The co-existence of organic pollutants and nanoparticles in the environment may lead to combined biological effects. The joint toxicity of pollutants and nanoparticles has been receiving increasing attention from researchers, but few studies have focused on soil biota due to the complexity of soil matrices. This study investigated the effects of tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) at 0, 5, and 25 mg/kg and nanoparticulate TiO₂ (nTiO₂) at 0, 500, and 2500 mg/kg in a 3 × 3 factorial arrangement of treatments for 28 days (d) on Eisenia fetida (earthworm). Compared with the control group (the 0 mg/kg TDCIPP + 0 mg/kg nTiO₂ treatment), all other single (TDCIPP or nTiO₂) and binary (TDCIPP + nTiO₂) treatments except for the single 500 mg/kg nTiO₂ treatment significantly reduced the weight gain rate of E. fetida. The binary treatments had significantly greater such effect than their corresponding single treatments, exhibiting a synergistic toxicity between TDCIPP and nTiO2 on the growth of E. fetida. Since TDCIPP and nTiO₂ had no significant effect on their concentrations in the soil or in E. fetida during binary exposure, the synergistic toxicity could be a result of the superimposition of the toxicity pathways of TDCIPP and nTiO₂. Transcriptomic analysis of E. fetida intestinal region revealed that exposure to 25 mg/kg TDCIPP or 2500 mg/kg nTiO₂ affected nutrient-related or cell apoptosis and DNA damage related genes, respectively; their co-exposure greatly inhibited genes related to nutrient digestion and absorption, while causing abnormal transcription of genes related to the development and maintenance of E. fetida's muscles, leading to synergistic toxicity. These findings provide new insights into the environmental risks of organophosphorus flame retardants, nanoparticles, and their co-exposure.

Asthma is a chronic respiratory disease that is highly sensitive to environmental pollutants, including engineered nanoparticles (NPs). Exposure to NPs has become a growing concern for human health, especially for susceptible populations. Toxicological studies have demonstrated strong associations between ubiquitous NPs and allergic asthma. In this review, we analyze articles that focus on adverse health effects induced by NPs in animal models of allergic asthma to highlight their critical role in asthma. We also integrate potential mechanisms that could stimulate and aggravate asthma by NPs. The toxic effects of NPs are influenced by their physicochemical properties, exposure dose, duration, route, as well as the exposure order between NPs and allergens. The toxic mechanisms involve oxidative stress, various inflammasomes, antigen presenting cells, immune cells, and signaling pathways. We suggest that future research should concentrate on establishing standardized models, exploring mechanistic insights at the molecular level, assessing the combined effects of binary exposures, and determining safe exposure levels of NPs. This work provides concrete evidence of the hazards posed by NPs in animals with compromised respiratory health and supports the modifying role of NPs exposure in allergic asthma. Graphical Abstract: