Life Cycle Impact Assessment of Solution Combustion Synthesis of Titanium Dioxide Nanoparticles and Its Comparison with More Conventional Strategies.

This paper represents the first attempt to quantitatively and reliably assess the environmental sustainability of solution combustion synthesis (SCS) with respect to other soft chemistry strategies, which are more conventionally employed in the preparation of engineered oxide nanomaterials, namely hydrolytic and non-hydrolytic sol-gel syntheses (i. e., HSGS and NHSGS). Indeed, although SCS is well known to rely on significant reduction in the energy as well as time required for the obtainment of the desired nanocrystals, its quantitative environmental assessment and a detailed comparison with other existing synthetic pathways represents an absolute novelty of high scientific desirability in order to pursue a more sustainable development in the inorganic chemistry as well as materials science research fields. TiO2 nanoparticles were selected as the material of choice, for the production of which three slightly modified literature procedures were experimentally reproduced and environmentally evaluated by the application of the comprehensive life cycle assessment (LCA) methodology. Particularly, SCS was compared from an environmental perspective with sol-gel approaches performed both in water and in benzyl alcohol. The results of the present study were also framed among those recently obtained in a systematic study assessing seven further chemical, physical, and biological routes for the synthesis of TiO2 nanoparticles, comprising also flame spray pyrolysis (typically used in industrial productions), highlighting and quantifying the excellent environmental performances of SCS.

Crystal structure determination of a lifelong biopersistent asbestos fibre using single-crystal synchrotron X-ray micro-diffraction.

The six natural silicates known as asbestos may induce fatal lung diseases via inhalation, with a latency period of decades. The five amphibole asbestos species are assumed to be biopersistent in the lungs, and for this reason they are considered much more toxic than serpentine asbestos (chrysotile). Here, we refined the atomic structure of an amosite amphibole asbestos fibre that had remained in a human lung for ∼40 years, in order to verify the stability in vivo. The subject was originally exposed to a blend of chrysotile, amosite and crocidolite, which remained in his parietal pleura for ∼40 years. We found a few relicts of chrysotile fibres that were amorphous and magnesium depleted. Amphibole fibres that were recovered were undamaged and suitable for synchrotron X-ray micro-diffraction experiments. Our crystal structure refinement from a recovered amosite fibre demonstrates that the original atomic distribution in the crystal is intact and, consequently, that the atomic structure of amphibole asbestos fibres remains stable in the lungs for a lifetime; during which time they can cause chronic inflammation and other adverse effects that are responsible for carcinogenesis. The amosite fibres are not iron depleted proving that the iron pool for the formation of the asbestos bodies is biological (haemoglobin/plasma derived) and that it does not come from the asbestos fibres themselves.

The Impact of Lipid Corona on Rifampicin Intramacrophagic Transport Using Inhaled Solid Lipid Nanoparticles Surface-Decorated with a Mannosylated Surfactant.

The mimicking of physiological conditions is crucial for the success of accurate in vitro studies. For inhaled nanoparticles, which are designed for being deposited on alveolar epithelium and taken up by macrophages, it is relevant to investigate the interactions with pulmonary surfactant lining alveoli. As a matter of fact, the formation of a lipid corona layer around the nanoparticles could modulate the cell internalization and the fate of the transported drugs. Based on this concept, the present research focused on the interactions between pulmonary surfactant and Solid Lipid Nanoparticle assemblies (SLNas), loaded with rifampicin, an anti-tuberculosis drug. SLNas were functionalized with a synthesized mannosylated surfactant, both alone and in a blend with sodium taurocholate, to achieve an active targeting to mannose receptors present on alveolar macrophages (AM). Physico-chemical properties of the mannosylated SLNas satisfied the requirements relative to suitable respirability, drug payload, and AM active targeting. Our studies have shown that a lipid corona is formed around SLNas in the presence of Curosurf, a commercial substitute of the natural pulmonary surfactant. The lipid corona promoted an additional resistance to the drug diffusion for SLNas functionalized with the mannosylated surfactant and this improved drug retention within SLNas before AM phagocytosis takes place. Moreover, lipid corona formation did not modify the role of nanoparticle mannosylation towards the specific receptors on MH-S cell membrane.

Structure Model and Toxicity of the Product of Biodissolution of Chrysotile Asbestos in the Lungs.

Asbestos is a commercial term indicating six natural silicates with asbestiform crystal habit. Of these, five are double-chain silicates (amphibole) and one is a layer silicate (serpentine asbestos or chrysotile). Although all species are classified as human carcinogens, their degree of toxicity is still a matter of debate. Amphibole asbestos species are biopersistent in the human lungs and exert their chronic toxic action for decades, whereas chrysotile is not biopersistent and transforms into an amorphous silica structure prone to chemical/physical clearance when exposed to the acidic environment created by the alveolar macrophages. There is evidence in the literature of the toxicity of chrysotile, but its limited biopersistence is thought to explain the difference in toxicity with respect to amphibole asbestos. To date, no comprehensive model describing the toxic action of chrysotile in the lungs is available, as the structure and toxic action of the product formed by the biodissolution of chrysotile are unknown. This work is aimed at fulfilling this gap and explaining the toxic action in terms of structural, chemical, and physical properties. We show that chrysotile's fibrous structure induces cellular damage, mainly through physical interactions. Based on our previous work and novel findings, we propose the following toxicity model: inhaled chrysotile fibers exert their toxicity in the alveolar space by physical and biochemical action. The fibers are soon leached by the intracellular acid environment into a product with residual toxicity, and the dissolution process liberates toxic metals in the intracellular and extracellular environment.

Biodurability and release of metals during the dissolution of chrysotile, crocidolite and fibrous erionite.

BACKGROUND: The mechanisms by which mineral fibers induce adverse effects in vivo are still not well understood. The mechanisms of fiber dissolution in the lungs and subsequent release of metals in the extracellular/intracellular environment must be taken into account. AIM: For the first time, the kinetics of release of metals during the acellular in vitro dissolution of chrysotile, crocidolite and fibrous erionite were determined. METHODS: In vitro acellular dissolution of chrysotile, crocidolite, and fibrous erionite-Na was conducted using a solution mimicking the phagolysosome environment active during the phagocytosis process (pH=4.5, at 37 °C). The kinetics of release of a representative selection of metals were determined over a period of three months. RESULTS: Despite the fact that the difference in Fe content between chrysotile and crocidolite is one order of magnitude, the much faster dissolution rate of chrysotile compared to crocidolite prompts greater release of available active surface Fe in the first weeks of the dissolution experiment and comparable amounts after 90 d. Such active iron may promote the formation of toxic hydroxyl radicals. The fast release of metals like Cr, Ni and Mn from chrysotile is also a source of concern whereas the release of V in solution is negligible. CONCLUSION: Because chrysotile undergoes fast dissolution with respect to crocidolite and fibrous erionite, it behaves like a carrier that releases its metals' cargo in the lung environment, mimicking the phenomenon that explains the toxicity of nanoparticles. Hence, the toxicity paradigm of a non biodurable fiber like chrysotile should also take into account the release of toxic metals in the intracellular/extracellular medium during the rapid dissolution process.