Malnutrition assessed by the mini nutritional assessment is associated with overall survival in patients with resectable non-small cell lung cancer.

The large-scale production and widespread use of plastic products have promoted the development of modern society [,,], but have also led to the persistent accumulation of plastic waste in the environment, where it can further fragment into microplastics (MPs) and nanoplastics (NPs) [,]. Current studies generally define plastic particles smaller than 5 mm as MPs, whereas smaller particles, usually less than 1 μm, are commonly classified as NPs. The World Health Organization has noted that the main routes of human exposure to MPs and NPs include dietary intake and inhalation [,]. Food, water, and air together constitute a continuous, low-dose, and long-term exposure background [,]. However, substantial uncertainties remain regarding human exposure levels, fate, and health risks [,,]. Compared with conventional chemical pollutants, the health risks of microplastics and nanoplastics (MNPs) are more complex []. On the one hand, MNPs are characterized by small particle size, large specific surface area, and abundant surface functional groups, which enable them to directly interact with the intestinal mucus layer, cell membranes, mitochondria, and immune cells [,,]. These interactions are particularly important for NPs, whose nanoscale dimensions may facilitate trans-epithelial transport, cellular uptake, organelle stress, and systemic distribution. In addition, MNPs surfaces can adsorb organic contaminants, heavy metals, as well as pathogen-associated molecular patterns, which further modulates the bioavailability and toxicokinetic profiles of co-occurring pollutants within biological organisms [,,,,]. Accordingly, MNPs function not only as inherent pollutants but also as effective carriers of exogenous contaminants. Their toxic effects are far beyond simple linear additivity, instead presenting as a pathological cascade involving intestinal barrier impairment, inflammatory exacerbation, and metabolic dysregulation. In recent years, the concept of gut-organ axis has offered an innovative holistic framework to decipher MNPs-triggered systemic toxicity [,]. The intestine serves not only as a key organ for nutrient absorption, but also as the body’s largest immune and microbial ecological interface []. Upon entry into the organism, MNPs initially interact with the intestinal mucus layer, resident microbiota, and epithelial cells within the intestinal lumen []. Intestinal microecological dysbiosis suppresses the expression of tight junction proteins and elevates intestinal barrier permeability. Subsequently, lipopolysaccharide (LPS), bile acids, short-chain fatty acids (SCFAs), tryptophan metabolites, arachidonic acid derivatives, and inflammatory mediators can target distal organs the portal vein, systemic circulation, and neuroendocrine pathways, ultimately initiating pathological responses across the gut-liver, gut-brain, gut-kidney, gut-lung, and gut-reproductive axes. Therefore, the central question is no longer whether MNPs can damage individual organs, but how intestinal injury is translated into systemic toxicity through interorgan communication.