Alterations in rat pulmonary phosphatidylcholines after chronic exposure to ambient fine particulate matter.

This study elucidated the underlying pathophysiological changes that occur after chronic ambient fine particulate matter (PM2.5) exposure via a lipidomic approach. Five male Sprague-Dawley rats were continually whole-body exposed to ambient air containing PM2.5 at 16.7 ± 10.1 μg m(-3) from the outside of the building for 8 months, whereas a control group (n = 5) inhaled filtered air. Phosphorylcholine-containing lipids were extracted from lung tissue and profiled using ultraperformance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). The phosphatidylcholine (PC) signal features of the two groups were compared using partial least squares discriminant analysis (PLS-DA) and Wilcoxon rank sum tests. The PC profile of the exposure group differed from that of the control group; the R(2)Y and Q(2) were 0.953 and 0.677, respectively, in the PLS-DA model. In the exposure group, a significant 0.66- to 0.80-fold reduction in lyso-PC levels, which may have resulted from repeated inflammation, was observed. Decreased surfactant PCs by 16% at most may indicate injuries to alveolar type II cells. Cell function and cell signalling are likely to be altered because the decrease in unsaturated PCs may reduce membrane fluidity. Accompanied by the decline in plasmenylcholines, decreased unsaturated PCs may indicate the attack of reactive oxygen species generated by PM2.5 exposure. The physiological findings conformed to the histopathological changes in the exposed animals. PC profiling using UPLC-MS/MS-based lipidomics is sensitive for reflecting pathophysiological perturbations in the lung after long-term and low concentration PM2.5 exposure.