Occupational exposure to cement dust and potential pulmonary and systemic effects

Introduction Cement production is a major source of occupational exposure to airborne particles, yet detailed characterization of exposure and associated health effects remains limited. Methods Emissions and worker exposures were assessed during clinker mineral production, cement grinding, and bagging using filter‐based sampling and direct‐reading instruments. The pulmonary toxicity of collected PM2.5 (particulate matter with an aerodynamic diameter <2.5 µm) was evaluated using both an in vitro model and in vivo mouse models. Results Personal full‐shift measurements showed average exposures to inhalable and respirable dust of 2.2 mg/m 3 and 0.058 mg/m 3 , respectively. Time‐resolved measurements demonstrated exposure to particles <300 nm, with a mean particle number concentration of 13,800 cm −3 and a lung‐deposited surface area concentration of 40 µm 2 /cm 3 . Most particles, by number concentration, were 50–60 nm. Calcium was the dominant constituent, with contributions from iron, aluminum, and magnesium. To assess potential health effects, PM2.5 samples from clinker production and cement bagging were administered to mice by intratracheal instillation, and responses were evaluated at 1, 3, and 28 days post‐exposure. Both materials induced mild pulmonary responses, with no marked cytotoxicity or tissue injury. Clinker PM2.5 elicited slightly stronger effects than cement PM2.5, including modest increases in bronchoalveolar lavage cell counts and macrophages at the latest time point, and an early pulmonary acute phase response. Intravital lung microscopy revealed rapid neutrophil recruitment following clinker PM2.5 exposure, indicating an early innate immune response. Conclusion The findings demonstrate that cement production workers were exposed to low levels of respirable particles. The collected PM2.5 samples induced mild pulmonary responses in vivo, with slight differences between particles from the clinker production and cement bagging sites.

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Journal
Frontiers in Toxicology
Published
2026-11-09
DOI
https://doi.org/10.3389/ftox.2026.1963820
Primary Topic
Air Quality and Health Impacts
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article
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article

Occupational exposure to cement dust and potential pulmonary and systemic effects

Camilla Abrahamsson, Markus Rehberg, Ulla Birgitte Vogel, Jorid Birkelund Sørli et al.
Frontiers in Toxicology
Air Quality and Health Impacts
article

Occupational exposure to cement dust and potential pulmonary and systemic effects

Camilla Abrahamsson, Markus Rehberg, Ulla Birgitte Vogel, Jorid Birkelund Sørli, Monica H. Kåredal, Pernille Høgh Danielsen, Johanna Samulin Erdem, Christina Isaxon, Trine Berthing, Maria Hedmer, Mathilde Sundberg, Guo Yang, Peng Lei
article en

Abstract

Introduction Cement production is a major source of occupational exposure to airborne particles, yet detailed characterization of exposure and associated health effects remains limited. Methods Emissions and worker exposures were assessed during clinker mineral production, cement grinding, and bagging using filter‐based sampling and direct‐reading instruments. The pulmonary toxicity of collected PM2.5 (particulate matter with an aerodynamic diameter <2.5 µm) was evaluated using both an in vitro model and in vivo mouse models. Results Personal full‐shift measurements showed average exposures to inhalable and respirable dust of 2.2 mg/m 3 and 0.058 mg/m 3 , respectively. Time‐resolved measurements demonstrated exposure to particles <300 nm, with a mean particle number concentration of 13,800 cm −3 and a lung‐deposited surface area concentration of 40 µm 2 /cm 3 . Most particles, by number concentration, were 50–60 nm. Calcium was the dominant constituent, with contributions from iron, aluminum, and magnesium. To assess potential health effects, PM2.5 samples from clinker production and cement bagging were administered to mice by intratracheal instillation, and responses were evaluated at 1, 3, and 28 days post‐exposure. Both materials induced mild pulmonary responses, with no marked cytotoxicity or tissue injury. Clinker PM2.5 elicited slightly stronger effects than cement PM2.5, including modest increases in bronchoalveolar lavage cell counts and macrophages at the latest time point, and an early pulmonary acute phase response. Intravital lung microscopy revealed rapid neutrophil recruitment following clinker PM2.5 exposure, indicating an early innate immune response. Conclusion The findings demonstrate that cement production workers were exposed to low levels of respirable particles. The collected PM2.5 samples induced mild pulmonary responses in vivo, with slight differences between particles from the clinker production and cement bagging sites.

Frontiers in ToxicologyVol. 8
National Institute of Occupational Health (NO), Lund University (SE), Helmholtz Zentrum München (DE), National Institute of Occupational Health (IN), German Center for Lung Research (DE), National Research Centre for the Working Environment (DK), Skåne University Hospital (SE), NanoLund (SE), Technical University of Denmark (DK)
Air Quality and Health Impacts
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