Carbon Soot Exposure Induces Hepatic Injury, Inflammatory Response, and Anxiety-Like Behaviour in Wistar Rats
Sonny Clement Okoseimiema
Department of Anatomy, Faculty of Basic Medical Sciences, University of Port Harcourt, Port Harcourt, Nigeria.
Chidinma Goodness Maduabuchi
Department of Anatomy, Faculty of Basic Medical Sciences, University of Port Harcourt, Port Harcourt, Nigeria.
Ibinabo Fubara Bob-Manuel *
Department of Anatomy, Faculty of Basic Medical Sciences, University of Port Harcourt, Port Harcourt, Nigeria.
Precious Ojo Uahomo
Department of Pharmacology and Therapeutics, Faculty of Basic Clinical Sciences, University of Abuja, Gwagwalada, FCT, Nigeria.
Paul Chikwuogwo Wokpeogu
Department of Anatomy, Faculty of Basic Medical Sciences, University of Port Harcourt, Port Harcourt, Nigeria.
*Author to whom correspondence should be addressed.
Abstract
Background: Exposure to carbon soot particulate matter from crude oil combustion is a growing environmental health concern, particularly in oil-producing regions. While respiratory effects are well known, systemic impacts on liver structure, inflammation, and behaviour remain poorly understood. This study evaluated hepatotoxic, inflammatory and neurobehavioural effects of PM₁₀ carbon soot in Wistar rats.
Methods: Forty male Wistar rats were assigned to control and three exposure groups (low: 2.131±0.207 mg/m³; moderate: 2.161±0.232 mg/m³; high: 2.278±0.221 mg/m³). Animals were exposed for 1 hour daily over 28 days. Liver tissues were collected at days 3, 7, 14, 21, and 28 from separate cohorts for histology (H&E) and tumor necrosis factor-alpha (TNF-α) ELISA. Anxiety-like behaviour was assessed using the elevated plus maze. Data were analyzed using one-way ANOVA with Tukey’s post-hoc test.
Results: Histological examination revealed progressive hepatic injury characterized by hepatocyte degeneration, necrosis, sinusoidal dilation, vascular congestion, and inflammatory infiltration, with severity increasing with both exposure duration and concentration. TNF-α levels increased steadily across exposed groups. Early elevations were observed at day 3 in the moderate (11.40±0.40 pg/mL) and high exposure groups (13.85±0.35 pg/mL) compared to control (8.30±0.20 pg/mL), followed by marked increases at day 7 (40.65±1.15 and 71.75±3.45 pg/mL, respectively). By day 21, TNF-α levels further increased to 116.50±3.50 pg/mL (moderate) and 204.50±7.50 pg/mL (high), reaching peak values at day 28 (266.00±39.00 and 295.00±23.00 pg/mL, respectively), compared to control (59.25±8.25 pg/mL). The low exposure group also demonstrated elevated TNF-α levels at day 28 (119.00±2.00 pg/mL). Behavioural assessment showed reduced open arm entries (1.08±0.08 vs 1.33±0.21) and open arm duration (7.00±1.51 s vs 10.67±5.64 s), alongside decreased closed arm duration (194.10±20.50 s vs 236.55±1.53 s), indicating increased anxiety-like behaviour in exposed animals. Additional behavioural alterations included increased central square duration (39.10±22.70 s) and altered rearing activity (15.86±4.68 in the moderate exposure group).
Conclusion: Carbon soot PM10 induces significant dose- and time-dependent hepatic injury, inflammatory activation, and anxiety-like behaviour. The atypical moderate-dose behavioural findings warrant further investigation. These results highlight systemic soot toxicity and indicate the need for environmental health interventions.
Keywords: Carbon soot, particulate matter (PM10), hepatotoxicity, tumor necrosis factor-alpha (TNF-α), anxiety-like behaviour, inflammation, air pollution/particulate exposure, Wistar rats