[Carbon nanotubes (CNT) and nanoparticles (NP): interaction with lung epithelium and other biological systems]

Abstract

Carbon nanotubes (CNT) and nanoparticles (NP) represent new classes of technological materials with innovative properties. Although inhalation is less likely for engineered nanomaterials (NM) compared with ambient or mineral dust particles, this can happen during bulk manufacture and handling of freely dispersable NP at workplace. Both environmental and engineered NP are able to cause oxidative stress, reactive oxygen species (ROS) generation, NF-kappaB activation, but some of the possible NM interactions with biological systems may result in additional forms of injury. NP can impair fagocytosis, can enhance macrophage sensitivity to chemotactic factors (MCP-1), thus worsening antigen-mediated inflammation. Metal NP (e.g. TiO2, Al2O3 and Fe3O4) can impair mitochondrial function, leading to a dramatic reduction of the intracellular glutathione pool, thus compromising cell viability and morphology. CNTs are a man-made form of crystalline carbon currently attracting intense research efforts because of their unique properties, that make them suitable for many uses in biomedicine and pharmacology. CNTs stimulate TNF-alpha production in the lung, inducing inflammatory reactions, but they can also cross cell membranes reacting with DNA and aminoacidic residues, leading to cell apoptosis. Larger CNTs could have features of conventional fibers and show the ability to stimulate mesenchymal cell growth and to cause lung granulomas formation and fibrotic reactions. These results suggest that NM are potentially hazardous to humans and that strict industrial hygiene measures should be taken to limit exposure during their manipulation.