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tumour necrosis factor alpha (Brown
et al.
, 2004). The cationic nanoparti-
cles, including gold and polystyrene, have shown to cause haemolysis and
blood clotting, while usually anionic particles are quite non-toxic. High
exposures to diesel exhaust particles (DEPs) by inhalation caused altered
heart rate in hypertensive rats interpreted as a direct effect of DEP on the
pacemaker activity of the heart (Hansen
et al.
, 2007). Exposure to single-
walled carbon nanotubes has also resulted in cardiovascular effects (Li
et al.
, 2007). The nanoparticles inhaled can gain access to the brain by
means of two different mechanisms, namely, transsynaptic transport after
inhalation through the olfactory epithelium and uptake through the blood-
brain barrier (Lockman
et al.
, 2004; Jallouli
et al.
, 2007).
In vitro
studies
have shown that multiwalled carbon nanotubes are capable of localizing
within and initiating an irritation response in human epidermal keratino-
cytes, which are a primary route of occupational exposure (Baroli
et al.
,
2007; Zvyagin
et al.
, 2008).
The change in the structural and physicochemical properties of nanopar-
ticles with a decrease in size could be responsible for numerous material
interactions that could lead to toxicological effects (Nel
et al.
, 2006); for
example, shrinkage in size may create discontinuous crystal planes that
increase the number of structural defects as well as disrupt the electronic
confi guration of the material and give rise to altered electronic properties
(Fig. 16.9). These changes could establish specifi c surface groups that could
function as reactive sites. Chemical composition of the materials is particu-
larly responsible for these changes and their importance. The surface groups
can make nanoparticles hydrophilic or hydrophobic, lipophilic or lipopho-
bic, or catalytically active or passive. These surface properties can lead to
toxicity by the interaction of electron donor or acceptor active sites (chemi-
cally or physically activated) with molecular oxygen (O
2
), and electron
capture can lead to the formation of the superoxide radical, which generates
additional reactive oxygen species (ROS) through Fenton chemistry
(Fig. 16.9).
Various studies have been carried out to investigate the adverse effects
of nanoparticle on the biological systems (N. Li
et al.
, 2003; Hoshino
et al.
,
2004; Li
et al.
, 2007; Baker
et al.
, 2008; Lyon
et al.
, 2006; Peters
et al.
, 2006)
and the interaction of nanoparticles with biological systems is represented
in Fig. 16.10. It has been demonstrated that carbon black nanoparticles
produce their increased infl ammatory effects via mechanisms other than
the leaching of soluble components from the particle surface. Transition
metals are an important source of free radicals, which are important in
PM10-stimulated lung infl ammation. Therefore, it is clear that nanoparticles
may exert their increased proinfl ammatory effects, at least in part, by modu-
lating intracellular calcium.
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