From: Airborne micro- and nanoplastics: emerging causes of respiratory diseases
Characteristics | Sample type | AMNPs type | The Sources of AMNPs | Shape | Size | Mechanism | References |
---|---|---|---|---|---|---|---|
Oxidative Imbalance | HPAEpiC and BEAS-2B cells | PS-MNPs | Commercially available beads | Not clear | 7.5, 15, and 30 µg/cm2 | Oxidative stress-induced mitochondrial damage can lead to ferroptosis | [121] |
A549 cells | PTFE-MNPs | Ground PTFE raw powder materials with 450 μm average particle size using a homogenize | Not clear | 31.7 ± 5.6 μm and 6.0 ± 2.1 μm | Activate ERK signaling pathways, ultimately leading to the generation of ROS and oxidative stress | [122] | |
HPAEpiC and BEAS-2B cells | PS-MNPs | Commercially available beads | Irregular geometric shape | 40Â nm | Disrupt redox balance, decrease levels of tight junction proteins, reduce levels of matrix metalloproteinase 9 and surfactant protein A, thereby impairing lung repair capacity and causing tissue damage | [125] | |
BEAS-2B cells | PS-MNPs | Commercially available beads | Spheres | 10 μm and 20 μm | Increased cell apoptosis, levels of MDA and iron content, decreased levels of key ferroxidases (GPX4 and FTH1), and mitochondrial changes | [13] | |
A549 cells, BEAS-2B cells and 5–8 weeks BALB/c mice | PE-, PP-, PS-, PVC-MNPs | Commercially available beads | PE, PS AND PVC are regular spheres but have non-uniform size, while PP displays irregular geometric shape | 6.5 μm−1 mm, 6.5–100 μm, 3–100 μm, and 6.5–25 μm | Disrupt the cellular redox homeostasis and prompt cellular senescence | [115] | |
A549 cells | PS-MNPs | Commercially available beads | Spheres | 1 and 5 μm | Reduce the integrity of the single-layer barrier and slowed down the regeneration in wound healing experiments | [98] | |
A549 cells | PS-MNPs | Commercially available beads | Spheres | 50Â nm | Induce significant increases in ROS production | [116] | |
A549 cells | PET-MNPs | Commercially available beads | Spheres | ≤ 20 nm | Oxidative stress induces a decrease in the mitochondrial membrane potential | [118] | |
Generation of inflammation | A549 cells | PTFE-MNPs | Ground PTFE raw powder materials with 450 μm average particle size using a homogenize | Not clear | 31.7 ± 5.6 μm and 6.0 ± 2.1 μm | Increase the secretion of IL−6 and TNF-α | [122] |
 | A549 cells | PS-MNPs | Commercially available beads | Not clear | 25 and 75 nm | Increase the secretion of NF-κB, TNF-α and IL−8 | [132] |
 | Mice | PP-MNPs | Precipitate a solution dissolved at 200 °C on a hot plate with PP beads and xylene solvent with ethanol | irregular fragments with a spherical shape | 0.66 ± 0.27 μm | The NF-κB pathway regulated by p38 phosphorylation as a result of mitochondrial damage | [12] |
 | Six-week-old male and female (n = 40; 20 males and 20 females) specific pathogen-free (SPF) Sprague-Dawley rats | PS-MNPs | Commercially available beads | Spheres | 0.10 μm | The lung tissue exhibited an increase in TGF-β and TNF-α that is dependent on exposure concentration | [131] |
 | BEAS-2B cells | PS-MNPs, NH2PS-MNPs, COOH-PS-MNPs | Commercially available beads | Spheres | 100 nm | Increase the expression and secretion of the pro-inflammatory cytokine IL-β | [129] |
 | C57BL/6 mice, BALB/c and ICR mice | PE-, PP-, PS-MNPs | Commercially available beads | Irregular geometric shape | 6.40 ± 1.48 μm for PP, 17.53 ± 2.11 μm for PS and 21.27 ± 6.07 μm for PE | Induce lung inflammation through the TLR4 pathway and raise levels of IL−1β in BALF and elevated levels of NLRP3, ASC, and Caspase−1 in the lung tissue | [133] |
 | ICR mice | PET-MNPs | Microplastics were prepared from polyethylene beads (5 mm) | Irregular geometric shape | 27.0 ± 10.9 μm | Not clear | [127] |
 | A549 cells | PS-MNPs | Commercially available beads | Spheres | 104.77 ± 1.47 nm | Increase the secretion of pro-inflammatory cytokines | [128] |
 | A549 cells | Plastic-waste derived MNPs | Were recovered in the laboratory from industrially recycled plastic granules | Irregular shape, encompassing fiber-like formations, with noticeable surface irregularities and structural flaws at the submicron level | ≤ 50 μm | Increase the secretion of IL−6 and IL−8 | [126] |
ER stress | BEAS-2B cells | PS-MNPs, NH2PS-MNPs, COOH-PS-MNPs | Commercially available beads | Spheres | 100 nm | The protein levels associated with the PERK-EIF2α and ATF4-CHOP pathways increased | [128] |
 | BEAS-2B cells | PS-MNPs | Commercially available beads | Spheres | 570 nm | Amino acids and TCA cycle intermediate metabolites | [119] |
 | BEAS-2B cells | PS-MNPs | Commercially available beads | Spheres | 10 μm and 20 μm | The elevation of IRE1α, PERK, XBP1S, and CHOP | [13] |
Apoptosis | A549 cells | PS-MNPs | Commercially available beads | Not clear | 25 nm and 70 nm | the expression of Bax/Bcl−2, DR5, caspase−3, caspase−8, caspase−9, and cytochrome c significantly upregulate, resulting in cell apoptosis | [132] |
 | A549 cells | Bap@PS-MNPs | Ground styrene materials | Spheres | 410–470 nm | lead to a significant decrease in mitochondrial membrane potential and involvement of mitochondria in the apoptotic pathway | [138] |
Autophagy cell death | BEAS-2B cells | PS-MNPs, NH2PS-MNPs, COOH-PS-MNPs | Commercially available beads | Spheres | 100Â nm | Inhibit the PI3K/Akt/mTOR pathway in cells. They in lysosomes and nuclear deformation can also be observed, resulting in autophagic cell death | [129] |
 | Human primary nasal epithelial cells | PET-MNPs | Self-preparation within the laboratory | Irregular geometric shape | 62.38 nm ± 3.51 μm | Increases in the expression levels of LC3-II and p62 proteins, altering the autophagy pathway | [139] |
 | A549 cells | PS-MNPs | Commercially available beads | Not clear | 20 nm | Increased autophagic activity, but limit to autophagic capacity | [140] |
Impact on LS | LS extracted from porcine lungs | PS-MNPs | Commercially available beads | Spheres | 500–1000 nm | It can quicken the process of ascorbic acid to dehydroascorbic acid conversion, which causes hydrogen peroxide (HOOH) to be produced in simulated LS, which raises the level of hydroxyl radicals (·OH) | [142] |
 | Simulated lung fluid | aged MNPs | Commercially available beads | Irregular geometric shape | 200 μm | Lipid peroxidation and protein degradation in LS | [143] |
 | BALB/c mice | PS-, PP-, PVC-MNPs | Self-preparation | PP-MNPs : irregular block like structure; PS-, PET-MNPs: crinkled flocculent morphology | PP-, PET-MNPs are all larger than 200 nm, while the PS-MNPs are around 52 nm | Particles adhered to the air-water interface and aggregated with the LS membrane | [144] |
 | Alveolar fluid | PS-, PET-, PP-, PE-, PVC-MNPs | Using melting-annealing approach to fabricate nanoplastics of different materials | Spheres | 10 nm and 5 nm | Once AMNPs have reached the alveolar air-water interface, they can disrupt the ultrastructure and fluidity of LS, which can interfere with LS’s regular biophysical function and lead to LS membrane collapse | [81] |
Microbiota dysbiosis | ICR male mice | AMNPs | Self-preparation within the laboratory | Not clear | 5 μm and 99 nm | The most closely linked to MP were nasal Staphylococcus and pulmonary Roseomonas, while the most closely linked to NP were nasal Prevotella and pulmonary unclassified bacteria. Both MP and NP were associated with nasal Staphylococcus, pulmonary Roseomonas, pulmonary Aggregatibacter, and pulmonary Bacillus | [145] |
 | 20 subjects from a Plastic Factory and the other 20 from Huanhuaxi Park | AMNPs | Realistic MNPS | Not clear | Not clear | Increase the abundance of nasal microbiota and decrease the abundance of beneficial microorganisms. It can also increase the abundance of intestinal microbiota | [146] |
 | 20 subjects from a Plastic Factory and the other 20 from Huanhuaxi Park | AMNPs | Realistic MNPS | Not clear | Not clear | Not only cause changes in the major microbial communities in the intestines and nose, but also alter the symbiotic relationship between intestinal and nasal microbiota | [147] |
Inhibition of cell proliferation | A549 cells | PS-MNPs | Commercially available beads | Spheres | 1 μm and 10 μm | Decrease in cell proliferation | [148] |
 | A549 cells | PS-MNPs | Commercially available beads | Not clear | 25 nm and 70 nm | Induce cell cycle arrest and have a substantial impact on cell viability | [132] |
Promotion of aging | MLE12 | PS-MNPs | Commercially available beads | Spheres | 100Â nm | circ_kif26b binds to miR-346-3p and co-regulates the target gene, p21 of miR-346-3p | [148] |
 | A549 cells, BEAS-2B cells and 5–8 weeks BALB/c mice | PVC-MNPs | Commercially available beads | PE, PS AND PVC are regular spheres but have non-uniform size, while PP displays irregular geometric shape | 6.5 μm−1 mm, 6.5–100 μm, 3–100 μm, and 6.5–25 μm | Increase the levels of ROS in A549 cells and the aging features induced by them can be largely reversed by antioxidant treatment. Increase in systemic inflammation levels can cause the accumulation of senescent cells | [115] |
Metabolism | HaCaT cells, A549cells and RAW 264.7 | ulfate-modified MNPs | Commercially available beads | Irregular geometric shape | 210 ± 4.63 nm | Human macrophages exposed to them can stimulate the accumulation of LDs in the cytoplasm, and the accumulated LDs are further transported and accumulated in lysosomes, leading to lysosomal damage and further differentiation of macrophages into foam cells | [150] |
 | BEAS−2B cells and RAW264.7 | PS-MNPs | Commercially available beads | Spheres | 100 nm | Cause cell damage by regulating prostaglandin B1 and other metabolites via the cGAS-STING pathway | [151] |
Induction of ferroptosis | BEAS-2B cells | PS-MNPs | Commercially available beads | Spheres | 100 and 200 nm | The HIF-1α/HO-1 signaling pathway plays an important role in regulating ferroptosis in lung injury | [152] |
Genetic toxicity | A549 cells | PET-MNPs | Was produced by grinding food containers | Spheres | 136Â nm | Increase the level of DNA strand breaks | [153] |
Impairment of lysosomal function | A549 cells | PS-MNPs | Commercially available beads | Not clear | 10 μm | Lysosomal dysfunction | [154] |
Damage to epithelial airway cell | Human and murine alveolar and airway-type organoids as well as air–liquid interface cultures derived from primary lung epithelial progenitor cells | PS-MNPs | Self-preparation within the laboratory | Fibers | 15 × 52 μm | Damage developing and/or repairing airways | [157] |
 | Primary rat alveolar epithelial monolayers | PS-MNPs | Commercially available beads | Not clear | 20, 100, 120 nm | Disrupt the characteristics of the alveolar epithelial barrier and involve changes in cellular transport pathways | [159] |
Immune responses | Not clear | AMNPs | Not clear | Not clear | Not clear | Insufficient response (immune suppression, increased susceptibility to infection and disease) and excessive response (pathological inflammation, allergies, autoimmune disorders) | [156] |
Sulfonamide resistance | KM mice | PET-MNPs | Locally purchased mineral water bottles were cut and mechanically broke into small particles with the aid of a kitchen blender | Not clear | 63.4 μm | Increase the relative abundance of multidrug genes | [158] |