RESUMEN
The effect of microplastics on the ecological environment and human health has become a topical issueï¼ and research on the risks and harmful effects of MPs on human health in particular has attracted widespread attention. Due to the characteristics of small sizeï¼ low degradabilityï¼ and easy migrationï¼ MPs continuously migrate from the environment to the human bodyï¼ and their main exposure pathways are oral ingestionï¼ inhalationï¼ and dermal contactï¼ with the main exposure media being foodï¼ drinking waterï¼ dustï¼ personal care productsï¼ etc. MPs have been detected in organsï¼ fluidsï¼ and excreta of digestiveï¼ respiratoryï¼ cardiovascularï¼ reproductive systemsï¼ etc. The abundance range of MPs in the human body is 0-1 206.94 particles per gram. After entering the human bodyï¼ MPs can cause cytotoxicityï¼ mitochondrial toxicityï¼ DNA damageï¼ cell membrane damageï¼ and other effects on human cells and organsï¼ leading to serious consequences such as local inflammationï¼ ecological imbalanceï¼ metabolic disordersï¼ etc.ï¼ in various systems. Owing to their small specific surface areaï¼ they can also adsorb pollutants such as heavy metalsï¼ organic pollutantsï¼ antibioticsï¼ pathogensï¼ and harmful microorganismsï¼ causing combined toxicity and immunotoxicity. In the endï¼ we highlighted general deficiencies in existing studies and provided directions for future research on the influence of MPs on human health.
Asunto(s)
Contaminantes Ambientales , Metales Pesados , Contaminantes Químicos del Agua , Humanos , Microplásticos , Plásticos , Contaminantes Químicos del Agua/análisisRESUMEN
Ocular surface diseases are common in the plateau city, Kunming China, the continued daily exposure to heavy metals in dust may be an important inducement. In this study, the 150 road dust samples from five functional areas in Kunming were collected. The concentrations, distribution, possible sources, and bioaccessibility of heavy metals were analyzed. The adverse effects of dust extracts on human corneal epithelial cells and the underlying mechanisms were also assessed. The concentrations (mg·kg-1) of As (19.1), Cd (2.67), Cr (90.5), Cu (123), Pb (78.4), and Zn (389) in road dust were higher than the soil background, with commercial and residential areas showing the highest pollution. Their bioaccessibility in artificial tears was As (6.59 %) > Cu (5.11 %) > Ni (1.47 %) > Cr (1.17 %) > Mn (0.84 %) > Cd (0.76 %) > Zn (0.50 %) > Pb (0.31 %). The two main sources of heavy metals included tire and mechanical abrasion (24.5 %) and traffic exhaust (21.6 %). All dust extracts induced cytotoxicity, evidenced by stronger inhibition of cell viability, higher production of ROS, and altered mRNA expression of antioxidant enzymes and cell cycle-related genes, with commercial- areas-2 (CA2)-dust extract showing the greatest oxidative damage and cell cycle arrest. Our data may provide new evidence that dust exposure in high geological background cities could trigger human cornea damage.
Asunto(s)
Polvo , Metales Pesados , Humanos , Polvo/análisis , Ciudades , Monitoreo del Ambiente , Cadmio , Plomo , Metales Pesados/toxicidad , Metales Pesados/análisis , China , Medición de RiesgoRESUMEN
Tris(2-chloroisopropyl) phosphate (TCPP) and Tris(2-chloroethyl) phosphate (TCEP) are the widely used organophosphorus flame retardants indoors and easily accessible to the eyes as the common adhesive components of dust and particle matter, however, hardly any evidence has demonstrated their corneal toxicity. In this study, the adverse effects of TCPP, TCEP, and TCPP + TCEP exposure on human corneal epithelial cells (HCECs) were investigated. The cell viability and morphology, intracellular reactive oxygen species (ROS), cell cycle, and the expressions of cell cycle and pyroptosis-related genes were assessed to explain the underlying mechanisms. Compared to individual exposure, co-exposure to TCPP20+TCEP20 showed higher cytotoxicity with a sharp decrease of >30% in viability and more serious oxidative damage by increasing ROS production to 110.92% compared to the control group. Furthermore, the cell cycle arrested at the S phase (36.20%) was observed after combined treatment, evidenced by the upregulation of cyclin D1, CDK2, CDK4, CDK6, p21, and p27. Interestingly, pyroptosis-related genes GSDMD, Caspase-1, NLRP3, IL-1ß, IL-18, NLRP1, and NLRC4 expressions were promoted with cell swelling and glowing morphology. Oxidative stress and cell cycle arrest probably acted as a key role in TCPP20+TCEP20-induced cytotoxicity and pyroptosis in HCECs. Our results suggested that TCPP20+TCEP20 co-exposure induced severer corneal damage, further illustrating its significance in estimating indoor health hazards to humans.