Seaton A, MacNee W, Donaldson K, Godden D
Department of Environmental and Occupational Medicine, University of Aberdeen, UK.
Lancet. 1995 Jan 21;345(8943):176-8. doi: 10.1016/s0140-6736(95)90173-6.
Epidemiological studies have consistently shown an association between particulate air pollution and not only exacerbations of illness in people with respiratory disease but also rises in the numbers of deaths from cardiovascular and respiratory disease among older people. Meta-analyses of these studies indicate that the associations are unlikely to be explained by any confounder, and suggest that they represent cause and effect. We propose that the explanation lies in the nature of the urban particulate cloud, which may contain up to 100000 nanometer-sized particles per mL, in what may be a gravimetric concentration of only 100-200 micrograms/m3 of pollutant. We suggest that such ultra-fine particles are able to provoke alveolar inflammation, with release of mediators capable, in susceptible individuals, of causing exacerbations of lung disease and of increasing blood coagulability, thus also explaining the observed increases in cardiovascular deaths associated with urban pollution episodes. This hypothesis is testable both experimentally and epidemiologically.
流行病学研究一直表明,空气中的颗粒物污染不仅与呼吸系统疾病患者病情加重有关,还与老年人心血管疾病和呼吸系统疾病死亡人数增加有关。对这些研究的荟萃分析表明,这些关联不太可能由任何混杂因素解释,表明它们代表因果关系。我们认为,解释在于城市颗粒物云的性质,每毫升可能含有多达100000个纳米级颗粒,而污染物的重量浓度可能仅为100-200微克/立方米。我们认为,这种超细颗粒能够引发肺泡炎症,释放出的介质在易感个体中能够导致肺部疾病加重并增加血液凝固性,从而也解释了与城市污染事件相关的心血管死亡人数增加的现象。这一假设在实验和流行病学上都是可检验的。