Pulmonary toxicity study in rats with PM10 and PM2.5: Differential responses related to scale and composition

Objection: To study the pollution of atmospheric particles at winter in Beijing and compare the lung toxicity which induced by particle samples from different sampling sites. Method: We collected samples from two sampling points during the winter for toxicity testing and chemical analysis. Wistar rats were administered with particles by intratracheal instillation. After exposure, biochemically index, esimmunity indexes, histopathology and DNA damage were detected in rat pulmonary cells. Result: The elements with enrichment factors (EF) larger than 10 were As, Cd, Cu, Zn, S and Pb in the four experiment groups. The priority control of the total concentration of polycyclic aromatic hydrocarbons (PAHs) in PM10 and PM2.5 of Near-traffic source was much higher than that of Far-traffic source, it demonstrated that near the traffic source of PAHs pollution was heavier than that of Far-traffic source, as it was close to main roads Beiyuan Road, motor vehicle emissions were much higher. The pathology of lung showed that the degree of inflammation was increased with the particle diameter minished, it was the same as the detection of biochemical parameters such as lactate dehydrogenase (LDH), Total antioxidant status(T-AOC) and total protein (TP) in BALF and inflammation cytokine(interleukin-1, interleukin-6 and tumor necrosis factor-alpha) in lung homogenate. The indexes of DNA damage including the content of DNA and Olive empennage of PM2.5 were significant higher than that of PM10 at the same surveillance point (P < 0.05), near-traffic particles were higher than the far-traffic particles at the same diameter, (P < 0.05). Conclusion: Near-traffic area particles had certain pollution at winter in Beijing. Meanwhile, atmospheric particulate matters on lung toxicity were related to the particles size and distance related sites which were exposed: smaller size, more toxicity; nearer from traffic, more toxicity. (C) 2010 Elsevier Ltd. All rights reserved.