Analysis of Carbon Nanoparticle Coatings via Wettability.

Wettability, typically estimated through the contact angle, is a fundamental property of surfaces with wide-ranging implications in both daily life and industrial processes. Recent scientific interest has been paid to the surfaces exhibiting extreme wettability: superhydrophobic and superhydrophilic surfaces, characterized by high water repellency and exceptional water wetting, respectively. Both chemical composition and morphology play a role in the determination of the wettability "performance" of a surface. To tune surface-wetting properties, we considered coatings of carbon nanoparticles (CNPs) in this study. They are a new class of nanomaterials synthesized in flames whose chemistry, dimension, and shape depend on combustion conditions. For the first time, we systematically studied the wettability of CNP coatings produced in a controlled rich ethylene/air flame stabilized over a McKenna burner. A selected substrate was intermittently inserted in the flame at 15 mm above the burner to form a thin coating thanks to a thermophoretic-driven deposition mechanism. The chemical-physical quality and the deposed quantity of the CNPs were varied by opportunely combing the substrate flame insertion number (from 1 to 256) and the carbon-to-oxygen ratio, C/O (from 0.67 to 0.87). The wettability of the coatings was evaluated by measuring the contact angle, CA, with the sessile drop method. When the C/O = 0.67, the CNPs were nearly spherical, smaller than 8 nm, and always generated hydrophilic coatings (CA < 35°). At higher C/O ratios, the CNPs reached dimensions of 100 nm, and fractal shape aggregates were formed. In this case, either hydrophilic (CA < 76°) or superhydrophobic (CA ~166°) behavior was observed, depending on the number of carbon nanoparticles deposed, i.e., film thickness. It is known that wettability is susceptible to liquid surface tension, and therefore, tests were conducted with different fluids to establish a correlation between the flame conditions and the nanostructure of the film. This method offers a fast and simple approach to determining mesoscale information for coating roughness and topographical homogeneity/inhomogeneity of their surfaces.

In vitro effects of combustion generated carbon dots on cellular parameters in healthy and cancerous breast cells.

Carbon nanomaterials are an inventive class of materials with wide applications in state-of-the-art bioimaging and therapeutics. They allow a broad range of tunable and integrated advantages of structural flexibility, chemical and thermal stability, upright electrical conductivity, and the option of scale-up and mass production. In the context of nanomedicine, carbon nanomaterials have been used extensively to mitigate the serious side effects of conventional chemotherapy and also to enable early cancer diagnostics, given their wide range of tunable properties. A class of carbon nanomaterials, called carbon dots (CDs) are small carbon-based nanoparticles and have been a valued discovery due to their photoluminescence, low photobleaching, and high surface area to mass ratio. The process of producing these CDs had so far been a high energy demanding process involving wet chemistry for purification. A one-step tunable production of luminescent CDs from fuel rich combustion reactors was recently presented by our group. In this paper, we explore the effects of these yellow luminescent combustion-generated CDs in MCF7 adenocarcinoma and MCF10a normal breast epithelial cells. We observed that these CDs, also at nontoxic doses, can affect basic cellular functions, such as cell cycle and proliferation; induce substantial changes on the physical parameters of the plasma membrane; and change the overall appearance of a cell in terms of morphology.

The Inhibition of Caspase-1- Does Not Revert Particulate Matter (PM)-Induced Lung Immunesuppression in Mice.

Background: Air pollution is becoming a threatening issue for human health. Many epidemiological studies relate air pollution index to adverse effects in terms of disease incidence and/or disease exacerbation. In our previous studies, we found air pollutants can induce the release of pro-inflammatory cytokines from human peripheral blood cells. To better understand, the effects of air pollution in the lung, we took advantage of an animal model. Experimental Approach: Mice were intratracheally and daily exposed to urban collected particulate matter (PM, PM10, and PM1) and to the sub-micrometric carbonaceous component, Soot. Results: We found that PM10, PM1, and Soot promoted lung inflammation associated to higher bronchial responsiveness and lower dilation together with an immunosuppressive lung environment, characterized by tolerogenic dendritic cells (DCs), macrophages and myeloid -derived suppressor cells (MDSCs), the latter two Arginase I positive. In support, higher recruitment of Treg associated to higher levels of IL-10 were detected in the lung of PM10, PM1, and Soot treated mice. This effect was not abolished by the administration of a caspase-1 inhibitor, Ac-Y-VAD, implying that the canonical inflammasome complex was not associated to PMx-induced lung immunosuppression in mice. Conclusion: Our study proves that PM exposure leads to an immunosuppressive lung environment in a caspase-1-independent manner, paving the way to understand the molecular and cellular mechanism/s underlying the establishment of some respiratory disorders according to the exposure to air pollution.

Chronic Obstructive Pulmonary Disease-Derived Circulating Cells Release IL-18 and IL-33 under Ultrafine Particulate Matter Exposure in a Caspase-1/8-Independent Manner.

Chronic obstructive pulmonary disease (COPD) is considered the fourth-leading causes of death worldwide; COPD is caused by inhalation of noxious indoor and outdoor particles, especially cigarette smoke that represents the first risk factor for this respiratory disorder. To mimic the effects of particulate matter on COPD, we isolated peripheral blood mononuclear cells (PBMCs) and treated them with combustion-generated ultrafine particles (UFPs) obtained from two different fuel mixtures, namely, pure ethylene and a mixture of ethylene and dimethylfuran (the latter mimicking the combustion of biofuels). UFPs were separated in two fractions: (1) sub-10 nm particles, named nano organic carbon (NOC) particles and (2) primarily soot particles of 20-40 nm and their agglomerates (200 nm). We found that both NOC and soot UFPs induced the release of IL-18 and IL-33 from unstable/exacerbated COPD-derived PBMCs. This effect was associated with higher levels of mitochondrial dysfunction and derived reactive oxygen species, which were higher in PBMCs from unstable COPD patients after combustion-generated UFP exposure. Moreover, lower mRNA expression of the repairing enzyme OGG1 was associated with the higher levels of 8-OH-dG compared with non-smoker and smokers. It was interesting that IL-18 and IL-33 release from PBMCs of unstable COPD patients was not NOD-like receptor 3/caspase-1 or caspase-8-dependent, but rather correlated to caspase-4 release. This effect was not evident in stable COPD-derived PBMCs. Our data suggest that combustion-generated UFPs induce the release of caspase-4-dependent inflammasome from PBMCs of COPD patients compared with healthy subjects, shedding new light into the biology of this key complex in COPD.

Exposure to sub-10nm particles emitted from a biodiesel-fueled diesel engine: In vitro toxicity and inflammatory potential.

OBJECTIVES: The inflammatory effects of organic sub-10nm particles generated and emitted from a diesel engine fueled with a biodiesel and a commercial diesel oil are analyzed in this paper. Diesel combustion is the major sources of ultrafine particles (UFP) in the environment, particularly in urbanized areas. In the last years, there is an increasing use of biomass-derived fuels because they are a renewable source of energy that may mitigate climate change through the reduction of net CO2 with respect to conventional fossil fuels. Although there is a general agreement on biofuels ability to reduce conventional pollutants, new and potentially harmful pollutants can be formed during biofuel combustion. In particular, the emission of sub-10nm particles is strongly increased with respect to that of larger soot particles. METHODS: Organic sub-10nm particles are separated from larger sizes particulate matter by collection in water suspension for toxicological and inflammatory tests. After exposure to sub-10nm particles, the effects on proliferation, apoptosis and secretion of cytokines, chemokines and growth factors networks production is analyzed in immortalized non-tumorigenic human dermal keratinocyte cell line (HaCaT) and human alveolar epithelial-like cells (A549). RESULTS AND CONCLUSION: Nanoparticles exert different cytotoxic effects in the two cell lines, suggesting that the dermal way of exposure is more sensitive than the inhalant way. These differences are most evident in the secretion of pro-inflammatory, angiogenic and proliferative cytokines and chemokines whose expression is more finely modulated in HaCaT cells compared to A-549 cells. Considering the size of these particles, it is important to promote the culture of prevention also for the dermal way in particularly exposed workers.

Human peripheral blood mononuclear cells (PBMCs) from smokers release higher levels of IL-1-like cytokines after exposure to combustion-generated ultrafine particles.

Ultrafine particles (UFP) generated by combustion processes are often associated with adverse health effects. However, little is known about the inflammatory processes generated by UFP that may underlie their toxicological activity. Murine macrophages (J774.1 cells) and human peripheral blood mononuclear cells (PBMCs) were used to evaluate the molecular mechanism underlying the pro-inflammatory activity of UFP. The addition of soot particles to J774.1 cells induced a concentration-dependent release of IL-1α, IL-1ß and IL-33 This effect was not associated with cell death and, in contrast to literature, was pronounced at very low concentrations (5-100 pg/ml). Similarly, UFP induced the release of IL-1α, IL-18 and IL-33 by PBMCs. However, this effect was solely observed in PBMCs obtained from smokers, as the PBMCs from non-smokers instead released higher levels of IL-10. The release of these cytokines after UFP exposure was caspase-1- and NLRP3 inflammasome-dependent in PBMCs from healthy smokers, whereas IL-1α release was calpain-dependent. These results show that UFP at very low concentrations are able to give rise to an inflammatory process that is responsible for IL-1α, IL-18 and IL-33 release, which is pronounced in PBMCs from smokers, confirming that these individuals are especially susceptible to inflammatory-based airway diseases once exposed to air pollution.