Acute and Recovery Phase Effects of Diesel Exhaust Particles on Lung and Brain in Mice

Abstract

Air pollution is recognized as a risk factor for neurodegenerative diseases, but the effects of acute exposure and subsequent recovery from traffic-related air pollution remain unclear. This study aimed to investigate the acute and recovery effects of diesel exhaust particle (DEP) exposure on central nervous system (CNS) toxicity. Six-week-old female C57BL/6NCrl mice received oropharyngeal aspiration of either 0 (vehicle control) or 50 µg/mouse of DEP twice a week for 3 weeks, with the acute group euthanized in week 4, and the recovery group undergoing behavioral tests in weeks 4 and 15 before being euthanized in week 16. DEP deposition in the lungs was estimated using the multiple-path particle dosimetry (MPPD) model, revealing 16.58% deposition, with 12.03% in the alveolar region, and clearance taking over 95 days. Mononuclear cell infiltration and DEP-laden macrophages were observed in lung tissues of both groups. Behavioral tests showed no significant differences between control and DEP groups in step-through latency, escape latency, quadrant area crossing time, or swimming velocity. Lipid peroxidation, indicated by malondialdehyde (MDA) levels, was significantly higher in the cerebellum and hippocampus of the acute exposure group (p < 0.05). Acute DEP exposure also significantly elevated Tau and p-Tau levels in the cortex (p < 0.05), but no significant changes were observed in the cerebellum and hippocampus. Histological analysis showed no significant pathological changes in the brain regions examined. The findings underscore the need for further research into the prolonged effects of DEP exposure and highlight the importance of addressing traffic-related air pollution to protect respiratory and neurological health.