Air pollutants cause changes in iron homeostasis through: 1) a capacity of the pollutant, or a metabolite(s), to complex/chelate iron from pivotal sites in the cell or 2) an ability of the pollutant to displace iron from pivotal sites in the cell. Through either pathway of disruption in iron homeostasis, metal previously employed in essential cell processes is sequestered after air pollutant exposure. An absolute or functional cell iron deficiency results. If enough iron is lost or is otherwise not available within the cell, cell death ensues. However, prior to death, exposed cells will attempt to reverse the loss of requisite metal. This response of the cell includes increased expression of metal importers (e.g. divalent metal transporter 1). Oxidant generation after exposure to air pollutants includes superoxide production which functions in ferrireduction necessary for cell iron import. Activation of kinases and phosphatases and transcription factors and increased release of pro-inflammatory mediators also result from a cell iron deficiency, absolute or functional, after exposure to air pollutants. Finally, air pollutant exposure culminates in the development of inflammation and fibrosis which is a tissue response to the iron deficiency challenging cell survival. Following the response of increased expression of importers and ferrireduction, activation of kinases and phosphatases and transcription factors, release of pro-inflammatory mediators, and inflammation and fibrosis, cell iron is altered, and a new metal homeostasis is established. This new metal homeostasis includes increased total iron concentrations in cells with metal now at levels sufficient to meet requirements for continued function.

空气污染物通过以下方式引起铁体内平衡的变化：1）污染物或代谢物从细胞关键部位复合/螯合铁的能力，或2）污染物从体内关键部位置换铁的能力。细胞。通过铁稳态的任何一种破坏途径，暴露于空气污染物后，螯合了先前用于基本细胞过程的金属。导致绝对或功能性细胞铁缺乏症。如果细胞内铁丢失过多或无法获得，则将导致细胞死亡。但是，在死亡之前，裸露的细胞将试图逆转必需金属的损失。细胞的这种反应包括金属导入物（例如二价金属转运蛋白1）表达的增加。暴露于空气污染物后产生的氧化剂包括超氧化物的产生，超氧化物的产生在细胞铁导入所需的亚铁还原中起作用。暴露于空气污染物后，细胞铁缺乏症（无论是绝对的还是功能性的）也导致激酶，磷酸酶和转录因子的活化以及促炎性介质的释放增加。最后，暴露于空气污染物最终导致发炎和纤维化，这是对铁缺乏症的组织反应，挑战了细胞的存活率。继进口商表达增加和亚铁减少，激酶和磷酸酶和转录因子的激活，促炎性介质的释放以及炎症和纤维化的反应之后，细胞铁被改变，并且建立了新的金属稳态。