Biomedical Engineering Reference
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toxic to humans. Experimental studies signified that CNTs have the potential to induce adverse
pulmonary effects, including alveolitis, fibrosis, and genotoxicity in epithelial cells. In vitro experi-
ments on rat lung epithelial cells showed that the acute pulmonary toxicity and the genotoxicity of
CNTs were reduced upon heating but restored upon grinding, suggesting that the intrinsic toxicity
of CNTs is mainly mediated by the presence of defective sites in their carbon framework [75,76].
After 30- and 60-day inhalation exposures, the pulmonary toxicity of MWCNTs was assessed
using biochemical indices in bronchoalveolar lavage fluid and pathological examinations [77]. It
was found that the aerosolized MWCNTs did not induce obvious pulmonary toxicities in the 30-day
exposure group, but induced severe pulmonary toxicity in the 60-day exposure group.
The drastic, dose-dependent cytotoxicity of SWCNTs was noticed in alveolar macrophages sepa-
rated from guinea pigs in vitro for 6 h. The macrophages exposed to SWCNTs or MWCNTs showed
characteristic features of apoptosis at different dosages, toxic responses being more with SWCNTs
than with the MWCNTs, quartz, or fullerene used in this study [48,78]. There are reports showing
contradictory results of CNT cytotoxicity to macrophages. The intratracheal or pharyngeal instilla-
tions of a SWCNT suspension in mice caused a persistent accumulation of CNT aggregates in the
lung, followed by the rapid formation of pulmonary granulomatous and fibrous tissues at the site; it
also produced cardiovascular toxicity. A brief account of toxicity issues associated with CNTs are
briefed in Table 11.1.
TABLE 11.1
Pulmonary Toxicities of SWCNTs and MWCNTs
Type of
CNT
Studies Performed on
Animal Species/Cells
Toxicity Noticed
Reference
SWCNTs
B6C3F1 mice
Generation of interstitial granulomas and associated lung injuries
[71]
C57BL mice
Production of granulomatous fibrosis with thickening of alveolar
walls, increment in count of alveolar type II cells and damage of
pulmonary cells
[74]
Albino Wistar rats
Formation of lung granuloma with approximately 15% death of
instilled rats within one day
[109]
C57BL mice
Production of pulmonary fibrous tissues with cardiovascular toxicity
[48]
C57BL mice
Raised count of inflammatory cells, raised LDH release, leukocytes
count, and raised levels of proinflammatory cytokines (tumor
necrosis factor-α (TNF-α) and interleukin-6, (IL-6)) with
enhanced profibrotic response
[74]
CR mice
Activation of alveolar macrophages, initiation of several chronic
inflammatory responses with severe granuloma
[70]
Trout fish
Severe respiratory toxicity including raised mucus secretion, bulged
mucocytes on gills with significantly increased ventilation rates
[73]
MWCNTs
Sprague-Dawley rats
Authors observed significant protein exudation on peritoneal side of
diaphragm with drastically increased inflammatory and fibrotic
response. Stimulated production of TNF-α was also reported
[66]
Albino Wistar rats
Alveolitis, fibrosis with genotoxicity in epithelial cells
[75]
Wistar rats
Acute pulmonary toxicity
[66]
Wistar rats/lung
epithelial cells
Adverse pulmonary effects, including alveolitis, fibrosis, and
genotoxicity in epithelial cells. In vitro experiments showed acute
pulmonary toxicity and the genotoxicity of CNTs
[76]
NR8383 and human
A549 lung cell lines
Formation of reactive oxygen species in rat macrophages
[60,72]
Epidermal keratinocytes
(HaCaTs) cells
Loss of cell viability, including ultrastructural and morphological
changes
[74]
 
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