39
mesothelium, which is covering many of internal organs (Takagi et al. 2008). The
most difficult question is probably related to long-term fate of nanoparticles.
Concerns have risen not only related to exposure to pure nanoparticles but also
related to exposure to nanomaterial based products. Toxicity assessment of sanding
dust of paint nanocomposites containing UV-Titan approved that their inflammatory
response is relatively higher as compared to pure UV-Titan (Saber et al. 2012).
There are some other studies showing that nanotubes cause cellular toxicity, oxidative stress, decrease in cell viability, and morphological, structural, and genetic
changes in epidermal cell cultures (Ding et al. 2005).
Since titanium dioxide and carbon black nanoparticles are one of most produced
chemicals, it is quite likely to be exposed to these materials in working environment. So, it is extremely important to know their potential risks. It is probable that
significant fraction of nanoparticles gets deposited in alveolar region of lungs.
Because clearance is low, this can result in long-term inflammation and in turn,
adverse health effects. Hougaard et al. showed that 24% of titanium dioxide is
detectable in lung tissue for 5 days, while 21% of particles can be detected for
25 days after exposure, which means slow clearance (Hougaard et al. 2010). Saber
et al. have shown that inflammation is strongly related to the total surface area of
deposited nanoparticles (Saber et al. 2011). Jackson et al. performed an experiment
on mice and reported that inhaled nanoparticles resulted in increase in the lungs
(Jackson et al. 2012). It has been shown that Printex 90, a form of carbon black, is
able to induce reactive oxygen species in vitro (Jacobsen et al. 2008). The material
may result in genetic damages (Jacobsen et al. 2011).
It has been observed that NPs smaller than 50 nm (administrated by intravenous
injection) reached quickly nearly all tissues and impart potentially toxic manifestations in various tissues; on the other hand, NPs greater than 50 nm (in particular
100–200 nm positively charged particles) are readily taken up by reticuloendothelial system (RES), which refrain their path to other tissues (Gatoo et al. 2014).
Although the clearance by reticulo endothelial system safeguards other tissues, it
makes reticulo endothelial system organs such as the liver and spleen as the main
targets of oxidative stress.
One of the most common effects of nanoparticle on biological system is the
induction of oxidative stress and inflammation. There are some theories relating
biological hazards to nanoparticles. Seaton et al. (1995) claimed that ultrafine particles are responsible for the inflammation in the lung (Seaton et al. 1995). The
inflammation obstructs blood flow by creating blood clots. This is mostly associated
with cardiovascular deaths. Another possible cell damage results from free radical
production via ionization events. It has been shown that higher catalytic activity of
nanoparticles led to higher production of free radicals and in turn cellular damage.
This hazard can be in various ways such as genotoxicity and cell death (Rahman
et al. 2002).
Buckminsterfullerene, structures of carbon atoms being about 1 nm, are expected
to be highly mobile due to their tiny size. They are currently being used in drugs and
targeted drug delivery, healthcare products, energy application, cosmetic products,
polymer adaptations, and sporting goods (Aschberger 2012). With the extensive
2 Nanomaterials and Human Health
mesothelium, which is covering many of internal organs (Takagi et al. 2008). The
most difficult question is probably related to long-term fate of nanoparticles.
Concerns have risen not only related to exposure to pure nanoparticles but also
related to exposure to nanomaterial based products. Toxicity assessment of sanding
dust of paint nanocomposites containing UV-Titan approved that their inflammatory
response is relatively higher as compared to pure UV-Titan (Saber et al. 2012).
There are some other studies showing that nanotubes cause cellular toxicity, oxidative stress, decrease in cell viability, and morphological, structural, and genetic
changes in epidermal cell cultures (Ding et al. 2005).
Since titanium dioxide and carbon black nanoparticles are one of most produced
chemicals, it is quite likely to be exposed to these materials in working environment. So, it is extremely important to know their potential risks. It is probable that
significant fraction of nanoparticles gets deposited in alveolar region of lungs.
Because clearance is low, this can result in long-term inflammation and in turn,
adverse health effects. Hougaard et al. showed that 24% of titanium dioxide is
detectable in lung tissue for 5 days, while 21% of particles can be detected for
25 days after exposure, which means slow clearance (Hougaard et al. 2010). Saber
et al. have shown that inflammation is strongly related to the total surface area of
deposited nanoparticles (Saber et al. 2011). Jackson et al. performed an experiment
on mice and reported that inhaled nanoparticles resulted in increase in the lungs
(Jackson et al. 2012). It has been shown that Printex 90, a form of carbon black, is
able to induce reactive oxygen species in vitro (Jacobsen et al. 2008). The material
may result in genetic damages (Jacobsen et al. 2011).
It has been observed that NPs smaller than 50 nm (administrated by intravenous
injection) reached quickly nearly all tissues and impart potentially toxic manifestations in various tissues; on the other hand, NPs greater than 50 nm (in particular
100–200 nm positively charged particles) are readily taken up by reticuloendothelial system (RES), which refrain their path to other tissues (Gatoo et al. 2014).
Although the clearance by reticulo endothelial system safeguards other tissues, it
makes reticulo endothelial system organs such as the liver and spleen as the main
targets of oxidative stress.
One of the most common effects of nanoparticle on biological system is the
induction of oxidative stress and inflammation. There are some theories relating
biological hazards to nanoparticles. Seaton et al. (1995) claimed that ultrafine particles are responsible for the inflammation in the lung (Seaton et al. 1995). The
inflammation obstructs blood flow by creating blood clots. This is mostly associated
with cardiovascular deaths. Another possible cell damage results from free radical
production via ionization events. It has been shown that higher catalytic activity of
nanoparticles led to higher production of free radicals and in turn cellular damage.
This hazard can be in various ways such as genotoxicity and cell death (Rahman
et al. 2002).
Buckminsterfullerene, structures of carbon atoms being about 1 nm, are expected
to be highly mobile due to their tiny size. They are currently being used in drugs and
targeted drug delivery, healthcare products, energy application, cosmetic products,
polymer adaptations, and sporting goods (Aschberger 2012). With the extensive
2 Nanomaterials and Human Health