Researchers from the Institute of Applied Ecology of the Chinese Academy of Sciences and Shengjing Hospital of China Medical University have examined the respiratory effects of inhaled nanoplastics and found that repeated exposure to nanoplastics can induce sustained pulmonary injury in mice.

The study was published in Ecotoxicology and Environmental Safety on March 12.

Nanoplastics are extremely small plastic particles typically less than one micrometer in size. Due to their low density, small particle diameter, and large surface area, they can remain suspended in the atmosphere for extended periods and be easily transported over long distances. These characteristics enable them to be inhaled through the respiratory system and subsequently deposited in lung tissue, posing potential risks to respiratory health. However, the toxic effects and underlying mechanisms of inhaled nanoplastics remain insufficiently understood, especially regarding continuous exposure and persistent toxicity after exposure cessation.

To address these knowledge gaps, the researchers led by Dr. XU Mingkai and Prof. LI Tiegang developed a mouse model of polystyrene nanoplastics (PS-NPs) inhalation exposure via intratracheal instillation. They exposed C57BL/6 mice (six to eight weeks old) to particles of 25, 100, and 500 nm at doses of 1 mg/kg and 5 mg/kg over a four-week period, followed by a two-week post-exposure observation phase.

The researchers found that the inhaled nanoplastics accumulated in the lung tissue of the mice and were translocated to distant organs, including the heart, liver, spleen, and kidneys, and reduced peripheral white blood cell counts. In the lungs, nanoplastic exposure disrupted the alveolar epithelial barrier, induced inflammatory responses and oxidative stress in lung tissue, impaired lung function, and promoted collagen deposition, thereby promoting the progression of pulmonary fibrosis. Pulmonary fibrosis is a progressive and chronic lung disease characterized by alveolar epithelial barrier injury and excessive collagen deposition, gradually impairing respiratory capacity.

The researchers also discovered that the toxic effects were strongly size-dependent, with smaller particles inducing greater toxicity. Furthermore, adverse effects persisted during the post-exposure period, suggesting that PS-NPs-induced injury is not easily reversible in the short term.

Further analysis revealed that macrophage polarization may contribute to the progression of PS-NP-induced pulmonary fibrosis. Macrophages are key effector and regulatory cells in particle-induced pulmonary pathology. They exhibit high plasticity and can polarize into classically activated (M1) or alternatively activated (M2) phenotypes. These phenotypes are closely associated with the progression of pulmonary fibrosis.

The researchers observed a shift in pulmonary macrophages from the M1 to the M2 phenotype, suggesting that this transition contributes to the development of fibrosis following nanoplastic exposure.