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Review
. 2020 Jul:34:101545.
doi: 10.1016/j.redox.2020.101545. Epub 2020 May 23.

Oxidative stress pathways of air pollution mediated toxicity: Recent insights

Roopesh Singh Gangwar  1 , Graham H Bevan  1 , Rengasamy Palanivel  1 , Lopa Das  1 , Sanjay Rajagopalan  2
Affiliations
Review

Oxidative stress pathways of air pollution mediated toxicity: Recent insights

Roopesh Singh Gangwar et al. Redox Biol. 2020 Jul.

Abstract

Ambient air pollution is a leading environmental cause of morbidity and mortality globally with most of the outcomes of cardiovascular origin. While numerous mechanisms are proposed to explain the link between air pollutants and cardiovascular events, the evidence supports a role for oxidative stress as a critical intermediary pathway in the transduction of systemic responses in the cardiovascular system. Indeed, alterations in vascular function are a critical step in the development of cardiometabolic disorders such as hypertension, diabetes, and atherosclerosis. This review will provide an overview of the impact of particulate and gaseous pollutants on oxidative stress from human and animal studies published in the last five years. We discuss current gaps in knowledge and evidence to date implicating the role of oxidative stress with an emphasis on inhalational exposures. We conclude with the identification of gaps, and an exhortation for further studies to elucidate the impact of oxidative stress in air pollution mediated effects.

Keywords: Air pollution; Lung inflammation; Oxidative stress; Particulate matter; Reactive oxygen species; Redox reaction.

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Conflict of interest statement

Declaration of competing interest The authors have no competing interests to declare.

Figures

Image 1
Graphical abstract
Fig. 1
Fig. 1
Particulate Matter Air Pollution: source and health effects. Air pollution standards were obtained from WHO 2005 air quality guidelines (http://apps.who.int/iris/bitstream/10665/69477/1/WHO_SDE_PHE_OEH_06.02_eng.pdf). PM2.5, particulate matter <2.5 μm; PM10, particulate matter <10 μm.
Fig. 2
Fig. 2
Schematic illustration of key changes in the lung inflammation in chronic PM2.5 exposure. Chronic exposure to PM2.5 results in release of inflammatory cytokines and chemokines in the blood circulation that leads to infiltration of Ly6chi monocytes in the lungs from bone marrow. Continual exposure to PM2.5 cause persistent inflammatory environment in the lungs that resulted in increased apoptosis of tissue resident alveolar macrophage and differentiated of recruited BM-monocytes into BM-alveolar macrophages.
See this image and copyright information in PMC

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