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

PM2.5 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 PM2.5 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 PM2.5 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-1ß (IL-1ß) significantly increased. These changes were accompanied with damage to the pathological structure of the rat lungs. After stopping PM2.5 exposure, the difference between the PM2.5 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 PM2.5, the levels of IL-6, IL-1ß, 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 PM2.5 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.

Volatile organic compounds in Shihezi, China, during the heating season: pollution characteristics, source apportionment, and health risk assessment.

From November 2018 to March 2019, the mixing ratios of 57 types of volatile organic compounds (VOCs) were measured using gas chromatography-mass spectrometry in Shihezi. The results depicted that the average mixing ratios of VOCs were 58.48 ppbv and alkanes (34.15 ppbv) showed the largest contribution, followed by ethyne (20.16 ppbv), alkenes (2.62 ppbv), and aromatics (1.55 ppbv). Based on the positive matrix factorization (PMF) model result, coal burning (39.83%), traffic-related exhaust (26.87%), liquefied petroleum gas/natural gas usage (LPG/NG) (17.32%), fuel evaporation and paint usage (9.02%), and industrial emission (6.96%) were distinguished. Secondary formation potential was applied to demonstrate the probability of secondary pollution; the results indicated that alkanes (27.30 ppbv) and alkenes (21.42 ppbv) played leading roles in ozone formation potential (OFP) and the contributions of alkanes (1.05 µg/m3) and aromatics (0.99 µg/m3) were nearly equal for secondary organic aerosol formation potential (SOAFP) under high-NOx condition. However, under a low-NOx condition, aromatics (2.12 µg/m3) dominated, and the contribution of alkanes (1.05 µg/m3) was lower. Monte Carlo simulation results showed that exposure to 1,3-butadiene and benzene may contribute potential carcinogenic risks to local residents; PMF results showed that reducing traffic-related and industrial emissions as well as coal burning was more effective in controlling carcinogenic risks. This study provides a crucial theoretical basis for decision-makers to minimize local air pollution more effectively.