Abstract

Although nanoparticles (NPs) have been used as simplified atmospheric particulate matter (PM) models, little experimental evidence is available to support such simulations. In this study, we comparatively assessed the toxic effects of PM and typical NPs (four carbonaceous NPs with different morphologies, metal NPs of Fe, Al, and Ti, as well as SiO2 NPs) on human lung epithelial A549 cells. The EC50 value of PM evaluated by cell viability assay was 148.7 μg/mL, closest to that of SiO2 NPs, between the values of carbonaceous NPs and metal NPs. All particles caused varying degrees of reactive oxygen species (ROS) generation and adenosine triphosphate (ATP) suppression. TiO2 NPs showed similar performance with PM in inducing ROS production (p < 0.05). Small variations between two carbonaceous NPs (graphene oxides and graphenes) and PM were also observed at 50 μg/mL. Similarly, there was no significant difference in ATP inhibition between carbonaceous NPs and PM, while markedly different effects were caused by SiO2 NP and TiO2 NP exposure. Our results indicated that carbonaceous NPs could be served as potential surrogates for urban PM. The identification of PM model may help us further explore the specific roles and mechanisms of various components in PM.

Highlights

  • Published: 22 December 2020Atmospheric particulate matter (PM) is a major environmental pollutant endangering human health

  • We examined the physicochemical properties of different particles and their toxic effects on cell viability, reactive oxygen species (ROS) generation, and adenosine triphosphate (ATP) synthesis, seeking to explore which NPs could be used as suitable surrogates for urban PM, if any

  • Our study provided experimental evidences that carbonaceous NPs could be used as surrogate models to study the toxic mechanisms of PM

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Summary

Introduction

Atmospheric particulate matter (PM) is a major environmental pollutant endangering human health. It can penetrate and deposit deep inside the lungs, initiate a local inflammation or attack remote tissues by translocated particles [1,2]. Epidemiological and toxicological studies have demonstrated that chronic exposure to PM may induce or aggravate a variety of diseases including asthma, stroke, ischemic heart disease, chronic obstructive pulmonary disease, and lung cancer [3,4,5]. PM varies greatly in particle size and surface property. There are numerous studies on the toxic effects of PM, its exact toxic components and the underlying mechanisms are largely unknown

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