via aerial exposure. Thus, besides through the roots (aquatic and soil exposure), the
interactions between atmospheric CNPs and plants through the leaves (i.e., aerial/
rain deposition) were examined to provide more comprehensive and informative
picture on the actual influences of CNPs contamination toward plants.
Findings highly suggested that CNPs could be adsorbed on and further incorporated in leaves through both powder and suspension spraying (Birbaum et al. 2010;
Hong et al. 2014; Jie et al. 2016; Ma et al. 2018; Salehi et al. 2017). An effective
uptake and translocation of CNPs through leaves to the plants tissues was observed
in Lactuca sativa (Ma et al. 2018), cucumber (Hong et al. 2014; Ma et al. 2017), and
Phaseolus vulgaris L. (Salehi et al. 2017), while contradicted results of Birbaum
et al. in maize plants were reported (Birbaum et al. 2010). In Ma et al., no significant
difference in plant growth between the control and group treated with foliar exposure
was detected (Ma et al. 2018). However, Hong et al. revealed that low concentrations
of CNPs (40 and 160 mg/L) in contact with leaves could interfere the enzyme
activities, whereas high concentration (320 mg/L) caused toxicity (Hong et al.
2014; Jie et al. 2016). These results were further evidenced by Salehi et al. through
morphological, proteomic, and metabolomic data (Salehi et al. 2017). These marked
differences could be related to the influencing factors such as the plant species, size
and type of CNPs, as well as environmental conditions (e.g., wind, moisture).
Particularly, the exposure route of airborne was suggested to pose a more marked
effect toward bean than soil exposure (Salehi et al. 2017). Besides, when exposed
through foliage, the differences in particle size were less significant compared to
root-based exposure (Jie et al. 2016). These strong differences are because CNPs
might be modulated by hydroponic cultures or soil factors such as pH, root exudates,
and microorganisms (Thill et al. 2006; Xu et al. 2018). Then, the bioavailability,
influenced by adsorption-desorption and mobility processes in soil, would be limited, thus decreasing the root uptake (Cornelis et al. 2011).
In addition to the plants, the increased ambient air concentrations of CNPs could
also contribute to the exposure of animals and humans. Most studies on the health
effects of CNPs pay attention to the lung cells, since the most likely route of
exposure is through inhalation (Cassee et al. 2011). The uptake of 20–50 nm
CNPs by human lung 3T3 fibroblasts was examined in vitro, and results showed
that CNPs internalization occurred linearly with exposure time at concentrations as
low as 100 ng/g cells (Limbach et al. 2005). The tissue distribution of inhaled CNPs
in rats was determined in a 28-day exposure study. After 6 h exposure, CNPs were
translocated to the liver, kidney, spleen, brain, testis, and epididymis (Geraets et al.
2012). The biotransformation of CNPs in the vasculature of rat’s brain was
conducted by EELS, and the ratio of Ce
3+ /Ce
4+ was not changed after 20 h (Hardas
et al. 2010). However, when the liver was tested by HRTEM after 90 days, CNPs
showed rounded edges and corners with the increased surface Ce
3+ (Graham et al.
2015), which was described as the basis of the genotoxicity toward human fibroblasts (Auffan et al. 2009). The toxic effects of CNPs on human mesothelioma were
examined by measuring metabolic activity and cell proliferation, which showed that
the metabolic activity and DNA content reduced by approximately 50% after 3 days
of exposure (Brunner et al. 2006).
Surface Properties and Environmental Transformations Controlling the. . .
181
interactions between atmospheric CNPs and plants through the leaves (i.e., aerial/
rain deposition) were examined to provide more comprehensive and informative
picture on the actual influences of CNPs contamination toward plants.
Findings highly suggested that CNPs could be adsorbed on and further incorporated in leaves through both powder and suspension spraying (Birbaum et al. 2010;
Hong et al. 2014; Jie et al. 2016; Ma et al. 2018; Salehi et al. 2017). An effective
uptake and translocation of CNPs through leaves to the plants tissues was observed
in Lactuca sativa (Ma et al. 2018), cucumber (Hong et al. 2014; Ma et al. 2017), and
Phaseolus vulgaris L. (Salehi et al. 2017), while contradicted results of Birbaum
et al. in maize plants were reported (Birbaum et al. 2010). In Ma et al., no significant
difference in plant growth between the control and group treated with foliar exposure
was detected (Ma et al. 2018). However, Hong et al. revealed that low concentrations
of CNPs (40 and 160 mg/L) in contact with leaves could interfere the enzyme
activities, whereas high concentration (320 mg/L) caused toxicity (Hong et al.
2014; Jie et al. 2016). These results were further evidenced by Salehi et al. through
morphological, proteomic, and metabolomic data (Salehi et al. 2017). These marked
differences could be related to the influencing factors such as the plant species, size
and type of CNPs, as well as environmental conditions (e.g., wind, moisture).
Particularly, the exposure route of airborne was suggested to pose a more marked
effect toward bean than soil exposure (Salehi et al. 2017). Besides, when exposed
through foliage, the differences in particle size were less significant compared to
root-based exposure (Jie et al. 2016). These strong differences are because CNPs
might be modulated by hydroponic cultures or soil factors such as pH, root exudates,
and microorganisms (Thill et al. 2006; Xu et al. 2018). Then, the bioavailability,
influenced by adsorption-desorption and mobility processes in soil, would be limited, thus decreasing the root uptake (Cornelis et al. 2011).
In addition to the plants, the increased ambient air concentrations of CNPs could
also contribute to the exposure of animals and humans. Most studies on the health
effects of CNPs pay attention to the lung cells, since the most likely route of
exposure is through inhalation (Cassee et al. 2011). The uptake of 20–50 nm
CNPs by human lung 3T3 fibroblasts was examined in vitro, and results showed
that CNPs internalization occurred linearly with exposure time at concentrations as
low as 100 ng/g cells (Limbach et al. 2005). The tissue distribution of inhaled CNPs
in rats was determined in a 28-day exposure study. After 6 h exposure, CNPs were
translocated to the liver, kidney, spleen, brain, testis, and epididymis (Geraets et al.
2012). The biotransformation of CNPs in the vasculature of rat’s brain was
conducted by EELS, and the ratio of Ce
3+ /Ce
4+ was not changed after 20 h (Hardas
et al. 2010). However, when the liver was tested by HRTEM after 90 days, CNPs
showed rounded edges and corners with the increased surface Ce
3+ (Graham et al.
2015), which was described as the basis of the genotoxicity toward human fibroblasts (Auffan et al. 2009). The toxic effects of CNPs on human mesothelioma were
examined by measuring metabolic activity and cell proliferation, which showed that
the metabolic activity and DNA content reduced by approximately 50% after 3 days
of exposure (Brunner et al. 2006).
Surface Properties and Environmental Transformations Controlling the. . .
181