Exposure to fine particulate matter induces self-recovery and susceptibility of oxidative stress and inflammation in rat lungs.

PM induces pulmonary inflammation via oxidative stress, and this role in the lungs is widely accepted, but studies on whether oxidative stress and inflammation can self-recover and be fully restored are limited. In this study, the oxidative stress and inflammation in the lungs of rats, which were first exposed to different PM dosages (0, 0.5, 3.0, and 15.0 mg/kg body weight) and different recovery days (0, 15, and 30 days) and then were exposed to the same PM dosages (30 mg/kg b.w.) after 30 days of recovery, were investigated. Results showed that the activity of superoxide dismutase (SOD) was significantly inhibited, and the levels of malondialdehyde (MDA), inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) significantly increased. These changes were accompanied with damage to the pathological structure of the rat lungs. After stopping PM exposure, the difference between the PM group and the control group gradually decreased with the extension of recovery time. However, when the rats were again exposed to the same dose of PM, the levels of IL-6, IL-1β, TNF-α, MDA, and iNOS were significantly increased, and the activities of SOD and GSH-Px were significantly inhibited in the high-dose group. And the high-dose group was accompanied by more severe lung pathological structural damage. Results showed that PM could induce oxidative stress and inflammatory damage in the lungs of rats, and these damages gradually recovered as exposure ceased, but increased lung susceptibility in rats.