Atmospheric fine particulate matter and epithelial mesenchymal transition in pulmonary cells: state of the art and critical review of thein vitrostudies

Exposure to fine particulate matter (PM2.5) has been associated with several diseases including asthma, chronic obstructive pulmonary disease (COPD) and lung cancer. Mechanisms such as oxidative stress and inflammation are well-documented and are considered as the starting point of some of the pathological responses. However, a number of studies also focused on epithelial-mesenchymal transition (EMT), which is a biological process involved in fibrotic diseases and cancer progression notably via metastasis induction. Up until now, EMT was widely reportedin vivoandin vitroin various cell types but investigations dealing within vitrostudies of PM(2.5)induced EMT in pulmonary cells are limited. Further, few investigations combined the necessary endpoints for validation of the EMT state in cells: such as expression of several surface, cytoskeleton or extracellular matrix biomarkers and activation of transcription markers and epigenetic factors. Studies explored various cell types, cultured under differing conditions and exposed for various durations to different doses. Such unharmonized protocols (1) might introduce bias, (2) make difficult comparison of results and (3) preclude reaching a definitive conclusion regarding the ability of airborne PM(2.5)to induce EMT in pulmonary cells. Some questions remain, in particular the specific PM(2.5)components responsible for EMT triggering. The aim of this review is to examine the available PM(2.5)induced EMTin vitrostudies on pulmonary cells with special emphasis on the critical parameters considered to carry out future research in this field. This clarification appears necessary for production of reliable and comparable results.