+ Site Statistics
References:
54,258,434
Abstracts:
29,560,870
PMIDs:
28,072,757
+ Search Articles
+ PDF Full Text Service
How our service works
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ Translate
+ Recently Requested

Oxidative stress-induced telomeric erosion as a mechanism underlying airborne particulate matter-related cardiovascular disease



Oxidative stress-induced telomeric erosion as a mechanism underlying airborne particulate matter-related cardiovascular disease



Particle and Fibre Toxicology 9: 21



Particulate matter (PM) pollution is responsible for hundreds of thousands of deaths worldwide, the majority due to cardiovascular disease (CVD). While many potential pathophysiological mechanisms have been proposed, there is not yet a consensus as to which are most important in causing pollution-related morbidity/mortality. Nor is there consensus regarding which specific types of PM are most likely to affect public health in this regard. One toxicological mechanism linking exposure to airborne PM with CVD outcomes is oxidative stress, a contributor to the development of CVD risk factors including atherosclerosis. Recent work suggests that accelerated shortening of telomeres and, thus, early senescence of cells may be an important pathway by which oxidative stress may accelerate biological aging and the resultant development of age-related morbidity. This pathway may explain a significant proportion of PM-related adverse health outcomes, since shortened telomeres accelerate the progression of many diseases. There is limited but consistent evidence that vehicular emissions produce oxidative stress in humans. Given that oxidative stress is associated with accelerated erosion of telomeres, and that shortened telomeres are linked with acceleration of biological ageing and greater incidence of various age-related pathology, including CVD, it is hypothesized that associations noted between certain pollution types and sources and oxidative stress may reflect a mechanism by which these pollutants result in CVD-related morbidity and mortality, namely accelerated aging via enhanced erosion of telomeres. This paper reviews the literature providing links among oxidative stress, accelerated erosion of telomeres, CVD, and specific sources and types of air pollutants. If certain PM species/sources might be responsible for adverse health outcomes via the proposed mechanism, perhaps the pathway to reducing mortality/morbidity from PM would become clearer. Not only would pollution reduction imperatives be more focused, but interventions which could reduce oxidative stress would become all the more important.

Please choose payment method:






(PDF emailed within 0-6 h: $19.90)

Accession: 036460578

Download citation: RISBibTeXText

PMID: 22713210

DOI: 10.1186/1743-8977-9-21


Related references

Air particulate matter induced oxidative stress and inflammation in cardiovascular disease and atherosclerosis: The role of Nrf2 and AhR-mediated pathways. Toxicology Letters 270: 88-95, 2017

Airborne fine particulate matter induced pulmonary inflammation as well as oxidative stress in neonate rats. Chinese Medical Journal 123(20): 2895-2900, 2011

Involvement of oxidative stress and calcium signaling in airborne particulate matter - induced damages in human pulmonary artery endothelial cells. Toxicology in Vitro 45(Pt 3): 340-350, 2017

DNA methylation: A critical epigenetic mechanism underlying the detrimental effects of airborne particulate matter. Ecotoxicology and Environmental Safety 161: 173-183, 2018

The spontaneously hypertensive rat as a model of human cardiovascular disease: evidence of exacerbated cardiopulmonary injury and oxidative stress from inhaled emission particulate matter. Toxicology and Applied Pharmacology 164(3): 250-263, 2000

Real-world exposure of airborne particulate matter triggers oxidative stress in an animal model. International Journal of Physiology, Pathophysiology and Pharmacology 2(1): 64-68, 2010

Oxidative stress as a screening metric of potential toxicity by nanoparticles and airborne [corrected] particulate matter. Inhalation Toxicology 20(9): 895, 2008

Is oxidative stress the pathogenic mechanism underlying insulin resistance, diabetes, and cardiovascular disease? The common soil hypothesis revisited. Arteriosclerosis, Thrombosis, and Vascular Biology 24(5): 816-823, 2004

Airborne Fine Particulate Matter Induces Oxidative Stress and Inflammation in Human Nasal Epithelial Cells. Tohoku Journal of Experimental Medicine 239(2): 117-125, 2017

Seasonal variation of particle-induced oxidative potential of airborne particulate matter in Beijing. Science of the Total Environment 579: 1152-1160, 2016

Evaluating the toxicity of airborne particulate matter and nanoparticles by measuring oxidative stress potential--a workshop report and consensus statement. Inhalation Toxicology 20(1): 75-99, 2008

Water-insoluble fraction of airborne particulate matter PM1 induces oxidative stress in human lung epithelial A549 cells. 2012

Effect of Particulate Matter Air Pollution on Cardiovascular Oxidative Stress Pathways. Antioxidants and Redox Signaling 28(9): 797-818, 2017

Water-insoluble fraction of airborne particulate matter (PM10 ) induces oxidative stress in human lung epithelial A549 cells. Environmental Toxicology 29(2): 226-233, 2014

Oxidative stress as a mechanism of added sugar-induced cardiovascular disease. International Journal of Angiology 23(4): 217-226, 2014