Titanium dioxide (TiO₂) nanoparticles (NPs) are manufactured worldwide in large quantities for use in a wide range of applications. TiO₂ NPs possess different physicochemical properties compared to their fine particle (FP) analogs, which might alter their bioactivity. Most of the literature cited here has focused on the respiratory system, showing the importance of inhalation as the primary route for TiO₂ NP exposure in the workplace. TiO₂ NPs may translocate to systemic organs from the lung and gastrointestinal tract (GIT) although the rate of translocation appears low. There have also been studies focusing on other potential routes of human exposure. Oral exposure mainly occurs through food products containing TiO₂ NP-additives. Most dermal exposure studies, whether in vivo or in vitro, report that TiO₂ NPs do not penetrate the stratum corneum (SC). In the field of nanomedicine, intravenous injection can deliver TiO₂ nanoparticulate carriers directly into the human body. Upon intravenous exposure, TiO₂ NPs can induce pathological lesions of the liver, spleen, kidneys, and brain. We have also shown here that most of these effects may be due to the use of very high doses of TiO₂ NPs. There is also an enormous lack of epidemiological data regarding TiO₂ NPs in spite of its increased production and use. However, long-term inhalation studies in rats have reported lung tumors. This review summarizes the current knowledge on the toxicology of TiO₂ NPs and points out areas where further information is needed.

Chromium has two main valence states: hexavalent chromium (Cr[VI]) and trivalent chromium (Cr[III]). Cr(VI), a well-established human carcinogen, can enter cells by way of a sulfate/phosphate anion-transport system, and then be reduced to lower-valence intermediates consisting of pentavalent chromium (Cr[V]), tetravalent chromium (Cr[IV]) or Cr(III) via cellular reductants. These intermediates may directly or indirectly result in DNA damage or DNA–protein cross-links. Although Cr(III) complexes cannot pass easily through cell membranes, they have the ability to accumulate around cells to induce cell-surface morphological alteration and result in cell-membrane lipid injuries via disruption of cellular functions and integrity, and finally to cause DNA damage. In recent years, more research, including in vitro, in vivo, and epidemiological studies, has been conducted to evaluate the genotoxicity/carcinogenicity induced by Cr(VI) and/or Cr(III) compounds. At the same time, various therapeutic agents, especially antioxidants, have been explored through in vitro and in vivo studies for preventing chromium-induced genotoxicity/carcinogenesis. This review aims to provide a brief update on the carcinogenicity of Cr(VI) and Cr(III) and chemoprevention with different antioxidants.

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