Gamer AO, Leibold E, van Ravenzwaay BThe in vitro absorption of microfine zinc oxide and titanium dioxide through porcine skin. Toxicol In Vitro 20:301-307

BASF Aktiengesellschaft, Department of Experimental Toxicology and Ecology, GVT Z 470, Carl-Bosch-Str. 38, D-67056 Ludwigshafen/Rhein, Germany.
Toxicology in Vitro (Impact Factor: 2.9). 05/2006; 20(3):301-7. DOI: 10.1016/j.tiv.2005.08.008
Source: PubMed


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.

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    • "Furthermore, it is in the viable skin where nanoparticles could be taken up by blood vessels for systemic distribution. Larger particles that tend to agglomerate, such as TiO 2 and ZnO, do not appear to present a hazard due to a lack of significant skin absorption (Gamer et al., 2006; Sadrieh et al., 2010; Cross et al., 2007; Zvyagin et al., 2008; Monteiro-Riviere et al., 2011). However , smaller particles less than 10 nm in size have been shown to occasionally reach the viable skin layers (Baroli et al., 2007). "
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    ABSTRACT: Nanomaterials are being used in cosmetic products for various effects. However, their use also raises potential safety concerns. Some of these concerns can be addressed by determining the type of nanomaterials used, as well as stability, potential for skin absorption, route of exposure, and how they are formulated in cosmetic products. There has been considerable effort internationally to harmonize approaches in order to address definitional issues and safety concerns related to the use of nanomaterials in cosmetic products. Copyright © 2015. Published by Elsevier Ltd.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 07/2015; DOI:10.1016/j.fct.2015.06.020 · 2.90 Impact Factor
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    • "In two cases TiO 2 NPs penetrated also to the stratum granulosum. Gamer et al. (2006) have investigated in vitro penetration of TiO 2 NPs in cosmetic formulations through porcine skin. TiO 2 NPs were detected on the outermost surface of the stratum corneum, but did not penetrate through porcine skin. "
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    ABSTRACT: Titanium dioxide nanoparticles (TiO2 NPs) have found many practical applications in industry and daily life. A widespread application of TiO2 NPs rises the question about safety of their use in the context of potential occupational, environmental and intentional exposure of humans and biota. TiO2 NPs easily enter the body through inhalation, cross blood-brain barrier and accumulate in the brain, especially in the cortex and hippocampus. Toxicity of these NPs and the molecular mechanisms of their action have been studied extensively in recent years. Studies showed that TiO2 NPs exposure resulted in microglia activation, reactive oxygen species production, activation of signaling pathways involved in inflammation and cell death, both in vitro and in vivo. Consequently, such action led to neuroinflammation, further brain injury. A, spatial recognition memory and locomotor activity impairment has been also observed. Copyright © 2015. Published by Elsevier Ltd.
    Toxicology in Vitro 04/2015; 29(5). DOI:10.1016/j.tiv.2015.04.004 · 2.90 Impact Factor
    • "Common in skin care products, ZnO nanoparticles (ZnO NPs) in particular have been the focus of numerous toxicity studies over the past decade. Although NPs are highly toxic in vitro (Brunner et al., 2006; Lin et al., 2009), their limited transport through the dermis would suggest a minimal health risk for the consumer via this route (Baroli et al., 2007; Gamer et al., 2006). Many manufacturing processes, however, result in dry, ultrafine particulate matter that could easily be aerosolized, making inhalation a potential route of entry. "
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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; 9(6):1-12. DOI:10.3109/17435390.2014.974709 · 6.41 Impact Factor
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