Devalia J L, Rusznak C, Wang J, Khair O A, Abdelaziz M M, Calderón M A, Davies R J
Department of Respiratory Medicine and Allergy, St. Bartholomew's Hospital, London, UK.
Toxicol Lett. 1996 Aug;86(2-3):169-76. doi: 10.1016/0378-4274(96)03687-9.
Epidemiological evidence suggests that an increase in liquid petroleum derived pollutants is associated with exacerbation of allergic airway disease, and that the effects of pollution may occur 1-2 days later. Laboratory based studies have demonstrated that the pollutants responsible for the adverse effects on respiratory health include nitrogen dioxide (NO2), sulphur dioxide (SO2), ozone (O3) and respirable particulates (PM10). More recently, studies of asthmatic individuals exposed to O3, NO2 and a combination of NO2 and SO2 have indicated that these agents increase the airway responsiveness of these individuals to inhaled allergen, and that this effect may be maximal 24 h after exposure to the pollutants. Studies investigating the putative mechanisms underlying the effects of these pollutants suggest that exposure to these agents may lead to perturbation of the airway epithelium and release of pro-inflammatory mediators from the epithelial cells, which then influence the activity of inflammatory cells, such as eosinophils.
流行病学证据表明,液态石油衍生污染物的增加与过敏性气道疾病的加重有关,且污染的影响可能在1 - 2天后出现。基于实验室的研究表明,对呼吸道健康产生不利影响的污染物包括二氧化氮(NO2)、二氧化硫(SO2)、臭氧(O3)和可吸入颗粒物(PM10)。最近,对暴露于O3、NO2以及NO2和SO2组合环境中的哮喘患者的研究表明,这些物质会增加这些患者气道对吸入性过敏原的反应性,且这种效应在接触污染物24小时后可能达到最大。调查这些污染物作用潜在机制的研究表明,接触这些物质可能导致气道上皮细胞紊乱,并促使上皮细胞释放促炎介质,进而影响炎症细胞(如嗜酸性粒细胞)的活性。