Nanoparticle Toxicology in Pulmonary Systems

Engineered nanoparticles, typically ranging from 1 to 100 nm in at least one dimension, present unique challenges to respiratory health owing to their high surface area, varied chemical composition and potential to reach deep lung compartments. Following inhalation, particles deposit along the airways and in the alveolar spaces, where they interact with epithelial cells and alveolar macrophages. Physicochemical properties such as surface functional groups, crystal structure, shape and solubility govern the generation of reactive oxygen species, membrane perturbation and the release of pro-inflammatory mediators. Persistent inflammation can lead to epithelial injury, pulmonary fibrosis and systemic acute phase responses that elevate cardiovascular risk. Translocation of particles or particle-derived ions across the air–blood barrier can provoke genotoxicity in extrapulmonary organs, notably the liver. Recent advances have elucidated quantitative relationships between surface-specific metrics, oxidative potential and biological endpoints, facilitating predictive models of hazard. Understanding the interplay between dose metrics, clearance mechanisms and host susceptibility remains essential to guide safe design and regulatory frameworks for nanomaterials in occupational and environmental settings.

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Nanoparticle Toxicology in Pulmonary Systems publication trend

The graph below shows the total number of articles in nanoparticle toxicology in pulmonary systems across all publications each year (not limited to Nature Index journals).

Technical terms

Reactive oxygen species (ROS): Chemically reactive oxygen-containing molecules that can damage cellular lipids, proteins and DNA.

Acute phase response (APR): Systemic inflammatory reaction characterised by altered production of acute-phase proteins such as serum amyloid A.

Bronchoalveolar lavage (BAL): Sampling technique in which fluid is instilled and recollected from the lower respiratory tract to assess inflammatory cells and mediators.

BET specific surface area (SSA): Measurement of total surface area per unit mass of a material, determined by gas adsorption methods.

Alveolar macrophage (AM): Resident immune cell in pulmonary alveoli responsible for clearance of particulates and orchestration of inflammatory responses.

References

1. Toxicity of carbon nanomaterials: A model to predict ROS production from easily measurable surface characteristics. Carbon (2025).
2. Acute phase response following pulmonary exposure to soluble and insoluble metal oxide nanomaterials in mice. Particle and Fibre Toxicology (2023).
3. Carbon black nanoparticle instillation induces sustained inflammation and genotoxicity in mouse lung and liver. Particle and Fibre Toxicology (2012).