Environmental Factors and Lung Cancer: Polycyclic Aromatic Hydrocarbon Content of Traffic Airborne PM2.5 and AhR Gene Expression

Abstract

PP-31-010 Background/Aims: Recent studies have provided increasing evidence that lung cancer incidence in different countries is associated with exposure to airborne PM2.5 of environmental motorcycle emitted particulates. Traffic-related airborne pollutants include polycyclic aromatic hydrocarbons (PAHs), are known activators for nuclear receptors like AhR and PPAR. The aim of this work is to investigate if exposure to PAHs from traffic PM2.5 would induce changes in expressions of related genes. Methods: We collected blood from traffic police officers in Northern Taiwan before and after they went on duty at the road cross-sections. We asked them to carry personal air samplers during the day of work, to collect PM2.5 particles to which they would be exposed. Afterwards, PAHs were extracted from these particles and analyzed with Gas Chromatograph-Mass Spectrometer. mRNA was extracted and converted into cDNA for gene expression analysis with Taqman systems. Expression of AhR, CYP1A1, CYP1A2, CYP1B1, TNF, IL-1, IL-6, IL-8, PPARα, and IL-10 were analyzed. Results: Ambient air PM2.5 concentrations ranged from 39.5 to 244.8 μg/m3. Most abundant PAH were acenaphthene, dibenzo(a,e)pyrene, naphthalene, and acenaphthylene, among 20 PAH species. AhR mRNA level either decreased or increased after exposure in 75% of the participants, and most of the subjects also had their IL-1, IL-6, IL-8, IL-10 gene levels altered in their post-shift levels compared to pre-shift levels (P < 0.05). Conclusion: PAHs from traffic PM2.5 may induce changes in expressions of AhR and related gene levels.