Function of PM2.5 in the pathogenesis of lung cancer and chronic airway inflammatory diseases

Oncol Lett. 2018 May;15(5):7506-7514. doi: 10.3892/ol.2018.8355. Epub 2018 Mar 26.


Previous research has identified that air pollution is associated with various respiratory diseases, but few studies have investigated the function served by particulate matter 2.5 (PM2.5) in these diseases. PM2.5 is known to cause epigenetic and microenvironmental alterations in lung cancer, including tumor-associated signaling pathway activation mediated by microRNA dysregulation, DNA methylation, and increased levels of cytokines and inflammatory cells. Autophagy and apoptosis of tumor cells may also be detected in lung cancer associated with PM2.5 exposure. A number of mechanisms are involved in triggering and aggravating asthma and COPD, including PM2.5-induced cytokine release and oxidative stress. The present review is an overview of the underlying molecular mechanisms of PM2.5-induced pathogenesis in lung cancer and chronic airway inflammatory diseases.

Keywords: DNA methylation; apoptosis; asthma; autophagy; chronic obstructive lung disease; cytokines; lung cancer; microRNA; microenvironment; oxidative stress; particulate matter 2.5; pathogenesis.

Publication types

  • Review