Metabolic dysregulations underlying the pulmonary toxicity of atmospheric fine particulate matter: focus on energy-producing pathways and lipid metabolism


Exposure to atmospheric fine particulate matter (PM2.5) is currently recognized as a leading cause and/or a serious aggravating factor of several respiratory diseases, such as chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, asthma, and lung cancer. Notably, pulmonary-altered metabolism has emerged as an important hallmark of those diseases, while a growing body of evidence shows that exposure to PM2.5 deeply modulates the bioenergetic profiles and metabolic pathways of lung cells. Hence, there is great interest in understanding how PM-induced metabolic dysregulations may contribute to pulmonary pathobiological events. Herein, in vitro and in vivo studies assessing the impact of PM2.5 on lung cells metabolism are reviewed, with emphasis on lung bioenergetics and lipid composition. Overall, there is compelling evidence that the metabolism of lung cells is an early target of PM2.5 exposure, with changes in metabolic pathways being observed at PM doses that do not cause extensive cell death or tissue injury. Hence, characterizing metabolic dysregulations associated with specific PM features and exposure conditions represents a valuable approach to further enlighten the toxicity mechanisms of PM2.5 and to identify novel biomarker signatures of air pollution exposure and health hazard.



subject category

Environmental Sciences & Ecology


Silva, TD; Alves, C; Oliveira, H; Duarte, IF

our authors


This work was developed within the scope of the projects CICECO-Aveiro Institute of Materials (UIDB/50011/2020, UIDP/50011/2020, and LA/P/0006/2020) and CESAM-Centre for Environmental and Marine Studies (UIDB/50017/2020 and UIDP/50017/2020 and LA/P/0094/2020) financed by national funds through the FCT/MEC (PIDDAC). LabEx DRIIHM is acknowledged in the scope of the project ATHEROFIT: Phytochemical-based metabolic immunomodulation to prevent/attenuate particulate mattermediated atherosclerosis (OHM-Estarreja/2019-2128). The authors are also thankful to the project SOPRO: Chemical and toxicological Source Profiling of particulate matter in urban air, POCI-01-0145FEDER-029574, funded by FEDER, through COMPETE2020 -POCI, and by national funds, through FCT/MCTES. T.D.S. acknowledges FCT for the doctoral grant (SFRH/BD/139647/2018).

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