Mechanism of lung injury caused by PM10 and ultrafine particles with special reference to COPD

Abstract

Particulate air pollution (particles with a 50% cut-off aerodynamic diameter of 10 µm (PM₁₀)) has strong associations with the adverse health events detected by epidemiological studies in chronic obstructive pulmonary disease patients in diverse geographical locations. Transition metals may determine the toxic effects of PM₁₀ through oxidative stress which may be injurious as shown by an increase in airspace epithelial permeability and may lead to inflammation through the activation of transcription factors for pro‐inflammatory genes in both macrophages and epithelial cells. Recently, the present authors have shown that particulate air pollution may cause further molecular events that enhance transcription factor activation by causing acetylation of histones leading to unwinding of deoxyribonucleic acid (DNA) enhancing transcription factor DNA binding and increasing transcription for pro-inflammatory genes.