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Open AccessJournal ArticleDOI

Free radical activity of PM10: iron-mediated generation of hydroxyl radicals.

TLDR
It is concluded that the free radical activity of PM10 particles is derived either from a fraction that is not centrifugeable on a bench centrifuge, or that the radical generating system is released into solution.
Abstract
The purpose of this study was to test the hypothesis that particulate matter < or = 10 microns in aerodynamic diameter (PM10) particles have the ability to generate free radical activity at their surface. We collected PM10 filters from the Edinburgh, United Kingdom, Enhanced Urban Network sampling site, removed particles from the filter, and tested their ability to cause free radical damage to supercoiled plasmid DNA. We found that the PM10 particles did cause damage to the DNA that was mediated by hydroxyl radicals, as shown by inhibition of the injury with mannitol. The PM10-associated hydroxyl radical activity was confirmed using a high-performance liquid chromatography-based assay to measure the hydroxyl radical adduct of salicylic acid. Desferrioxamine abolished the hydroxyl radical-mediated injury, which suggests that iron was involved. Analysis of PM10 filters confirmed the presence of large amounts of iron and leaching studies confirmed that the PM10 samples could release substantial amounts of Fe(III) and lesser amounts of Fe(II). To investigate the size of the particles involved in the hydroxyl radical injury, we centrifuged the suspension of PM10 to clarity, tested the clear supernatant, and found that it had all of the suspension activity. We conclude, therefore, that the free radical activity is derived either from a fraction that is not centrifugeable on a bench centrifuge, or that the radical generating system is released into solution.

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Citations
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Journal ArticleDOI

Air Pollution and Cardiovascular Disease A Statement for Healthcare Professionals From the Expert Panel on Population and Prevention Science of the American Heart Association

TL;DR: The purpose of this statement is to provide healthcare professionals and regulatory agencies with a comprehensive review of the literature on air pollution and cardiovascular disease and practical recommendations for healthcare providers and their patients are outlined.
Journal ArticleDOI

Airborne particulate matter and human health: toxicological assessment and importance of size and composition of particles for oxidative damage and carcinogenic mechanisms

TL;DR: The evaluation of most of these studies shows that the smaller the size of PM the higher the toxicity through mechanisms of oxidative stress and inflammation, and Associations between chemical compositions and particle toxicity tend to be stronger for the fine and ultrafine PM size fractions.
Journal ArticleDOI

Oxidative stress-induced DNA damage by particulate air pollution.

TL;DR: Oxidative stress-induced DNA damage appears to an important mechanism of action of urban particulate air pollution and related biomarkers and personal monitoring may be useful tools for risk characterization.
Journal ArticleDOI

Pulmonary Oxidative Stress, Inflammation and Cancer: Respirable Particulate Matter, Fibrous Dusts and Ozone as Major Causes of Lung Carcinogenesis through Reactive Oxygen Species Mechanisms

TL;DR: The role of ROS and oxidative stress in the production of mediators of pulmonary inflammation and mechanisms of carcinogenesis are presented and pulmonary cancer initiation and promotion is linked to a series of biochemical pathways of oxidative stress.
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Inhaled particles and lung cancer. Part A: Mechanisms.

TL;DR: Since most of the proposed molecular mechanisms underlying particle‐related carcinogenesis have been derived from in vitro studies, there is a need for future studies that evaluate the implication of these mechanisms for in vivo lung cancer development and transgenic and gene knockout animal models may provide a useful tool.
References
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Journal ArticleDOI

Particulate air pollution and acute health effects

TL;DR: It is suggested that ultra-fine particles in the nature of the urban particulate cloud are able to provoke alveolar inflammation, with release of mediators capable, in susceptible individuals, of causing exacerbations of lung disease and of increasing blood coagulability, thus also explaining the observed increases in cardiovascular deaths associated with urban pollution episodes.
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Systemic oxidative stress in asthma, COPD, and smokers.

TL;DR: Smoking, acute exacerbations of COPD, and asthma are associated with a marked oxidant/ant antioxidant imbalance in the blood, associated with evidence of increased oxidative stress, and the decreased antioxidant capacity in plasma may result from different mechanisms in these conditions.
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Pulmonary Retention of Ultrafine and Fine Particles in Rats

TL;DR: Both acute instillation and subchronic inhalation studies showed that ultrafine particles at equivalent masses access the pulmonary interstitium to a larger extent than fine particles (integral of 250 nm).
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Association of particulate air pollution and acute mortality: involvement of ultrafine particles?

TL;DR: Ultrafine particles are always present in the urban atmosphere and it is suggested that they play a role in causing acute lung injury in sensitive parts of the population.
Journal ArticleDOI

Health effects of particulate air pollution: time for reassessment?

TL;DR: It is concluded that respirable particulate air pollution is likely an important contributing factor to respiratory disease and increased cardiopulmonary disease mortality in developed world cities.
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