Chronic Inhalation of Carbon Soot PM2.5 Induces Weight Loss and Cerebellar Cytoarchitectural Disruption in Humans: A Scientific Perspective on Wistar Rats
Sonny Clement Okoseimiema, Precious Ojo Uahomo
International Neuropsychiatric Disease Journal · pp. 27–39 · Published 5 Apr 2025
10.9734/indj/2025/v22i3478Abstract
Background: Carbon soot particulate matter (PM2.5) from crude oil combustion poses significant health risks; however, its systemic and neurological effects remain understudied. This study investigated the impact of chronic carbon soot PM2.5 inhalation on body weight and cerebellar cytoarchitecture in Wistar rats. Methods: Twenty-eight male Wistar rats were acclimatized and randomized into four groups: one control group and three experimental groups exposed to different PM2.5 concentrations (1.221 ± 0.169, 1.290 ± 0.214, and 1.282 ± 0.235 mg/m³) via a whole-body inhalation system for 4 hours/day over 28 days. Body weight was recorded daily, and cerebellar tissues were processed histologically using hematoxylin and eosin (H&E) staining post-sacrifice, whereas body weight data were analyzed using ANOVA and Tukey’s post hoc test (p<0.05). Results: Control rats exhibited normal weight gain (120.10 ± 2.00 g to 140.20 ± 3.05 g). All the PM2.5-exposed groups presented significant weight loss, which was most pronounced in Experimental Group 3 (113.15 ± 1.56 g to 105.80 ± 1.56 g, p<0.05). Histological analysis revealed dose-dependent cerebellar damage: mild vacuolation in Group 1, Purkinje cell degeneration in group 2, and severe cytoarchitectural disruption (pyknotic granular cells, necrosis) in group 3. Conclusion: Chronic carbon soot PM2.5 exposure induces systemic toxicity (weight loss) and progressive cerebellar neurodegeneration in a dose-dependent manner. These findings underscore the urgent need for stricter air quality regulations in regions with high industrial emissions and highlight the potential role of PM2.5 in metabolic and neurological disorders.
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