Aggregation kinetics of polystyrene nanoplastics in gastric environments: Effects of plastic properties, solution conditions, and gastric constituents.

Nanoplastics are inevitably ingested into human gastric environment, wherein their aggregation kinetics and interactions with gastric constituents remain unclear. This study investigated the early-stage (20 min) and long-term (1-6 h) aggregation kinetics of four commonly-found polystyrene nanoplastics (PSNPs) including NP100 (100-nm), A-NP100 (100-nm, amino-modified), C-NP100 (100-nm, carboxyl-modified), and NP500 (500-nm) under gastric conditions. Five simulated human gastric fluids (SGFs) including SGF1-3 (0-3.2 g/L pepsin and 34.2 mM NaCl), SGF4 (400 mM glycine), and SGF5 (nine constituents), three pH (2, fasted state; 3.5, late-fed state; and 5, early-fed state), and 1-100 mg/L PSNPs were examined. Aggregation rates ranked NP100 > A-NP100 ≈ C-NP100 > NP500, SGF5 > SGF4 > SGF3 > SGF2 > SGF1, and pH 2 > 3.5 > 5. Increasing PSNP concentration enhanced aggregation rate up to 13.82 nm/s. Aggregation behavior generally followed the Derjaguin-Landau-Verwey-Overbeek (DLVO) theory. Pepsin, glycine, and proteose-peptone strongly influenced PSNP stability via electrostatic interaction and steric hindrance imparted by protein corona. Freundlich isotherm suggested that PSNPs adsorbed organic constituents following lysozyme > porcine bile > proteose-peptone > pepsin > glycine > D-glucose, inducing changes in constituent structure and PSNP properties. These findings provide insights on the transport of nanoplastics in the gastric environments.

Toxicity of micro(nano)plastics with different size and surface charge on human nasal epithelial cells and rats via intranasal exposure.

Micro (nano)plastics (MNPs) have become emerging environmental contaminants, yet their toxicity and systemic effects via intranasal exposure remain unclear. This study investigated the in vitro toxicity of thirteen polystyrene MNPs with different surface functionalization (carboxylic (C-PS), amino (A-PS), and bare (PS)) and sizes (20-2000 nm) on human nasal epithelial cells (HNEpCs) at 10-1250 µg/mL as well as their in vivo toxicity to rats via intranasal administration at 125 µg/mL. The in vitro study showed that PS20, PS50, A-PS50, PS500, and A-PS500 significantly inhibited cell viability, which was dependent on particle concentration. A-PS induced higher cytotoxicity than C-PS and PS, and most MNPs inhibited cell proliferation after 24-h. Flow cytometry analysis suggested that PS induced cell apoptosis, while A-PS caused cell necrosis. MNPs were phagocytosed by HNEpCs and entered nucleus. The in vivo study showed that MNPs inhibited dietary behaviors of rats. Histological analysis indicated that PS20, PS200, and A-PS50 thinned out nasal mucosa. Immunohistochemical analysis revealed that exposure to PS20, PS200, and A-PS50 enhanced expression of transient receptor potential cation channel subfamily M (melastatin) member 8 (TRPM8). Systemic effects including hepatocyte cytoplasmic vacuolation and renal tubule dilatation were observed. The results suggested that nasal inhalation of MNPs may disturb energy metabolism and damage upper respiratory tract, liver, and kidneys.