Environmental Risks of Nanomaterials - Nanotechnologies for Water Environment Applications - page 598

chemical anti-oxidants delayed macrophage aggregation responses. Shvedova et al.
(2003) reported that SWCNTs caused oxidative stress and cellular toxicity to human
epidermal keratinocytes. The oxidative stress was characterized by the formation of free
radicals, the accumulation of peroxide products, antioxidant depletion, and loss of cell
viability. Stimulating inflammatory is directly proved by skin cell culture experiments.
Cui et al. (2005) showed that SWCNTs inhibited human embryo kidney cell
proliferation, and decreased cell adhesion to the culture dish.
NMs absorbed into humans or animals by any route may cause cytotoxicity
effects, which damage DNA and protein synthesis, prevent or hinder cell division and
eventually lead to cell death. Clinic and experimental studies suggest that alveolar
translocation of NPs leads to circulatory access and allows NMs to distribute themselves
throughout the body, including the vasculature, heart, liver, spleen, and bone marrow. It
may be explained by NMs access to the blood circulation (Brook et al., 2004).
Meanwhile, dermal exposure to NMs occurs regularly. Mobility of NM-protein
complexes may lead to boosting of primary and secondary immune responses by
changing the antigen presentation function of dendritic cells.
Metal oxide NPs such as SiO 2 (Chen et al., 2004), TiO 2 (Rehn et al., 2003) and
ZnO (Gordon et al., 1992) caused pulmonary inflammation in rats. Inhalation studies of
metal oxides such as TiO 2 produced deleterious effects in rodents. Rats and mice
exposed to ultrafine TiO 2 at 10mg·m -3 resulted in pulmonary inflammation
characterized by increased numbers of macrophages and neutrophils (Bermudez et al.,
2004). The animals also retained particles in the lung for a long time after the exposure,
with 57% and 45% of the original dose (rats and mice, respectively) remaining after 52
weeks. In another study, rats exposed to ultrafine TiO 2 for two years experienced
increases in lung tumors, and agglomerates of TiO 2 particles exerted toxic effects on
alveolar macrophages (Heinrich et al., 1995). These studies suggest that exposure to
nano-TiO 2 caused rapid and sustained release of ROS, and mitochondrial depolarization,
depleted cell ATP levels, and stimulated an oxidative burst in the microglia and neurons.
Some NPs, such as CeO 2 , have been demonstrated to enter the digestive gland cells of
blue mussels and cockles by endocytosis (Moore et al., 1997). Study showed that
quantum dots were taken into the cytoplasm of eukaryotes (Chan et al., 1998).
Table 17.1 shows some results of the studies on the toxic effects of NMs. As a
surrogate to human beings, Lam et al. (2004) exposed mice to single walled carbon
nanotubes (SWCNT), and their lung injury was observed within 7 to 90 days. The mice
exposed to the highest dose (0.5 mg) experienced over 55% mortalities within 7 days of
exposure, although this may be attributed to metal toxicity because of nickel and yttrium
impurities in the SWCNTs. The mice also showed the SWCNT aggregated to form
carbon fibers in the lung. Within less than 7 days, clinically significant inflammation
was presented in the lung. These symptoms were more pronounced in mice by 90 days,