Particulate matter-induced epigenetic changes and lung cancer

Abstract

Background and aims: Lung cancer is the leading cause of cancer death worldwide. Cigarette smoking is the well-known risk factor for lung cancer. Epidemiological studies suggest that air pollution, especially particulate matter (PM) exposure, is associated with increased lung cancer risk and mortality independent of cigarette smoking.

Methods: English-language publications focusing on PM, epigenetic changes, and lung cancer were reviewed. The epigenome serves as an interface between the environment and the genome. PM is one of the environmental factors that can cause epigenetic changes. The epigenome serves as an interface between the environment and the genome. Some of the epigenetic changes lead to increased disease susceptibility and progression. In cardiovascular disease and asthma, the association between PM exposure and the disease specific epigenetic changes has been identified. In lung cancer, the epigenetic changes in DNA methylation, histone modification and microRNA expression are commonly found, but the specific link between PM exposure and lung cancer remains incompletely understood.

Results: The results of epidemiological studies indicate the important effects of PM exposure on lung cancer. PM2.5 is consistently associated with the increased lung cancer risk and mortality. Based on the epidemiological associations between PM exposure and lung cancer, PM-induced epigenetic changes may play important roles in the pathogenesis of lung cancer.

Conclusion: In this review, we focus on the current knowledge of epigenetic changes associated with PM exposure and lung cancer. Better understanding of the link between PM exposure and lung cancer at the epigenomic level by comprehensive comparison approach may identify lung cancer early detection biomarkers and novel therapeutic targets.

Keywords: epigenetic changes; lung cancer; particulate matter.

Figure 1.

Epigenetic changes associated with PM exposure. PM2.5 is small enough to be aspirated into alveoli, to be absorbed either by alveolar macrophage or direct translocation into extracellular matrix and vascular endothelial cells, and to be transported into the systemic circulation. The circulating PM2.5 may induce epigenetic changes and systemic inflammation. PM2.5 exposure decreases DNA methylation of LINE-1, decreases DNMT1 and increased DNMT3B expression. PM10 exposure increases HAT activity and cigarette smoke decreases HDAC2 activity. PM2.5 exposure is associated with miRNA changes related to multiple inflammatory pathways.