Jing Cong

Microplastics (MPs) can modify the partitioning, uptake, and biological effects of co‐occurring contaminants, yet zebrafish studies have reported markedly divergent combined responses. This critical review evaluates co‐exposure to MPs and metals, pesticides, or antibiotics using two complementary dimensions: confidence in interaction classification and confidence in mechanistic attribution. Across the 86 original research studies, only 12 (13.9%) met the high‐confidence criteria for interaction classification and 13 (15.1%) for mechanistic attribution, whereas 28 (32.6%) and 41 (47.7%), respectively, provided limited evidence. Claims of synergy or antagonism are considered robust only when supported by concentration–response data, an explicit additivity model, and quantitative uncertainty analysis. Mechanistic interpretation distinguishes external contaminant partitioning from internal delivery. Sorption to MPs may lower freely dissolved concentrations and produce sequestration, increase internal exposure when ingestion is followed by biologically relevant release, or coexist with stronger toxicity caused by particle‐induced sensitization. Across contaminant classes, the observed outcomes are influenced by chemical speciation and ionization, particle size and aging, matrix chemistry, exposure route, gastrointestinal release, tissue burden, and developmental stage. Concentration addition and independent action remain useful reference models, but applications based only on nominal concentrations are difficult to interpret when MPs alter the biologically effective dose, exposure route, or host susceptibility. Future studies should combine complete factorial and concentration–response designs with measurements of freely dissolved, particle‐associated, gastrointestinally bioaccessible, and tissue‐associated fractions, together with chronic, route‐specific exposure and toxicokinetic analyses.

Metabolic dysfunction–associated steatotic liver disease is associated with a growing global health burden with increasing prevalence in both adult and pediatric populations. Emerging evidence suggests that the origins of steatotic liver disease may trace back to early life, with the gut microbiota serving as a critical mediator in this developmental programming. This review synthesizes current knowledge on maternal-infant gut microbiota transmission and its role in shaping long-term liver health through the gut-liver axis. We examined key maternal factors, including delivery mode, feeding of breast milk, diet, metabolic status, and antibiotic exposure, that profoundly influence infant microbiota assembly. The critical window of microbiota establishment during the first 1000 days shapes intestinal barrier function, immune development, and metabolic pathways that persist into adulthood. Mechanistically, early dysbiosis contributes to metabolic dysfunction–associated steatotic liver disease pathogenesis through multiple interconnected pathways, including compromised intestinal barrier integrity facilitating endotoxemia, altered short-chain fatty acid production affecting energy metabolism and inflammation, disturbed bile acid signaling disrupting metabolic homeostasis, and epigenetic modifications potentially shaping long-term susceptibility. We critically evaluated emerging microbiota-targeted interventional strategies during pregnancy and infancy, including probiotics, human milk oligosaccharide supplementation, and synbiotic approaches, highlighting their potential for disease prevention. This review uniquely integrates concepts of developmental origins with detailed gut-liver axis mechanisms, emphasizing the maternal-infant microbial continuum as an underexplored but promising target for preventing metabolic liver disease. While significant research challenges remain, particularly in establishing causality and developing personalized interventions, modulation of the early gut microbiome offers an innovative preventive strategy against the rising tide of metabolic dysfunction–associated steatotic liver disease, potentially disrupting the intergenerational cycle of metabolic disease.