Hazard potential of perovskite solar cell technology for potential implementation of "safe-by-design" approach.

The perovskite solar cell (PSC) is a rapidly advancing solar technology with high efficiencies and low production costs. However, as the PSC contains methylammonium lead iodide (CH3NH3PbI3, MAPbI3) in the light-harvesting active layer, addressing the safety issue of PSCs is an important prerequisite for its commercialization. In this study, the potential hazards of the PSC were investigated with consideration of Pb species released from PSC using an ecotoxicity, cytotoxicity, chronic toxicity, and genotoxicity battery assay. PSC and its degradation products can cause significant toxicity, with PSC being more toxic than the individual degradation products. The order of ecotoxicity and cytotoxicity was found to be Pb2+ > PSC > PbI2 = PbO. Aquatic toxicity of PSC and its degradation products was suggested by Daphnia magna acute, chronic, and genotoxicity results. The current study highlights the non-negligible hazard potentialities of the PSC and its degradation products, as evidenced by our ecotoxicity and cytotoxicity battery assay. Our study indicates that great caution should be taken in the mass production of PSCs and could facilitate proper risk assessment. Based on our study, some considerations on the implementation of the "safe-by-design (SbD)" approach for the sustainable development of PSC technology can be formulated.

Tuning the Structural Color of a 2D Photonic Crystal Using a Bowl-like Nanostructure.

Structural colors of the ordered photonic nanostructures are widely used as an effective platform for manipulating the propagation of light. Although several approaches have been explored in attempts to mimic the structural colors, improving the reproducibility, mechanical stability, and the economic feasibility of sophisticated photonic crystals prepared by complicated processes continues to pose a challenge. In this study, we report on an alternative, simple method for fabricating a tunable photonic crystal at room temperature. A bowl-like nanostructure of TiO2 was periodically arranged on a thin Ti sheet through a two-step anodization process where its diameters were systemically controlled by changing the applied voltage. Consequently, they displayed a broad color distribution, ranging from red to indigo, and the principal reason for color generation followed the Bragg diffraction theory. This noncolorant method was capable of reproducing a Mondrian painting on a centimeter scale without the need to employ complex architectures, where the generated structural colors were highly stable under mechanical or chemical influence. Such a color printing technique represents a potentially promising platform for practical applications for anticounterfeit trademarks, wearable sensors, and displays.

Magnetite- and maghemite-induced different toxicity in murine alveolar macrophage cells.

The unique properties of nanoparticles and biological systems are important factors affecting the biological response following nanoparticle exposure. Iron oxide nanoparticles are classified mainly as magnetite (M-FeNPs) and maghemite (NM-FeNPs). In our previous study, NM-FeNPs induced autophagic cell death in RAW264.7, a murine peritoneal macrophage cell line, which has excellent lysosomal activity. In this study, we compared the toxicity of M-FeNPs and NM-FeNPs in MH-S, a murine alveolar macrophage cell line, which has relatively low lysosomal activity. At 24 h post-exposure, M-FeNPs decreased cell viability and ATP production, and elevated the levels of reactive oxygen species, nitric oxide, and pro-inflammatory cytokines to a higher extent than NM-FeNPs. Damage of mitochondria and the endoplasmic reticulum and the down-regulation of mitochondrial function and transcription-related genes were also higher in cells exposed to M-FeNPs than in cells exposed to NM-FeNPs (50 µg/ml). In addition, cells exposed to M-FeNPs (50 µg/ml) showed an increase in the number of autophagosome-like vacuoles, whereas cells exposed to NM-FeNPs formed large vacuoles in the cytosol. However, an autophagy-related molecular response was not induced by exposure to either FeNPs, unlike the results seen in our previous study with RAW264.7 cells. We suggest that M-FeNPs induced higher toxicity compared to NM-FeNPs in MH-S cells, and lysosomal activity plays an important role in determining cell death pathway.

ERK pathway is activated in bare-FeNPs-induced autophagy.

Iron oxide nanoparticles (FeNPs) are known to be one of the most biocompatible and safe nanoparticles. However, their long-term persistence remains a problem, and macrophages play as an important mediator in continuous stimulation of the immune system due to biopersistence of nanoparticles. In the present study, we identified the mechanisms underlying the uptake and toxicity of bare-FeNPs using RAW264.7 cells, a mouse peritoneal macrophage cell line. The bare-FeNPs penetrated the cell membrane through electrostatic interactions together with the general phagocytic pathway. At 24 h after exposure, they distributed freely in the cytosol or within autophagosome-like vacuoles. Bare-FeNPs induced decrease in the cell viability along with the cell cycle arrest in G1 phase. In addition, they increased the generation of ROS and the secretion of NO and TNF alpha as well as the expression of SOD-1 and SOD-2 proteins, which are an antioxidant. While the mitochondrial calcium level, the intensity of labeled mitochondria, and ATP production decreased, the levels of autophagy-related proteins such as p62, beclin 1, ATG5, and LC3B increased in a dose-dependent manner together with the levels of ATF 3, p-EGFR, and p-ERK proteins. However, the level of p-JNK protein clearly decreased. TEM images also showed that damaged organelle exist within autophagosome-like vacuoles with bare-FeNPs. On the basis of these results, we suggest that bare-FeNPs induce autophagy by initiating oxidative stress in RAW264.7 cells. Furthermore, ERK, but not JNK, pathway is activated in bare-FeNPs-induced autophagy.