The in vitro absorption of microfine zinc oxide and titanium dioxide through porcine skin.
ABSTRACT Microfine metallic oxides such as titanium dioxide or zinc oxide have been found to be highly protective against harmful UV rays. Because their long-term use could potentially lead to health effects if significant amounts of these microfine metallic oxides would be absorbed through the skin, the in vitro absorption of microfine zinc oxide and titanium oxide in cosmetic formulations through porcine skin was investigated. In the experiments with a microfine zinc oxide formulation, the mean total recoveries of Zn were in the range from 102% to 107% of the total Zn applied. Virtually the total amount of applied Zn was recovered in the first five tape strips. The amounts of Zn found in the skin membrane and the receptor fluid were comparable in untreated, vehicle treated or test substance treated skin preparations. The absorption-time plots from diffusion cells treated with the vehicle did not differ from those treated with the ZnO containing formulation. In the experiments with microfine titanium dioxide formulations T-Lite SF-S and T-Lite SF, mean total recoveries of Ti ranged from 98% to 100% and 86% to 93% of the total Ti applied, respectively. Virtually the total amount of applied Ti could be removed from the skin surface by washing. The amounts of titanium found in the tape strips and skin preparations were in the order of the analytical determination limit. No Ti was found in the receptor fluid at any sampling time. The results show that neither zinc or titanium ions nor microfine zinc oxide or titanium dioxide particles were able to penetrate porcine stratum corneum. Therefore, from the absence of internal exposure we conclude that their use in sunscreens does not pose a health risk.
Chapter: Chapter 11 - Skin[Show abstract] [Hide abstract]
ABSTRACT: The role of the skin as a potential route of exposure to nanomaterials is described in the present chapter. Most studies suggest minimal skin penetration and little to no systemic exposure. However, they also show that nanoparticle (NP) size, shape, charge, surface properties, and vehicle as well as animal species are very important determinants as to whether or not NP can traverse through the rate-limiting lipid barrier of the stratum corneum. Long-term in vivo studies in humans or animals are desperately needed because in vitro cell systems and differences in animal species present several limitations to a complete understanding of NP penetration through the skin. This will be a major challenge in understanding the safety of nanomaterials.Adverse Effects of Engineered Nanomaterials, Edited by Shvedova, Bengt FadeelAntonio PietroiustiAnna A, 01/2012: pages 185-207; Academic Press., ISBN: 9780123869401
Archives des Maladies Professionnelles et de l Environnement 11/2013; 74(5):488-498. DOI:10.1016/j.admp.2013.05.003 · 0.09 Impact Factor
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ABSTRACT: Abstract The increasing risk of incidental exposure to nanomaterials has led to mounting concerns regarding nanotoxicity. Zinc oxide nanoparticles (ZnO NPs) are produced in large quantities and have come under scrutiny due to their capacity to cause cytotoxicity in vitro and potential to cause harm in vivo. Recent evidence has indicated that ZnO NPs promote autophagy in cells; however, the signaling pathways and the role of ion release inducing toxicity remain unclear. In this study, we report that ZnO NPs are immunotoxic to primary and immortalized immune cells. Importantly, such immunotoxicity is observed in mice in vivo, since death of splenocytes is seen after intranasal exposure to ZnO NPs. We determined that ZnO NPs release free Zn(2+) that can be taken up by immune cells, resulting in cell death. Inhibiting free Zn(2+) ions in solution with EDTA or their uptake with CaCl2 abrogates ZnO NP-induced cell death. ZnO NP-mediated immune cell death was associated with increased levels of intracellular reactive oxygen species (ROS). ZnO NP death was not due to apoptosis, necroptosis or pyroptosis. Exposure of immune cells to ZnO NPs resulted in autophagic death and increased levels of LC3A, an essential component of autophagic vacuoles. Accordingly, ZnO NP-mediated upregulation of LC3A and induction of immune cell death were inhibited by blocking autophagy and ROS production. We conclude that release of Zn(2+) from ZnO NPs triggers the production of excessive intracellular ROS, resulting in autophagic death of immune cells. Our findings suggest that exposure to ZnO NPs has the potential to impact host immunity.Nanotoxicology 11/2014; DOI:10.3109/17435390.2014.974709 · 7.34 Impact Factor