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Microplastics (MPs) are widely identified as emerging hazards causing considerable eco-toxicity in terrestrial ecosystems, but the impacts differ in different ecosystem functions among different chemical compositions, morphology, sizes, concentrations, and experiment duration. Given the close relationships and trade-offs between plant and soil systems, probing the "whole ecosystem" instead of individual functions must yield novel insights into MPs affecting terrestrial ecosystems. Here, a comprehensive meta-analysis was employed to reveal an unambiguous response of the plant-soil-microbial system to MPs. Results showed that in view of plant, soil, and microbial functions, the general response patterns of plant and soil functions to MPs were obviously opposite. For example, polyethylene (PE) and polyvinyl chloride (PVC) MPs highly increased plant functions, while posed negative effects on soil functions. Polystyrene (PS) and biodegradable (Bio) MPs decreased plant functions, while stimulating soil functions. Additionally, low-density polyethylene (LDPE), PE, PS, PVC, Bio, and granular MPs significantly decreased soil microbial functions. These results clearly revealed that MPs alter the equilibrium of the plant-soil-microbial system. More importantly, our results further revealed that MPs tended to increase ecosystem multifunctionality, e.g., LDPE and PVC MPs posed positive effects on ecosystem multifunctionality, PE, PS, and Bio MPs showed neutral effects on ecosystem multifunctionality. Linear regression analysis showed that under low MPs size (<100 µm), ecosystem multifunctionality was gradually reduced with the increased size of MPs. The response of ecosystem multifunctionality showed a concave shape pattern along the gradient of experimental duration which was lower than 70 days. More importantly, there was a threshold (i.e., 5% w/w) for the effects of MPs concentration on ecosystem multifunctionality, i.e., under low concentration (< 5% w/w), ecosystem multifunctionality was gradually increased with the increased concentration of MPs, while ecosystem multifunctionality was gradually decreased under high concentration (i.e., > 5% w/w). These findings emphasize the importance of studying the effects of MPs on plant-soil-microbial systems and help us identify ways to reduce the eco-toxicity of MPs and maintain environmental safety in view of an ecology perspective. [Display omitted] • MPs posed opposite effects on plant and soil functions. • Soil microbial functions endured more severe damage from MPs. • MPs are likely to cause positive effects on ecosystem multifunctionality. • Impacts of MPs on EMF are type, size, concentration and duration dependency. [ABSTRACT FROM AUTHOR]

Carbon black nanoparticles (CBNPs) and cadmium (Cd) are major components of various air pollutants and cigarette smoke. Autophagy and inflammation both play critical roles in understanding the toxicity of particles and their components, as well as maintaining body homeostasis. However, the effects and mechanisms of CBNPs and Cd (CBNPs-Cd) co-exposure on the human respiratory system remain unclear. In this study, a CBNPs-Cd exposure model was constructed to explore the respiratory toxicity and combined mechanism of these chemicals on the autophagy-lysosome pathway in the context of respiratory inflammation. Co-exposure of CBNPs and Cd significantly increased the number of autophagosomes and lysosomes in human bronchial epithelial cells (16HBE) and mouse lung tissues compared to the control group, as well as the groups exposed to CBNPs and Cd alone. Autophagic markers, LC3II and P62 proteins, were up-regulated in 16HBE cells and mouse lung tissues after CBNPs-Cd co-exposure. However, treatment with Cq inhibitor (an indicator of lysosomal acid environment) resulted in a substantial decreased co-localization fluorescence of LC3 and lysosomes in the CBNPs-Cd combination group compared with the CBNPs-Cd single and control groups. No difference in LAMP1 protein expression was observed among the exposed groups. Adding 3 MA alleviated inflammatory responses, while applying the Baf-A1 inhibitor aggravated inflammation both in vitro and in vivo following CBNPs-Cd co-exposure. Factorial analysis showed no interaction between CBNPs and Cd in their effects on 16HBE cells. We demonstrated that co-exposure to CBNPs-Cd increases the synthesis of autophagosomes and regulates the acidic environment of lysosomes, thereby inhibiting autophagy-lysosome fusion and enhancing the inflammatory response in both 16HBE cells and mouse lung. These findings provide evidence for a comprehensive understanding of the interaction between CBNPs and Cd in mixed pollutants, as well as for the prevention and control of occupational exposure to these two chemicals. • CBNPs and Cd co-exposure increases inflammation in respiratory epithelial cells. • CBNPs and Cd co-exposure targets autophagosome formation and autophagy-lysosomal fusion. • CBNPs and Cd co-exposure disrupts the lysosomal acidic environment. • CBNPs and Cd co-exposure aggravates inflammation by blocking autophagic flux. [ABSTRACT FROM AUTHOR]