It has been concluded that acute CNPs exposure from hours up to 1 day via the
inhalation route might induce cytotoxicity via oxidative stress and would lead to a
chronic inflammatory response, while the levels of exposure concentration are orders
of magnitude higher than the real condition in the environment (Yokel et al. 2014).
An inhalation study in mice exhibited that at an aerosol concentration of 2 mg/m
3 for
7, 17, or 28 days, CNPs can induce pulmonary and extrapulmonary toxicity
(Aalapati et al. 2014). When a truly nanoscale aerosol exposure atmosphere was
used, inflammation of neutrophils after 24 h exposure was observed, while the
markers of pulmonary response returned to the control levels 84 days post-exposure
(Demokritou et al. 2013). Fall et al. (2007) also explored the biological influence of
engine emissions using a CNPs fuel additive compared to that of a reference fuel and
an organotypic culture of lung slices from rat. The authors demonstrated that the
biological impacts of CNPs fuel additive are very limited and there was no influence
of CNPs aerosol on lung tissue viability. Similarly, Park et al. (2008a) also concluded that no effects were observed on the viability of the lung tissue slices when
exposed to a continuous flow of CNPs aerosol. However, with longer exposure
duration, accumulation can occur and lead to a dose that causes adverse health
effects. Regrettably, there is no data on the inhalation toxicity of chronic exposure
to CNPs under realistic conditions.
In summary, CNPs could penetrate the leaf surface through aerosol exposure,
while their translocation through the leaf tissue and adverse effects are contradictory
among studies under various test conditions. Besides, pulmonary exposure to high
concentrations of CNPs led to pulmonary inflammation and alveolar interstitial
fibrosis. Considering the risks that atmospheric CNPs could be directly stored in
or adsorbed by the fruit of plants, the skin or lung, studies are needed to determine
the chronic threat for environmental and human health through trophic transfer and
inhalation.
4 Chemical Transformation of CNPs Core and Associated
Effects on Toxicity
The formation of environmentally relevant Ce species described in Sect. 3 has been
investigated to partly evaluate the impact of such transformations on toxicity. In
some cases, these transformations may promote toxicity potential (e.g., dissolution
reactions that produce excessive ROS) (Seal 2008). In other cases, these transformations have been shown to reduce effects (e.g., the formation of CePO 4
decreased the cytotoxicity of CNPs toward wastewater biofilm (Xu et al. 2018)
and plants (Zhang et al. 2016). Some transformations can potentially limit CNPs
persistence in the environment (e.g., dissolution and redox reactions). Importantly,
many transformations are slow or irreversible and cannot necessarily be predicted
using thermodynamics. Thus, some main transformations are discussed in more
in-depth in the following sections.
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G. You et al.
inhalation route might induce cytotoxicity via oxidative stress and would lead to a
chronic inflammatory response, while the levels of exposure concentration are orders
of magnitude higher than the real condition in the environment (Yokel et al. 2014).
An inhalation study in mice exhibited that at an aerosol concentration of 2 mg/m
3 for
7, 17, or 28 days, CNPs can induce pulmonary and extrapulmonary toxicity
(Aalapati et al. 2014). When a truly nanoscale aerosol exposure atmosphere was
used, inflammation of neutrophils after 24 h exposure was observed, while the
markers of pulmonary response returned to the control levels 84 days post-exposure
(Demokritou et al. 2013). Fall et al. (2007) also explored the biological influence of
engine emissions using a CNPs fuel additive compared to that of a reference fuel and
an organotypic culture of lung slices from rat. The authors demonstrated that the
biological impacts of CNPs fuel additive are very limited and there was no influence
of CNPs aerosol on lung tissue viability. Similarly, Park et al. (2008a) also concluded that no effects were observed on the viability of the lung tissue slices when
exposed to a continuous flow of CNPs aerosol. However, with longer exposure
duration, accumulation can occur and lead to a dose that causes adverse health
effects. Regrettably, there is no data on the inhalation toxicity of chronic exposure
to CNPs under realistic conditions.
In summary, CNPs could penetrate the leaf surface through aerosol exposure,
while their translocation through the leaf tissue and adverse effects are contradictory
among studies under various test conditions. Besides, pulmonary exposure to high
concentrations of CNPs led to pulmonary inflammation and alveolar interstitial
fibrosis. Considering the risks that atmospheric CNPs could be directly stored in
or adsorbed by the fruit of plants, the skin or lung, studies are needed to determine
the chronic threat for environmental and human health through trophic transfer and
inhalation.
4 Chemical Transformation of CNPs Core and Associated
Effects on Toxicity
The formation of environmentally relevant Ce species described in Sect. 3 has been
investigated to partly evaluate the impact of such transformations on toxicity. In
some cases, these transformations may promote toxicity potential (e.g., dissolution
reactions that produce excessive ROS) (Seal 2008). In other cases, these transformations have been shown to reduce effects (e.g., the formation of CePO 4
decreased the cytotoxicity of CNPs toward wastewater biofilm (Xu et al. 2018)
and plants (Zhang et al. 2016). Some transformations can potentially limit CNPs
persistence in the environment (e.g., dissolution and redox reactions). Importantly,
many transformations are slow or irreversible and cannot necessarily be predicted
using thermodynamics. Thus, some main transformations are discussed in more
in-depth in the following sections.
182
G. You et al.