Ocular surface and systemic responses to repeated carbon black exposure across different durations in a rat model.

Carbon black (CB), a carbonaceous component of particulate matter, has been implicated in ocular toxicity, yet the biological effects associated with varying exposure durations remain unclear. This study investigated exposure-duration-associated changes in the ocular surface-tear unit and systemic responses following CB exposure in a rat model. Sprague-Dawley rats were topically exposed to CB for 1 day, 5 days, or 4 weeks. Ocular surface injury was assessed by rose bengal and corneal fluorescein staining and conjunctival hyperemia. Tear parameters included matrix metalloproteinase-9 (MMP-9), lactate dehydrogenase (LDH), histamine, lactoferrin, vascular endothelial growth factor (VEGF), and tear secretion. Corneal, conjunctival, and lacrimal gland tissues were examined for inflammatory mediators, sirtuin 1 (SIRT1) expression, and lacrimal gland senescence, while systemic responses were assessed by serum immunoglobulin E (IgE) and IgG levels. CB induced ocular surface injury across exposure durations. Tear MMP-9 increased after intermediate and prolonged exposure, whereas LDH and VEGF elevations were confined to the longest exposure duration. Tear secretion showed a non-significant increase at the early time point, followed by a decline. At the late stage, CB was associated with enhanced ocular inflammation, reduced tissue SIRT1 expression, and lacrimal gland senescence. Systemically, serum IgE increased after prolonged exposure, whereas IgG increased only at the intermediate time point. Collectively, these findings suggest that sustained ocular exposure to CB disrupts ocular surface and tear homeostasis, accompanied by local inflammation, senescence-associated changes, and IgE-dominant systemic immune modulation, highlighting the ocular surface-tear unit as a vulnerable site under carbonaceous exposure.