A Study on Acute Injury from Single Exposure to Diesel Exhaust Particles in Mice

Objective To investigate the acute injury caused by single intratracheal instillation (IT) of diesel exhaust particles (DEP) in mice.

Methods The DEP particle size, polycyclic aromatic hydrocarbons (PAHs) and metals absorbed in DEP were measured by scanning mobility particle sizer, gas chromatography-mass spectrometry, and inductively coupled plasma mass spectrometry, respectively. A total of 108 male C57BL/6 J mice were randomly divided into DEP group and control group, with 54 mice in each group. Mice in the DEP and control groups received single IT of DEP (100 μg, dissolved in PBS + 0.05% Tween-80) and PBS + 0.05% Tween-80, respectively. Eighteen mice (9 in DEP and 9 in control) were sacrificed at each time point of 0.5, 6, 12, 24, 48 and 72 h after IT.Samples were collected for analyses of blood biochemistry and acute lung injury biomarkers.

Results The particle sizes of 84.3% DEP were below 100 nm. Among the PAHs adsorbed on DEP, carcinogenic and non-carcinogenic PAHs accounted for 38.1% and 61.9%, respectively. A total of 30 metals were detected on DEP, of which Na, Ca, Al, and Fe were the most abundant. Blood biochemical tests showed transient increases in alanine aminotransferase, aspartate aminotransferase, total bile acid, and triglyceride in mice after DEP exposure, indicating liver injury. In the serum and the liver, serum amyloid A (SAA) increased from 6 to 24 h and C-reaction protein (CRP) increased at 6 h, indicating acute phase response (APR). In the lungs, surfactant protein A (SPA) increased from 0.5 to 72 h and Club cell protein (CC16) increased from 6 to 48 h, indicating lung injury.

Conclusion Single DEP exposure causes APR and transient lung injury in mice.