC2, EC5 > EC3, EC4). Minimal effects were associated with OC and OC1. Associations between carbon subfractions and BP were negligible. Associations with non-carbonaceous components and trace elements were generally non-significant or of negligible effect size.
conclusionsThese findings are the first to describe associations between acute cardiovascular responses and thermally resolved carbon subfractions. We report that cardiovascular responses to PM2.5 carbonaceous materials appear to be driven by EC and its EC1 fraction.
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