Linking ambient particulate matter pollution effects with oxidative biology and immune responses

Abstract

Exposure to combustion-related particulate matter (PM), at concentrations experienced by populations throughout the world, contributes to pulmonary and cardiac disease through multiple mechanistic pathways that are complex and interdependent. Current evidence supports an interactive chain of events linking pollution-induced pulmonary and systemic oxidative stress, inflammatory events, and translocation of particle constituents with an associated risk of vascular dysfunction, atherosclerosis, altered cardiac autonomic function, and ischemic cardiovascular and obstructive pulmonary diseases. Because oxidative stress is believed to play such an instrumental role in these pathways, the capacity of particulate pollution to cause damaging oxidative reactions (the oxidative potential) has been used as an effective exposure metric, identifying toxic components and sources within diverse ambient PM mixes that vast populations are subjected to-from traffic emissions on busy roads in urban areas to biomass smoke that fills homes in rural areas of the developing world.

Developmental neurotoxicity of inhaled ambient ultrafine particle air pollution: Parallels with neuropathological and behavioral features of autism and other neurodevelopmental disorders

“…VM is a clinical indicator of disrupted white matter development [80,81] and can be accompanied by significant cognitive deficits [113]. Based on its well-known inflammatory properties [137], UFP exposures would be expected to activate brain microglia, resulting in the release of proinflammatory cytokines [138-140] that could lead to hypomyelination via toxicity to oligodendrocytes, the myelinating cells of the brain [141]. Indeed, particular vulnerability of premyelinating olidgodendrocytes to such consequences of microglial activation has been described [142,143].…”

Oxidative Stress and Cardiovascular Risk: Obesity, Diabetes, Smoking, and Pollution

“…DE inhalation attenuates vasodilation in response to both endothelium-dependent and nitric oxide donor drugs, but not in response to vasodilators acting via smooth muscle cell receptors; a profile that is suggestive of NO scavenging by O 2 − free radicals (143,206). Exposure to C-DEAP is known to cause a compensatory increase and to eventually deplete antioxidant concentrations in respiratory tract lining fluids and pulmonary cells (207). Likewise, inhalation of DE alters the expression of several antioxidant pathways in peripheral blood monocytes (208).…”

“…The lung lining fluids surrounding pulmonary epithelial cells in vivo provide an early defense against acute exposure to inhaled pollutants. However, prolonged or repeated exposure leads to depletion of antioxidants in cell surfactants and changes in pulmonary cell function (207). The gases within C-DEAP can modify blood constituents in the pulmonary circulation, although the precise mechanism by which the oxidative “signal” is carried or transferred to peripheral organs requires further investigation (159).…”

Protective effects of chebulic acid on alveolar epithelial damage induced by urban particulate matter

“…In this study we showed that CA affects epithelial monolayer integrity and paracellular permeability [37]. In addition, the alveolar epithelium participates in immune responses to UPM [38]. So, we focused on disruption of the alveolar epithelial barrier function caused by proinflammatory cytokines and intracellular ROS induced by UPM.…”