Bioavailability of Nickel in Single‐Wall Carbon Nanotubes

Abstract

The world-wide nanotechnology movement is devoting a rapidly growing literature on biological interactions of carbon nanotubes (CNTs), however the conflicting data have emerged about the biocompatibility and toxicity of carbon nanotubes, and there is no consensus on the overall risk to human health (Hurt et al., 2006; Smart et al., 2006). To resolve this issue, further study is needed, with particular emphasis on understanding the material features of carbon nanotubes, such as size, shape, surface chemistry, and metals content, and we hypothesize that some of the conflicting toxicity data are due to real sample-to-sample variation in these material properties. It is also unclear whether carbon nanotube catalyst residues can trigger these toxicity mechanisms due to apparent encapsulation of the nickel within carbon shells. Nickel, the majority component in Ni-Y catalysts commonly used in the commercial synthesis of single-wall nanotubes (SWNTs) (Journet et al. 1997), is an established human carcinogen that induces gene silencing and hypoxia signaling through mechanisms involving intracellular nickel cation. The early toxicology literature includes nickle effects in SWNT by Lam et al, nickel nanoparticles and mostly nickel compounds such as nickel subsulfide (Lam et al. 2004; Zhang et al. 1998; Costa et al. 2005). Models of nickel induced respiratory tumors suggests that cellular bioavailability of nickel (the delivery of Ni (II) ions to the nucleus of target epithelial cells) is the major determinant for the carcinogenicity of nickel. A key material science question, therefore, is whether sufficient Ni (II) ion can be released from CNT samples. Moreover, the ability of various nickel compounds to be taken up by cells directly influences intracellular nickel levels, and their carcinogenic activity is proportional to cellular uptake(Oller et al., 1997; Costa et al., 1980). Soluble nickel ions can be transported directly, and insoluble or relatively insoluble nickel compounds can be taken up as particles by endocytosis or phagocytosis. Phagocytosis/endocytosis of poorly soluble nickel compounds such as Ni