A multi-omics investigation of pulmonary and hepatic toxicity induced by polyamide and polyacrylonitrile microplastics via ingestion and inhalation exposures.

Microplastics (MP) are pervasive environmental contaminants in human habitats. Polyamide (PA) and polyacrylonitrile (PAN) MP, frequently shed from synthetic textiles, can enter the human body. However, their potential respiratory and hepatic toxicity remain largely unexplored. This study investigated the pulmonary toxicity of airborne PA and PAN MP, as well as the hepatotoxicity of foodborne PA and PAN MP. Airborne PA and PAN MP induced respiratory microbial dysbiosis, serum and pulmonary metabolic perturbations, hepatic transcriptomic deregulation, and pulmonary toxicity. Similarly, foodborne PA and PAN MP triggered intestinal microbial and metabolic disruptions, serum metabolic disturbances, hepatic transcriptomic perturbations, and hepatotoxicity. Distinct critical toxicity pathways were associated with different MP exposures: arachidonic acid metabolism for airborne PA; choline metabolism in cancer and cAMP signaling pathway for airborne PAN; riboflavin metabolism and neuroactive ligand-receptor interaction for foodborne PA; and steroid hormone biosynthesis and central carbon metabolism in cancer for foodborne PAN. The findings demonstrate that airborne PA and PAN MP perturb the respiratory microbiota-lung axis and cause pulmonary toxicity, whereas foodborne PA and PAN MP interfere with the intestinal microbiota-intestine-liver axis and induce hepatotoxicity. These findings advance the hazard assessment of PA and PAN MP, while highlighting the critical need to reduce exposure to these pervasive environmental contaminants.