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In response to highly concentrated PM 2.5 , impairments in TLR4, NOX2, and neutrophil cytosolic factor 1 (p47 phox ) have mostly been observed to promote vascular function, decrease ROS generation, and decrease inflammatory vasculature monocyte infiltration exposures by inhalation (153, 169)

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It has been suggested that monotonous, near-continuous acquaintance with air contamination promotes atherosclerosis and recurrent occurrences, considering that air impurity revelation happens across a lifetime (110)

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