Perfluorooctanoic acid in indoor particulate matter triggers oxidative stress and inflammation in corneal and retinal cells

Abstract

To investigate the particle size distribution of particulate matter and the concentration of specific perfluorinated compounds in indoor dust samples from several locations. Then, we used cell-based assays to investigate the effect of perfluorinated compounds on human corneal epithelial (HCEpiC), endothelial cells (HCEC) and retinal pigment epithelial cells (RPE). Indoor dust samples were collected at five different locations and PM50–10, PM10–2.5, and PM2.5–1 were fractionized. The presence and levels of 8:2 fluorotelomer alcohol, 10:2 fluorotelomer alcohol, and perfluorooctanoic acid were detected by gas chromatography–mass spectrometry. The effect of perfluorooctanoic acid on the activation of reactive oxygen species, transepithelial resistance as well as the expression of interleukin (IL)-6 and IL-8 were determined. The basolateral media of human corneal epithelial or human corneal endothelial cells were used to treat human corneal endothelial or retinal pigment epithelial cells, respectively to indicate the potential of ocular surface inflammation may result in retinal inflammation. Among perfluorinated compounds, only perfluorooctanoic acid was detected in all indoor dust samples. Perfluorooctanoic acid had the highest concentration among all perfluorinated compounds in the samples. Exposure to perfluorooctanoic acid impaired tight junction sealing and increased the levels of reactive oxygen species in human corneal epithelial cells. In human corneal epithelial cells, secretion of IL-6 and IL-8 in both apical and basolateral media was promoted significantly by perfluorooctanoic acid treatment. Stimulation with the basolateral media from perfluorooctanoic acid-treated human corneal epithelial cells induced inflammation in human corneal endothelial cells. The treatment of retinal pigment epithelial cells with the basolateral media from stimulated human corneal endothelial cells also elicited the secretion of proinflammatory cytokines. The results indicate that perfluorooctanoic acid exposure impaired the tight junction of corneal cells and caused inflammatory reactions in the retina. Exposure of the cornea to perfluorooctanoic acid contained in particulate matter might induce oxidative stress and inflammation in the retina and represent a risk factor for age-related macular degeneration.

Particulate Matter Elevates Ocular Inflammation and Endoplasmic Reticulum Stress in Human Retinal Pigmented Epithelium Cells

“…Furthermore, induction of the ocular hypoxic response may also be closely related to the disruption of epithelial tight junction integrity [ 57 ]. Ocular epithelial tight junctions have been shown to be affected by various stress conditions, including increased inflammation [ 58 ], hypoxia [ 57 ], and unfolded protein responses [ 59 ].…”

Urban Aerosol Particulate Matter Promotes Necrosis and Autophagy via Reactive Oxygen Species-Mediated Cellular Disorders that Are Accompanied by Cell Cycle Arrest in Retinal Pigment Epithelial Cells

“…Several genetic and environmental risk factors for AMD lead to inflammation, anatomical changes, and dysfunction in the retina, which can eventually lead to loss of vision [34]. Recently, it has been reported that air pollutants are considered one of the environmental risk factors for AMD and are involved in ROS overload by oxidative stress, which can lead to RPE cell death [19,24].…”

“…One animal study demonstrated that PM induces edema in retina [23]. More recently, Tien et al [24] published results showing that perfluorooctanoic acid contained in PM induces oxidative stress and inflammation in the retinal pigment epithelium (RPE) and acts as a risk factor for AMD. In 2020, another study suggested that glial fibrillary acidic protein (GFAP), a hallmark of glial activation in accordance with neural damage, is markedly expressed by long-term exposure to UPM [16].…”

Recent Advances in Our Understanding of Age-Related Macular Degeneration: Mitochondrial Dysfunction, Redox Signaling, and the Complement System

“…In addition, light exposure, particularly in the form of UV radiation and blue light, which can induce ROS formation, has been linked to AMD and considered a possible factor in disease onset or progression [49][50][51][52]. Moreover, specific chemical substances, such as perfluorooctanoic acid found in indoor particulate matter, have been identified as potential inducers of oxidative stress and may be regarded as risk factors for AMD [53]. The impact of gender on the occurrence of AMD is a subject of debate.…”