Effect of Nanoparticles and Environmental Particles on a Cocultures Model of the Air-Blood Barrier

Bengalli, Rossella; Mantecca, Paride; Camatini, M; Gualtieri, Maurizio

doi:10.1155/2013/801214

Cited by 31 publications

(27 citation statements)

References 36 publications

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“…The potential high deposited doses in the lungs reported here raise concerns for adverse health effects (Bengalli et al, 2013; Michael et al, 2013) as more than 52% of those inhaled particles deposit in the alveoli and 26% in the respiratory bronchioles. Specifically, particle deposition in the lung would be approximately 4 and 16 μg/m 2 for 15- and 60-min PEPs exposures, respectively.…”

Section: Discussionmentioning

confidence: 92%

Development and characterization of an exposure platform suitable for physico-chemical, morphological and toxicological characterization of printer-emitted particles (PEPs)

Pirela¹,

Pyrgiotakis²,

Bello

et al. 2014

Inhalation Toxicology

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An association between laser printer use and emissions of particulate matter (PM), ozone and volatile organic compounds has been reported in recent studies. However, the detailed physico-chemical, morphological and toxicological characterization of these printer-emitted particles (PEPs) and possible incorporation of engineered nanomaterials into toner formulations remain largely unknown. In this study, a printer exposure generation system suitable for the physico-chemical, morphological, and toxicological characterization of PEPs was developed and used to assess the properties of PEPs from the use of commercially available laser printers. The system consists of a glovebox type environmental chamber for uninterrupted printer operation, real-time and time-integrated particle sampling instrumentation for the size fractionation and sampling of PEPs and an exposure chamber for inhalation toxicological studies. Eleven commonly used laser printers were evaluated and ranked based on their PM emission profiles. Results show PM peak emissions are brand independent and varied between 3000 to 1 300 000 particles/cm3, with modal diameters ranging from 49 to 208 nm, with the majority of PEPs in the nanoscale (<100 nm) size. Furthermore, it was shown that PEPs can be affected by certain operational parameters and printing conditions. The release of nanoscale particles from a nano-enabled product (printer toner) raises questions about health implications to users. The presented PEGS platform will help in assessing the toxicological profile of PEPs and the link to the physico-chemical and morphological properties of emitted PM and toner formulations.

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Section: Discussionmentioning

confidence: 92%

Development and characterization of an exposure platform suitable for physico-chemical, morphological and toxicological characterization of printer-emitted particles (PEPs)

Pirela¹,

Pyrgiotakis²,

Bello

et al. 2014

Inhalation Toxicology

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“…In several studies THP-1 monocytes or PMA-differentiated THP-1 monocytes (THP-1 macrophages), have been included in the apical or basolateral compartment [43,48]. The apical compartment in such tri-culture models has been exposed to crystalline silica [49,50], particulate matter [51,52], diesel exhaust particles (DEP) [43,53,54] as well as NPs, including SiNPs [53] and silver (Ag) NPs and nanowires [48,55,56]. The most common biological endpoints include barrier function, cytotoxicity and pro-inflammatory responses in the apical and basolateral compartment, with some studies reporting endothelial responses [49,[53][54][55][56][57], others not [53,55].…”

Section: Introductionmentioning

confidence: 99%

Pro-inflammatory effects of crystalline- and nano-sized non-crystalline silica particles in a 3D alveolar model

et al. 2020

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Background: Silica nanoparticles (SiNPs) are among the most widely manufactured and used nanoparticles. Concerns about potential health effects of SiNPs have therefore risen. Using a 3D tri-culture model of the alveolar lung barrier we examined effects of exposure to SiNPs (Si10) and crystalline silica (quartz; Min-U-Sil) in the apical compartment consisting of human alveolar epithelial A549 cells and THP-1-derived macrophages, as well as in the basolateral compartment with Ea.hy926 endothelial cells. Inflammation-related responses were measured by ELISA and gene expression. Results: Exposure to both Si10 and Min-U-Sil induced gene expression and release of CXCL8, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-1α (IL-1α) and interleukin-1β (IL-1β) in a concentration-dependent manner. Cytokine/chemokine expression and protein levels were highest in the apical compartment. Si10 and Min-U-Sil also induced expression of adhesion molecules ICAM-1 and E-selectin in the apical compartment. In the basolateral endothelial compartment we observed marked, but postponed effects on expression of all these genes, but only at the highest particle concentrations. Geneexpressions of heme oxygenase-1 (HO-1) and the metalloproteases (MMP-1 and MMP-9) were less affected. The IL-1 receptor antagonist (IL-1RA), markedly reduced effects of Si10 and Min-U-Sil exposures on gene expression of cytokines and adhesion molecules, as well as cytokine-release in both compartments. Conclusions: Si10 and Min-U-Sil induced gene expression and release of pro-inflammatory cytokines/adhesion molecules at both the epithelial/macrophage and endothelial side of a 3D tri-culture. Responses in the basolateral endothelial cells were only induced at high concentrations, and seemed to be mediated by IL-1α/β released from the apical epithelial cells and macrophages.

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“…Moreover, ultrafine particles (UFPs ≤0.1 µm) are able to over-pass the lung clearance process and enter into the alveolar epithelium [10], [11], thus increase the possibility of their translocation through the alveolar blood barrier (ABB) [12], [13] and involving UFPs in cardiopulmonary diseases [14] and induction of neuroinflammation [15], [16].…”

Section: Introductionmentioning

confidence: 99%

Repeated Intratracheal Instillation of PM10 Induces Lipid Reshaping in Lung Parenchyma and in Extra-Pulmonary Tissues

et al. 2014

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Adverse health effects of air pollution attributed mainly to airborne particulate matter have been well documented in the last couple of decades. Short term exposure, referring to a few hours exposure, to high ambient PM10 concentration is linked to increased hospitalization rates for cardiovascular events, typically 24 h after air pollution peaks. Particulate matter exposure is related to pulmonary and cardiovascular diseases, with increased oxidative stress and inflammatory status. Previously, we have demonstrated that repeated intratracheal instillation of PM10sum in BALB/c mice leads to respiratory tract inflammation, creating in lung a condition which could potentially evolve in a systemic toxic reaction. Additionally, plasma membrane and tissue lipids are easily affected by oxidative stress and directly correlated with inflammatory products. With this aim, in the present investigation using the same model, we analyzed the toxic potential of PM10sum exposure on lipid plasma membrane composition, lipid peroxidation and the mechanisms of cells protection in multiple organs such as lung, heart, liver and brain. Obtained results indicated that PM10 exposure led to lung lipid reshaping, in particular phospholipid and cholesterol content increases; concomitantly, the generation of oxidative stress caused lipid peroxidation. In liver we found significant changes in lipid content, mainly due to an increase of phosphatidylcholine, and in total fatty acid composition with a more pronounced level of docosahexaenoic acid; these changes were statistically correlated to lung molecular markers. Heart and brain were similarly affected; heart was significantly enriched in triglycerides in half of the PM10sum treated mice. These results demonstrated a direct involvement of PM10sum in affecting lipid metabolism and oxidative stress in peripheral tissues that might be related to the serious systemic air-pollution effects on human health.

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Effect of Nanoparticles and Environmental Particles on a Cocultures Model of the Air-Blood Barrier

Cited by 31 publications

References 36 publications

Development and characterization of an exposure platform suitable for physico-chemical, morphological and toxicological characterization of printer-emitted particles (PEPs)

Development and characterization of an exposure platform suitable for physico-chemical, morphological and toxicological characterization of printer-emitted particles (PEPs)

Pro-inflammatory effects of crystalline- and nano-sized non-crystalline silica particles in a 3D alveolar model

Repeated Intratracheal Instillation of PM10 Induces Lipid Reshaping in Lung Parenchyma and in Extra-Pulmonary Tissues

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