Krishna M T, Chauhan A J, Frew A J, Holgate S T
University of Southampton, UK.
Rev Environ Health. 1998 Jan-Jun;13(1-2):59-71.
The health effect of atmospheric pollution is causing increasing public concern. Several controlled human-exposure studies have clearly. shown that oxidant pollutants, including ozone, nitrogen dioxide, and diesel exhaust, induce an acute inflammatory response in human airways. The main component of this response involves the influx of polymorphonuclear leukocytes (PMN) and is mediated via the upregulation of transcription factors NF-kappa B, AP-1, and NF-IL6; leukocyte-endothelial adhesion molecules, and chemokine secretion, including IL-8 and Gro-alpha. The results of recent studies also suggest that short-term exposure to ozone leads to neurogenic inflammation by causing damage to the bronchial epithelium and stimulating subepithelial sensory nerves to release substance P. In addition, such exposures lead to the consumption of endogenous antioxidants that are present in the airway lining fluid. Studies in asthmatics have shown that oxidant pollutants, including ozone and nitrogen dioxide, induce PMN influx in the airways and potentiate responses to inhaled aero-allergens. This article will review various studies addressing the toxicological mechanisms underlying oxidant pollutant-induced airways injury.
大气污染对健康的影响日益引起公众关注。多项人体对照暴露研究已明确表明，包括臭氧、二氧化氮和柴油废气在内的氧化性污染物会在人体气道中引发急性炎症反应。该反应的主要成分涉及多形核白细胞（PMN）的流入，并通过转录因子NF-κB、AP-1和NF-IL6的上调、白细胞-内皮粘附分子以及趋化因子分泌（包括IL-8和Gro-α）介导。近期研究结果还表明，短期接触臭氧会通过损伤支气管上皮并刺激上皮下感觉神经释放P物质而导致神经源性炎症。此外，此类暴露会导致气道内衬液中内源性抗氧化剂的消耗。对哮喘患者的研究表明，包括臭氧和二氧化氮在内的氧化性污染物会诱导气道中的PMN流入，并增强对吸入性空气过敏原的反应。本文将综述针对氧化性污染物所致气道损伤潜在毒理学机制的各类研究。
