Particulate matters (PMs) are significant components of air pollution in the urban environment. PMs with aerodynamic diameter less than 2.5 μm (PM2.5) can penetrate to the alveolar area and introduce numerous compounds to the pneumocystis that can initiate inflammatory response. There are several questions about this exposure as follows: does PM2.5-induced inflammation lead to a specific disease? If yes, what is the form of the progressed disease? This systematic review was designed and conducted to respond to these questions. Four databases, including Web of Science, Scopus, PubMed, and Embase, were reviewed systematically to find the related articles. According to the included articles, the only available data on the inflammatory effects of PM2.5 comes from either in vitro or animal studies. Both types of studies have shown that the induced inflammation is type I and includes secretion of proinflammatory cytokines. The exposure duration of longer than 28 weeks was not observed in any of the reviewed studies. However, as there is not a specific antigenic component in the urban particulate matters and based on the available evidence, the antigen-presenting is not a common process in the inflammatory responses to PM2.5. Therefore, neither signaling to repair cells such as fibroblasts nor over-secretion of extracellular matrix (ECM) proteins can occur following PM2.5-induced inflammation. These pieces of evidence weaken the probability of the development of fibrotic diseases. On the other hand, permanent inflammation induces the destruction of ECM and alveolar walls by over-secretion of protease enzymes and therefore results in progressive obstructive effects.
Keywords: Air pollution; COPD; Emphysema; Idiopathic pulmonary fibrosis; Inflammation; PM2.5.