Neurotoxic effects of polystyrene nanoplastics on memory and microglial activation: Insights from in vivo and in vitro studies.

Nanoplastics, arising from the fragmentation of plastics into environmental pollutants and specialized commercial applications, such as cosmetics, have elicited concerns due to their potential toxicity. Evidence suggests that the oral ingestion of nanoplastics smaller than 100 nm may penetrate the brain and induce neurotoxicity. However, comprehensive research in this area has been hampered by technical challenges associated with the detection and synthesis of nanoplastics. This study aimed to bridge this research gap by successfully synthesizing fluorescent polystyrene nanoplastics (PSNPs, 30-50 nm) through the incorporation of IR-813 and validating them using various analytical techniques. We administered PSNPs orally (10 and 20 mg/kg/day) to mice and observed that they reached brain tissues and induced cognitive dysfunction, as measured by spatial and fear memory tests, while locomotor and social behaviors remained unaffected. In vitro studies (200 µg/mL) demonstrated a predominant uptake of PSNPs by microglia over astrocytes or neurons, leading to microglial activation, as evidenced by immunostaining of cellular markers and morphological analysis. Transcriptomic analysis indicated that PSNPs altered gene expression in microglia, highlighting neuroinflammatory responses that may contribute to cognitive deficits. To further explore the neurotoxic effects of PSNPs mediated by microglial activation, we measured endogenous neuronal activity using a multi-electrode array in cultured hippocampal neurons. The application of conditioned media from microglia exposed to PSNPs suppressed neuronal activity, which was reversed by inhibitors of microglial activation. Our findings offer detailed insights into the mechanisms by which nanoplastics damage the brain, particularly emphasizing the potential environmental risk factors that contribute to cognitive impairment in neurodegenerative diseases.

Survival of human coronavirus 229E at different temperatures on various food-contact surfaces and food and under simulated digestive conditions.

The COVID-19 pandemic caused by SARS-CoV-2 has had a major impact on human health and the global economy. Various transmission possibilities of SARS-CoV-2 have been proposed, such as the surface of food in the cold chain and food packaging, as well as the fecal-oral route, although person-to-person contact via droplets and aerosols has been confirmed as the main route of transmission. This study evaluated the survivability of HCoV-229E, a SARS-CoV-2 surrogate, in suspension, on food-contact surfaces and on food at various temperatures, and in simulated digestive fluids by TCID50 assay. In suspension, HCoV-229E survived after 5 days at 20 °C with a 3.69 log reduction, after 28 days at 4 °C with a 3.07 log reduction, and after 12 weeks at -20 °C with a 1.18 log reduction. On food-contact surfaces, HCoV-229E was not detected on day 3 on stainless steel (SS), plastic (LDPE), and silicone rubber (SR) at 20 °C with a 3.28, 3.24 and 3.28 log reduction, respectively, and survived after 28 days on SS and LDPE at 4 °C with a 3.13 and 2.88 log reduction, respectively, and survived after 12 weeks on SS, LDPE, and SR at -20 °C with a 1.92, 1.32 and 1.99 log reduction, respectively. On food, HCoV-229E was not detected on day 3 on lettuce and day 4 on chicken breast and salmon at 20 °C with a 3.61, 3.26 and 3.08 log reduction, respectively, and on day 14 on lettuce and day 21 on chicken breast and salmon at 4 °C with a 3.88, 3.44 and 3.56 log reduction, respectively. The virus remained viable for 12 weeks in all foods at -20 °C with 2-2.47 log reduction. In addition, in simulated digestive fluid experiments, HCoV-229E was relatively resistant in simulated salivary fluid (SSF; pH 7, 5), fed state simulated gastric fluid (FeSSGF; pH 3, 5, 7), and fasted state simulated intestinal fluid (FaSSIF; pH 7). However, the virus was less tolerant in fasted state simulated gastric fluid (FaSSGF; pH 1.6) and fed state simulated intestinal fluid (FeSSIF; pH 5). Therefore, this study suggested that HCoV-229E remained infectious on various food-contact surfaces and foods; in particular, it survived longer at lower temperatures and survived depending on the pH of the simulated digestive fluid.

Inactivation methods for human coronavirus 229E on various food-contact surfaces and foods.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the cause of the COVID-19 outbreaks, is transmitted by respiratory droplets and has become a life-threatening viral pandemic worldwide. The aim of this study was to evaluate the effects of different chemical (chlorine dioxide [ClO2] and peroxyacetic acid [PAA]) and physical (ultraviolet [UV]-C irradiation) inactivation methods on various food-contact surfaces (stainless steel [SS] and polypropylene [PP]) and foods (lettuce, chicken breast, and salmon) contaminated with human coronavirus 229E (HCoV-229E). Treatments with the maximum concentration of ClO2 (500 ppm) and PAA (200 ppm) for 5 min achieved >99.9% inactivation on SS and PP. At 200 ppm ClO2 for 1 min on lettuce, chicken breast, and salmon, the HCoV-229E titers were 1.19, 3.54, and 3.97 log10 TCID50/mL, respectively. Exposure (5 min) to 80 ppm PAA achieved 1.68 log10 reduction on lettuce, and 2.03 and 1.43 log10 reductions on chicken breast and salmon, respectively, treated with 1500 ppm PAA. In the carrier tests, HCoV-229E titers on food-contact surfaces were significantly decreased (p < 0.05) with increased doses of UV-C (0-60 mJ/cm2) and not detected at the maximum UV-C dose (Detection limit: 1.0 log10 TCID50/coupon). The UV-C dose of 900 mJ/cm2 proved more effective on chicken breast (>2 log10 reduction) than on lettuce and salmon (>1 log10 reduction). However, there were no quality changes (p > 0.05) in food samples after inactivation treatments except the maximum PAA concentration (5 min) and the UV-C dose (1800 mJ/cm2).