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410 Potential Impacts of Nanomaterials
(Gelis et al., 2003). On the other hand, TiO is also a well-known pho-
2
tocatalyst (see Chapter 5).
TiO absorbs UVA light, catalyzing the generation of reactive oxygen
2
species, such as superoxide anion radicals, hydrogen peroxide, free
hydroxyl radicals, and singlet oxygen in aqueous media. These hydroxyl
radicals are known to initiate oxidation. Using chemical methods, it
has been shown that TiO sunscreen samples catalyze the photo-
2
oxidation of some organic substrate (e.g., phenol) (Dunfort et al., 1997).
Because of its photocatalytic properties, TiO has been applied in the
2
environment and wastewater as a disinfectant. Recently, TiO was used
2
as a photosensitizer for photodynamic therapy for endobronchial and
esophageal cancers.
Several studies have shown that the cytotoxicity of nano-sized TiO 2
was very low or negligible as compared with other nanoparticles (Peters
et al., 2004; Yamamoto et al., 2004; Zhang et al., 1998), and size alone
was not the effective predictor of cytotoxicity (Yamamoto et al., 2004).
Other studies have evaluated the effects of five different nanoscaled
particles (PVC, TiO , SiO , Co, Ni) on endothelial cell function and via-
2
2
bility. TiO nanoparticles did not show significant cytotoxic or inflam-
2
matory effects, although some proinflammatory effects were observed
in human endothelial cells (Peters et al., 2004).
As TiO reflects and scatters UVB and UVA in sunlight, nano-sized
2
TiO is used in numerous sunscreens. However, it has been noted that
2
sunlight-illuminated TiO catalyses DNA damage both in vitro and in
2
human cells. These results may be relevant to the overall effects of sun-
screens because without UV irradiation, DNA damage was not observed
(Dunfort et al., 1997).
nanoparticles have been shown to be photogenotoxic, but little
TiO 2
information has been published on the genotoxic properties of unirra-
diated TiO nanoparticles. Studies have reported that TiO nanoparti-
2
2
cles can induce apoptosis and micronuclei formation, these changes are
known to reveal numerical and/or structural chromosomal damage in
Syrian hamster embryo fibroblast (Rahman et al., 2002).
In the absence of photoactivation, nanoscale TiO (10 and 20 nm) in
2
the anatase form can induce lipid peroxidation and oxidative DNA
damage, and increase cellular nitric oxide and hydrogen peroxide
levels in BEAS-2B, a human bronchial epithelial cell line. Fpg (for-
mamidopyrimidine [fapy]-DNA glycosylase)-digestible DNA adducts
were detected in treatment with anatase TiO (10 nm) particles, but
2
oxidative DNA damage was not detected with >200 nm particles. The
size of the particles and the crystalline form are extremely important
factors as 200 nm rutile size particles can induce oxidative DNA
damage. Concomitantly, levels of cellular melanodialdehyde (MDA), a
major end-product of lipid peroxidation, increased following 10 and 20 nm

