In vitro pulmonary and vascular effects induced by different diesel exhaust particles

Bengalli, Rossella; Zerboni, Alessandra; Marchetti, Sara; Longhin, Eleonora; Priola, Marco; Camatini, Marina; Mantecca, Paride

doi:10.1016/j.toxlet.2019.01.017

Cited by 35 publications

(25 citation statements)

References 36 publications

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“…In particular, we evidence that the epithelial-mesenchymal transition (EMT) may be regulated by STAT3 and related genes (HES1, HMOX1, IL6, IL24 and VEGF); the oncogene KRAS may be a key node in determining UFP effects by upregulating the expression of EREG; and finally, the hypoxia inducible-factor-1a (HIF1a) may play a central role in UFP-related endothelial dysfunction. Building up on these results, we also show the ability of UFP to induce endothelial modification after exposure of lung epithelial cells to UFP [113] suggesting the relevance of cell signaling on endothelium modification and the possible onset of relevant effects at the cardiovascular level. Again, the cardiovascular effects of combustion particles are well documented [114,115], but the importance of second messengers in determining the onset of these health issues is poorly understood.…”

Section: Ultrafine Pmsupporting

confidence: 63%

Fifteen Years of Airborne Particulates in Vitro Toxicology in Milano: Lessons and Perspectives Learned

Longhin

Mantecca

Gualtieri

2020

IJMS

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Air pollution is one of the world’s leading environmental causes of death. The epidemiological relationship between outdoor air pollution and the onset of health diseases associated with death is now well established. Relevant toxicological proofs are now dissecting the molecular processes that cause inflammation, reactive species generation, and DNA damage. In addition, new data are pointing out the role of airborne particulates in the modulation of genes and microRNAs potentially involved in the onset of human diseases. In the present review we collect the relevant findings on airborne particulates of one of the biggest hot spots of air pollution in Europe (i.e., the Po Valley), in the largest urban area of this region, Milan. The different aerodynamic fractions are discussed separately with a specific focus on fine and ultrafine particles that are now the main focus of several studies. Results are compared with more recent international findings. Possible future perspectives of research are proposed to create a new discussion among scientists working on the toxicological effects of airborne particles.

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Section: Ultrafine Pmsupporting

confidence: 63%

Fifteen Years of Airborne Particulates in Vitro Toxicology in Milano: Lessons and Perspectives Learned

Longhin

Mantecca

Gualtieri

2020

IJMS

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“…For morphological analysis, cells were seeded on a cover slide at a concentration of 1.5*10 5 cells/well, cultured for 24 h and then exposed to NPs for further 24 h. At the end of the treatment, cells were processed for hematoxylin-eosin (HE) staining, as previously described in [27]. The slides were observed on an optical microscope (Zeiss-Axioplan, Carl Zeiss Microscopy GmbH, Jena, Germany), and pictures were acquired using an AxioCam MRc5 digital camera and processed using AxioVision Real 4.8 software (Carl Zeiss Solutions, Jena, Germany).…”

Section: Methodsmentioning

confidence: 99%

In Vitro Toxicity of TiO2:SiO2 Nanocomposites with Different Photocatalytic Properties

et al. 2019

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The enormous technological relevance of titanium dioxide (TiO2) nanoparticles (NPs) and the consequent concerns regarding potentially hazardous effects that exposure during production, use, and disposal can generate, encourage material scientists to develop and validate intrinsically safe design solution (safe-by-design). Under this perspective, the encapsulation in a silica dioxide (SiO2) matrix could be an effective strategy to improve TiO2 NPs safety, preserving photocatalytic and antibacterial properties. In this work, A549 cells were used to investigate the toxic effects of silica-encapsulated TiO2 having different ratios of TiO2 and SiO2 (1:1, 1:3, and 3:1). NPs were characterized by electron microscopy and dynamic light scattering, and cell viability, oxidative stress, morphological changes, and cell cycle alteration were evaluated. Resulting data demonstrated that NPs with lower content of SiO2 are able to induce cytotoxic effects, triggered by oxidative stress and resulting in cell necrosis and cell cycle alteration. The physicochemical properties of NPs are responsible for their toxicity. Particles with small size and high stability interact with pulmonary cells more effectively, and the different ratio among silica and titania plays a crucial role in the induced cytotoxicity. These results strengthen the need to take into account a safe(r)-by-design approach in the development of new nanomaterials for research and manufacturing.

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“…Pb 2+ does not induce inflammation individually, just like Cr(VI), but it is revealed that the co-existence of these two species in PM 2.5 caused cytotoxicity in lung cells [ 228 ]. The traffic-related PM is also reported to induce inflammation in both lymphocytes and lung cells [ 229 ], where the induction effect is stronger for PM with higher PAHs levels [ 230 ]. Additionally, the in vitro low dose exposure of rat lung to silica particles for 24 h exhibited inflammatory response [ 231 ], while the in vivo long-term, repeated and high-concentration diesel exhaust exposures of rats showed chronic inflammation [ 219 ].…”

Section: Health Effects Associated With Pm Invasionmentioning

confidence: 99%

“…It is found that the presence of traffic-related PM led to an increase of ROS generation and oxidative DNA damage in human lymphocytes, alveolar epithelial adenocarcinoma cells [ 229 ], and type II lung epithelial A549 cells [ 235 ]. The extent of oxidative stress, cytotoxicity and epithelial activation on pulmonary cells induced by diesel exhaust particles increased with the content of PAHs [ 230 ]. Soltani et al .…”

Section: Health Effects Associated With Pm Invasionmentioning

confidence: 99%

Interactions of particulate matter and pulmonary surfactant: Implications for human health

Wang

Liu

Zeng

2020

Advances in Colloid and Interface Science

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Particulate matter (PM), which is the primary contributor to air pollution, has become a pervasive global health threat. When PM enters into a respiratory tract, the first body tissues to be directly exposed are the cells of respiratory tissues and pulmonary surfactant. Pulmonary surfactant is a pivotal component to modulate surface tension of alveoli during respiration. Many studies have proved that PM would interact with pulmonary surfactant to affect the alveolar activity, and meanwhile, pulmonary surfactant would be adsorbed to the surface of PM to change the toxic effect of PM. This review focuses on recent studies of the interactions between micro/nanoparticles (synthesized and environmental particles) and pulmonary surfactant (natural surfactant and its models), as well as the health effects caused by PM through a few significant aspects, such as surface properties of PM, including size, surface charge, hydrophobicity, shape, chemical nature, etc. Moreover, in vitro and in vivo studies have shown that PM leads to oxidative stress, inflammatory response, fibrosis, and cancerization in living bodies. By providing a comprehensive picture of PM-surfactant interaction, this review will benefit both researchers for further studies and policy-makers for setting up more appropriate regulations to reduce the adverse effects of PM on public health.

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In vitro pulmonary and vascular effects induced by different diesel exhaust particles

Cited by 35 publications

References 36 publications

Fifteen Years of Airborne Particulates in Vitro Toxicology in Milano: Lessons and Perspectives Learned

Fifteen Years of Airborne Particulates in Vitro Toxicology in Milano: Lessons and Perspectives Learned

In Vitro Toxicity of TiO2:SiO2 Nanocomposites with Different Photocatalytic Properties

Interactions of particulate matter and pulmonary surfactant: Implications for human health

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