Previous studies have indicated that engineered nanomaterials can be transferred through the food chain. However, their potential ecotoxicity to the environment is not fully understood. Here, we systematically evaluated the physiological behavior and toxicity of polyvinylpyrrolidone (PVP)-coated silver nanoparticles (AgNPs) using a food chain model from Escherichia coli (E. coli) to Caenorhabditis elegans (C. elegans). Our results demonstrated that AgNPs accumulated in E. coli could be transferred to the C. elegans, and AgNPs were clearly distributed in the gut lumen, subcutaneous tissue and gonad. After being transferred to C. elegans through the food chain, the accumulated AgNPs caused serious toxicity to the higher trophic level (C. elegans), including effects on germ cell death, reproductive integrity and life span. Relative to larger particles (75 nm), small AgNPs (25 nm) more easily accumulated in the food chain and exhibited a stronger toxicity to the higher trophic level. More importantly, both the AgNPs that had accumulated in C. elegans through the food chain and the resulting impairment of germ cells could be transferred to the next generation, indicating that AgNP can cause genetic damage across generations. Our findings highlight that nanomaterials pose potential ecotoxicity to ecosystems via transport through the food chain.

Particulate matter 2.5 (PM2.5) is a widely known atmospheric pollutant which can induce the aging-related pulmonary diseases such as acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD) and interstitial pulmonary fibrosis (IPF). In recent years, with the increasing atmospheric pollution, airborne fine PM2.5, which is an integral part of air pollutants, has become a thorny problem. Hence, this study focused on the effect of PM2.5 on cellular senescence in the lung, identifying which inflammatory pathway mediated PM2.5-induced cellular senescence and how to play a protective role against this issue. Our data suggested that PM2.5 induced time- and concentration-dependent increasement in the senescence of A549 cells. Using an inhibitor of cGAS (PF-06928215) and an inhibitor of NF-κB (BAY 11-7082), it was revealed that PM2.5-induced senescence was regulated by inflammatory response, which was closely related to the cGAS/STING/NF-κB pathway activated by DNA damage. Moreover, our study also showed that the pretreatment with selenomethionine (Se-Met) could inhibit inflammatory response and prevent cellular senescence by hindering cGAS/STING/NF-κB pathway in A549 cells exposed to PM2.5. Furthermore, in vivo C57BL/6J mice model demonstrated that aging of mouse lung tissue caused by PM2.5 was attenuated by decreasing cGAS expression after Se-Met treatment. Our findings indicated that selenium made a defense capability for PM2.5-induced cellular senescence in the lung, which provided a novel insight for resisting the harm of PM2.5 to human health.