Molecular mechanisms of dust-induced lung disease: exploring the role of physicochemical composition and cellular pathways
- 1School of Civil and Environmental Engineering, Water Research Centre, The University of New South Wales, Sydney, NSW 2052 Australia
Abstract
Background: Respirable dust and fibres in occupational settings are major contributors to lung dysfunction, imposing a significant societal burden. Following the ban on asbestos in most countries, silica and coal mine dust have emerged as primary concerns due to their abundance and persistence in workplace dust. Exposure to dust containing these elements has been strongly linked to pulmonary fibrosis and lung cancer.
Main body: Extensive research has explored the molecular mechanisms underlying respirable occupational dust-induced cytotoxicity and immune dysregulation. The toxic effects of respirable occupational dust and fibres are largely induced by oxidative stress, mitochondrial dysfunction, lysosomal damage, inflammasome activation and immune suppression. These exposures can trigger multiple cell death pathways, including ferroptosis, necrosis, and pyroptosis. While sharing common toxicological features, silica, coal dust, and asbestos exhibit distinct toxic effects on various pulmonary cell types involved in fibrosis and cancer progression. The immunological consequences of dust exposure are profound, as dust-induced activation of macrophages and neutrophils, together with natural killer (NK) cell dysfunction, sustains chronic inflammation and disrupts epithelial repair and fibroblast regulation, thereby promoting fibrosis and tumorigenesis. Although no curative treatments exist for pulmonary fibrosis, especially coal workers’ pneumoconiosis and silicosis, this review also discusses emerging therapeutic approaches, such as antifibrotic agents and immunotherapy, aimed at mitigating lung fibrosis and lung cancer.
Conclusion: This review summarises recent findings on the toxicological mechanisms underlying respirable occupational dust- and fibre-induced lung diseases, with a focus on crystalline silica, and coal dust and asbestos, especially those bearing reduced iron minerals. By highlighting both cellular toxicity and immunological effects, as well as potential therapeutic strategies, this work provides insights into current trends, challenges, and future research directions in the study of respirable occupational dust- and fibre-induced lung diseases.
Related
- Editorial: Molecular and cellular mechanisms of type 2 immunity-related disorders: allergic diseases and beyond
- Commercial Oat‐Based Cosmetic Ingredients Promote Antioxidant Capacity and Reduce Inflammatory Markers in Skin Cellular Stress Models: An Insight Into Molecular Mechanisms In Vitro
- Exploring the Phytochemical Composition of Bitter Melon Fruit and Molecular Responses to Its Extract in U87 MG Glioblastoma Cells
- Gamete Cryopreservation: Molecular Mechanisms of Cellular Injury and Epigenomic Alterations in Human and Animal Models
- Cellular Senescence in Ocular Surface Diseases: Molecular Mechanisms and Therapeutic Perspectives
BibTeX
@article{sun2026molecular,
title = {{Molecular mechanisms of dust-induced lung disease: exploring the role of physicochemical composition and cellular pathways}},
author = {Yingying Sun and T. David Waite},
journal = {Particle and Fibre Toxicology},
year = {2026},
month = aug,
doi = {10.1186/s12989-026-00696-3},
url = {https://doi.org/10.1186/s12989-026-00696-3},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Molecular mechanisms of dust-induced lung disease: exploring the role of physicochemical composition and cellular pathways
AU - Yingying Sun
AU - T. David Waite
PY - 2026
DA - 2026/08/07
JO - Particle and Fibre Toxicology
DO - 10.1186/s12989-026-00696-3
UR - https://doi.org/10.1186/s12989-026-00696-3
AB - Background: Respirable dust and fibres in occupational settings are major contributors to lung dysfunction, imposing a significant societal burden. Following the ban on asbestos in most countries, silica and coal mine dust have emerged as primary concerns due to their abundance and persistence in workplace dust. Exposure to dust containing these elements has been strongly linked to pulmonary fibrosis and lung cancer. Main body: Extensive research has explored the molecular mechanisms underlying respirable occupational dust-induced cytotoxicity and immune dysregulation. The toxic effects of respirable occupational dust and fibres are largely induced by oxidative stress, mitochondrial dysfunction, lysosomal damage, inflammasome activation and immune suppression. These exposures can trigger multiple cell death pathways, including ferroptosis, necrosis, and pyroptosis. While sharing common toxicological features, silica, coal dust, and asbestos exhibit distinct toxic effects on various pulmonary cell types involved in fibrosis and cancer progression. The immunological consequences of dust exposure are profound, as dust-induced activation of macrophages and neutrophils, together with natural killer (NK) cell dysfunction, sustains chronic inflammation and disrupts epithelial repair and fibroblast regulation, thereby promoting fibrosis and tumorigenesis. Although no curative treatments exist for pulmonary fibrosis, especially coal workers’ pneumoconiosis and silicosis, this review also discusses emerging therapeutic approaches, such as antifibrotic agents and immunotherapy, aimed at mitigating lung fibrosis and lung cancer. Conclusion: This review summarises recent findings on the toxicological mechanisms underlying respirable occupational dust- and fibre-induced lung diseases, with a focus on crystalline silica, and coal dust and asbestos, especially those bearing reduced iron minerals. By highlighting both cellular toxicity and immunological effects, as well as potential therapeutic strategies, this work provides insights into current trends, challenges, and future research directions in the study of respirable occupational dust- and fibre-induced lung diseases.
SN - 1743-8977
ER -