Roles of oxidative stress in signaling and inflammation induced by particulate matter

Abstract

This review reports the role of oxidative stress in impairing the function of lung exposed to particulate matter (PM). PM constitutes a heterogeneous mixture of various types of particles, many of which are likely to be involved in oxidative stress induction and respiratory diseases. Probably, the ability of PM to cause oxidative stress underlies the association between increased exposure to PM and exacerbations of lung disease. Mostly because of their large surface area, ultrafine particles have been shown to cause oxidative stress and proinflammatory effects in different in vivo and in vitro studies. Particle components and surface area may act synergistically inducing lung inflammation. In this vein, reactive oxygen species elicited upon PM exposure have been shown to activate a number of redox-responsive signaling pathways and Ca(2+) influx in lung target cells that are involved in the expression of genes that modulate relevant responses to lung inflammation and disease.

An epidemiological appraisal of the association between heart rate variability and particulate air pollution: a meta-analysis

“…Since air particulates can provoke oxidative stress and an inflammatory response in the lung and heart,57 oxidative stress is a potentially important cellular mechanism. A study by Schwartz et al 58 concluded that the effects of PM 2.5 on HF seemed to be mediated by reactive oxygen.…”

Impact of air pollution on oxidative DNA damage and lipid peroxidation in mothers and their newborns

“…Oxidative stress results from an imbalance between the formation of reactive oxygen species (ROS) and the ability of the organism to readily detoxify the reactive intermediates or to repair the resulting damage (Mazzoli-Rocha et al, 2010). Oxidative damage to cellular macromolecules (nucleic acid, lipids and proteins) is associated with the development of cancer, respiratory tract and cardiovascular diseases (Yang and Omaye 2009), neurodegenerative diseases (Andersen 2004) as well as ageing (Evans et al, 2004).…”

Patterns of Retention of Particulate Matter in Lung Tissues of Patients With COPD

“…47 A reason for lung cell (such as epithelial and macrophage) activation and damage following PM exposure is via oxidative stress pathways. 48 Tuder and colleagues 49 have shown that apoptosis predominates in lung regions of oxidative stress. We postulate that the reduction in the volume fraction of PM in lung tissues in subjects with severe COPD is due to apoptosis 44,47 of these tissues, possibly due to the burden of PM in these tissues.…”