Ambient particulate matter exposure causes visual dysfunction and retinal neuronal degeneration

Abstract

PM2.5 pollution is related to neurotoxic and vascular effects in eye diseases such as glaucoma. This study investigates the adverse effects of PM2.5 exposure on visual function and retinal neurons. A versatile aerosol concentration enrichment system was used to expose mice to either control air or PM2.5 polluted air. Six months after PM2.5 exposure, visual function was measured by electroretinography (ERG). Hematoxylin and eosin staining and immunofluorescence staining were used for histopathological analysis. Protein markers of apoptosis, astrocytic reactivity, inflammatory cytokines, lipid peroxidation, protein nitration and DNA damage response were quantified with ELISA, western blot or detected using immunofluorescence and immunohistochemistry. After six months of exposure, PM2.5-exposed mice responded poorly to light stimuli compared with those exposed to the control air. PM2.5 exposure caused retinal thinning and reduction in the expression of retinal ganglion cell-selective marker RNA-binding protein with multiple splicing (RBPMS). Further, positive TUNEL staining was observed in the inner nucleus and outer nuclear layers of the retinae after exposure to PM2.5, which was accompanied by the activation of apoptosis signaling molecules p53, caspase-3 and Bax. PM2.5 induced the release of inflammatory cytokines including tumor necrosis factor-α and cleaved interleukin-1β. Furthermore, increased levels of 8-OHdG and γ-H2AX in the mouse retinea were indicative of DNA single and double strand breaks by PM2.5 exposure, which activated PARP-1 mediated DNA damage and repair. In conclusion, this study demonstrates sub-chronic systemic exposure to concentrated PM2.5 causes visual dysfunction and retinal neuronal degeneration. Data availabilityThe datasets during and/or analyzed during the current study available from the corresponding author on reasonable request.