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Size-partitioning of an urban aerosol to identify particle determinants involved in the proinflammatory response induced in airway epithelial cells.

Ramgolam K, Favez O, Cachier H, Gaudichet A, Marano F, Martinon L, Baeza-Squiban A - Part Fibre Toxicol (2009)

Bottom Line: However the respective involvement of coarse, fine and ultrafine particles in health effects is still unclear.In presence of a recombinant endotoxin neutralizing protein, the GM-CSF release induced by particles is reduced for all size-fractions, with exception of the ultra-fine fraction which response is not modified.The different aerosol size-fractions were found to display important chemical differences related to the various contributing primary and secondary sources and aerosol age.

View Article: PubMed Central - HTML - PubMed

Affiliation: Univ Paris Diderot, Paris 7, Laboratory of Molecular and Cellular Responses to Xénobiotics, Unit of Functional and Adaptive Biology affiliated to CNRS, 5 rue Thomas Mann, case courrier 7073, 75013 Paris, France. baeza@univ-paris-diderot.fr.

ABSTRACT

Background: The contribution of air particles in human cardio-respiratory diseases has been enlightened by several epidemiological studies. However the respective involvement of coarse, fine and ultrafine particles in health effects is still unclear. The aim of the present study is to determine which size fraction from a chemically characterized background aerosol has the most important short term biological effect and to decipher the determinants of such a behaviour.

Results: Ambient aerosols were collected at an urban background site in Paris using four 13-stage low pressure cascade impactors running in parallel (winter and summer 2005) in order to separate four size-classes (PM0.03-0.17 (defined here as ultrafine particles), PM0.17-1 (fine), PM1-2.5(intermediate) and PM2.5-10 (coarse)). Accordingly, their chemical composition and their pro-inflammatory potential on human airway epithelial cells were investigated. Considering isomass exposures (same particle concentrations for each size fractions) the pro-inflammatory response characterized by Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) release was found to decrease with aerosol size with no seasonal dependency. When cells were exposed to isovolume of particle suspensions in order to respect the particle proportions observed in ambient air, the GM-CSF release was maximal with the fine fraction. In presence of a recombinant endotoxin neutralizing protein, the GM-CSF release induced by particles is reduced for all size-fractions, with exception of the ultra-fine fraction which response is not modified. The different aerosol size-fractions were found to display important chemical differences related to the various contributing primary and secondary sources and aerosol age. The GM-CSF release was correlated to the organic component of the aerosols and especially its water soluble fraction. Finally, Cytochrome P450 1A1 activity that reflects PAH bioavailability varied as a function of the season: it was maximal for the fine fraction in winter and for the ultrafine fraction in summer.

Conclusion: In the frame of future regulations, a particular attention should thus be paid to the ultrafine/fine (here referred to as PM1) fraction due to their overwhelming anthropogenic origin and predominance in the urban aerosol and their pro-inflammatory potential.

No MeSH data available.


Related in: MedlinePlus

Sampling and experimental strategy overview. Particles were sampled with four 13 stage low pressure Dekati impactors running in parallel for 22 to 98 h according to samples (Step 1). For chemical analysis (Step A), gravimetry, ions and carbon content were determined on each stage filter. For biological analysis, filters were gathered to constitute 4 PM-size fractions (PM0.03–0.17, PM0.17–1, PM1–2.5, PM2.5–10). They were briefly sonicated directly in 600 μL culture medium (Step 2). HBECs were exposed for 24 hrs to the different PM-size fractions (Step 3) either at the same volume of particle suspension (isovolume exposure) or at the same concentration of particle suspension (isomass exposure). After exposure, GM-CSF release was measured in the culture medium and cell viability was assessed using a propidium iodide (PI) assay (Step 4). Specific short samplings (20 min) were performed to collect particles on specific supports for transmission electron microscopy (TEM) observations (step B).
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Figure 6: Sampling and experimental strategy overview. Particles were sampled with four 13 stage low pressure Dekati impactors running in parallel for 22 to 98 h according to samples (Step 1). For chemical analysis (Step A), gravimetry, ions and carbon content were determined on each stage filter. For biological analysis, filters were gathered to constitute 4 PM-size fractions (PM0.03–0.17, PM0.17–1, PM1–2.5, PM2.5–10). They were briefly sonicated directly in 600 μL culture medium (Step 2). HBECs were exposed for 24 hrs to the different PM-size fractions (Step 3) either at the same volume of particle suspension (isovolume exposure) or at the same concentration of particle suspension (isomass exposure). After exposure, GM-CSF release was measured in the culture medium and cell viability was assessed using a propidium iodide (PI) assay (Step 4). Specific short samplings (20 min) were performed to collect particles on specific supports for transmission electron microscopy (TEM) observations (step B).

Mentions: Fine particles are commonly defined as particles with aerodynamic equivalent diameters (AED) below 2.5 μm. For Paris aerosols, a pilot study indicated that the AED threshold between fine and coarse particles might actually be around 1 μm [18]. For this reason, four size classes were investigated: PM0.03–0.17 (ultrafine (UF), LPI stages 1–3), PM0.17–1 (fine (F), stages 4–7), PM1–2.5 (intermediate (I), stages 8–9), and PM2.5–10 (coarse (C), stages 10–12) as presented in Figure 6 (step 1).


Size-partitioning of an urban aerosol to identify particle determinants involved in the proinflammatory response induced in airway epithelial cells.

Ramgolam K, Favez O, Cachier H, Gaudichet A, Marano F, Martinon L, Baeza-Squiban A - Part Fibre Toxicol (2009)

Sampling and experimental strategy overview. Particles were sampled with four 13 stage low pressure Dekati impactors running in parallel for 22 to 98 h according to samples (Step 1). For chemical analysis (Step A), gravimetry, ions and carbon content were determined on each stage filter. For biological analysis, filters were gathered to constitute 4 PM-size fractions (PM0.03–0.17, PM0.17–1, PM1–2.5, PM2.5–10). They were briefly sonicated directly in 600 μL culture medium (Step 2). HBECs were exposed for 24 hrs to the different PM-size fractions (Step 3) either at the same volume of particle suspension (isovolume exposure) or at the same concentration of particle suspension (isomass exposure). After exposure, GM-CSF release was measured in the culture medium and cell viability was assessed using a propidium iodide (PI) assay (Step 4). Specific short samplings (20 min) were performed to collect particles on specific supports for transmission electron microscopy (TEM) observations (step B).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2667424&req=5

Figure 6: Sampling and experimental strategy overview. Particles were sampled with four 13 stage low pressure Dekati impactors running in parallel for 22 to 98 h according to samples (Step 1). For chemical analysis (Step A), gravimetry, ions and carbon content were determined on each stage filter. For biological analysis, filters were gathered to constitute 4 PM-size fractions (PM0.03–0.17, PM0.17–1, PM1–2.5, PM2.5–10). They were briefly sonicated directly in 600 μL culture medium (Step 2). HBECs were exposed for 24 hrs to the different PM-size fractions (Step 3) either at the same volume of particle suspension (isovolume exposure) or at the same concentration of particle suspension (isomass exposure). After exposure, GM-CSF release was measured in the culture medium and cell viability was assessed using a propidium iodide (PI) assay (Step 4). Specific short samplings (20 min) were performed to collect particles on specific supports for transmission electron microscopy (TEM) observations (step B).
Mentions: Fine particles are commonly defined as particles with aerodynamic equivalent diameters (AED) below 2.5 μm. For Paris aerosols, a pilot study indicated that the AED threshold between fine and coarse particles might actually be around 1 μm [18]. For this reason, four size classes were investigated: PM0.03–0.17 (ultrafine (UF), LPI stages 1–3), PM0.17–1 (fine (F), stages 4–7), PM1–2.5 (intermediate (I), stages 8–9), and PM2.5–10 (coarse (C), stages 10–12) as presented in Figure 6 (step 1).

Bottom Line: However the respective involvement of coarse, fine and ultrafine particles in health effects is still unclear.In presence of a recombinant endotoxin neutralizing protein, the GM-CSF release induced by particles is reduced for all size-fractions, with exception of the ultra-fine fraction which response is not modified.The different aerosol size-fractions were found to display important chemical differences related to the various contributing primary and secondary sources and aerosol age.

View Article: PubMed Central - HTML - PubMed

Affiliation: Univ Paris Diderot, Paris 7, Laboratory of Molecular and Cellular Responses to Xénobiotics, Unit of Functional and Adaptive Biology affiliated to CNRS, 5 rue Thomas Mann, case courrier 7073, 75013 Paris, France. baeza@univ-paris-diderot.fr.

ABSTRACT

Background: The contribution of air particles in human cardio-respiratory diseases has been enlightened by several epidemiological studies. However the respective involvement of coarse, fine and ultrafine particles in health effects is still unclear. The aim of the present study is to determine which size fraction from a chemically characterized background aerosol has the most important short term biological effect and to decipher the determinants of such a behaviour.

Results: Ambient aerosols were collected at an urban background site in Paris using four 13-stage low pressure cascade impactors running in parallel (winter and summer 2005) in order to separate four size-classes (PM0.03-0.17 (defined here as ultrafine particles), PM0.17-1 (fine), PM1-2.5(intermediate) and PM2.5-10 (coarse)). Accordingly, their chemical composition and their pro-inflammatory potential on human airway epithelial cells were investigated. Considering isomass exposures (same particle concentrations for each size fractions) the pro-inflammatory response characterized by Granulocyte Macrophage-Colony Stimulating Factor (GM-CSF) release was found to decrease with aerosol size with no seasonal dependency. When cells were exposed to isovolume of particle suspensions in order to respect the particle proportions observed in ambient air, the GM-CSF release was maximal with the fine fraction. In presence of a recombinant endotoxin neutralizing protein, the GM-CSF release induced by particles is reduced for all size-fractions, with exception of the ultra-fine fraction which response is not modified. The different aerosol size-fractions were found to display important chemical differences related to the various contributing primary and secondary sources and aerosol age. The GM-CSF release was correlated to the organic component of the aerosols and especially its water soluble fraction. Finally, Cytochrome P450 1A1 activity that reflects PAH bioavailability varied as a function of the season: it was maximal for the fine fraction in winter and for the ultrafine fraction in summer.

Conclusion: In the frame of future regulations, a particular attention should thus be paid to the ultrafine/fine (here referred to as PM1) fraction due to their overwhelming anthropogenic origin and predominance in the urban aerosol and their pro-inflammatory potential.

No MeSH data available.


Related in: MedlinePlus