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<p>Airborne nanoplastics (NPs) are increasingly recognized as an emerging respiratory health concern because their small size enables deposition in the distal lung, where they can interact directly with the alveolar microenvironment. However, the sequence of mechanisms linking their initial physicochemical interactions to chronic pulmonary outcomes remains insufficiently defined. This review integrates recent evidence to propose a mechanistic framework connecting early biophysical barrier disruption with intracellular stress signaling and progressive lung pathology. We discuss how inhaled NPs may destabilize lung surfactant (LS) structure and function and acquire biological coronas that modify their cellular interactions and uptake. We then examine how lysosomal dysfunction, impaired mitophagy, and mitochondrial damage amplify oxidative stress and promote the release of mitochondrial danger signals, leading to activation of cGAS-STING and the NLRP3 inflammasome. These events contribute to sterile inflammation, pyroptotic signaling, ferroptotic cell death, and profibrotic remodeling. Particular attention is given to epithelial injury, fibroblast metabolic reprogramming, and immune dysregulation as key processes that may underlie asthma exacerbation and pulmonary fibrosis. Finally, we highlight current knowledge gaps, including the limited relevance of short-term high-dose models to chronic low-dose inhalation scenarios, and discuss priorities for future research, biomarker development, and mechanism-based intervention strategies.</p> Graphical abstract <p></p>

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Inhalation toxicity of nanoplastics: mechanistic insights from biophysical barrier disruption to chronic lung diseases

  • 期刊论文

  • 发表日期：

    2026年6月27日

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  • Mi-kyung Song,
  • Kyuhong Lee

摘要

Airborne nanoplastics (NPs) are increasingly recognized as an emerging respiratory health concern because their small size enables deposition in the distal lung, where they can interact directly with the alveolar microenvironment. However, the sequence of mechanisms linking their initial physicochemical interactions to chronic pulmonary outcomes remains insufficiently defined. This review integrates recent evidence to propose a mechanistic framework connecting early biophysical barrier disruption with intracellular stress signaling and progressive lung pathology. We discuss how inhaled NPs may destabilize lung surfactant (LS) structure and function and acquire biological coronas that modify their cellular interactions and uptake. We then examine how lysosomal dysfunction, impaired mitophagy, and mitochondrial damage amplify oxidative stress and promote the release of mitochondrial danger signals, leading to activation of cGAS-STING and the NLRP3 inflammasome. These events contribute to sterile inflammation, pyroptotic signaling, ferroptotic cell death, and profibrotic remodeling. Particular attention is given to epithelial injury, fibroblast metabolic reprogramming, and immune dysregulation as key processes that may underlie asthma exacerbation and pulmonary fibrosis. Finally, we highlight current knowledge gaps, including the limited relevance of short-term high-dose models to chronic low-dose inhalation scenarios, and discuss priorities for future research, biomarker development, and mechanism-based intervention strategies.

Graphical abstract