Sub-chronic Inhalation of Wood Smoke PM2.5 Induces Ocular and Pulmonary Inflammation Via Upregulation of TNF-α/IL-6 in a Rat Model

Inflammation and oxidative stress triggered by oculo-pulmonary injury caused by wood smoke PM2.5 (WSPM2.5) exposures are still poorly investigated. The purpose of this study was to investigate the cytotoxicity mechanism of PM2.5 exposure in the eyes and lungs of experimental rats. Thirty-two adult male Wistar rats were arbitrarily divided into four (n = 8) groups. The inaugural group (control) was excluded from WS exposure, whereas Groups II (WS10mins), III (WS 20 mins) and IV (WS30mins) were exposed to WSPM2.5 (1234.8 ± 1.0 µg/m³) for 10, 20, and 30 minutes/day, respectively, for 30 days. Histological, biochemical, and gene expression analyses were conducted to evaluate oxidative stress, inflammation, and tissue injury using markers such as pro-inflammatory cytokines, Tumor Necrosis Factor-α (TNF-α) and Interleukin-6 (IL-6), and malondialdehyde (MDA). Thirty days of subchronic exposure to wood smoke PM2.5 caused eye and lung toxicity characterized by keratinization, complete loss of the retinal layers, hyperplasia of alveolar cells, enlargement of air spaces, thrombosis, and inflammation of the alveoli and perivascular space as a result of cellular injury. This was correlated with increased MDA levels and insflammatory cytokines (IL-6 and TNF-α) expression in exposed rats compared with the unexposed group. These findings imply that WSPM2.5 exposure can trigger inflammation and oxidative damage, leading to ocular and pulmonary toxicity in exposed rats.