PDF(Pubmed)
Abstract：
The central issue of this review are inflammatory changes that take place in the mucous membranes of the respiratory tract as a result of inhaled pollutants. Of particular relevance are dusts, SO(2), ozone, aldehydes und volatile organic compounds. Bioorganic pollutants, especially fragments of bacteria and fungi, occur predominantly in indoor dusts. They activate the toll-like/IL-1 receptor and lead to the activation of the transcription factor NF-κB for the release of numerous proinflammatory cytokines. Metals are predominant in ambient air dust particles. They induce the release of reactive oxygen species that cause damage to lipids, proteins and the DNA of the cell. As well as NF-κB, transcription factors that foster proliferation are activated via stress activated protein kinases. Organic compounds such as polycyclic aromatic hydrocarbons and nitroso-compounds of incomplete combustion processes activate additional via the cytosolic arylhydrocarbon receptor for detoxification enzymes. Sulphur dioxide leads to acid stress, and ozone to oxidative stress of the cell. This is accompanied by the release of proinflammatory cytokines via stress activated protein kinases. Aldehydes and volatile organic compounds activate the vanilloid receptor of trigeminal nerve fibres and induce a hyperreactivity of the mucous membrane via the release of nerve growth factors. The mechanisms described work synergistically and lead to a chronic inflammatory reaction of the mucous membranes of the upper respiratory tract that is regularly demonstrable in inhabitants of western industrial nations. It is unclear whether we are dealing here with a physiological inflammation or with an at least partially avoidable result of chronic pollutant exposure.
摘要：
这篇综述的中心问题是吸入污染物导致呼吸道粘膜发生的炎症变化。特别相关的是灰尘，SO(2),臭氧,醛和挥发性有机化合物。生物有机污染物,尤其是细菌和真菌的碎片，主要发生在室内灰尘中。它们激活toll样/IL-1受体并导致转录因子NF-κB的激活，以释放许多促炎细胞因子。金属在环境空气尘埃颗粒中占主导地位。它们诱导活性氧的释放，导致脂质受损，蛋白质和细胞的DNA。以及NF-κB,促进增殖的转录因子通过应激激活的蛋白激酶被激活。有机化合物如多环芳烃和不完全燃烧过程的亚硝基化合物通过胞质芳香烃受体额外激活解毒酶。二氧化硫导致酸胁迫,和臭氧对细胞的氧化应激。这伴随着促炎细胞因子通过应激激活的蛋白激酶的释放。醛类和挥发性有机化合物激活三叉神经神经纤维的香草素受体，并通过释放神经生长因子诱导粘膜的高反应性。所描述的机制协同作用，并导致上呼吸道粘膜的慢性炎症反应，这在西方工业国家的居民中经常表现出来。目前尚不清楚我们在这里处理的是生理炎症还是慢性污染物暴露的至少部分可避免的结果。
