Keywords: 
• gasoline engine exhaust /
• PM_2.5 /
• mice /
• chemical composition /
• exposure chamber /
• inflammatory factor /
• pathological injury

Abstract: Motor vehicle exhaust is one of the main sources of PM_2.5 pollution in China. Long-term exposure to vehicle exhaust causes damage to animal respiratory system and other organs. To explore the effects of long-term exposure to gasoline-burning vehicle exhaust on lung tissue damage in mice, 51 male 8-week-old SPF-class ICR mice were randomly divided into 7 groups. Among them, one air control group (6 mice); three control groups: 0.5 h control group (5 mice), 1 h control group (8 mice), and 2 h control group (8 mice); three gasoline exhaust exposure groups: 0.5 h exposure group (8 mice), 1 h exposure group (8 mice), and 2 h exposure group (8 mice). Mice were exposed to gasoline engine exhaust in homemade chambers for 0.5 h, 1 h, and 2 h daily. After 95 days of exposure, the mice were sacrificed and their lung tissues were measured for inflammatory factors interleukin-6 (IL-6), lactate dehydrogenase (LDH), tumor necrosis factor-α (TNF-α), and transform growth factor β (TGF-β), and pulmonary pathology sections were made for HE staining. During the exposure experiment, the behavioural characteristics of the mice were observed and the concentrations of O₂, NO_x, NO₂, NO, SO₂ and CO in the exposure chamber were determined. In addition, PM_2.5 gasoline vehicle exhaust particles were collected and analysed for concentrations of water-soluble anions (F^-, Cl^-, NO₂^-, NO₃^-, SO₄^2-), water-soluble cations (Na⁺, NH₄⁺, Ca²⁺, K⁺, Mg²⁺), organic carbon (OC) and elementary carbon (EC), seven heavy metals (Cu, Ni, Mn, Zn, Pb, As, Cr) and 16 polycyclic aromatic hydrocarbons (PAHs). The results showed that: (1) Among the chemical species analyzed in the subchronic exposure chamber, the OC concentration was the highest, accounting for 75.5% of the total chemical concentration in PM_2.5; followed by EC, accounting for 22.9%; and then anion and cation, accounting for 1.11% and 0.27%, respectively. (2) The mice in the three exposed groups were less active. After 5-8 minutes of exposure, they entered sleep or rest, with the respiratory rate decreased, and these behaviours can reduce the damage from gasoline exhaust emissions. (3) There was no significant difference for weight growth rate between the parallel exposure and control groups, but the growth rate of the 2 h exposure group was significantly lower than that of the 2 h control group, and the 2 h exposure group has a weight decline tendency at the 14th week. (4) Compared with the control group, TNF-α in the 0.5 h exposure group and IL-6 in the 1 h exposure group were significantly increased, indicating that exposure to gasoline exhaust gases induced mouse lung inflammation injury, with increased secretion of IL-6 and TNF-α. With the prolongation of exposure time, IL-6 and TNF-α were significantly lower in the 2 h exposure group than that in the 1 h exposure group and 0.5 h exposure group respectively, which indicates that the lungs of the mice were seriously injured and the immunity was seriously reduced, with no positive anti-inflammatory response. (5) Histopathological observation showed that pulmonary congestion was more serious in the three exposure groups than in the control groups, a large number of lymphocytes and neutrophils infiltrated, and the alveolar interstitial hyperplasia was obvious, showing a gradient difference of damage aggravation with time. (6) Long-term exposure of gasoline vehicle exhaust can cause lung injury in mice, and the degree of damage to lung tissue increases with increasing exposure time.