tests (cytotoxicity, human bioaccessibility, and oxidative potential). They classified
the toxicity of particles as CdCl 2 > CdO > CuO > PbO > ZnO > PbSO 4 > Sb 2 O 3 .
Several studies revealed elevated levels of heavy metal(loid)s in blood upon human
exposure to airborne dust/PM (Acton 2012; Li et al. 2015). Uzu et al. (2011a, b)
evaluated human Pb toxicity and bioaccessibility after its emissions from a Pb
recycling plant. They reported that the process Pb-PM displayed differences in
granulometry, metal content, and percentage of inhalable fraction depending on
their origin (refining, furnace, and emissions) and PM size (PM 10 , PM 2.5 , PM 1 ,
and PM 0.1 ). They reported that the finest Pb-PM 1 induced the most significant
pro-inflammatory effect in human bronchial epithelial cells.
Heavy metal(loid)s are considered as highly harmful to the human even at low
levels of exposure. This is because of the fact that humans do not have an effective
tolerance or excretion mechanism for these metal(loid)s. Metal-PM generates ROS
(reactive oxygen species) in human beings and induces different associated diseases
(Valavanidis et al. 2005). When human beings are exposed to metal-PM, oxidative
stress rises pulmonary pathology through airway inflammation (Ghio et al. 2012).
Squadrito et al. (2001) found the induction of ROS when heavy metal(loid)-enriched
PM is deposited in the lungs after inhalation from the atmosphere. These ROS,
overproduced due to heavy metal(loid) toxicity, cause oxidative stress and deleterious effects at the deposition site (Fryzova et al. 2018). Apart from direct ROS
generation by the airborne PM, ROS can also be generated by interacting with the
cells on which PM is deposited such as epithelial cells of lungs and pulmonary
macrophages (Santibáñez-Andrade et al. 2017; Valavanidis et al. 2013).
One of the main toxic effects of heavy metal(loid)s deposition inside the human
body is induced by their ability to bind to biomembrane structures, modifying their
function. For example, Pb has been reported to react with thiol (SH) groups,
resulting in damage to glutathione (GSH) (Gurer-Orhan et al. 2004). Glutathione
is a cellular antioxidant and plays a key role to scavenge ROS by taking part in
bio-reductive reactions (Shahid et al. 2017a). In this way, GSH protects cells from
oxidative stress. Thus, metal-PM ingestion into the human body is linked with
oxidative stress, which is generally considered a secondary mechanism of metalPM toxicity (Cho et al. 2005; Uzu et al. 2011b). Numerous studies have confirmed
the association of metal-PM ingestion with oxidative stress by using both in vitro
biological assays (respiratory epithelial or macrophages cells) (Baulig et al. 2004)
and cellular assays (Dithiothreitol test) (Cho et al. 2005).
7 Management Strategies to Reduce Air Contamination
by Metal-PM
Keeping in view the health risks associated with the atmospheric contamination
and deposition of metal-PM on terrestrial ecosystem, it is highly necessary to
control and manage the atmospheric environment. The management of atmospheric
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M. Shahid et al.
the toxicity of particles as CdCl 2 > CdO > CuO > PbO > ZnO > PbSO 4 > Sb 2 O 3 .
Several studies revealed elevated levels of heavy metal(loid)s in blood upon human
exposure to airborne dust/PM (Acton 2012; Li et al. 2015). Uzu et al. (2011a, b)
evaluated human Pb toxicity and bioaccessibility after its emissions from a Pb
recycling plant. They reported that the process Pb-PM displayed differences in
granulometry, metal content, and percentage of inhalable fraction depending on
their origin (refining, furnace, and emissions) and PM size (PM 10 , PM 2.5 , PM 1 ,
and PM 0.1 ). They reported that the finest Pb-PM 1 induced the most significant
pro-inflammatory effect in human bronchial epithelial cells.
Heavy metal(loid)s are considered as highly harmful to the human even at low
levels of exposure. This is because of the fact that humans do not have an effective
tolerance or excretion mechanism for these metal(loid)s. Metal-PM generates ROS
(reactive oxygen species) in human beings and induces different associated diseases
(Valavanidis et al. 2005). When human beings are exposed to metal-PM, oxidative
stress rises pulmonary pathology through airway inflammation (Ghio et al. 2012).
Squadrito et al. (2001) found the induction of ROS when heavy metal(loid)-enriched
PM is deposited in the lungs after inhalation from the atmosphere. These ROS,
overproduced due to heavy metal(loid) toxicity, cause oxidative stress and deleterious effects at the deposition site (Fryzova et al. 2018). Apart from direct ROS
generation by the airborne PM, ROS can also be generated by interacting with the
cells on which PM is deposited such as epithelial cells of lungs and pulmonary
macrophages (Santibáñez-Andrade et al. 2017; Valavanidis et al. 2013).
One of the main toxic effects of heavy metal(loid)s deposition inside the human
body is induced by their ability to bind to biomembrane structures, modifying their
function. For example, Pb has been reported to react with thiol (SH) groups,
resulting in damage to glutathione (GSH) (Gurer-Orhan et al. 2004). Glutathione
is a cellular antioxidant and plays a key role to scavenge ROS by taking part in
bio-reductive reactions (Shahid et al. 2017a). In this way, GSH protects cells from
oxidative stress. Thus, metal-PM ingestion into the human body is linked with
oxidative stress, which is generally considered a secondary mechanism of metalPM toxicity (Cho et al. 2005; Uzu et al. 2011b). Numerous studies have confirmed
the association of metal-PM ingestion with oxidative stress by using both in vitro
biological assays (respiratory epithelial or macrophages cells) (Baulig et al. 2004)
and cellular assays (Dithiothreitol test) (Cho et al. 2005).
7 Management Strategies to Reduce Air Contamination
by Metal-PM
Keeping in view the health risks associated with the atmospheric contamination
and deposition of metal-PM on terrestrial ecosystem, it is highly necessary to
control and manage the atmospheric environment. The management of atmospheric
94
M. Shahid et al.