Table 3.
Studies on effect (human health and environment) of various types of nanoparticles
| Reference | Type of nanoparticle | Biomarker/model used | Toxicity/harmful impacts of nanoparticle |
|---|---|---|---|
| Inorganic-based Nanoparticles | |||
| Ahamed et al. [31] | Bismuth oxide (Bi2O3) | MCF-7 cell line (a human breast cancer cell line with estrogen, progesterone, and glucocorticoid receptors) |
• Reduces cell viability • Induces membrane damage Dose-dependently • Oxidative stress • Reactive Oxygen Species generation |
| Eom & Choi [32] | Fumed and porous Silicon dioxide (SiO2) | Human bronchial epithelial cell (Beas-2) |
• Oxidative stress • Induction of heme oxygenase-1 (HO-1) |
| Bengalli et al. [33] | Copper (CuO) and Zinc oxide (ZnO) | Reconstructed human epidermis model and fibroblast monolayer | • Deeply affect the epidermal tissue and the underlying dermal cells upon trans-epidermal permeation |
| Ferraro et al. [34] | Titanium dioxide (TiO2) | Human neuroblastoma (SH-SY5Y) cell line |
• Reactive Oxygen Species generation • Apoptosis • Induction of endoplasmic (ER) stress • Neurotoxicity |
| Gambardella et al. [35] | Silicon dioxide (SiO2) | Sea urchin Paracentrotus lividus sperms |
• Reduced toxicity • Neurotoxic damage • Decrease of acetylcholinesterase (AChE) expression • No effect on fertilization capability • Induced of toxic effect on the offspring |
| Yusefi-Tanha et al. [30] | Zinc oxide (ZnO) | Soil samples and Soybean seeds |
• Oxidative stress • Significant particle size-, morphology-, and concentration-dependent influence on seed yield and lipid peroxidation |
| Oh et al. [36] | Citrate-coated silver (Ag) | Human embryonic stem cell (hESC) |
• Oxidative stress • Dysfunctional neurogenesis |
| Zhao et al. [37] | Silicon dioxide (SiO2) | Lung bronchial epithelial cells (BEAS-2B) |
• Disturbs global metabolism • Oxidative stress • Generation of reactive oxygen species • Significantly perturbs mitochondrial dysfunction-related GSH metabolism and pantothenate and coenzyme A (CoA) biosynthesis • Causes abnormality in mitochondrial structure and mitochondrial dysfunction |
| Ying et al. [38] | Superparamagnetic Iron oxide (SPIO) | A3 human T lymphocytes | • Causes concentration-dependent nanotoxicity |
| Jing et al. [39] | Copper oxide (CuO) | Lung adenocarcinoma cells (A549 cells) and human bronchial epithelial cells (HBEC) |
• Significantly reduced cell viability • Increased lactate dehydrogenase (LDH) release • Reactive Oxygen species and IL-8 generation |
| Lojk et al. [40] | Silicon dioxide (SiO2), Titanium dioxide (TiO2), Silver (Ag), Polyacrylic acid (PAA) coated cobalt ferrite (CoFe2O4) | Human neuroblastoma (SH-SY5Y) cell |
• Neurotoxicity • Reactive Oxygen species formation • Membrane damage • Autophagy dysfunction for TiO2 P25 NPs • Decrease of cell viability for TiO2 FG NPs |
| Tsai et al. [41] | Titanium dioxide (TiO2) and Cerium dioxide (CeO2) | BEAS-2B epithelial cell |
• TiO2 induces apoptosis and hypersecretion of mucus • CeO2 NPs reduce cytosolic Ca2+ changes and mitochondrial damage caused by TiO2 NPs |
| Sramkova et al. [42] | Titanium dioxide (TiO2), Silicon dioxide (SiO2), magnetite (Fe3O4) and gold (Au) | Human renal proximal tubule epithelial TH1 cell line |
• None of the NPs induced any DNA strand breaks and oxidative DNA lesions regardless of the exposure (static and dynamic conditions) • No cytotoxicity was observed, except for Fe3O4NPs |
| Bell et al. [43] | Silicon dioxide (SiO2) |
SH-SY5Y human neuroblastoma (ATCC CRL-2266) Human epithelial type-2 (HEp-2) cells (ATCC CCL-23) |
• Destabilizes mitochondrial membrane potential • stimulates reactive oxygen species production • Promotes cytotoxicity |
| Akhtar et al. [44] | Silicon dioxide (SiO2) | Human lung epithelial cells (A549 cells) |
• Lower concentration: o Induction of reactive oxygen species o Membrane damage • Higher concentration: o Reactive oxygen species generation o GSH depletion |
| Gaiser et al. [27] | Silver (Ag) and cerium oxide (CeO2) |
Aquatic species: Daphnia magna neonates, fish, Carp (Cyprius carpio) Human model: C3A human hepatocyte cell line and caco-2 human intestinal epithelial cells |
• Ag is more cytotoxic than CeO2 • Both particles when in diet have the potential to enter the body following ingestion |
| Dankers et al. [45] | CeO2, Mn2O3, CuO, ZnO, Co3O4, and WO3 | Lung epithelium and dendritic cells | • Metal oxide NPs elicit minimal proinflammatory effects |
| Chen et al. [46] | Zinc oxide (ZnO) | Human umbilical vein endothelial cells (HUVECs) |
• ZnO induces significant cellular ER stress • Higher doses of ZnO induces apoptosis |
| Patil et al. [47] | Titanium dioxide (TiO2) and zinc oxide (ZnO) | Lung fibroblast (MRC5) | • Impedes genomic DNA hypomethylation |
| Mohamed et al. [48] | Silicon dioxide (SiO2) | Human monocytic leukemia cell line THP-1 and human alveolar epithelial (A549) cell line |
• Low degree of cytotoxicity at all concentrations • Stress-related cellular response at high concentrations |
| Mancuso & Cao [14] | Copper oxide (CuO) | Human bone marrow mesenchymal stem cells (hBMMSCs) |
• Bigger sizes exhibit significant cytotoxicity at all concentrations • Micro-sized particles exhibit very low cytotoxicity at the same concentration |
| Alshatwi et al. [49] | Aluminium oxide (Al2O3) | Human mesenchymal stem cells (hMSCs) |
• Dose-dependent decreased cell viability • Decreased mitochondrial membrane potential with increasing concentrations after 24 exposures • Down-regulation in the expression of the antioxidant enzyme SOD • Did not induce apoptosis • Dose-dependent oxidative stress |
| Baber et al. [50] | Two amorphous silica coated (MagSilica 85, MagSilica 50) and uncoated iron oxide NPs (Fe3O4) | BEAS-2B (immortalized normal human bronchial epithelium) |
• Little to no indications of cytotoxicity • No induction of inflammatory response/oxidative stress |
| Corbalan et al. [51] | Amorphous Silicon dioxide (SiO2) | Blood |
• Induced an upregulation of selectin P expression and glycoprotein IIb/IIIa activation on the platelet surface membrane • Platelet aggregation |
| Branica et al. [52] | Zinc oxide (ZnO) | Blood (Human lymphocyte) | • Higher concentrations increase cytogenetic damage and intracellular Zn2+ levels in lymphocytes |
| Gurunathan et al. [53] | Platinum (Pt) | Human acute monocytic leukemia (THP-1) macrophages |
• Decreased cell viability and proliferation • Induces cell death • Oxidative stress • Mitochondrial dysfunction • Endoplasmic reticulum stress (ERS) • Proinflammatory responses |
| Hussain et al. [54] | Cerium dioxide (CeO2) | Human peripheral blood monocytes | • CeO2 NPs at non-cytotoxic concentrations neither modulate pre-existing inflammation nor prime for subsequent exposure to lipopolysaccharides in human monocytes from healthy subjects |
| Zerboni et al. [55] | Zinc oxide (ZnO) and Cupper oxide (CuO) | Human alveolar epithelial cells, A549 | • The presence of diesel exhaust particles (DEP) introduces new physicochemical interactions able to increase the cytotoxicity of ZnO and to reduce that of CuO NPs |
| Zielinska et al. [56] | Silver (Ag) | Human fetal osteoblast cells (hFOB 1.19) |
• Cell death • Reactive oxygen species production |
| Rajiv et al. [57] | Cobalt (II, III) oxide (Co3O4); Iron (III) oxide (Fe2O3), Silicon dioxide (SiO2), and Aluminium oxide (Al2O3) | Human lymphocytes |
• Co3O4 NPs showed a decrease in cellular viability and an increase in cell membrane damage followed by Fe2O3, SiO2, and Al2O3 NPs in a dose-dependent manner • Oxidative stress • Lipid peroxidation • Depletion of catalase • Reduced glutathione • Superoxide dismutase |
| Alarifi et al. [58] | Copper oxide (CuO) | Human skin epidermal cell line (HaCaT; passage no. 20) |
• Decrease in cell viability • Reduction in glutathione and induction in lipid peroxidation, catalase, and superoxide dismutase • Apoptosis • Necrosis • Induces DNA damage mediated by oxidative stress |
| Sun et al. [59] | Zinc oxide (ZnO), Fe2O3, Iron (II, III) oxide (Fe3O4), Magnesium oxide (MgO), Aluminium oxide (Al2O3), Copper (II) oxide (CuO) | Human cardiac microvascular endothelial cells (HCMECs) |
• Fe2O3, Fe3O4, and Al2O3 NPs did not have significant effects on cytotoxicity, permeability, and inflammation response • ZnO, CuO, and MgO NPs produced cytotoxicity at a concentration-dependent and time-dependent manner and elicited permeability and inflammation response in HCMECs |
| Tolliver et al. [60] | Titanium dioxide – (TiO2), Zinc oxide – (ZnO), Copper oxide – (CuO), Manganese oxide (Mn2O3), Iron oxide – (Fe2O3), Nickel oxide – (NiO), Chromium oxide – (Cr2O3) | Human lung cancer cell model (A549) |
• All NPs aside from Cr2O3 and Fe2O3 showed a time- and dose-dependent decrease in viability • All NPs significantly inhibited cellular proliferation • Apoptosis • Cell cycle alteration in the most toxic NPs |
| Rothen-Rutishauser et al. [61] | Cerium oxide (CeO2) | Adenocarcinomic human alveolar basal epithelial (A549) cell line |
• Generation of oxidative DNA damage • Causes tightness of the lung cell monolayer • Dose-dependent cellular response |
| Benameur et al. [62] | Cerium Oxide (CeO2) | Human dermal fibroblasts |
• Genotoxicity • Reactive oxygen species production • Lower doses of CeO2 did not induce significant cytotoxicity • Induces lipid peroxidation and decline of cellular glutathione level at concentrations above 0.00006 M |
| Gojova et al. [63] | Cerium oxide (CeO2) | Human aortic endothelial cells (HAECs) | • Causes very little inflammatory response even at higher doses |
| Lee et al. [29] | Zinc oxide (ZnO) |
Natural soil and seedlings of buckwheat |
• The effect of ZnO NPs on soil bacterial depends on the presence of plants • The soil–plant interactive system helps to decrease the toxic effects of ZnO nanoparticles on the rhizobacteria population relative to soil systems not containing plants |
| Hildebrand et al. [64] | Magnetite (Fe3O4) and palladium magnetite (Pd/Fe3O4) |
1) Human cell lines: Colon adenocarcinoma cells, CaCo-2 (HTB-37), Human keratinocyte cells, (HaCaT) 2) Fish cell line: Rainbow trout gills (RTgill-W1) cell line |
• No initiation of reactive oxygen species production • Little impact on the viability of colon adenocarcinoma cells, human keratinocyte cells, and the rainbow trout gills cell line • No toxic effect was found |
| Lai et al. [65] | Titanium dioxide (TiO2) | Human astrocytoma and human fibroblasts |
• Induces cell death • Apoptosis • Necrosis |
| Ahamed et al. [66] | Copper oxide (CuO) | Human lung epithelial cells (A 459) |
• Dose-dependent reduction in cell viability • Induces oxidative stress • Depletion of glutathione • Induction of lipid peroxidation, Catalase and superoxide dismutase • Induces cellular damage (indicated by the expression of Hsp70, the first tier biomarker of cellular damage) |
| Vergaro et al. [67] | Titanium dioxide (TiO2) | Human bronchial epithelial cells (BEAS-2B) | • Induces a low photo reactivity and a toxic effect lower than Aeroxide P25 of the nano-TiO2 powders |
| Dávila-Grana et al. [68] | Zinc oxide (ZnO), Titanium dioxide (TiO2), Cerium dioxide (CeO2), Aluminium oxide (Al2O3), Yttrium (III) oxide (Y2O3) | Jurkat cell line |
• The combination of nanoparticles induces changes in cell signalling mediated by the MAPKs and nuclear factor-κB (NF-κB) • Al2O3 NPs had a protective effect when combined with the ZnO NPs • CeO2 and Y2O3 Nps induced a synergistic effect on the toxicity and p38 activation • TiO2 nanoparticles increase the toxicity induced by ZnO nanoparticles but reduced the phosphorylation of the signalling proteins |
| Pierscionek et al. [69] | Cerium oxide (CeO2) | Human lens epithelial cells |
• Epithelial cells can sustain normal growth when exposed to lower concentrations of nanoceria • Induces genotoxicity when exposed for longer periods |
| Rafieepour et al. [70] | Magnetite iron oxide (Fe3O4), polymorphous silicon dioxide (P-SiO2) | Adenocarcinomic human alveolar basal epithelial (A549) cell line |
• Reduces cell viability • Reduces cellular glutathione content and mitochondrial membrane potential • Increases reactive oxygen species generation in both single and combined exposures of Fe3O4 and P-SiO2 • The toxic effects of combined exposure to these NPs were less than the single exposures |
| Ickrath et al. [71] | Zinc oxide (ZnO) | Human mesenchymal stem cells (hMSC) |
• Induces cytotoxic effect at higher concentrations of 50mcg/mL • Induces genotoxic effects in hMSC exposed to between 1 and 10mcg/mL ZnO-NP |
| Radeloff et al. [72] | Iron oxide (Fe3O4) | Human adipose tissue derived stromal cells (hASCs) | • No effect on the physiological functions of human adipose tissue derived stromal cell (hASCs) |
| Jin et al. [73] | Zinc oxide (ZnO) | Zebrafish larvae and human neuroblastoma cells SH-SY5Y |
• Smaller sizes of ZnO showed slightly higher toxicity than the larger sizes • Long ZnO NRs (l-ZnO NRs) harbours a remarkably potential risk for the onset and development of Parkinson’s disease at relatively high doses |
| Kumari et al. [74] | Cerium oxide (CeO2) | Human neuroblastoma cell line (IMR32) |
• Induces size- and dose-dependent toxicity (oxidative stress and genotoxicity) • CeO2 did not induce toxicity below 100 mg/mL concentration • IMR32 cells are less sensitive to CeO2 NPs |
| Fernández-Bertólez et al. [75] | Silica-coated iron oxide nanoparticles (SiO2) | Human glioblastoma A172 cells |
• Cytotoxicity (cell cycle disruption and cell death induction) • Rarely induces genotoxic effects • No alteration in the DNA repair process |
| Gliga et al. [76] | Nickel (Ni), nickel oxide (NiO) | Human bronchial epithelial cell line (BEAS-2B) |
• Long-term exposures (six weeks) changes gene expressions • Induces DNA strand breaks and alter cell cycle after six weeks of repeated exposure • Nickel causes no effect on cell transformation (ability to form colonies in soft agar) or cell motility |
| Kennedy et al. [77] | Iron oxide (Fe3O4), zinc oxide (ZnO), Yttrium oxide (Y2O3), and cerium oxide (CeO2) | Human aortic endothelial cells (HAECs) |
• Induces oxidative stress • Zinc oxide more toxic than yttrium oxide • No effect on HAECs when exposed to Iron oxide and cerium oxide |
| Schanen et al. [78] | Titanium dioxide and cerium dioxide (TiO2 and CeO2) | PBMC blood product | • Low dose exposures modulate human innate and adaptive immunity (i.e., dendritic cells activation and primary CD4 T helper cell differentiation state) |
| Seker et al. [79] | Zinc oxide (ZnO) | Human periodontal ligament fibroblast cells (hPDLFs) |
• Causes cell index decrease at concentrations of 50 to 100lg/mL • Induces changes in cell morphology • Induces harmful effects on cell viability and membrane integrity • Necrosis • Cell death (in terms of morphological change or cellular shrinkage) at doses higher than 50lg/mL • Cytotoxicity depends on duration of exposure and concentration |
| Könen-Adıgüzel & Ergenel [80] | Cerium dioxide (CeO2) | Human blood lymphocytes | • Induces genotoxicity even at 3–24 h exposure under in vitro conditions |
| Henson et al. [81] | Cupric (II) oxide (CuO), Polyvinylpyrrolidone (PVP) coated NPs | A three-dimensional model of the human small intestine, EpiIntestinalTM(SMI-100) | • Induces dose- and time-dependent viability of human cells |
| Gojova et al. [82] | Iron oxide (Fe2O3), Yttrium oxide (Y2O3), and Zinc oxide (ZnO) | Human aortic endothelial cells (HAECs) |
• All three types of nanoparticles are internalized into HAECs and are often found within intracellular vesicles • No inflammatory response after exposure to Fe2O3 • Y2O3 and ZnO nanoparticles elicit pronounced inflammatory response |
| Alarifi et al. [83] | Zinc Oxide (ZnO) | Human skin melanoma (A375) cells |
• Decrease in cell viability • Causes morphological changes • Induces oxidative stress • Reactive oxygen species generation • Depletion of the antioxidant, glutathione • Induces DNA damage at higher concentrations |
| Ãkerlund et al. [84] | Nickel (Ni) and nickel oxide (NiO) | Human bronchial epithelial cells (HBEC) | • Causes a release of inflammatory cytokines from exposed macrophages |
| Jiménez-Chávez et al. [85] | Titanium dioxide and Zinc oxide (TiO2 and ZnO) | Human alveolar epithelial cells (A549) |
TiO2: • Shows a higher persistence in cell surface and uptake • Induces sustained inflammatory response (by means of TNF-Î ± , IL-10, and IL-6 release) • Induces reactive oxygen species generation ZnO: • Shows a modest response and low number in cell surface Both TiO2 and ZnO: • Concentration-dependent reduction in SP-A levels at 24 h of exposure to both TiO2 and ZnO • Cellular damage • Loss of lung function |
| Hussain & Garantziotis [86] | Cerium dioxide (CeO2) | Primary human monocytes |
• Apoptosis (involving mitochondrial damage) • Causes a loss in membrane potential • Induces mitochondrial relocation of BAX • Induces modulation in autophagic events |
| Abudayyak et al. [87] | Bismuth Oxide—Bi (III) oxide (Bi2O3) |
a) HepG2 human hepatocarcinoma cells (ATCC HB-8065) b) Caco-2 human colorectal adenocarcinoma cells (ATCC HTB-37) c) A549 human lung carcinoma cells (ATCC CCL-185) |
• Induces apoptosis in HepG2 • Induces necrosis in A549 and Caco-2 cells • Causes significant changes in the levels of glutathione (GSH), malondialdehyde (MDA), and 8-hydroxydeoxyguanine (8-OHdG) in HepG2 and Caco-2 cells, except A549 cell |
| Fahmy et al. [88] | Copper/copper oxide (Cu/CuO) | Human diploid lung fibroblast normal cell lines (WI-38 cell) and human epithelial lung carcinoma cell lines (A549 cells) |
• Suppresses proliferation and cell viability • Cause DNA damage • Induces generation of reactive oxygen species • Induces oxidative stress |
| Božinović et al. [89] | Molybdenum trioxide (MoO3) | Human keratinocyte (HaCaT) cell line | • Short exposure (up to 1 h) of keratinocytes to MoO3 has no significant impact on cell survival |
| Ahamed et al. [90] | Iron oxide (Fe3O4) | Skin epithelial A431 and lung epithelial A549 cell lines |
• Induces dose-dependent cytotoxicity (indicated by reduction in cell viability lactate dehydrogenase leakage assays) • Induces dose-dependent oxidative stress • Induces reactive oxygen species • Induces lipid peroxidation • Causes DNA damage in high concentrations • Up-regulates the protein expression level of cleaved caspase-3 |
| Pelclova et al. [91] | Titanium dioxide (TiO2) | Exhaled breath condensate (EBC) and urine |
• Induces elevation of Leukotrienes (LT) levels • Induces inflammation and potential fibrotic changes in the lungs |
| Valdiglesias et al. [92] | Zinc oxide (ZnO) | Human neuroblastoma SHSY5Y cell line |
• Apoptosis • Decreases cell viability • Induces cell cycle alterations • Induces micronuclei production • Induces H2AX phosphorylation and DNA damage |
| Verdon et al. [93] | Silver (Ag), Zinc oxide (ZnO), Copper oxide (CuO), Titanium dioxide (TiO2) |
1) Human acute myeloid leukemia suspension cell line, HL-60 2) Primary neutrophils from human blood |
• Ag and CuO nanoparticles stimulate neutrophil activation • TiO2 do not induce neutrophil response in either cell type • ZnO induces activation of HL-60 cells but does not activate primary cells |
| Siddiqui et al. [94] | Nickel oxide (NiO) | Cultured human airway epithelial (HEp-2) and human breast cancer (MCF-7) cells |
• Apoptosis • Cytotoxicity • Reactive Oxygen species generation • Oxidative stress • generation and oxidative stress • Dietary antioxidant curcumin can effectively abrogate NiO NP-induced toxicity |
| Park et al. [95] | Cerium oxide (CeO2) | Human lung epithelial cells (BEAS-2B) |
• Causes cell death • Reactive oxygen species production • Glutathione (GSH) decrease • Induces oxidative stress-related genes (e.g., heme oxygenase-1, catalase, glutathioneS-transferase, and thioredoxin reductase) • Apoptosis |
| Fakhar-e-Alam et al. [96] | Zinc oxide (ZnO) | Melanoma cells and human foreskin fibroblasts |
• Induces reactive oxygen species production after UV-A-irradiation • Causes loss of mitochondrial membrane potential • Induces significant loss of cell viability |
| Hackenberg et al. [97] | zinc oxide (ZnO) | Human mucosa of the inferior nasal turbinate | • Repetitive exposure to low concentrations of ZnO-NPs results in persistent or ongoing DNA damage |
| Andujar et al. [98] | Welding-related NPs (essentially, Iron (Fe), Manganese (Mn), Chromium (Cr) oxide) | The lung of arc welders exposed to fume-issued NPs |
• Induce the production of a pro-inflammatory secretome • All, but magnetite NPs, induce an increased migration of macrophages • NP-exposed macrophage secretome has no effect on human primary lung fibroblasts differentiation |
| Sharma et al. [99] | Zinc oxide (ZnO) | Human hepatocarcinoma cell line (HepG2) |
• Decreases cell viability • Apoptosis • Induces DNA damage • Production of reactive oxygen species • Decreases mitochondria membrane potential • Activates JNK and p38 • Induces p53-Ser15 phosphorylation |
| Senapati et al. [100] | Zinc oxide (ZnO) | Human monocytic cell line, THP-1 |
• Induces oxidative and nitrosative stress • Causes an increase in inflammatory response (via activation of redox sensitive NF-kB and MAPK signalling pathways) |
| Carbon-based Nanoparticles | |||
| Vlaanderen et al. [101] | Multi-walled carbon nanotubes (MWCNTs) | Breathing zone measurement of inhalable particulate matter, whole blood samples, and assessment of lung function of workers |
• Significant upward trends for immune markers C–C motif ligand 20 (p = .005), basic fibroblast growth factor (p = .05), and soluble IL-1 receptor II (p = .0004) with increasing exposure to MWCNTs • Effect on lung health and immune system |
| Asghar et al. [102] | Carbon Nanotubes (CNT), Graphene Oxide (GO) | Human sperm |
• Both SWCNT-COOH and reduced GO Causes no effect to sperm viability at lower concentrations • SWCNT-COOH generates significant reactive superoxide species at a higher concentration • Reduced graphene oxide does not initiate reactive species in human sperm |
| Periasamy et al. [103] | Carbon nanoparticles (CNPs) | Human mesenchymal stem cells (hMSCs) | • Reduces cell viability |
| Beard et al. [104] | Carbon nanotubes and nanofibers (CNT/F) | Sputum and blood |
Inhalable rather than respirable CNT/F associated with: • Fibrosis • Inflammation • Oxidative stress • Cardiovascular biomarkers |
| Zhang et al. [105] | Single Wall Carbon nanotube (SWCNT) | Human ovarian cancer cell line OVCAR3 |
• Sensitises OVCAR3 cells to the chemotherapeutic compound paclitaxel (PTX) resulting in increased cell death • Apoptosis |
| de Gabory et al. [106] | Double-Walled Carbon Nanotubes (DWCNTs) | Human nasal epithelial cells (HNEpCs) |
• Dose-dependent decrease in cell metabolic activity and cell growth • Stimulation of mucus production • Significant increase in Reactive Oxygen Species • Increased effect after 12-day exposure |
| Eldawud et al. [107] | Single Wall Carbon nanotubes (SWCNTs) | Immortalised human lung epithelial cell (BEAS-2B) |
• Reducing cell viability • Changes cell structure, cycle and cell–cell interactions |
| Pacurari et al. [108] | Multi-walled carbon nanotubes (MWCNTs) | Human microvascular endothelial cells (HMVEC) |
• Increase in endothelial monolayer permeability and migration in HMVEC • Induces endothelial cell permeability • Production of reactive oxygen species • Actin filament remodelling |
| Reamon-Buettner et al. [109] | Multi-walled carbon nanotubes (MWCNTs) | Human peritoneal mesothelial cells LP9 |
• Inhibition of cell division • Induces premature cellular senescence |
| Phuyal et al. [110] | Multi-walled carbon nanotubes (MWCNTs) | Human bronchial epithelial 3-KT (HBEC-3KT) cells | • Alters both the proteome and the lipidome profiles of the target epithelial cells in the lung |
| Witzmann & Monteiro-Riviere [111] | Multi-walled carbon nanotubes (MWCNTs) | Cryopreserved neonatal human epidermal keratinocytes |
• Alters the protein expression in epithelial cells • Significant effect on the expression of cytoskeletal elements |
| Snyder et al. [112] | Multi-walled carbon nanotubes (MWCNTs) | Human bronchial epithelial primary cells |
• Negatively impacts the ability of human airway epithelium to form a monolayer barrier • Altered cell morphology • Cytoskeletal disruption |
| Snyder et al. [113] | Multi-walled carbon nanotube (MWCNTs) | Human bronchial epithelial cells (BECs) | • Causes mitochondrial dysfunction that leads to mitophagy |
| Ghosh et al. [28] | Multi-walled carbon nanotubes (MWCNTs) | Allium cepa bulbs |
• Cyto-genotoxicity • Induces significant DNA damage • Induces micronucleus formation • Chromosome aberration • Internucleosomal fragments formation, indicative of apoptotic cell death |
| Yu et al. [114] | Multi-walled carbon nanotubes (MWCNTs) | Immortalized human mesothelial cell line (Met-5A) |
• Causes significant cytotoxic effects on Met-5A cells • Higher concentrations induce cellular membrane permeability and disturbance of mitochondrial metabolism • No significant toxic effect at low concentrations • Reactive oxygen species formation |
| Rizk et al. [115] | Multi-walled carbon nanotube (MWCNTs) | Normal human dermal fibroblast (NHDF) cells |
• Induces induced massive loss of cell viability • DNA damage • Programmed cell death |
| Jos et al. [116] | Single wall carbon nanotubes (SWCNTs) | Human Caucasian colon adenocarcinoma (Caco-2) cell line |
• Increase in Lactate dehydrogenase (LDH) leakage • Cytotoxicity • Protein content only modified at higher concentrations |
| Vankoningsloo et al. [117] | Multi-walled carbon nanotubes (MWCNTs) |
1) Immortalised human keratinocytes (IHK) 2) SZ95 sebocytes 3) Reconstructed human epidermises (RHE) |
• Induces cytotoxicity in human keratinocytes • No cytotoxic effects in SZ95 sebocytes or in stratified epidermises reconstructed in vitro |
| Herzog et al. [118] | Single-walled carbon nanotubes (SWCNTs), Carbon black (CB) |
1) Human lung epithelial cells (A549) 2) Normal human primary bronchial epithelial cells (NHBE) |
• Low oxidative stress • Cell responses are strongly dependent on the vehicle used for dispersion • The presence of dipalmitoyl phosphatidylcholine (DPPC) increased intracellular reactive oxygen species (ROS) formation |
| Müller et al. [119] | Single-walled carbon nanotubes (SWCNTs) and Titanium dioxide (TiO2) | Human epithelial lung cells (A549), human monocyte-derived macrophages (MDMs) and monocyte-derived dendritic cells (MDDCs) |
• SWCNTs and TiO2 can penetrate into A549, MDMs, and MDDCs • Induces the production of reactive oxygen species |
| Baktur et al | Single-walled Carbon nanotubes (SWCNTs) | Human alveolar epithelial cells (A549) |
• Enhances Interleukin-8 (IL-8) expression in the presence of serum • Induces changes in IL-8 expression |
| Basak et al. [120] | Multi-walled carbon nanotubes (MWCNTs) and TiO2 nanobelts (TiO2-NB) | Human colorectal adenocarcinoma cells | • Cytotoxicity |
| Patlolla et al. [121] | Multi-walled carbon nanotubes (MWCNTs) | Normal human dermal fibroblast cells (NHDF) |
• Dose-dependent toxicity • Massive loss of cell viability through DNA damage • Cell death |
| Dahm et al. [122] | Carbon nanotubes and nanofibers (CNT/F) |
Sputum samples Scanning electron microscopy (SEM) |
• Industrial workers are exposed to the toxic effect of carbon nanotubes at the workplace |
| Fatkhutdinova et al. [123] | Multi-walled carbon nanotubes (MWCNTs) | Blood and sputum samples from workers |
• Induction of pro-inflammatory cytokines (IL-6, TNF-α, and IL-1β) • Induction of KL-6 (a serological biomarker for interstitial lung disease) • Accumulation of inflammatory and fibrotic biomarkers in biofluids of workers manufacturing MWCNTs |
| Zhao et al. [124] |
Multi-walled carbon nanotubes (MWCNTs) i.e., three commercially available MWCNTs, namely XFM4, XFM22, and XFM34 (diameters XFM4 < XFM22 < XFM34) |
Human umbilical vein endothelial cells (HUVECs) |
• XFM4 induced a significantly higher level of cytotoxicity than XFM22, and XFM34 • HUVECs internalized more XFM4 • XFM4 induces cytokine release, monocyte adhesion, and intracellular reactive oxygen species level • XFM4 exposure reduces the expression of autophagic genes autophagy-related 7 (ATG7), autophagy-related 12 (ATG12), and beclin 1 (BECN1) • Causes autophagy dysfunction and endoplasmic reticulum stress |
| Öner et al. [125] | Multi-walled carbon nanotubes (MWCNTs) and Single-walled carbon nanotubes (SWCNTs) | Human bronchial epithelial cells (16HBE) |
• MWCNTs induce a single hypomethylation at a CpG site and gene promoter region • No change in DNA methylation after the recovery period for MWCNTs • SWCNTs or amosite induce hypermethylation at CpG sites after sub-chronic exposure |
| Luanpitpong et al. [126] | Carbon nanotubes (CNT) | Non-tumorigenic human lung epithelial cells |
• Induces Cancer Stem-like cells (CSC) in lung epithelial cells • Induces specific stem cell surface markers CD24 low and CD133 high that are associated with SWCNT-induced CSC formation and tumorigenesis |
| Shvedova et al. [127] | Carbon nanotubes (CNT)—Multi-walled carbon nanotubes (MWCNTs) |
Air Sample Peripheral whole blood |
• Causes significant changes in the non-coding RNAs (ncRNA) and coding messenger RNAs (mRNA) expression profiles • Cell cycle regulation/progression/control • Apoptosis and proliferation • Potential to trigger pulmonary and cardiovascular effects • Potential to induce carcinogenic outcomes in humans |
| Domenech et al. [128] | Carbon-based nanoparticles: Graphene oxide (GO), Graphene nanoplatelets (GNPs) | Human colorectal adenocarcinomas (Caco-2, ATCC HTB-37) |
• No oxidative damage induction was detected, either by the DCFH-DA assay or the FPG enzyme in the comet assay • Both GO and GNPs induce DNA breaks • Induces weak anti-inflammatory response |
| Wang et al. [129] | Single-walled carbon nanotubes (SWCNT) and multi-walled carbon nanotubes (MWCNTs) | Primary human Small Airway epithelial Cells (SAECs) |
• Increases cell proliferation • Induces anchorage-independent growth • Causes cell invasion and angiogenesis |
| Mukherjee et al. [130] | Graphene oxide (GO) | human bronchial epithelium (BEAS-2B) cells |
• Causes mitochondrial dysfunction after a 48-h exposure • Causes engagement of apoptosis pathways after longer exposure periods (i.e., 28 days) • Causes down regulation of genes belonging to the inhibitor of apoptosis protein (IAP) family |
| Pérez et al. [131] | Reduced graphene oxide (rGO) | Human airway epithelial (BEAS-2B) cells | • Medium-term rGO exposure does not have significant effects on the DNA methylation patterns of human lung epithelial cells |
| Xu et al. [132] | Single-walled carbon nanotubes (SWCNT) | Pulmonary surfactant monolayer (PSM) |
• Inhalation toxicity of SWCNTs is largely affected by their lengths • Short SWCNTs increases inflammatory response • Longer SWCNTs causes severe lipid depletion and PSM-rigidifying effect |
| Gasser et al. [133] | Multi-walled carbon nanotubes (MWCNTs) |
Human monocyte derived macrophages (MDM) monocultures A sophisticated in vitro model of the human epithelial airway barrier |
• Increases reactive oxygen species levels • Decreases intracellular glutathione depletion in MDM • Decreases the release of Tumour necrosis factor alpha (TNF-Î ±) • Induces apoptosis • Increases the release of the release of Interleukin-8 (IL-8) |
| Di Cristo et al. [134] | Graphene Oxide (GO) | EpiAirway™ tissues (AIR-100, PE6-5), a 3D mucociliary tissue model of the primary human bronchial epithelium |
• Elicits proinflammatory response after 2 weeks exposure • Causes moderate barrier impairment • Induces autophagosome accumulation (resulting from blockade of autophagy flux) • Prolonged exposures increase the risk of pulmonary infections and/or lung diseases |
| Chortarea et al. [135] | Carbon nanotubes (CNTs) | Human (alveolar) epithelial A549 cell line with human monocyte-derived dendritic cells (MDDCs) and macrophages (MDMs) | • Repeated exposures to lung cell cultures at the Air–Liquid Interface, elicit a limited biological impact over a three-day period |
| Lee et al. [26] | Graphene oxide (GO) | Workplace air samples |
• Minimum release of graphene or other particles during manufacturing based on real-time aerosol monitoring • Negligible exposure to graphene based on personal and area sampling for the Total Suspended Particles (TSP) and elemental carbon (EC) |
| Both Inorganic-based and Carbon-based Nanoparticles | |||
| Phuyal et al. [21] | Titanium dioxide (TiO2) and multi-walled carbon nanotubes (MWCNTs) | Human bronchial epithelial (HBEC-3KT) cell line |
• Low cytotoxicity in short-term tests • Cell proliferation affected in long-term exposure |
| Shalini et al. [22] | Zinc oxide (ZnO) and nanorods | Human peripheral blood lymphocytes (HPBL) |
• Genotoxicity in smaller ZnO NPs • Cytotoxic effect in larger microparticles and microrods • Higher level of oxidative potential and reactive oxygen species generation capacity in ZnO NPs and nanorods |
| Simon-Deckers et al. [23] | Aluminium oxide (Al2O3), Titanium dioxide – (TiO2), Multi-walled carbon nanotubes (MWCNTs) | A549 human type II lung epithelium cell line |
• Carbon nanotubes are more toxic than metal oxide NPs • Both nanotubes and NPs rapidly enter into cells, and distribute in the cytoplasm and intracellular vesicles |
| Inorganic-based and Polymer Nanoparticles | |||
| Setyawati et al. [24] | Titanium dioxide (TiO2), Terbium-doped gadolinium oxide (Tb-Gd2O3), and Poly (lactic-co-glycolic acid) (PLGA) | Human neonatal foreskin fibroblast cell line (BJ) |
TiO2 and Tb-Gd2O3: • Dose-dependent cytotoxicity • Promotes genotoxicity via DNA damage PLGA nanoparticles: • Did not induce significant cytotoxic or genotoxic effects on BJ |
| Polymer Nanoparticles | |||
| Nishu et al. [25]., 2020 | Poly lactic-co-glycolic acid (PLGA) |
Nitrosomonas europaea KCTC 12270 bacterium Nitrospira moscoviensis bacterium |
• Reduce nitrification in both cultures of nitrifying strains and in microbial communities in soil samples |