PM-bound organic compounds from residential coal combustion: levels and toxicological effects

[EN] Residential coal combustion is a significant source of airborne particulate matter, which has been linked to adverse health effects. This study investigates the in vitro toxicity (MTT, fluorometric intracellular ROS, flow cytometry, and FITC Annexin V) and the composition of PM10-bound organics...

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Detalles Bibliográficos
Autores: Figueiredo, Daniela Filipa Rodrigues, Vicente, Estela Alexandra Domingos, Calvo Gordaliza, Ana Isabel, Evtyugina, Margarita, Fraile Laiz, Roberto, Oliveira, Helena Cristina Correia de, 1976-, Alves, Célia dos Anjos
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2026
País:España
Institución:Universidad de León
Repositorio:BULERIA. Repositorio Institucional de la Universidad de León
OAI Identifier:oai:buleria.unileon.es:10612/26352
Acceso en línea:https://www.sciencedirect.com/science/article/pii/S1352231025006168
https://hdl.handle.net/10612/26352
Access Level:acceso abierto
Palabra clave:Física
Química
Toxicología
Biological responses
Environmental exposure
Indoor air pollution
Organic tracers
Polycyclic aromatic hydrocarbons
2509.02 Contaminación Atmosférica
3214 Toxicología
2391 Química Ambiental
2503.07 Geoquímica Orgánica
Descripción
Sumario:[EN] Residential coal combustion is a significant source of airborne particulate matter, which has been linked to adverse health effects. This study investigates the in vitro toxicity (MTT, fluorometric intracellular ROS, flow cytometry, and FITC Annexin V) and the composition of PM10-bound organics (gas chromatography-mass spectrometry) of PM samples collected indoors and outdoors during coal combustion, as well as in the absence of the combustion source. Higher average PAH concentrations were detected indoors during coal burning, compared to outdoor and indoor concentrations without stove operation, with average levels over 8 and 10 times higher, respectively. PAHs with higher molecular weights constituted the largest amount of indoor PM10 samples, with indeno[1,2,3-cd]pyrene as the most abundant compound. Several compounds such as levoglucosan, phthalimide, oxidized Irgafos 168, phenyl compounds, dicarboxylic acids, and fatty acids exhibited lower concentrations or were absent in outdoor/background air but were prevalent during indoor coal burning. In vitro assays using A549 cells have shown that indoor samples collected during coal combustion induced cytotoxicity and oxidative stress. The cell cycle analysis revealed a significant increase in the Gap 1 (G1) phase and a decrease in the S (DNA synthesis) phase, pointing towards cell cycle arrest. The FITC Annexin V assay showed a marked increase in necrotic cell populations, suggesting persistent DNA damage or failure in DNA repair that hinders replication and transcription. Cell viability showed strong negative correlations with several PM-bound organic compounds, including dicarboxylic acids (p < 0.01), phenolic compounds such as vanillin, vanillic acid, and syringic acid (p < 0.01), and resin acids, particularly dehydroabietic acid (p < 0.01). Cell cycle arrest was significantly correlated with PAHs (p < 0.01) and phytane (p < 0.01). ROS levels were also correlated with PAHs, including phenanthrene and p-terphenyl (p < 0.01), as well as with glyceridic compounds and dicarboxylic acids (p < 0.01). These results underscore the critical need for targeted strategies to mitigate health risks associated with indoor coal combustion in European settings