Abstract
Age-related macular degeneration (AMD) is one of common causes of severe loss of vision in elder population. Oxidative stress in retinal pigment epithelium (RPE) plays the principal role in AMD. Considering the bio-accumulative and lipid-solubility, we focus one crucial oxidative stress trigger on environmental pollutants: polycyclic aromatic hydrocarbons (PAHs) in respirable particulate matter, PM2.5-1 (diameter 2.5-1μm), from municipal solid waste (MSW) incinerator. MSW fly ash sample contained 1.795% respirable PM (diameter<10μm), including 0.128% of PM2.5-1, which was classified by Dekati® Low Pressure Impactor. Then, PAHs in PM2.5-1 quantified by GC-MS were 11.3 ppm. To identify if PAHs in PM2.5-1 is a risky factor of AMD, EC50, ROS, transepithelial electrical resistance, immunofluorescence staining and variation of genomic expression were measured. PAHs and PM2.5-1 both induced ROS progressed the oxidative stress in ARPE-19 cells. Moreover, they both interfered the integrity of the tight junction protein, ZO-1, at REP monolayer. On the other hand, our results demonstrated the expression levels of CCL2, CRP, CXCL1, CXCL12, ITGB2, MMP14, and C7 in ARPE-19 cells were up-regulated whereas the levels of CLU, CFI, and C3aR1 were down-regulated after PAHs exposed. These variation of genomic expression was regarded as an indicator of severe CNV, inflammation and uncontrolled complement activity. In conclusion, all findings suggested an association between PAHs exposure and development of AMD.