A549 as an In Vitro Model to Evaluate the Impact of Microplastics in the Air

Airborne microplastics raise significant concerns due to their potential health impacts. Having a small size, larger surface area, and penetrative ability into the biological system, makes them hazardous to health. This review article compiles various studies investigating the mechanism of action of...

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Main Authors: Chman Shahzadi, Alessandra Di Serafino, Eleonora Aruffo, Alessandra Mascitelli, Piero Di Carlo
Format: Article
Language:English
Published: MDPI AG 2023-09-01
Series:Biology
Subjects:
Online Access:https://www.mdpi.com/2079-7737/12/9/1243
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author Chman Shahzadi
Alessandra Di Serafino
Eleonora Aruffo
Alessandra Mascitelli
Piero Di Carlo
author_facet Chman Shahzadi
Alessandra Di Serafino
Eleonora Aruffo
Alessandra Mascitelli
Piero Di Carlo
author_sort Chman Shahzadi
collection DOAJ
description Airborne microplastics raise significant concerns due to their potential health impacts. Having a small size, larger surface area, and penetrative ability into the biological system, makes them hazardous to health. This review article compiles various studies investigating the mechanism of action of polystyrene micro- and nanoplastics affecting lung epithelial cells A549. These inhalable microplastics damage the respiratory system, by triggering a proinflammatory environment, genotoxicity, oxidative stress, morphological changes, and cytotoxic accumulation in A549 cells. PS-NP lung toxicity depends on various factors such as size, surface modifications, concentration, charge, and zeta potential. However, cellular uptake and cytotoxicity mechanisms depend on the cell type. For A549 cells, PS-NPs are responsible for energy imbalance by mitochondrial dysfunction, oxidative stress-mediated cytotoxicity, immunomodulation, and apoptosis. Additionally, PS-NPs have the ability to traverse the placental barrier, posing a risk to offspring. Despite the advancements, the precise mechanisms underlying how prolonged exposure to PS-NPs leads to the development and progression of lung diseases have unclear points, necessitating further investigations to unravel the root cause. This review also sheds light on data gaps, inconsistencies in PS-Nos research, and provides recommendations for further research in this field.
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spelling doaj.art-bac3d871706541ca931ea1c8b544155b2023-11-19T09:39:01ZengMDPI AGBiology2079-77372023-09-01129124310.3390/biology12091243A549 as an In Vitro Model to Evaluate the Impact of Microplastics in the AirChman Shahzadi0Alessandra Di Serafino1Eleonora Aruffo2Alessandra Mascitelli3Piero Di Carlo4Center of Advanced Studies and Technology (CAST), University of “G. d’ Annunzio” Chieti Pescara, 66100 Chieti, ItalyCenter of Advanced Studies and Technology (CAST), University of “G. d’ Annunzio” Chieti Pescara, 66100 Chieti, ItalyCenter of Advanced Studies and Technology (CAST), University of “G. d’ Annunzio” Chieti Pescara, 66100 Chieti, ItalyCenter of Advanced Studies and Technology (CAST), University of “G. d’ Annunzio” Chieti Pescara, 66100 Chieti, ItalyCenter of Advanced Studies and Technology (CAST), University of “G. d’ Annunzio” Chieti Pescara, 66100 Chieti, ItalyAirborne microplastics raise significant concerns due to their potential health impacts. Having a small size, larger surface area, and penetrative ability into the biological system, makes them hazardous to health. This review article compiles various studies investigating the mechanism of action of polystyrene micro- and nanoplastics affecting lung epithelial cells A549. These inhalable microplastics damage the respiratory system, by triggering a proinflammatory environment, genotoxicity, oxidative stress, morphological changes, and cytotoxic accumulation in A549 cells. PS-NP lung toxicity depends on various factors such as size, surface modifications, concentration, charge, and zeta potential. However, cellular uptake and cytotoxicity mechanisms depend on the cell type. For A549 cells, PS-NPs are responsible for energy imbalance by mitochondrial dysfunction, oxidative stress-mediated cytotoxicity, immunomodulation, and apoptosis. Additionally, PS-NPs have the ability to traverse the placental barrier, posing a risk to offspring. Despite the advancements, the precise mechanisms underlying how prolonged exposure to PS-NPs leads to the development and progression of lung diseases have unclear points, necessitating further investigations to unravel the root cause. This review also sheds light on data gaps, inconsistencies in PS-Nos research, and provides recommendations for further research in this field.https://www.mdpi.com/2079-7737/12/9/1243nanoplasticspolystyreneA549alveolar epithelial cellsair pollutants
spellingShingle Chman Shahzadi
Alessandra Di Serafino
Eleonora Aruffo
Alessandra Mascitelli
Piero Di Carlo
A549 as an In Vitro Model to Evaluate the Impact of Microplastics in the Air
Biology
nanoplastics
polystyrene
A549
alveolar epithelial cells
air pollutants
title A549 as an In Vitro Model to Evaluate the Impact of Microplastics in the Air
title_full A549 as an In Vitro Model to Evaluate the Impact of Microplastics in the Air
title_fullStr A549 as an In Vitro Model to Evaluate the Impact of Microplastics in the Air
title_full_unstemmed A549 as an In Vitro Model to Evaluate the Impact of Microplastics in the Air
title_short A549 as an In Vitro Model to Evaluate the Impact of Microplastics in the Air
title_sort a549 as an in vitro model to evaluate the impact of microplastics in the air
topic nanoplastics
polystyrene
A549
alveolar epithelial cells
air pollutants
url https://www.mdpi.com/2079-7737/12/9/1243
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